REPTILES CLASSIFICATION, EVOLUTION AND SYSTEMS

VENOMOUS SNAKES - ENVENOMING,

THERAPY

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 REPTILES CLASSIFICATION, EVOLUTION AND SYSTEMS

VENOMOUS SNAKES - ENVENOMING,

THERAPY

JIRI VALENTA

Nova Science Publishers, Inc.

New York
2nd revised edition (1st edition in Czech: Galen Publishing, Prague 2008)
Photos: Ing Vladislav T. Jirousek - www.zoo-foto.cz, Petr Velensky, Dr Jiri Valenta
Figures: Karel Vavra
List of venomous snakes, zoological cooperation: Dr Ivan Rehak, CSc.

Copyright 2010 by Nova Science Publishers, Inc.

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Valenta, Jiri, 1960- Venomous snakes : envenoming, therapy / Jiri Valenta. -- 2nd rev. ed.
p. cm.
Includes bibliographical references and index.
ISBN 978-1-61209-217-1 (eBook)

Published by Nova Science Publishers, Inc.  New York

 CONTENTS

Preface vii
Introduction ix
List of Abbreviations xiii
Chapter 1 Zoological Basis 1
Chapter 2 Epidemiology of Snakebites 17
Chapter 3 Snake Venoms 27
Chapter 4 Snake Antivenoms 51
Chapter 5 Snakebite: Therapy and Prevention 59
Chapter 6 Envenoming and Snakebite Treatment in Specific Snake Groups 85
Chapter 7 List of Venomous Snakes 235
Glossary 289
Authors Affiliation 301
Index 303
Pictures 323
 PREFACE

This is a comprehensive monograph on the problems of intoxication incurred by snake

venom. This publication is primarily intended for those at all levels of health care, for
members of rescue teams, surgeries and emergency hospitals, as well as specialized
workplaces and intensive care units. Providing didactic instructions for first aid and treatment
procedures, information is also presented on venomous snakes, the fundaments of their
morphology and behavior, snakebite prevention, the composition of snake venom, symptoms
of envenoming, plus first aid in the event of snakebite for non-professionals, travelers, terrain
biologists, and breeders. This book features an updated alphabetical list of types and sub-
types of all venomous snakes, including their home ranges, as well as a comprehensive index,
list of abbreviations, glossary, and color picture insert with one hundred photographs of
venomous snakes.
 INTRODUCTION
Few creatures in the history of man have attracted more attention than snakes. One of the
first attempts to describe a snake in literature can be found in the Bible, where it is described
in the Old Testament as more shrewd than any of the wild animals that the Lord God had
made (Gn 3:1). The serpent is shown as a deceiver, luring Man to fall by eating from the
Tree of Life, for which Adam and Eve were banished from the Garden of Eden. For doing so,
the snake is castigated by God with punishments it bears still. The Lord God said to the
serpent, Because you have done this, cursed are you above all the wild beasts and all the
living creatures of the field! On your belly you will crawl and dust you will eat all the days of
your life. And I will put hostility between you and the woman and between your offspring and
her offspring; her offspring will attack your head, and you will attack her offsprings heel.
(Gn 3:14-15). As is evident from the Old Testament, the snake acts neither as Satan nor for
him at this point. Indeed, it does so on its own behalf, saying to Eve, Surely you will not die,
for God knows that when you eat from it your eyes will open and you will be like divine
beings who know good and evil. (Gn 3:4-5) In no case should this be viewed as temptation
or a satanic notion, but rather as a step towards another stage of evolution for mankind. In
fact, let this be the start of the biblical serpents reformation. After all, it was only an enticer,
for did not Woman perform what was forbidden?
The cult of the snake has played a part or is visible in many cultures, religions, and
traditions. Examples not only include cave paintings in Spain and France, but also others by
the Bushmen of South Africa and Australian aborigines, as well as in prehistory and more
recent times.
Mention should be made of the vital role played by the cobra in the history of Egypt. Its
intrinsic link to the cult of Imhotep - the builder and healer - was in the form of Ureus. This
sacred serpent became a potent symbol of the divinity and power of Egyptian pharaohs,
indeed it was the insignia of the kings - the headband shaped as an upright cobra with an
outstretched hood. Furthermore, snakes were important as ritual animals in antiquity: be it in
the Greek rooms of healing known as asclepieions, or Roman temples to Vesta, where snakes
were kept by the Vestal Virgins. The serpent symbolized fruitfulness and wisdom both for the
antique world and ancient Egypt.
Greek myths attribute the origin, or at least the occurrence of snakes in North Africa, to
the hideous and deadly creature of Medusa as a result of her death at the hand of Perseus,
poetically described by Ovid as: For the one achieved high heaven, and the other, (as he
bore the viperous monster-head) on sounding wings hovered a conqueror in the fluent air,
over sands, Libyan, where the Gorgon-head dropped clots of gore, that, quickening on the
x Jiri Valenta

ground, became unnumbered serpents; fitting cause to curse with vipers that infested land.
(Metamorphoses, Book IV, Ovidius Naso, Brooks More edition, Cornhill Publishing Co.,
1922)
Elsewhere, the role of god was assigned to the serpent in Aztec culture, thereby
transformed into the feathered serpent known as Quetzalcoatl. Moreover, snakes proliferate in
Asian religions. According to myth, it was a snake - probably the king cobra - that revealed
the meaning of life and faith to Buddha. Other examples include the Indian god Vishnu, who
rested upon the body of a multiheaded cobra in the sea of milk, whilst Shiva wears a cobra
wrapped around his neck. Some temples in Kangra Valley, North India, are dedicated to
ngas, deities in the form of great snakes, which are depicted with cobra fans on their heads.
Moreover, many places in India celebrate certain days of the year that are consecrated to
cobras. One fable tells that killing a snake, especially a cobra, will bring trouble that must be
redressed via a ritual, something which rural Indians still abide by today.
Therefore, the role of snakes in the history of mankind is evident, much like their
influence on the state of the human mind. The fear of snakes is incomparable to anything
posed by other animals. Beside arachnophobia - the fear of spiders, ophidiophobia, which
refers to the fear of snakes, is the widest form of pathological reaction to animals. In heavily
affected persons, it is not restricted to exclusion of a real threat; feelings can also be
associated with just seeing an animal or merely a depiction of one. Sometimes fear is
amplified by a physical experience, as in a vegetative response. Whether such extreme
reactions are determined by evolution (phylogeny) or are genetic in nature remains unclear. It
might even be stated that snakes create feelings of fear in zoo-based primates, including apes.
Nevertheless, the epidemiology of snakebites in children reveals a certain lack of fear and
respect for venomous snakes, which is probably due to unfamiliarity or assurance. Whatever
the case, attempts at physical exposure to snakes, as observed in certain children, did not
reveal any connection with atavism or a satisfactory educational influence. However,
indigenous peoples, such as in Africa, commonly associate fear with snakes and usually
consider any such creature as highly venomous. Responses like these are easily substantiated;
in addition to a lack of education and information, it is natural that any tribesperson
attempting to be heroic by belittling the danger of venomous snakes would not survive long in
the wild.
Why is that snakes are so mythologized? Answering this question is not simple. There
may be several factors involved: their venomousness, the imminent mortal danger, and
potential loss of life or impact on health even following a minor bite; these are sure to be
amongst the most important to humans. In fact, it is these which distinguish snakes from other
much larger animals that pose a threat to Man, creatures whose attack would result in visible
physical devastation to tissue, unlike the godlike bite of a venomous snake, and explaining
this is far from easy. Consequently, a number of other points must have contributed to placing
snakes in this most lofty of positions. Returning to one of the factors listed earlier, venom
causes prey to be killed by a single rapid bite, added to which snakes are able to devour catch
many times bigger than their mouths, plus they move without legs, even in trees and
underground. However, such explanations are insufficient when investigating the
extraordinary interest snakes possess for humans, which can but underline their truly mythical
nature.
A host of folk tales are associated with snakes. For example, the Czech version of
Goldilocks, by K J Erben, boasts a hero with the magic ability to understand animal speech
 Introduction xi

after eating some snake meat. In the 19th and early 20th centuries, notions abounded in rural
communities of snakes biting their tails and rolling down hills, and of a snake wedding
complete with the crowning of a queen. The superstition of snakes sipping milk from cows is
also widespread, although it is plain that snakes do not actually drink milk and visit cowsheds
only to get warm and catch rodents. Another falsehood is that snakes are slimy and clammy,
but this is true of eels and yet they are not generally despised by people. Moreover, the myth
of snakes hypnotizing prey is just that - only a myth. If a snakes prey were to be paralyzed
via hypnosis, the snakes ability to see their potential catch would weaken. Nevertheless,
rumors and misconceptions like these continue to shape how snakes are perceived.
Despite the reverence held for snakes by some ethnic groups, the eating of their meat
does occur amongst the indigenous peoples of a number of African, Asian, and South
American countries, as well as being served as a delicacy in local restaurants. This trade in
meat - catching, selling, and consuming it - relates mostly to larger non-venomous snakes like
pythons and boas, but even venomous snakes such as cobras are not immune to such
treatment. Snake meat itself is said to be delicious and reminiscent of fine game or chicken.
The entrails of creatures are used in soup, including a Chinese immunity-boosting variety
made of snake gall bladders. Other uses of venomous snakes in gastronomy include special
alcoholic beverages called snake liquor and health potions, which are produced by pickling
venomous snakes in spirit, an example being Japanese mamushi sak.
Alongside all manner of myths, cults and superstitions, a real interest in venoms has
developed, be it causes, duration and possible therapy. Notes on the effects and treatment of
snakebites, in addition to the use of venom as medicine, appear in Egyptian papyruses, as well
as in works by Aristotle, Nicandros of Colophon, Plinius, Hippocrates, Celsus, Pedanius
Dioscorides, Galenus, and Avicenna. In the Renaissance period, snakebites were investigated
by the French scientists Ambroise Par and Jacques Grvin. The first ever work of
methodology conducted on venomous snakes was produced by a Florence physician,
Francesco Redi (1621-1697), which outlined the venom apparatus of snakes. This served as
the foundation for a later study on animal toxinology by Italian Felice Fontana (1720-1805).
At the cusp of the 20th century and in the years that followed, interest in such work rose
dramatically, accompanied by an increasing number of studies dedicated to toxins, toxinology
and the therapy of envenoming-related cases. However, not every scientific paper was wholly
based on reality. The threats associated with the venomous nature of snakes, which in Central
Europe relates to the rather less venomous common viper, used to be largely overestimated in
the otherwise reliable literature of the day, and still is to a point at the present. A venerable
Czech journal, Vesmir, published the following in 1895: To prevent the terrible
consequences of snakebite, the aid given below shall be used. First, venom should be
eliminated from the wound, which is done by cutting off the place so affected and dripping
ammonia, chromic acid, fuming nitric acid, or tincture of iodine into the wound; alternatively
the wound may be burnt using a hot iron Using such a therapeutic procedure, no one
would wonder at such terrible consequences.
To some extent, the special position reserved for snakes in the human psyche may also
have a bearing on the attraction of capturing and keeping snakes. It cannot be ignored that the
act of owning snakes possesses vague phallic connotations, or at least lends their owners
some kudos based on their reptiles alleged or very real risk. Some might even acquire a
snake based on the single fact it is highly perilous or mortally so.
xii Jiri Valenta

However, reflecting on the various qualities of breeders and owners should not serve as a
distraction. In general, such people are well-informed enthusiasts and lovers of nature in all
its bounty, which certainly includes snakes. They expand our horizons by building upon
present knowledge on snake behavior and reproduction, requirements and habits, as well as
via regrettable cases of bites caused by misfortune or careless handling.
Within the period of six months, I was bitten by a number of reptiles including the black
mamba, the African boomslang, the cobra, and the rattlesnake. I found myself at ICU four
times. Several times, venom was sprayed into my eyes. Nevertheless, I always pulled through
without any lasting effects (Marais, 1995). J. Marais is surely one of the foremost snake
experts and keepers, although such incomprehension of the danger posed by a snakebite is by
no means recommended. In stark contrast, the following comment by Czech herpetologist
Zdenek Vogel is full of wisdom, Keepers of this kind of reptile should never get used to
their snakes more than the snakes can get used to them. Any bravura or snake charming are
unacceptable in the husbandry of snakes... All sorts of such intimacies with cobras,
rattlesnakes and other dangerous reptiles will eventually lead to the cemetery. Which is in
my particular case, speaking from personal experience, ...or at least intensive care.
 LIST OF ABBREVIATIONS
AAPCC American Association of Poison Control Center
ACE angiotensin-converting enzyme
ACh acetylcholine
AChE acetylcholinesterase
ADPase adenosine diphosphatase
AF Afrikaans
ALI/ARDS acute lung injury / acute respiratory distress syndrome
ALT alanine aminotransferase
APC activated protein C
APTT activated partial thrombin time
ASA acetyl salicylic acid, e.g. Acylpyrin
AST aspartate aminotransferase
AT antithrombin III
AV-block atrioventricular block. Failure of conduction from atria to ventricles.
app. approximately
BP blood pressure
CC creatine cinase
CLD certain lethal dose, see also LD100
CNS central nervous system
CPAP continuous positive airway pressure
CRP C-reactive protein
CRRT continual renal replacement therapy: hemofiltration, hemodialysis
CVF cobra venom factor
D-dim D-dimer, fibrin degradation product
Da Dalton, atomic mass unit
DIC disseminated intravascular coagulation
DRC Democratic Republic Congo
DTX dendrotoxins
ECG electrocardiograph
EEG electroencephalograph
EN English
ES Spanish
EVLW extravascular lung water
Fab Fab (fragment antigen binding) fragments
xiv Jiri Valenta

FBG fibrinogen
FDP fibrin degradation products
FF (FV, FVII,) coagulation factors
FPA fibrinopeptide A
FPB fibrinopeptide B
FR French
FTL fatal time limit
GIT GI tract, gastrointestinal tract
GMT glutamyl transpeptidase
Hb hemoglobin
Hct hematocrit; the ratio of blood volume that is red blood cells
HE Hebrew
HF hemorrhagic factors
ICU intensive care unit
IM intra musculum, within a muscle
INR international normalized ratio, a method for reporting PT results
IP intra peritoneam, within the peritoneal cavity
IV intra venam, within a vein
in part. partially
in vivo experimentation using a whole, living organism
JA Japanese
kat katal, SI unit of catalytic activity
kDa kilodalton, atomic mass unit
LD lactate dehydrogenase
LD0 median or average dose at which no mortality occurs, see also MLD
LD50 lethal dose 50%
LD100 lethal dose 100%, see also CLD
LMT last mortality time
LMWH low molecular weight heparin
MB fraction muscle brain fraction of CC
MLD minimal lethal dose: a maximum quantity that will kill no animal
MODS multiple organ dysfunction syndrome
nACh Nicotinic acetylcholine receptors
ng nanogram, SI unit of mass
p.o. per os, orally
PAF platelet-activating factor
PAI plasminogen activator inhibitor
PAWP pulmonary artery wedge pressure
PF1.2 prothrombin fragment 1.2
PGI2 prostaglandin I2
PI pressure immobilization bandage
PKS plasmatic coagulation system
PLA2 phospholipase A2
PLT platelets
PT Portuguese
PT prothrombin time
 List of Abbreviations xv

RSA The Republic of South Africa

RT reptilase time
RU Russian
SC sub cutam, subcutaneous
sp. singular abbreviation for species, used when the actual specific
name cannot or need not be specified
ssp. subspecies
syn. synonym
TAT thrombin-antithrombin complex
TEG thromboelastography; a method of testing the efficiency of blood
coagulation
TESS Toxic Exposure Surveillance System
TNF tumor necrosis factor
tPA tissue plasminogen activator
TT thrombin time
U urea
UFH unfractionated heparin
VFN 1. LF UKVseobecna fakultni nemocnice 1. lekarske fakulty Univerzity
Karlovy v Praze (General Teaching Hospital of the First Medical
Faculty, Charles University, Prague)
vs. versus
vWF von Willebrand factor
WHO World Health Organization
Chapter 1

ZOOLOGICAL BASIS
1.1. EVOLUTION AND PHYLOGENY OF SNAKES
Where snakes actually originate from still is unclear. Unquestionably, they belong to the
squamates order of scaled reptiles; their relationship to lizards is also beyond dispute. The rise
of snakes specific physical configuration is usually linked to hypothetical predecessors that
led a subterranean life or inhabited cracks. However, alternative hypotheses concerning the
aquatic ancestors of snakes also exist, winning increasing support from experts. Snakes are
presumed to have evolved from anguimorphous, most probably varanid-like lizards within the
process of diversification of ancestral scaled reptiles, in the Late Jurassic period about 150
million years ago. The oldest known fossil relics believed to be most likely related to snakes
are highly fragmentary and come from the Early Cretaceous, which are over 120 million
years old. The merging of the Lower and Middle Cretaceous produced Pachyrhachis
problematicus in Israel, a very intriguing marine squamate reptile. Ranked as a member of the
mosasaur family by some experts, this reptile is assumed to be an early snake with the
remnants of rear legs. Thus, Pachyrhachis may support the idea of snakes originating from
marine varanid-like lizards.
Described from the Algerian Middle Cretaceous from strata nearly 100 million years old,
Lapparentophis defrennei can be indisputably considered a snake - most probably one of
terrestrial form. In addition, other species appeared, for instance Simoliophis, supposedly a
water snake. Any exact phylogenetic ranking of these prehistoric examples referred to as
Cholophidia remains unclear for the moment. Shortly afterwards, the first family appeared:
false coral snakes, Aniliidae; this monotypic group of a single species has survived until
today. From the Upper Cretaceous, when apparently an important adaptive radiation of
primeval snakes occurred, fossil documentation shows that snakes increased in diversity,
although interpretation of their phyletic relationships greatly varies. A higher number of
lineages may have originated, from which many more recently became extinct without any
evolutionary successors. Genera that appeared at that time include Madtsoia and Gigantophis,
members of a highly successful and widespread snake group that in some places (Wonambi
genus in Australia) survived until the Pleistocene. These reptiles resemble later large boid
snakes in the size and shape of their body. Sometimes considered an important phylogenetic
node, Dinilysia, a reptile similar to a boa, is another Late Cretaceous form to emerge from
Patagonia.
2 Jiri Valenta

It was at the beginning of the Tertiary period when monumental forms resembling
pythons or boas proliferated, while in the later Eocene the family of boas (Boidae) appeared,
including genera that were either very close to recent members or still survive today (such as
Charina). Evidence has been produced as regards members of the recent Tropidophiidae
family as well. The earliest documented blind snakes (Scolecophidi) also come from the
Eocene. In addition, the most archaic forms of so-called modern snakes Caenophidia
appeared for the first time, from an ancestral relationship of extant wart snakes
(Acrochordoidea) and ancient Colubroidea snakes, and maybe even the first colubrid snakes,
Colubridae.
However, climatic changes at the meeting of the Eocene and Oligocene periods, along
with less favorable conditions in the course of the Oligocene, brought about a vast reduction
in prehistoric Eocene snake fauna, resulting in fundamental changes in its taxonomical
structure. While some of the archaic lineages died out and Booidea and related forms shrank
to some extent, Caenophidia took the lead and later developed at an enormous rate in the
Miocene, which lasted until modern times. It is clear the evolution of snakes as such did not
proceed independently, but in accord with the general transformation of the natural world at a
time of climatic change, and in close correlation with alterations in other fauna as well,
reflecting the changing pressure of rivalry in predators and their adversaries, and responding
to diverse availability of diet. Even in the Oligocene, over 30 million years ago, colubrid
snakes (Colubridae) were expanding throughout Asia, Europe, and North America. The
oldest elapid snakes (Elapidae) in fossil records appeared in the Lower Miocene in Europe
over 20 million years ago (Palaeonaja); more recent Miocene findings also show them
inhabiting a number of places around North America, Europe, and Asia. Moreover, it is the
Miocene period when vipers (Viperidae) first appear in fossil records over 20 million years
old, these being snakes that soon proliferated as well. For instance, Vipera antiqua, a smaller
close relative of the recent V. ammodytes, ranged throughout Europe as long ago as the lower
Miocene together with V. platyspondyla, a snake closely related to the recent V. xanthina.
Throughout the Miocene adaptive radiation of modern snakes, numerous extant colubrid,
elapid and viperid genera or species evolved. In Europe, not only were there colubrid and
viperid species as more recently, but even elapids and boids could be found.
Pliocene snake fauna already featured high diversity and taxonomic similarity to that of
recent times, developments which were further affected by Pleistocene glaciations as well as
marine transgressions and shrinkage. All of the above was accompanied by changes in snake
fauna populations in different parts of the world, resulting in the map of zoogeographical
distribution of snakes and their taxonomical structure as it is known today. Currently, snakes
are present on every continent except Antarctica, including a number of islands.
Approximately 3,000 species have been described to date, mostly colubroids (Colubroidea),
in addition to the most abundant family in terms of species, Colubridae, which covers elapids
(Elapidae), viperids (Viperidae), and the less-numerous Atractaspididae family including
burrowing asps and other snakes.
The exact time when snakes became venomous is not known. However, indications of
venomousness existed as long ago as the Cretaceous Period in the Pachyrhachis genus that
can be considered a sister taxon linked to all extant snakes. This is noteworthy as it suggests
in some snake lineages venomousness could have present in their earliest evolutionary
phases. After all, laboratory experiments with saliva from recent non-venomous snakes with
archaic origins indicate a certain level of toxicity. Nevertheless, venomousness, as is
 Zoological Basis 3

understand from a practical aspect, only exists in colubroids (Colubroidea) within the variety
of contemporary snakes. The presence of venom secretion from modified salivary glands in
the upper jaw may even have been a common trait from the very start, being apparently one
of the reasons for the extraordinary evolutionary success of these snakes. The non-existence
of venom secretion in some colubrids might obviously be only a secondary feature. In
colubroid snakes, the process of evolution was accompanied by extensive modifications to the
venomous gland, as well as the growth and development of specialized venom-delivering
apparatus. The wonderful adaptive radiation of these snakes brought about venom-specialist
families, namely in two basic parallel lineages: the solenoglyphous (viperids, Viperidae) and
proteroglyphous (elapid snakes, Elapidae). Since the Miocene period, these two families have
presented two successful alternative approaches in maximizing the potential of snake venom.

1.2. TAXONOMY OF SNAKES

Snake taxonomy is far from being completed and stable. Views of the mutual
relationships of taxonomy groups as well as particular genera are still being developed and
altered. Even today, further species are still being discovered, a number of which await
detailed scientific description, and some former species have been newly classified amongst
subspecies as a result of greater insight on their morphology. Increased knowledge and these
new findings on the classification of such snakes have also brought about changes to the
scientific names of genera and species.
Moreover, splits in high-level taxonomy groups like families and subfamilies are not
always apparent and delineating them is an unfinished chapter. For example, true sea snakes
are either placed within the elapid family (Elapidae) or under the separate Hydrophiidae
family, the sea krait subfamily (Laticaudinae) is also placed under a separate family; the
crotalids (Crotalidae) are still maintained as forming a separate group by some authors, whilst
elapid subfamilies are sometimes not listed at all due to their ambiguity. Similar problems
exist in the vast colubrid family (Colubridae), which will most probably be segregated and
rearranged at some point. Creating permanent and clear classification within such diversity as
has evolved on the Earth through the ages is definitely not an easy task, and may prove nigh
on impossible.
Furthermore, according to new findings from animal genome research, the Darwinist
understanding of a relationship based on morphology resemblance probably does not reflect
reality in terms of development and genetics. It cannot be predicted that future generations
will see an entirely altered taxonomy based on new rules respecting evolution and
relationships in a superior way.
The brief overview of venomous snake classification given below shows the recent
position of snakes in the animal system in addition to their general mutual relationships. It
should be born in mind that contemporary taxonomy knowledge indicates a monophyletic
status of many of the taxa listed, namely Colubrinae, Lamprophiinae, Natricinae, and
Elapinae. They greatly resemble polyphyletic or paraphyletic taxa instead, meaning their
nature is collective and merely temporary. Therefore, they will have to be re-classified,
although existing knowledge on the relevant phyletic relationships still does not allow for
taking such a step with the necessary responsibility.
4 Jiri Valenta

From a practical point of view, certain problems have arisen caused by dramatic recent
development in the field of snake taxonomy. This is reflected in a large number of changes in
nomenclature published in parallel (e.g. segregating genera, shifting taxa between subspecies
and species levels, creating synonyms for previously described taxa and relocating species
under different genera), as traced by a small number of specialists. Naturally, publications in
toxicology define subjects under study following recent systematics, and on many occasions
they are err on the conservative side by employing names long established. The persistence of
the nomenclature is relatively high in relevant statistics, as well as amongst manufacturers of
antivenoms and, more generally, in the awareness of the public, including snake owners. Any
vehement acceptance of alterations in taxonomy would actually be counterproductive.
Therefore, a certain conservative approach has been maintained in the snake nomenclature
used herein; notes on the possible occurrence of older or more recent synonyms are given
where important.

Position of Snakes within the Zoological System and Overview of Families

Containing Species of Venomous Species

Class: Reptilia - Reptiles

Subclass: Lepidosauria

Order: Squamata - Scaled reptiles

Suborder: Ophidia, Serpentes - Snakes

There are 14 families under the title of non-venomous snakes, and 4 families of a
venomous type are listed below under the Colubroidea superfamily:

Superfamily: Colubroidea - Colubroid snakes

Family: Colubridae - Colubrid snakes

Venomous species are found in five colubrid subfamilies out of total of seven:
Colubrinae (about 650 species), Homalopsinae (35+ species), Lamprophiinae (205+
species), Natricinae (195+ species), and Xenodontinae (540+ species).

Family: Atractaspididae - Burrowing asps

Subfamily: Atractaspidinae - Burrowing asps (17 species)
Subfamily: Aparallactinae (40+ species)

Family: Elapidae - Elapids

Subfamily: Elapinae (130+ species)
Subfamily: Hydrophiinae (165+ species)

Family: Viperidae - Viperids

Subfamily: Azemiopinae (1 species)
 Zoological Basis 5

Subfamily: Viperinae (65+ species)

Subfamily: Crotalinae (about 155 species)

+ stands for or more (e.g. if any subspecies are considered species by other authors)

1.3. MORPHOLOGY OF SNAKES

Anatomically, the skeletons of snakes (Ophidia or Serpentes) lack limbs, with vestiges of
such retained in more primitive groups like boids. The kinetic and extendable skull of the
snake features a large number of articulations, the facial part joined flexibly with the lower
section of the braincase and loose ligaments on the left and right of the lower jaw. The skull
configuration allows for ingestion of large prey by dilating the jaws and pushing via alternate
movements of their right and left sides. The backbone may consist of over 300 vertebrae with
ribs that articulate with the same.
Snakes are variable in length, ranging from 15 cm up to 10 m. The largest snake ever
found was an Asian reticulated python (Python reticulatus) caught in 1912, with a length of
32 feet and 9.5 inches (999.49 cm.) Nevertheless, the South American forests are believed to
host much longer specimens of large anacondas, which are non-venomous snakes. Among
venomous examples, the king cobra (Ophiophagus hannah) reigns when it comes to length,
with a documented size of 560 cm, followed by the black mamba (Dendroaspis polylepis) at
430 cm, and the coastal taipan (Oxyuranus scutellatus) at 380 cm. The heaviest venomous
snake is the large eastern diamond-backed rattlesnake (Crotalus adamanteus) that weighs 10
kg and inhabits North America.
The western blackhead snake (Tantilla planiceps), a member of the colubrid family
(Colubridae), which has rear fangs and is found in the southwest of America, seems to be the
least venomous snake. It can grow up to 15 cm in length and feeds on worms, centipedes and
insects.
A well-muscled body, flexible skeleton and moving ribs enable snakes to move forward
using variations of motion of lateral undulation, rectilinear movement, and that resembling a
concertina, as well as side-winding on loose ground. The actual speed of movement snakes
can achieve is often overstated. The fastest snake, which is the mamba, can move at around
12 to 15 kph, i.e. equivalent to a slight jog. It is true that some places exist in the African bush
so dense with shrubs that people cannot reach such a speed. However, the notion of a mamba
chasing a man is completely absurd. The brisk attack of this snake, much like that of the
cobra, would be performed over a shorter distance, 1 to 3 m at the most, with mans
inattention the reason for being bitten rather than impeded motion. A snake capable of such
speed is most likely to escape before being seen. Nevertheless, the motion of large vipers,
especially those with a robust body like the Bitis genus, is slow and hesitant. Therefore, a
person could stumble across one at close range, meaning a higher probability of attack due to
the snake sensing an imminent threat.
Again, the speed of a snake attacking its prey or defending itself is often exaggerated.
The measured speed of charge of the European viper after forming an S-coil in the frontal
part of its body lasts about 0.1 s, which equals the speed of attack of 2 mps at a maximum
6 Jiri Valenta

distance of 20 cm. However, during such a period the viper has to open its mouth, erect its
fangs, bite, and discharge its venom all at the same time. In fact, there is often a double strike.
The process described above may not be fully maintained when acting in defense, in which an
assault is only hinted at by the snake but not fully performed, including the bite and discharge
of venom; this chiefly applies to the Viperid family (Viperidae).
Snakeskin is entirely covered in scales of different shapes and is dry to the touch, with a
texture resembling slightly rough upholstery. Some snakes, saw-scaled vipers listed under the
Echis genus for example, can rub their sharp lateral scales against each other, employing such
behavior to warn a disturbing presence by creating sound. The same goes for the bony rattle
at the tips of tails of rattlesnakes belonging to the Crotalus and Sistrurus genera. The rattle
consists of free moving ossified segments, which are added to continuously each time the
snake sheds its skin. The shape, size, and number of scales are often used to identify a genus
or species. The outer horny layer of snakeskin called slough or exuvia is removed and
replaced by a new one on a periodical basis.
The eyelids of snakes are transparent and fused, hence they have a fixed stare. The pupil
is either in the shape of a ring or an upright slot, and only in extraordinary cases is it slotted
horizontally. The ring and larger pupils are usually seen in snakes with diurnal activity, while
slotted and small ring pupils tend to be features of nocturnal snakes. In some tree colubrids, a
horizontally slotted pupil serves to enhance panoramic binocular sight, essential when it
comes to properly focusing on prey. In fact, snakes perceive stationary items very badly,
which is the reason for the swinging motion that can sometimes be observed: they are
attempting to move their eyes towards their prey. This is also why an animal being hunted
stiffens instinctively.
The tongues of snakes are forked, allowing for chemosensory sensual recognition by the
creatures. The tongue can transmit chemical olfactory perceptions via a microscopic quantity
of matter, or even merely molecules, into the highly developed vomeronasal or Jacobsons
organ, these being palate cavities equipped with sensory epithelium. Furthermore, the
olfactory organ is used to perceive smells.
The snakes of the Crotalinae subfamily possess a special auxiliary organ that cannot be
found in any other animal: thermal receptors formed by a pair of small cup-shaped cavities
placed in the upper jaw and covered with a thermo-sensitive membrane. This organ provides
exact stereotactic information for detecting a source of heat at temperatures of only 0.2 - 0.5
o
C above that of the ambient atmosphere, facilitating a snake to detect prey in even complete
darkness. A blinded rattlesnake will strike its prey in 98% of cases, whilst only 27% of strikes
are successful after the thermal receptors have been covered. A similar sensory organ is found
in non-venomous boid snakes as well. In addition, it seems it is even possessed by some
venomous colubrids like Dromophis, Malpolon, Psammophis, and Rhamphiophis; however,
the pits are placed on the vertex in such snakes.
The auditory organ has changed in order to capture vibrations from the ground instead of
analyzing sound waves. These vibrations are sensed by scales on the belly, intercostal space
structures and lower jaw, the latter which vibrates the quadrate bone, with all such impulses
being transmitted to stapes and nerve endings. Consequently, snakes are deaf in the human
sense, and any attempts at driving away venomous snakes by noisy behavior while on a
family trip out is senseless but commonplace. Research made on this organ has revealed that
coughing or gunshots do not disturb snakes, although a cat walking or even a piece of paper
falling onto a writing pad is registered immediately.
 Zoological Basis 7

One general misconception is that snakes bathe in blinding summer sunshine. Despite the
fact that sunbathing is a normal form of thermoregulatory behavior among many snakes,
namely those from colder regions, snakes are mostly unable to tolerate harsh sunlight and
high temperatures. For the majority, ideal temperatures lie between 25oC and 30oC, and they
cannot cope with anything exceeding 40oC. Any exposure to hot sun is acceptable only for a
few minutes. Indeed, if left for several dozen minutes in the sun, a snake will die even at
lower temperatures. In hot climates, in the rocks, desert, and savannah, snakes hide during the
day and come out to hunt at night. The same goes for South and Central European vipers in
extremely hot summer months, hence spending a night out under the stars and unprotected by
a tent in such a season can pose a threat in certain localities. If temperatures permanently fall
below 20oC, snakes become torpid and slow down their motions. As a result, it is common
practice to artificially cool large or dangerous snakes in order to handle them better, e.g. by
using a refrigerator.

1.4. THE VENOM APPARATUS IN SNAKES

Depending on venom production and use, venomous animals can be referred to as
cryptotoxic, i.e. not possessing any specific venom producing apparatus, and phanerotoxic,
those with the presence of a specific organ, i.e. a venomous gland.
The cryptotoxic group features beetles, such as soldier beetles termed cantharids,
molluscs, e.g. natural oysters in the summer, certain fish species in their reproductive period
or if their diet includes venomous plankton, and other creatures.
In the animals deemed phanerotoxic a venom-delivering apparatus may be absent or
present. This trait is used to classify them as passive toxic animals possessing no delivery
mechanism, or active toxic animals with a venom-delivering apparatus.
Those that are passive toxic feature an open duct of venom glands on the surface of the
skin, examples being frogs and toads, newts and salamanders.
Venomous snakes are active phanerotoxic animals. They have a specialized venom-
producing organ, a venomous gland and, with some rare exceptions, a delivery mechanism in
form of venomous fangs.
In snakes, venom is produced in a venom gland - glandula venenosa - that has developed
from the salivary gland (glandula maxillaris) in the upper jaw; it is placed behind the salivary
gland but deeper under the surface. It forms part of the digestive tract of snakes. The role of
venom is not only to kill or immobilize prey, but also to facilitate digestion. In the majority of
snakes, the size of the venomous gland largely exceeds that of the saliva gland. Indeed, it can
extend from the eye up to the end of a snakes skull and, in some viperid snakes, it can even
stretch up to the neck. In the front section of the venomous gland, there is a slime gland
containing secretion probably designed to prevent spontaneous discharge of venom in
combination with a flap in its channel. The system opens through a duct placed in a mucous
fold near the fang channel on the base of a fang.
Fangs have developed from non-grooved teeth of the upper jaw. Snakes can be
differentiated on the basis of teeth morphology, stage of development, and location in the
upper jaw to Aglypha, which comes from the Greece glyph, i.e. the groove, featuring non-
differentiated teeth of the same length without longitudinal grooves or hollows, and
8 Jiri Valenta

Glyphodonta with certain teeth furnished with grooves or hollows connected with the venom
gland. (Figure 1.)
Aglyphous snakes cover so-called non-venomous varieties like pythons, boas and many
elapid snakes.
Nevertheless, as many as two thirds of Colubridae seem to have developed the venomous
gland, referred to as Duvernoys gland, or a rudimentary form of it along the sides of the
upper jaw. Even though these snakes have not evolved any injection mechanism, bites from
such a non-venomous snake may very occasionally cause a limited response due to the
small amount of the gland content that is spontaneously discharged to the snakes oral cavity.
Glyphodont snakes are venomous snakes with a venom-injecting mechanism. They can
be placed into one of three groups depending on the shape and location of their fangs.

Figure 1. Types of fangs (edited according to Kurka et al., 1984),a - Opisthoglyphous, b -

Proteroglyphous, c Solenoglyphous, I - Pulp cavity, II - Venom groove, III - Venom duct, IV - Orifice
of venom duct

Opistoglypha. These are snakes with rear fangs featuring a rather shallow groove in the
front of their fangs, these being larger than the rest of their teeth. They are placed at the end
of the upper jaw, mostly behind the eyes, although they can be even located closer in some
snakes, generally in the middle of the jaw. The snakes of this group are members of
venomous genera belonging to the Colubridae family. Although the venom mechanism is
rather primitive, Duvernoys gland opens above the venom teeth, thus ensuring the transfer of
venom to the body of prey. Their venom is quite effective. It is most necessary for tree
dwelling and bird hunting snake species to make sure they immediately kill or immobilize
 Zoological Basis 9

their prey. Any further pursuit would be impossible in this type of habitat. Nevertheless, there
are still some opisthoglyphous colubrid genera, such as Rhabdophis, that are neither bound to
trees nor can be termed ornithophagous snakes. Biting humans is, however, rare. Penetrating
the human skin with rear fangs would require the jaws to open at a very wide angle, and the
application of any significant amount of venom via a shallow channel is improbable from
such a brief and shallow bite. From this point of view, boigas are more dangerous snakes with
their fangs placed towards to the centre of the jaw.
Proteroglypha. These snakes feature relatively small fangs placed at the front of the
upper jaw along its sides in front of other maxillary teeth. The fangs have a deep groove at the
front, which in some snake genera are encased in the form of channel. As Proteroglyphous
snakes are unable to fully control venom application using special muscles, they mostly hold
onto their prey in their jaws following a bite, injecting venom by repeatedly manipulating the
jaws. A similar situation may occur if a human is bitten due to a defensive action. There have
even been reports of snake fangs remaining in a wound after the creature itself has been
removed following an attack. The Proteroglypha group covers elapid snakes (Elapidae),
examples including cobras, mambas, kraits, taipans, sea snakes and sea kraits.
Certain cobra species can defend themselves by spraying venom, which is called spitting;
by opening its mouth, a snake reveals short fangs with openings at the front and discharges
the venom through these slots under high pressure. In fact, the droplets produced might carry
as far as a distance of several meters. Thus, the term spitting is rather inadequate to express
this kind of action. In addition, it is uncertain as to the target of the snake - the face or, more
precisely, the eyes of the individual that caused disturbance. The conical shape of the droplets
of venom might hit the eyes, just as they would any other part of the body within range.
Solenoglypha. These snakes comprise advanced groups possessing large folded fangs
along the sides of the front part of the upper jaw. The fangs include a fully closed channel
which forms a cavity. Venom is injected very promptly and in a manner well controlled by
muscles of the venomous gland. Snakes like these mostly attack by means of a rapid strike
immediately after forming an S-coil from the front part of their bodies. Afterwards, the
mouth opens, and with fangs erect, venom is injected into the resultant wound. Then the
snake retreats swiftly, without further gripping the prey in its jaws. However, such an attack
may be repeated, and any prey that does not die on the spot or is immobilized and unmoving
is pursued. A defensive attack from these snakes may not always be complete, i.e. involving a
perfect bite and application of sufficient venom, although the manner in which it is conducted
is similar. Snakes can very probably distinguish between their hunting and defending
behavior: in over a half of bites made upon defense, either zero or a minimal quantity of
venom is discharged. The Solenoglypha include viperid snakes (Viperidae): night adders,
vipers, and rattlesnakes. (Figure 2)
Special fangs have evolved in the Atractaspididae family which are used to hunting in
narrow corridors and dens. To be able to hit their prey, they can turn and eject their front
fangs to one side and perform an attack by a swift side stab without opening their mouths. A
similar action proceeds when a snake is grasped some distance below its head and defends
itself, it can stab the hand grasping it by rapidly shaking its head to either side.
The fangs are covered by a mucous fold pulled over them. In the course of time, fangs are
renewed in most snakes, with new pairs growing behind the older and larger ones. Indeed, it
is no exception to find several fangs in a row, for instance in the Bitis genus of vipers, where
10 Jiri Valenta

up to six successive fangs can be found in Bitis gabonica, also visible in bite marks on
humans.

Figure 2. Types of venom apparatus and fangs in snakes a - Aglyphous, b - Opisthoglyphous, c -

Proteroglyphous, d Solenoglyphous.

Fang size may greatly vary; in smaller proteroglyphous snakes, they can grow to a mere 2
or 3 mm. In sea snakes and sea kraits, fangs are usually unable to penetrate neoprene diving
suits. However, the erectile fangs of larger vipers and rattlesnakes can reach several
 Zoological Basis 11

centimeters in length, the record holder being the Gabon viper (Bitis gabonica) which boasts
fangs 4-5 cm long.

1.5. DISTRIBUTION OF VENOMOUS SNAKES

Venomous snakes inhabit a major part of the Earths surface, be it dry land or sea.
Nevertheless, places without snakes do actually exist as well. In general, they involve cold
regions with an adverse climate, or islands that snakes could not reach by migrating through
evolution or via the intervention of humans.
In the southern hemisphere, snakes do not inhabit Antarctica, the entire territory of Chile,
which was blocked to them from the east due to the Andes Mountains causing a barrier; then
there are the Galpagos Islands, New Zealand and Madagascar. As regards Oceania, they live
in Polynesia, Micronesia, the New Hebrides, the Loyalty Islands and the Hawaiian Islands.
Nonetheless, sea snakes are found in the territory of the Pacific Ocean, but they do not extend
to the Atlantic Ocean. The most southerly venomous snake is one of the lanceheads
(Bothrops), with its territory extending as far as Tierra del Fuego.
In the northern hemisphere, the situation is more complicated from a geographical point
of view. The northerly limitation on territory in Europe and Asia, which affects the common
viper (Vipera berus), is defined by the Arctic Circle. The creature also does not live in the far
northern regions of Norway, Sweden, Finland and Russia, but can occasionally appear in the
polar circle. Its home range continues throughout Asia, and ends below the 60th parallel north
of Sakhalin Island. To the west, this species does not inhabit Ireland, Iceland and Greenland.
In North America, the territory of venomous snakes approximately follows the 50th parallel,
which is the US and Canadian border, where they can be found practically only in the vicinity
of the Great Lakes and on certain islands around eastern Canada.

Figure 3. Global distribution of venomous snakes (freely edited according to Kornalik, 1967). The light
gray sections indicate the approximated home ranges of marine snakes The white areas are territories
estimated to be free of venomous snakes.
12 Jiri Valenta

Within the colder parts of the territory, venomous snakes cannot be found on the Cape
Verde Islands, the Canary Islands, the Balearic Islands, or in Corsica, Sardinia, Malta, Crete
and on other Greek islands. In terms of Central America, they do not occur on any Caribbean
island except Tobago, Trinidad, Saint Lucia and Martinique, where venomous snakes do
reside; see Figure 3.
As already mentioned, sea snakes inhabit neither the Atlantic Ocean nor the
Mediterranean Sea, but occur in the Indian and Pacific Ocean. Most of them dwell in the
waters that stretch between the Gulf of Persia and Indo-Chinese and Australian regions. Some
extend over the Pacific Ocean as far as the US coast.
Regarding elevation, most snakes inhabit localities below 2,000-2,500 meters above sea
level; but even here there are some exceptions. For example, the common viper (Vipera
berus) may ascend to 3,000 meters above sea level in the Alps and Scandinavian mountains,
and the central plateau dusky rattlesnake (Crotalus triseriatus) of Central America is able to
live as high up as 4,400 meters above sea level. The Himalayan pit viper (Gloydius
himalayanus), a dweller of forests, holds the record for altitude, as 3,000 - 4,000 meters is
usual for it, but this snake has even been discovered at a height of 5,300 meters, at the very
edge of a glacial zone.
Although venomous snakes have adapted to living in nearly any habitat globally,
particular groups of these snakes prefer specific types of landscapes. For example, Viperinae
snakes favor quite dry and open ground, often wooded areas in sub-mountainous and
mountainous ranges with sand or stony substrates. With some exceptions, the Gabon and
rhinoceros vipers avoid dense forested enclaves with restricted sunlight. However, Atheris,
one of the Viperinae genera, has specialized in hunting and dwelling in trees and bushes.
Crotalinae snakes have similar requirements concerning landscape: they reside in
savannahs, sparse woodland and thickets in the sub-mountains and mountains of America and
Asia. However, there are exceptions to the rule in this group as well. Several lancehead
(Bothrops) and Asian pit viper (Trimeresurus) species are frequent inhabitants of forests and
their surroundings, while some species of the Agkistrodon genus prefer proximity to water.
Unlike the viperids (Viperidae), most elapid (Elapidae) species seem to consider ideal
habitats to be damp or dense tropical forests, or at the very least the environs of such, as do a
number of Asian cobra species of Naja and Ophiophagus genera, as well as coral snakes of
the Micrurus genus.
However, African cobras and mambas largely inhabit localities of grass savannahs in
addition to shrubby and sparse bush environments, with cobras living a terrestrial life and
mambas as tree dwellers. Similar dry or even partial desert locations are resided in by some
Australian coral snakes, too.
Sea snakes that once again belong to the group of elapid snakes (Elapidae) largely prefer
salt water; they are less common in brackish waters and rare in fresh waters.
The Atractaspididae snakes family members lead an intriguing way of life - they inhabit
tunnels and dens underground, where they also hunt.
Boigas, venomous colubrids, are chiefly tree or shrub dwellers, while damp and forested
enclaves prevail as far as Natricinae snakes are concerned.
 Zoological Basis 13

1.6. ETHOLOGY BASIS, HUNTING, ATTACKS AND DEFENSE

When hunting, venomous snakes use solely their venom apparatus. A snakebite thereby
means immediate or delayed paralysis, immobilization and eventual death to prey. Therefore,
the venom mechanism and toxins are tailored to the type of hunting and intended prey.
Some of the Atractaspididae snakes, more specifically, burrowing asps (Atractaspis),
which hunt for rodents in narrow tunnels underground, can slightly open their mouths by
releasing the lower jaw and lash out with their long fangs by shifting the head aside and
moving backward. A similar method is also used in defense; when gripped behind its head,
the snake can stab with its fangs, employing side movements of its head and jaws.
The venomous arboreal colubrids Thelotornis and Dispholidus, which principally hunt
birds and chameleons, possess rear fangs and toxins effective enough for birds. The rear
position of their fangs poses some limitation for these snakes in that their prey has to be rather
small, as the angle of the open mouth does not always allow for larger animals to be bitten
successfully. Nonetheless, they are efficient predators with good motional skills and eyesight,
essential qualities for this style of hunting. The effective toxins kill prey in a very short time
due to hunted animals being held in the snakes mouth, this is in addition to frequently being
grasped by the creatures coiled body. If prey is let go of too soon, it could escape to beyond
the snakes reach. Considering the position of the fangs in the rear part of the upper jaw,
envenoming a human via a defensive bite would be technically too complicated for most
representatives of the Colubridae family. With this in mind, boigas are the most dangerous
snakes, with their fangs placed in the middle of their upper jaw.
Elapid snakes (Elapidae) are mostly terrestrial animals that hunt small mammals, frogs,
lizards and other reptiles, although this family does includes marine piscivorous snakes.
These representatives excel in terms of motional skills and are able to paralyze prey very
swiftly owing to their venom, which contains effective neurotoxins. Most of them hold their
prey in their mouths, pumping venom into the animal by repeatedly clasping their jaws -
much like chewing - as venom discharge is not controlled by the muscles of the venomous
gland. In coral snakes, cobras for instance, the speed of movement over solid surfaces and
that of potential attack should be paid heed to by snake keepers and hunters. When in danger,
a large cobra is capable of performing an assault over a distance of several meters in just
fractions of a second. However, the speed and aggressiveness of the mamba (Dendroaspis) is
often overstated. Even though mambas are probably the quickest snakes - the velocity and
level of threat involved is described in the snake morphology chapter - popular belief of their
pace is based on myth. While it is true that a bite from a mamba proves mortal without
treatment due to the content of neurotoxins, it is still not ranked highly in snake envenoming
epidemiology in its home territories. When snake collecting in south-east Senegal, only four
black mamba (Dendroaspis polylepis) individuals were captured out of total 1,280 snakes.
Considering the fact this snake is not very rare, a possible explanation may be timely escape
from the area under survey. Much like other snakes, mambas are not keen on making contact
with humans, and intentional attacks on people are not listed amongst their behavioral traits.
Any possible case of a mamba approaching a man might be explained as inquisitive behavior.
They will attack only if sensing a threat, just like any other snake, although the swiftness of
this action can exceed the response of humans.
14 Jiri Valenta

Marine coral snakes - sea snakes and sea kraits - are hunters of small fish largely in the
vicinity of coral reefs. They may often follow or pursue divers, occasionally with even close
physical contact taking place in form of twining around legs. Nonetheless, occurrences of
snakebite are rare, in fact, their fangs are so small they are incapable of penetrating a
neoprene diving suit, and defensive biting is not typical of these snakes. Moreover, there are
instances on record of children playing with sea snakes washed up on beaches, but no child
has been bitten. It is more usual for fishermen to come into contact with sea snakes, although
such individuals are at risk of snakebite to some extent anyway.
The viperid family (Viperidae), an advanced snake taxon in terms of evolution, can hunt
prey by swift and sometimes repeated bites using erected fangs. They do not hold prey in
their mouths as the bitten animal is subsequently pursued. Viperids venom is a complex of
toxins and enzymes affecting a number of vital systems, meaning death to their prey even if
the attack is rather unsuccessful. The biting of humans by viperids, namely vipers (Viperinae)
is nothing rare in the wild. The higher rate of incidence is caused by the lesser speed of the
viper. While elapid snakes (Elapidae) can mostly escape from humans very quickly, vipers do
so much slower, whilst some species, like the Bitis genus, show little enthusiasm to get away.
This can expose such snakes to direct contact with humans much more often. Attacking prey
and defensive attacks in viperids follow certain rules and procedures, see chapter 1.3
Morphology of snakes. The anatomical configuration of the venom mechanism, as well as the
ability to differentiate between predation and defense is discernable in viperids by a high rate
of so-called dry bites - those where venom is not released - and mere warnings of a strike as a
deterrent.
To put off an enemy, snakes employ the most basic sound they can emit - a hiss - despite
not being able to hear. In addition, saw-scaled vipers (Echis) and rattlesnakes (Crotalus) have
another method of warning by sound. When threatened, the Echis viper emits a crisp or
strident (sharp) sound by rubbing together coils of its body, which is covered in thick ridged
scales. The use of the rattle on the tail of rattlesnakes (Crotalus) serves the same purpose. The
speculation that this is a passive form of audible defense to deter herds of running animals in
an open plain should not be ruled out. Other forms of deterrence include visibly enlarging the
body. This is performed by cobras by erecting and typically extending the ribs in the front
part of the body to form a hood, whereas the Gabon viper (Bitis gabonica) inflates its neck.
Another example is the opening of the mouth to display the different color inside, which
could function so as to make the creature more visible and simulate an attack. For instance, as
the names suggest, the inner part of mouth of the western cottonmouth (Agkistrodon
piscivorus leucostoma) is white, and in the black mamba (Dendroaspis polylepis) it is black.
The speed and behavior of venomous snakes relates to the safe distance one can stand
from them as well as estimating the potential of attack. The swifter the snake is when moving
and performing an attack, added to which the physically larger the creature, the greater the
distance that must be kept for safetys sake. In cobras and mambas, this can be up to several
meters depending on the size of the snake. Considering the 4-meter black mamba
(Dendroaspis polylepis) or the king cobra (Ophiophagus hannah) of 5 meters, these snakes, if
ideally positioned, are able to carry out a surprise attack over a distance of nearly two meters
without any prior movement. Compared to the species above, the lesser Vipera and Cerastes
genera, or even the rapid saw-scaled vipers (Echis), prove incapable of placing a bite at a
distance of over 50 cm. Such a short distance can be considered safe with the lazy Gabon
viper as well, in spite of its size, unless it is poised in a threatening position. However, the
 Zoological Basis 15

information above definitely cannot not be applied to the large and short-tempered Crotalus
and Bothrops genera, which are capable of a flying attack of over 1 meter from a point of
attack, despite their mighty bodies.
When determining a distance to be kept from a snake, the poise of the creature is crucial.
A safe distance from a snake that is lying outstretched, escaping or quietly resting is sure to
be reduced and any attack is less probable, unlike in the case of a viper coiled up with its head
elevated and ready to strike, a rattlesnake that has formed the typical coil at the front part of
its body or an erect cobra threatening to attack.
When kept in a terrarium, an attacking snake protects itself and its limited territory. In
fact, keeping any form of safe distance is practically impossible. The apparent calm of the
hidden snake should not be mistakenly relied upon, and placing ones hands inside the
terrarium in the presence of the snake is likely to wind up in a bite.
Another form of defense employed by snakes and animals alike is that of protective
coloring. Spotting the black mamba or a Trimeresurus snake in tree branches, the Gabon
viper in fallen leaves or the Levantine viper (Vipera lebetina) in stony and sandy
environments is sure to require a lot of attention.
In addition, certain snakes, the ringhals (Hemachatus hemachatus) for instance, feature
an ability to play dead, known as thanatosis, when the snake lies on its back, exposing its
lighter underside, coiling up and opening its mouth. The snakes mouth hangs free in order to
resemble bleeding. This puts potential aggressors off due to gathering carrion, although even
snakes in this position can prove dangerous to hunters or curious individuals, as they can,
nevertheless, bite.
Naturally, escape is the snakes principal and initial form of defense and, as mentioned
earlier, when walking around normally, one would hard pushed to actually see a snake even if
the area is rife with them. After all, snakes do not crave attention.

REFERENCES
FELIX, J., et al. Hadi. 2. vyd. Praha : Statni zemedelske nakladatelstvi, 1981, 155 pp. (in
Czech)
GAISLER, J. Zoologie obratlovcu. Praha : Academia, 1983, pp. 307-314. (in Czech)
HAYES, WK., LAVIN-MURCIO, P., KARDONG, KV. Delivery of Duvernoys secretion
into prey by the brown tree snake, Boiga irregularis (Serpentes: Colubridae). Toxicon,
1993, 31, No. 7, pp. 881-887.
HEGNER, D. Jedovai hadi v prirode a terariich. Uvaly : Ratio, 1999, 188 pp. (in Czech)
MATTISON, CH. Hadi. Praha : Ottovo nakladatelstvi, 2001, 192 pp. (in Czech)
KORNALIK, F. Zivocisne toxiny. Praha : SZN, 1967, 288 pp. (in Czech)
KURKA, A., PFLEGER, V. Jedovat ivoichov. Praha : Academia, 1984, 165 pp. (in
Czech)
MARAIS, J. Fascinujici svet hadu. Praha : Rebo Productions, 1995, 143 pp. (in Czech)
MEIER, J., STOCKER, KF. Biology and distribution of venomous snakes of medical
importance and the composition of snake venoms. In MEIER, J., WHITE, J. (Eds),
Handbook of clinical toxicology of animal venoms and poisons. Boca Raton: CRC Press,
1995, pp. 364-412.
16 Jiri Valenta

REHAK, I. O jedovatosti nejedovatych uzovek. Ziva, 1990, 38, No. 3, pp. 130-131. (in
Czech)
REHAK, I. Evoluce, fylogeneze a taxonomie hadu. Terarista, 1991, 2, No. 3-4, p. 18. (in
Czech)
REHAK, I. Soucasne nazory na klasifikaci hadu. Terarista, 1991, 2, No. 3-4, pp. 18-20. (in
Czech)
REHAK, I. Distribution, ecology and variability of snakes in Czechoslovakia. In KORSOS,
Z., KISS I. (Eds), Proc. Sixth Ord. Gen. Meet. S.E.H. Budapest 1991, 1992, pp. 383-388.
REHAK, I. Serpentes - Hadi, Hady. In BARUS, V., OLIVA, O. (Eds.), Plazi - Reptilia. Praha
: Academia, 1992, pp. 106-172. (in Czech)
STCKLIN, R., CRETTON, G. The ultimate database on venomous animals, snakes. CD-
rom, Geneva : Atheris Laboratories, 1998.
TRAPE, JF., PISON, G., GUYAVARCH, E., et al. High mortality from snakebite in south-
eastern Senegal. Trans R Soc Trop Med Hyg, 2001, 95, No. 4, pp. 420-423.
VALENTA, J., SIMAK, J. Intoxikace zivocisnymi jedy. In Pokorny, J. (Ed.), Urgentni
medicina. Praha : Galen, 2004, pp. 258-264. (in Czech)
VOGEL, Z. Zezivota plazu prazske zoologicke zahrady. Praha : Orbis, 1953, 84 pp. (in
Czech)
Chapter 2

EPIDEMIOLOGY OF SNAKEBITES
2.1. EPIDEMIOLOGICAL NOTES
Information on epidemiological indicators, incidence, mortality, and morbidity of
snakebites is not comprehensive both within particular countries and globally. There are
several reasons for this. Due to the limited numbers of venomous snakes, there is such a low
incidence of snakebites and subsequent morbidity in European countries that neither sparks
statistical concern nor interest from medical circles. Information on the total number of
envenomed individuals cannot be obtained, and actually tracing such people within health
institutions is practically impossible. The only data available is on patients dealt with by
toxinology centers or hospitalized at particular institutions. Thus, the numbers obtained
officially that relate to incidence and morbidity are probably highly understated.
The situation in developing Asian and African rural countries where dangerous snakes
frequently occur is of a completely different nature. The effects of snakebites are significant
in terms of epidemiology; however, the reporting and screening systems are either not
uniform in style, are not adhered to or do not exist at all. Moreover, a number of affected
persons are not subject to therapy in health institutions, as they seek assistance from
traditional indigenous healers, which may be true in up to 80% of cases, or, worst of all,
cannot make it to a distant hospital before the severe venom deals them a fatal blow. It is
estimated that in developing nations where distances from hospitals are very large, only 50%
of all envenomed individuals are within reach of medical care. Therefore, the incidence,
morbidity and mortality figures obtained in such regions are substantially lower than the
estimated and exact amounts.
Even in countries with well-developed systems of medical services and those governing
the reporting of statistics, such as the USA, epidemiological data is not uniform, and the
numbers of snakebites unreported and untreated in official medical institutions is assumed to
be high as well. Again, official incidence and morbidity figures are certainly lower than those
of reality.
With this in mind, epidemiological works from most countries are often elaborated and
subject to estimates largely produced on evidence from health institutions and consultation
centers, in addition to surveys on families from randomized areas.
In most cases, snakebites by venomous snakes are associated with farming; less
frequently, trips in the wild, either temporary or permanent, are involved. In these cases,
18 Jiri Valenta

lower limbs are the most frequent localization of the bite compared to upper limbs. The
numbers of attacks vary according to season.
In industrially developed nations, a certain quantity of snakebites and envenomings are
consequences of exotic venomous snakes being kept captive. In the 1990s, exotic snakes were
responsible for 21% of snakebites in Utah, the USA. In the Czech Republic, the percentage of
attack by exotic venomous snakes accounted for over 40% of the total number, according to
consultations at the Toxinology Center of Prague. However, while the numbers of visitations
following snakebites by the common viper probably do not match the incidence of actual
snakebites, the figures obtained for snakebites by exotic varieties are very close to those of
incidence. Therefore, the real percentage of envenoming cases by snakes kept in captivity is
likely to be lower. Substantially lower numbers of envenomings by exotic snakes - a mere 4%
- are provided in reports by the American Association of Poison Control Centers (AAPCC),
within the Toxic Exposure Surveillance System (TESS), for the periods of 1999 and 2000.
Amongst snake holders, the upper limbs are typical areas affected by bites, the usual
reasons including work in terrariums in the presence of snakes, the feeding of young snakes
and inadequate handling of a snake itself.

2.2. EUROPE
Generally, the importance of the snakebite in terms of epidemiology is minimal for
Europe, which also is implied by the statistics available. Envenomings are chiefly caused by
vipers of the Vipera genus: the common viper (V. berus), the nose-horned viper (V.
ammodytes) and the asp viper (V. aspis). Except for the European portion of Turkey (the rock
viper V. xanthina), snakebites by other European dwelling vipers of the same genus, as well
as those carried out by venomous colubrids like Malpolon monspessulanus, are rather rare.
A relatively high snakebite incidence has been recorded in Sweden, which might have
been influenced by the system of reporting to the Swedish Toxinology Center. The territories
of the common viper (V. berus), are inhabited by 5.3 million people, i.e. 63% of the Swedish
population. In 1985-1989, 4,269 incidents resulted in consultation around Sweden. According
to other data sources, occurrence is around 1,300 cases a year, with about 12% of those
affected being hospitalized; which is equal to the number of 136 patients with zero mortality
that were hospitalized in 1975 and that of morbidity: 2.6 per 100,000 inhabitants a year, as
reported. However, in 1911-1978, a total of 44 cases of death as a consequence of being
bitten by a common viper were recorded.
For Finland, the numbers reported are much higher: morbidity of 4.1 per 100,000
inhabitants and mortality of 0.02 per 100,000 inhabitants a year; which means 0.5% of fatal
cases.
In Italy, 2,329 cases of envenomings were recorded in 1980-1984, out of which 62%
were asymptomatic cases and 885 persons showed symptoms of envenoming; 3 patients died.
The estimated total numbers are as follows: incidence of snakebites 5 per 100,000
persons, morbidity of 1 per 100,000 and mortality of 0.01-0.04 per 100,000 inhabitants a
year. In terms of fatal cases, the figure is 0.1-0.6%.
 Epidemiology of Snakebites 19

Spains data shows a morbidity of 1.4-4 per 100,000 inhabitants and mortality of 0.006-
0.02 per 100,000 inhabitants a year; which means some 0.6-1.8% of fatalities via
envenoming.
In France, the approximate annual incidence of snakebites is 2.5 per 100,000 people,
morbidity is below 0.5 per 100,000 people; about 0.3% of those affected die.
The United Kingdom reports 200 hospitalizations a year, with a current mortality rate of
zero. Morbidity is currently a mere 0.1 per 100,000 inhabitants a year. In 1950-1972, England
and Wales recorded only a single fatal case; within the UK, only 14 cases of death as a result
of envenoming by the common viper were reported in the last 100 years.
A very low morbidity rate and zero mortality is reported by Switzerland.
In Poland, there is relatively high percentage of deaths: 1.1%, which is equal to that of
Israel, where they report l.3%; however, attacks were performed by much more serious
snakes in terms of toxinology. The Polish information might be, and probably is, greatly
affected by incomplete or understated morbidity data.
In the Czech Republic, several dozens of snakebites by the common viper are reported
annually. The cases of snakebites by exotic venomous snakes are decreasing compared to the
past, with several incidents registered a year. However, some of them involve life-threatening
envenomings that require therapy utilizing severe medication. No fatal case in connection
with a snakebite by the viper or any other species has been recorded by the Toxinology
Center within 15 years.
For the European population of 730 million people, estimated total numbers involve
25,000 snakebites, 8,000 cases with symptoms of envenoming, and 30-50 fatal cases a year,
i.e. 0.37 to 0.62% of those envenomed, which equals the incidence of 3.24 bites per 100,000
inhabitants a year, a morbidity of 1.1 per 100,000 inhabitants a year, and mortality of 0.004-
0.006 per 100,000 European inhabitants a year.

2.3. THE MIDDLE EAST

As in North America, the cases of scorpion bites prevail over those by snakes in this
region, with dangerous venomous snakes including the Vipera and Macrovipera genera, such
as the Palestine viper (V. palestinae), rock viper (V. xanthina) and Levantine viper (M.
lebetina). These snakes take the greatest share of the reported envenomings. Other vipers of
the Cerastes, Pseudocerastes and Vipera genus are insignificant due to their lower toxicity.
In this region, the estimated total quantity of snakebites amounts to 20,000 per 160
million inhabitants, of which there are 15,000 envenomings and a mortality rate of
approximately 100 cases a year. The numbers above correspond to this high incidence and
morbidity; however, they are not quite in correlation with the data provided for Israel, where
morbidity is 3-5 cases per 100,000 inhabitants, while mortality reaches 0.3 per 100,000
inhabitants, which means 1.3% of fatal cases. Estimated total incidence amounts to 12.5 cases
per 100,000 inhabitants a year, a morbidity rate of 9.4 patients per 100,000 inhabitants a year,
and mortality of 0.06 per 100,000 inhabitants a year, which makes for 0.6% of lethal cases
from the total number of envenomed patients.
20 Jiri Valenta

2.4. AFRICA
The African countries are considered among those assumed to have much understated
prevalence of statuses associated with snakebites for the reasons listed above. The major
representatives of Africas epidemiologically most serious snakes involve the saw-scaled
vipers of the Echis genus, i.e. E. ocellatus and E. leucogaster, the African puff adder (Bitis
arietans); the black and white cobra (Naja melanoleuca) and the black-necked spitting cobra
(N. nigricollis), mambas (Dendroaspis sp.) and the West-African night adder (Causus
maculatus). As for the north-eastern part of the continent, similarly as in the Middle East,
there is the Levantine viper (Macrovipera lebetina).
The factors responsible for the high morbidity and mortality values in the developing
agricultural countries involve abundance of toxinologically dangerous snakes, a long time of
delay due to the poor availability and quality of health facilities, lacking medicaments and
antivenoms, and also erudition of the personnel, which is not always satisfactory.
Nigeria reports the incidence of 497-600 snakebites per 100,000 inhabitants a year with
12% of fatal cases, which means mortality of nearly 60 cases per 100,000 inhabitants a year.
Up to 10% of beds in hospitals occupied in the country involve cases of snake envenoming.
The type of envenoming by Echis snakes with its severe symptoms of hemocoagulation
failure requiring an intensive and highly-specialized approach is by no means co-responsible
for the high rate of mortality in certain regions of Nigeria - especially that related to children -
that reaches up to 16%.
A similar situation exists in Benin, where the estimated incidence is 450 snakebites per
100,000 inhabitants a year with a lethality rate of 5.6%. Nonetheless, official reports provide
only unreal rates of 70 snakebites per 100,000 inhabitants a year, with a lethality rate of 1%.
In Senegal, they report mortality following a snakebite 11.7-14 cases per 100,000
inhabitants a year. In Ghana, 86 snakebites per 100,000 inhabitants a year occur, with bites
largely caused by Echis snakes, with a lethality rate reaching up to unbelievable 28%.
Kenya reports the incidence of 150 snakebites per 100,000 inhabitants a year with the
mortality rate of 6.7 per 100,000 inhabitants a year; nevertheless, it is assumed that 70% of
those affected will not visit any health institution at all, which modifies the provided data to a
great extent.
Higher morbidity and lethality rates exist in Cte d'Ivoire: 130-400 cases of envenoming
per 100,000 inhabitants a year, with 2% to 28% of fatalities.
Generally, estimated total numbers involve 1 million bites by venomous snakes a year for
the African population counting 760 million people, with one half, i.e. about 500,000 people,
that showed symptoms of envenoming, of which 20,000 people a year die. Such numbers
correspond to the incidence of 131 bites per 100,000 inhabitants a year, a morbidity of 65
patients per 100,000 inhabitants a year, and mortality of 2.6 victims per 100,000 inhabitants a
year. Fatalities involve about 2% from the number of bitten and 4% from envenomed patients.
 Epidemiology of Snakebites 21

2.5. ASIA
A number of Asian countries including India share a similar situation as those of Africa,
with resulting high morbidity and mortality of snakebites. The number of deaths, which is
25,000 to 30,000 annually as provided by some authors, seems to be understated.
In Asia, especially in India, snakes co-responsible for the cases of dangerous envenoming
involve the Russells viper (Daboia russelli), saw-scaled viper (Echis carinatus), Indian cobra
(Naja naja) for the Asian cobras, Indian krait (Bungarus caeruleus) and banded krait (B.
fasciatus) for kraits, and Malayan pit viper (Calloselasma rhodostoma).
Certain Indian and Pakistan localities report the incidence of 163 snakebites - largely by
E. carinatus and D. russelli - per 100,000 inhabitants a year with a morbidity of 70 cases per
100,000 inhabitants a year and mortality of 2.4 cases per 100,000 inhabitants a year, where
lethality ranges from 1.7% to 20% of cases. In the Indian State of Maharashtra, snakebites kill
over 1,000 people per year.
In Sri Lanka, they estimate 60,000 bites with 900 fatal cases a year. Provided rates of
mortality make 5.6, and even 18 cases in some places per 100,000 inhabitants a year. 40% of
the envenomings involve snakebites from the Russels viper (D. russelli), while 35% cases
goes on the account of the Indian cobra (N. naja).
With 2,000 fatal cases a year, death following a bite from D. russelli occupies the place 5
on the list of causes of death in Burma (Myanmar). The mortality in this country seems to be
the highest throughout Asia, thus probably around the globe; nevertheless, such high numbers
might be influenced by the higher quality of reporting system compared to that of other Asian
regions. The 70% of fatalities in this country is caused by the Russels viper (D. russelli),
largely at work in rice fields.
In Japan, the incidence varies from 10 to 500 snakebites per 100,000 inhabitants a year
depending on the region, with Asian pit vipers of the Trimeresurus genus responsible for the
most of cases, with morbidity of 0.2 to 120 cases per 100,000 inhabitants a year, and 0.8% to
1% of fatalities. The variance in the figures is determined by the climatic differences between
the northern and the southern part of the country, with increased incidence of snakebites and
morbidity southwards.
In general, some 4 million snakebites from venomous snakes a year are estimated for the
Asian population of 3.5 billion people, where symptoms of envenoming are present in one
half of the cases, i.e. 2 million, and a total number of deaths is 100,000, which involves the
incidence of 114 snakebites per 100,000 inhabitants a year, morbidity of 57 cases per 100,000
inhabitants a year, and mortality of 2.9 victims per 100,000 inhabitants a year. Fatalities
involve 2.5% of the bitten persons and 5% of the envenomed patients.

2.6. NORTH AMERICA

Even though the territory of Canada and the USA is inhabited by a number of highly
dangerous venomous snakes, incidence and morbidity and mainly mortality figures are very
low. The reason is that the situation is 180 degrees different from that of Africa and Asia:
snake localities are limited and less-inhabited, good health services are promptly available,
22 Jiri Valenta

and the quality level of final treatment of envenoming is very high. Deaths in this area are
largely caused by delays or cases of refused therapy by patients.
The North Americas dangerous snakes are largely the rattlesnakes (Crotalus), which for
the USA namely involves the western diamond-backed rattlesnake (C. atrox) and eastern
diamond-backed rattlesnake (C. adamanteus).
Within the USA and Canada, they estimate about 45,000 bites from venomous snakes a
year, which includes 10,000 cases of envenoming and 6,500 to 7,000 cases of people seeking
medical help. Approximately 5 to 15 people a year die from snake envenoming. The
snakebite incidence is variable depending on the region from 0.7 to 15 per 100,000
inhabitants a year, morbidity ranges from 0.5 to 5 patients per 100,000 inhabitants a year, and
mortality is 0.005 to 0.01 victims per 100,000 inhabitants a year. There are about 0.1-1.6%
fatalities a year. However, numbers of envenomings reported by the American Association of
Poison Control Centers (AAPCC) in the framework of the Toxic Exposure Surveillance
System (TESS) are substantially lower: only 1,729 cases in the wild and 80 cases by exotic
snakes held in captivity are provided for 1999; in 2000, there were 1,918 cases of
envenoming caused by local snakes and 83 envenomings by exotic snakes.

2.7. CENTRAL AND SOUTH AMERICA

This vast region with diverse habitats is ranged by venomous snakes throughout the most
of its territory. Mexican savannahs that involve sandy and rocky habitats are rich in
rattlesnakes (Crotalus): C. atrox and C. durissus durissus. For South America, the snakes of
the highest concern in terms of epidemiology include the South American rattlesnake
(Crotalus durissus terrificus), Micrurus snakes, and lanceheads like the common lancehead
(Bothrops atrox), jararaca (B. jararaca), jararacussu (B. jararacussu) and South American
bushmaster (Lachesis muta). In Mexico, the indicators are supposed to be higher than those of
North America, with about 100 mortal cases alone.
In Brazil, the incidence of snakebites is 350 to 450 per 100,000 inhabitants a year.
Morbidity ranges from 6.8 to 192 cases per 100,000 inhabitants a year, and mortality is 0.4-5
deaths per 100,000 inhabitants a year; fatal cases number 0.4% - 6.5%. The wide ranges
above are determined by specific localities; figures for the forest will naturally increase.
In the Brazilian epidemiological analysis of cases in the last 100 years (1901 to 2000),
Bochner and Struchiner (2003) provide lanceheads (Bothrops) as snakes mainly responsible
for snakebites and overall lethality of 0.45%, where 1.87% of snakebites were caused by
rattlesnakes (Crotalus), 0.95% by bushmasters (Lachesis), 0.52% by coral snakes of the
Micrurus genus and 0.31% by lanceheads (Bothrops).
In Costa Rica, the morbidity is estimated to 20-35 cases per 100,000 inhabitants a year,
and mortality to 0.2-1.2 per 100,000 inhabitants a year. Lethality ranges from 2.3% to 3.3%
of the cases. Nevertheless, a survey carried out in the populations of indigenous people
showed that the epidemiology indicators in the region would be possibly much higher.
The Ecuador situation can be outlined as that of high lethality of the cases - as much as
5.4% of patients treated in hospitals and 6.3% of people treated at home will die. In forest
localities, the incidence can reach up to 1,000 snakebites per 100,000 inhabitants a year.
Morbidity within country is 16-30 cases per 100,000 inhabitants a year, and mortality is 1.8
 Epidemiology of Snakebites 23

per 100,000 inhabitants a year. The highest fatality is reported from Venezuela: 6.5% of
cases.
The estimated total numbers for the population of 400 million inhabitants in Central and
Southern America are 300,000 snakebites, 150,000 cases of envenomings, and 5,000 mortal
cases per year, which involves the incidence of 75 snakebites per 100,000 inhabitants a year,
morbidity of 37 cases per 100,000 inhabitants a year, and mortality of 1.25 deaths per
100,000 inhabitants a year. Overall lethality is 1.6% of the bitten persons and 3.2% of the
envenomed patients.

2.8. AUSTRALIA AND OCEANIA

Within the Australian and Oceanian territory, terrestrial venomous snakes are in fact
limited only to Australia including Tasmania and the islands located in the north of the
continent. New Zealand and most of other Pacific islands are not inhabited by venomous
snakes at all. Naturally, the Pacific and Indian Ocean are home ranges of marine venomous
snakes. Even though venoms in these animals are highly effective, the epidemiological
relevance is quite low: snakebites are not very frequent, concerning mostly local fishermen.
The snakebite incidence specified by Australian reports is 3-18 cases of snakebite per
100,000 inhabitants a year, a mean morbidity of 4 envenomings per 100,000 inhabitants a
year, and mortality in connection with a snakebite of 0.03 deaths per 100,000 inhabitants a
year. Thus, several envenomings per year present mortal cases. In the period from 1981 to
1991, total 18 envenomed persons died in Australia, with 11 deaths caused by brown snakes,
Pseudonaja and 4 deaths caused by tiger snakes, Notechis; 2 affected persons succumbed to
snakebites of taipans (Oxyuranus) and a single person died from the snakebite caused by a
death adder (Acanthophis). However, not every death is recorded. The snakes of the
Pseudonaja genus are considered the most dangerous as their venoms can cause immediate
collapse and sudden death.
In Papua-New Guinea, the incidence is much higher with 215-526 bites per 100,000
inhabitants a year, the recorded morbidity relatively lower with 3-82 cases per 100,000
inhabitants, and the mean mortality high with 7.9 deaths per 100,000 inhabitants a year.
In general, 10,000 snakebites, 3,000 envenomings and 200 deaths a year are estimated for
the Australian and Oceanian population of 20 million people, which involves the incidence
of 50 snakebites, 15 envenomings and 1 death per 100,000 inhabitants a year.

2.9. WORLD-WIDE FIGURES

A total of strikes by venomous snakes for the global population of 5.85 billion people are
estimated to 5.4 million, of which the number of envenomings is approximately 2.7 million of
cases (see Fig 4). Reported numbers of deaths as a result of snakebites range from 20,000
(Warrell, 1993) to 50,000 (Swaroop et Grab, 1954) or even up to 125,000 (Chippaux, 1998)
cases per year. However, the lower estimations seem to be understated based on the reasons
mentioned above, i.e. the high number of untreated and unreported cases world-wide. The
WHO (World Health Organization) Report from 1979 is in accord with the calculation above,
24 Jiri Valenta

stating 250,000 deaths a year as a result of strikes by venomous animals, namely snakes and
scorpions. Provided that 50% of the cases were caused by venomous snakes, the numbers
approximately match Chippauxs estimations.

Figure 4. Global incidence of envenomings following snakebites (freely edited according to Chippaux,
1998) (Dark: more than 100 envenomings; midle: 25-100 envenomings; mild: less than 25
envenomings per 100,000 inhabitants a year).

REFERENCES
BOCHNER, R., STUCHINER, CJ. Snake bite epidemiology in the last 100 years in Brazil:
a rewiew. Cad Saude Publica, Rio de Janeiro 2003, 19, No. 1, pp. 7-16.
HABIB, AG., GEBI, UI., ONYEMELUKWE, GC. Snake bite in Nigeria. Afr J Med Sci,
2001, 30, pp. 171-178.
CHIPPAUX, JP. Snake-bites: appraisal of the global situation. Bulletin of the World Health
Organization, 1998, 76, No. 5, pp. 515-524.
ISMAIL, M., MEMISH, ZA. Venomous snakes of Saudi Arabia and the Middle East: a
keynote for travellers. Int J of Antimikrob Agents, 2003, 21, pp. 164-169.
KARLSON-STIBER, C., PERSSON, H. Antivenom treatment in Vipera berus envenoming -
report of 30 cases. J Intern Med, 1994, 235, pp. 57-61.
KURKA, A, PFLEGER, V. Jedovati izivocichove, Praha : Academia, 1984, 165 s. (in Czech)
MARAIS, J. Fascinujici svet hadu. Praha : Rebo Productions, 1995, 143 s. (in Czech)
MEIER, J., WHITE, J. (Eds.). Handbook of clinical toxicology of animal venoms and
poisons. Boca Raton : CRC Press, 1995, 752 p.
PERSSON, H., IRESTEDT, B. A study of 136 cases of adder bite treated in Swedish
hospitals during one year. Acta Med Scand, 1981, 210, No. 6, pp. 433-439.
POZIO, E. Venomous snake bites in Italy: epidemiological and clinical aspects. Trop Med
Parasit, 1988, 39, pp. 62-66.
REID, HA. Adder bites in Britain. Br Med J, 1976, 2, No. 6028, pp. 153-156.
SEKOGUCHI, S., NIKAI, T., SUZUKI, Y., et al. Kinin-releasing enzyme from the venom of
Bitis arietans (Puff Adder). Biochim Biophys Acta, 1986, 884, No. 3, p. 502-509.
 Epidemiology of Snakebites 25

SUTHERLAND, SK. Death from snake bite in Australia 1981-1991. Med J Aust, 1992, 157,
No. 11-12, pp. 740-746.
SWAROOP, S., GRAB, B. Snakebite mortality in the world. Bull World Health Organ, 1954,
10, pp. 35-76.
WARRELL, DA. Venomous bites and stings in the tropical world. Med J Aust, 1993, 159,
No. 11-12, pp. 773-779.
Chapter 3

SNAKE VENOMS
3.1. SNAKE VENOMS - PHYSICAL TRAITS AND COMPOSITION
Snake venom produced and stored in venom glands is a viscous liquid of either a white,
yellow color, or of a dark orange hue depending on the species, age, and condition of the
snake. Fresh native venom can be clear, or polluted with the epithelia of ducts and mucin
floccules. The operation and effectiveness of a liquid venom has certain time limits. Under
normal temperatures, the destruction of toxins takes place outside the venom apparatus, which
in part is caused by proteolytic enzymes of the animal and by bacterial activity. On average,
fresh venom accounts for only one third of the weight of the same as dry matter.
For laboratory and pharmaceutical purposes, some venomous snake species are kept on
farms, where their venom is collected artificially on a routine basis. The fangs of a snake,
which is held behind the head, are made to bite through a cellophane cover on a beaker, into
which the venom is drained. The venom draining process is accelerated by gently
manipulating the venom gland or by soft electrical impulses. Alternatively, venom can be
collected without the need for piercing the cover of a vessel but by opening a snakes mouth
and carrying out pressure maneuvers. After completing the collecting process, the venom
must be immediately modified, which is usually done by centrifugation and subsequent
drying. Lyophilized venom may then be stored over longer periods, such as in the order of
years or decades. However, some components lose some partial effectiveness during the
process of preparing the dry matter, while the activity of others diminishes during storage.
Nevertheless, any loss of effectiveness in fresh venom is something which should not be
relied upon, as some components maintain their function even up to a certain level of
destruction. For example, cases of envenoming have been recorded during post mortem
examinations on dead snakes or via other types of handling of the same, even a long time
after death.

3.2. EFFECTIVENESS OF SNAKE VENOMS

Only about 10-20% of snake species are venomous. However, this does not mean that all
of them are actually dangerous in every circumstance, as some of them are unable to inject
venom via a defensive bite due to their jaws being small or the fangs being inadequately
located. Meanwhile, others can only cause nausea or slight symptoms of envenoming as a
28 Jiri Valenta

result of the quantity of venom and its properties, and only a few of the remainder cause
serious envenoming with potentially fatal consequences.
Snake venoms combine dozens of biologically active components, protein-based toxins
and enzymes, polypeptide and peptide toxins, polysaccharides, low molecular substances, and
ions. The active substances of venoms may be classified subject to their chemical make-up,
thus forming two groups: toxins and enzymes.
Toxins consist of peptides, polypeptides and proteins lacking enzymatic activity with
molecular weights usually below the range of 3 to 30 kDa. They attack specific targets; most
frequently, these involve membrane receptors of target cells in particular systems. The effect
of the toxins is determined by the quantity of the toxin and target receptors, and is fully dose-
specific. Venoms rich in toxins are found in elapids (Elapidae).
Enzymes are substances based on proteins too, but their molecular weight is frequently
higher than 30 kDa. Some enzymes feature a lower level of immunogenicity, which is often
combined with low molecular glycosylation. The intensity of an enzyme effects is
significantly influenced by the time of action, in addition to concentration. Enzymes form the
key elements of venoms in viperids (Viperidae).
The severity of a snakebite will depend on the toxicity of the venom, type of systemic
effect, quantity ingested, and the speed of its release into tissues and systems, i.e. penetration
into the hypodermis and muscular matter, as well as the organs via vascular or lymphatic
systems.
For snake venom effectiveness, the main parameters include the toxicity of the venom.
To facilitate comparison of toxicity, venom quantity related to the weight of the victim needs
to be provided. A dose is determined in vivo to kill 50% of the group of animals envenomed,
which mostly comprise mice; this quantity is referred to as LD50. In the past, other labels
existed: the so-called LD0 (MLD - minimal lethal dose) - the maximum dose that would kill
no animals; and LD100 (CLD - certain lethal dose), the minimum dose with 100% lethality
(see chart 1). The velocity of effect together with a venoms potency can be represented by
two values: FTL (Fatal Time Limit) - the duration to the death of the first animal; and LMT
(Last Mortality Time) - the duration to the death of the last animal. According to WHOs
recommendations from 1981, hemorrhagic and necrotizing venoms are tested by the size of
the zone affected on day 1 and day 3 following intradermal application.
The greatest toxicity, defined as LD100 for mice, belongs to certain sea snakes, e.g. the
common sea snake (Enhydrina schistosa) and other elapids, the coastal taipan (Oxyuranus
scutellatus), the mainland tiger snake (Notechis scutatus), and the Indian cobra (Naja naja).
Probably the highest toxic potency can be assigned to the venom of other taipans - the inland
taipan (Oxyuranus microlepidotus), a snake also known under a synonym - Parademansia
microlepidota, which is capable of creating toxicity four times greater than that of the coastal
taipan.
The complex nature of snake venoms pre-determines the variability of some traits of the
same to some extent.
In addition to the primary or standard type of effect, which is specific to genus or species,
variability exists in the composition of particular components, therefore, many times in
immunogenicity of venom as a complex. A certain level of variation in toxin composition can
be recorded within the particular species inhabiting different regions and, in fact, a single
region. The actual make-up of snake venom changes within ontogenesis as well, and
variations might possibly depend on the season. Contrary to expectation, a bite by a young
 Snake Venoms 29

snake is dangerous, as toxins in young snakes can be more effective than those of adults. The
possible reasons for this include compensation for their lower speed or poor hunting skills.
Another similar factor relates to the greater probable effectiveness of snake venom in early
spring following winter hibernation, for instance, in the common viper.
Just like the exact composition of venom within a species, the quantity produced also
varies. In large species, the amount is naturally higher (see chart 2). It also depends on the
condition of the snake, and the addition of saliva to venom, which may differ.
The action of the venom that occurs following a snakebite depends upon its quantity and
composition. Aside from venom toxin potency and venom quantity in venomous apparatus,
the factors responsible for the severity of snakebite envenoming in humans include the
quantity of venom injected into a wound (see chart 3). In terms of the amount of venom,
envenoming by large Crotalus species and certain cobras, such as Naja haje, can be highly
dangerous and might prove even lethal, although these snakes do not compare to the common
viper (Vipera berus) when it comes to effectiveness in relation to quantity, the latter giving
bites resulting in very low morbidity and mortality. Finally, bites by snakes boasting a high
number of effective venom components are the most dangerous. The lethality rate for
envenoming without any subsequent treatment is 50% for the common death adder
(Acanthophis antarcticus), 73% for the South American rattlesnake (Crotalus durissus
terrificus), and even 100% for the coastal taipan (Oxyuranus scutellatus).

Chart 1. LD100 for 100 g of mice SC

Common seasnake (Enhydrina schistosa 0.015 mg

Coastal taipan Oxyuranus scutellatus 0.017
Indian cobra Naja naja 0.020
Mainland tiger snake Notechis scutatus 0.024
Black mamba Dendroaspis polylepis 0.060
Common death adder Acanthophis antarcticus 0.070
Eastern green mamba Dendroaspis angusticeps 0.080
South American rattlesnake Crotalus durissus 0.110
Southern coral snake Micrurus frontalis 0.250
Common viper Vipera berus 0.250
Red-bellied black snake Pseudechis porphyriacus 0.280
Egyptian cobra Naja haje 0.400
African puff adder Bitis arietans 0.600
Jararaca Bothrops jararaca 0.700
Southern copperhead Agkistrodon contortrix 1.100
Jararacussu Bothrops jararacusu 1.750
Western diamond-backed rattlesnake Crotalus atrox 1.900
Common lancehead Bothrops atrox 3.100

Chart 2. Quantity of dry venom in one collection from an adult snake

Western diamond-backed rattlesnake Crotalus atrox 1,500 mg

Western cottonmouth Agkistrodon piscivorus 1,100
Gabon viper Bitis gabonica 1,000
Red diamond rattlesnake Crotalus ruber 700
Coastal taipan Oxyuranus scutellatus 400
30 Jiri Valenta

Chart 2. (Continued)

South American rattlesnake Crotalus durissus 300

Common death adder Acanthophis antarcticus 230
Russells viper Daboia russelli 200

Chart 3. Lethal doses for a human and a maximum quantity of venom in mg

of dry matter

Human lethal Max. quantity of No. of doses

dose venom
Coastal taipan Oxyuranus scutellatus 5 400 80
Indian cobra Naja naja 10-17 230 20
Eastern diamond-backed rattlesnake 60 1,000 16
Crotalus adamanteus
South American rattlesnake Crotalus 24 300 13
durissus
Southern coral snake Micrurus frontalis 15 60 4
Common seasnake Enhydrina schistosa 3.5 15 4
Common viper Vipera berus 15 10 0

Viperidae, which are solenoglyphous snakes, regulate to some degree the quantity of
venom released. Therefore, a snakebite may not be always accompanied by envenoming,
even when delivering a perfect defense bite. Within a single species, a fluent transition exists
from warning bites without envenoming, known as dry bites, up to serious or even lethal
snakebites, all being determined by the amount of venom injected.
In proteroglyphous elapids (Elapidae), which boost venom discharge following a bite by
chewing, the quantity of venom injected may be reduced. Therefore, the process of
envenoming is weakened due to the short duration of a bite in instances of brief attack or
immediate separation of the snake.
The minimum incidence of envenoming following a bite by venomous colubrids
(Colubridae) cannot be put down to a low rate of toxin effectiveness, as it is rather high in
certain groups. However, opistoglyphous colubrids have a very small quantity of venom
available, in addition to which they hardly ever achieve a full bite and do not discharge a
significant amount of venom through their rear fangs, thereby lacking the capacity of
delivering a defensive bite.
Generally, envenomation numbers are estimated to be approximately fewer than one half
of actual bites. Snakebites by Pseudonaja snakes feature the highest incidence of
envenomation (80%); the lowest seeming to be that of Echis species - a mere 10% (Theakston
et al., 2003).
Injecting venom into well-perfused tissue, or even directly into the vascular system, is
hazardous. In this respect, rapid death has been described in humans following attacks by the
Indian cobra (Naja naja), within 15 minutes, and the South American rattlesnake (Crotalus
durissus) within 10 minutes. Another essential element in cases of venom injection into well-
perfused tissue or the vascular system is the composition of venom. When neurotoxins
prevail, the resultant effect does not depend on differences in toxicity according to the route
 Snake Venoms 31

of penetration. The venom of the Indian cobra (Naja naja) will act on a mouse in virtually the
same quantity whether applied subcutaneously or intravenously. Conversely, venoms of
lanceheads, such as the jararaca (Bothrops jararaca) and common lancehead (B. atrox) with
their hemocoagulation and hemorrhagic activities, are frequently more effective when spread
within the circulation system if applied intravenously compared to subcutaneous application.
Furthermore, a toxins effectiveness does not prove identical for all victims. The relative
non-susceptibility or, more precisely, a decreased susceptibility to venom exists within related
groups of snakes. Conversely, snake venom is phylogenetically formed for maximum effect
in relation to potential prey and hunting methods. For example, venom toxins of tree-dwelling
colubrids are highly effective on birds, whereas a vipers venom works well on small rodents,
etc. The venom of the African boomslang (Dispholidus typus) is lethal to a pigeon, starting
from a dose of 0.0002 mg, while the equivalent dose for a mouse weighing 100 g is 0.8 mg.
The role of venom does not only involve safe and fast paralyzation, immobilization, or
killing of prey, the proteolytic components within the venom also ensure enzymatic
destruction of tissue shortly following injection, thus facilitating the subsequent process of
digestion.
In general, the effect of venom is identical in both animals and humans. Neurotoxicity is
displayed by muscular paralysis, kallikrein enzymes and other vasodilation components
produce hypotension, and hemocoagulation affecting substances by hemocoagulation
dysfunction. Nevertheless, dissimilarities in action exist, determined by the quantity of toxins
in relation to the weight of the victim. The most potent neurotoxins present in the venom of
mambas (Dendroaspis) are capable of paralyzing small prey practically immediately, while
for humans the process of envenoming proceeds successively from the dysfunction of cranial
nerves to the main effect on respiratory muscles in the order of several dozen minutes.
Neurotoxins of some viperids (Viperidae), for example the Russels viper (Daboia
russelli) or the South American rattlesnake (Crotalus durissus terrificus), which are partly
responsible for killing prey and immobilization, are usually displayed in humans by
insignificant dysfunction in the area of cranial nerves, and any such effect may not be at all
apparent. The most distinct difference in action of a dose of toxin, depending on weight of the
victim, can be seen in venoms with an effect on hemocoagulation. The majority of them cause
prey to die immediately from hemocoagulation due to their remarkable prothrombotic
potency. However, some of the essentially prothrombotic enzymes in venom stimulate
pathophysiological processes, which will, on the contrary, result in either eventual increased
hemorrhage or death by exsanguination. This mechanism of action presents one of the main
causes for morbidity and mortality in humans when envenomed by snakes, for example,
following a snakebite by the Echis viper, which practically never happens when hunting in
the wild.

3.3. CLASSIFICATION OF SNAKE VENOMS AND THEIR EFFECTS

3.3.1. Classification by Type, Site, and Severity of Envenoming

The type of effects of toxin and human envenoming can be outlined depending on
localized or the systemic level of symptoms and their severity. This way, results in terms of
32 Jiri Valenta

the general destructive effect of venom components on tissues can be differentiated from
specific effects on particular systems. The destruction caused by enzymes and toxins will be
expressed by damage at either a localized (i.e. necrosis) or systemic level, such as
myonecrosis, damage to the capillary system with subsequent extravasation, hypotension, and
shock. Systemic specific damage then principally involves neural tissue, neuromuscular
junctions, conductive apparatus of the heart and myocardium, platelets, the plasma
coagulation system, effects on renal structures, etc.
With this in mind, the three basic types of envenoming that follow can be identified:

Type 1: Enzymatic type. Largely with local symptoms, tissue damage, extra vascular
transfers of water, and the development of edema, as well as hypotension, even shock.
Symptoms are largely subject to the actions of enzymes.
Type 2: Toxin type. This brings about a systemic effect, which is predominantly more
serious, with minor local traces. Symptoms are largely subject to actions of toxins.
Type 3: Combined type. Both localized and systemic effects are distinguishable, with
either the former or latter dominating depending on the case in question. Symptoms are
determined by the action of both enzymes and toxins. Unfortunately, neither the severity of
envenoming nor the nature of the damage, i.e. toxin effect, can be evident from this
classification method.

3.3.2. Classification by Systemic Effect and Symptoms of Envenoming

In most cases, toxins and, consequently, in part the clinical symptoms of envenoming can
be differentiated according to the system they affect. The severity of envenoming is
determined by the level of influence, damage to failure of organs or systems. In addition,
using this key to categorize toxins has its advantages. One type of a toxin can often contribute
towards damage to several systems. Phospholipase A2 (PLA2), the isoenzymes which damage
various tissues, systems, and organs, serves as an example. Due to its enzymes that can act,
for instance, as presynaptic neurotoxins, results show locally destructive activities, damage to
endothelium, and the exertion of a number of other activities.
However, a single clinical system or organ can be affected and caused detriment to by a
number of types of toxins of a different nature and method of effect; examples include venom
components that affect the cardiovascular apparatus by acting on the conductive apparatus of
the heart, myocardium, vessel resistance, and vessel wall integrity. They do so via totally
diverse biochemical and pathophysiological mechanisms, starting with dysrhythmia and
extending to extravascular hypotension.

3.3.2.1. Venom Components with Localized Effects

The snake venom substances that act locally are principally of enzymatic type. Their
destructive action does not specifically target certain types of tissues, but it tends to focus on
molecules forming such tissues. Protein-degrading enzymes, i.e. proteolytic enzymes, are
referred to as proteinases (proteases), with representatives classified depending on the nature
of the active centre of the enzyme: aspartate, cysteine and serine proteinases, and
metalloproteinases. Endopeptidases destruct proteins by lysis of inner peptide chains, while
exopeptidases degrade the ends of the peptidic chains. Other hydrolytic enzymes in snake
 Snake Venoms 33

venom include those that cleave lipids, phospholipids, saccharides, polysaccharides, and
nucleic acids. Hyaluronidases (hyases) are enzymes that contribute towards destroying
mucopolysaccharide components of tissues through hydrolysis.
Other components with a localized effect include a number of PLA2 forms, hemorrhagins
of variable enzymatic and non-enzymatic contents, and myotoxins. However, the action of
such components involved in effects of the most severe localized type often becomes
widespread, resulting in the development of primary intravascular hemolysis via the
destruction of erythrocyte walls, damage to endothelium, including extravasation, and deep
myolysis.
Locally acting enzymes chiefly cause intradermal bleeding, damage to tissue and necrosis
within the bitten site, just like necrotoxins do, but they impact in a general way too, i.e.
myodestruction, myoglobinuria, renal failure, extravasation and hemorrhaging . A varying
quantity of these enzymes is present in virtually any venomous snake, with a clinically
significant concentration in venoms of viperid snakes (Viperidae), i.e. members of Bitis,
Daboia, Echis, and Macrovipera genera, and also the Crotalinae subfamily, namely the
Crotalus genus. In addition, localized effects of venoms are caused by some elapid snakes
(Elapidae), for instance several cobras of the Naja genus. Furthermore, localized detriment
can be also caused by cytotoxic polypeptides without enzymatic activity.

Types of Enzymes with Localized Effects - Examples:

* Alanin aminotransferase, L-alanin molecule degradation.
* Phospholipases, phospholipid-destructing hydrolases, e.g. phospholipase A2 (PLA2).
* Acetylcholinestherase, acetylcholine-degrading hydrolytic enzymes.
* Alcalic and acid phosphatase, phosphoester decomposition.
* 5-nucleotidase, 5-ribonucleotide destruction.
* Phosphodiesterase, 5-nucleotide elimination from oligonucleotide molecules.
* Desoxyribonuclease and ribonuclease, cleavage of DNA and RNA.
* Hyaluronidase, cleavage of hyaluron acid and its salts contained in tissues.
* Non-specific proteases, hydrolysis of casein, hemoglobin, and gelatine molecules.
* Elastase, hydrolysis of elastin.
* Hemorrhagic proteases, collagen destruction.
* Collagenases, collagen proteolytic degradation.

3.3.2.2. Venom Components with Neurotoxic Activities

In most cases, neurotoxins cause a reversible effect on neuromuscular transmission,
which is exhibited by progressive muscular paralysis. The symptoms of muscular paralysis
primarily start in the region of the cranial nerves with ptosis, ophtalmophlegia, hazy or double
vision, dysarthria, dysphagia featuring increased salivation, and facial muscle weakness.
In more serious cases, a weakness in limbs and loss of deep tendon reflexes spread, most
severely resulting in paralysis of respiratory muscles. In some cases, the onset of neurotoxic
symptoms has been recorded after just several minutes, but in others 6-10 hours following a
bite. Death caused by suffocation under full consciousness will ensue unless respiratory
support is offered. Several neurotoxins may also have a local anesthetic effect, revealed
through paralysis of sensitive nerves at the wound.
Neurotoxins form a significant portion of venom in elapids (Elapidae). In that of other
families, these components are present in a lesser quantity and have a considerably reduced
34 Jiri Valenta

effect. In vipers (Viperinae), neurotoxins bearing a clinically apparent effect are found in the
Russels viper (Daboia russelli), common viper (the Vipera berus bosniensis subspecies), asp
viper (Vipera aspis), and others. As for Crotalinae members, a significant neurotoxic activity
has been reported from the South American rattlesnake (Crotalus durissus terrificus).
Generally, two basic types of neurotoxins - presynaptic and postsynaptic - are recognized.
The majority of neurotrophic components in snake venom are grouped under one of these.

Presynaptic Neurotoxins
Presynaptic neurotoxins may partially be responsible for the disorder of conduction, or
transmission of impulses on neuromuscular end-plates in particular, but presumably on other
types of neural connections as well.
PLA2 are the main type of presynaptic neurotoxins. The mechanisms of all presynaptic
effects of neurotoxins still have not been fully explained. They include blocking potassium,
sodium, and calcium channels of the terminal axon, as well as damage to or destruction of the
axon, with the resultant release of acetylcholine (ACh) from neural endings and its
subsequent absence, including disorder or complete blocking of transmission, which might
even be irreversible.
In most cases, the onset of symptoms will be delayed; they rarely occur sooner than 1 to 2
hours after a snakebite. The developing symptoms of the effect of toxins cannot be influenced
by an antivenom; they will only abate after some time based on the repair of relevant terminal
axons. Considering the possible irreversibility of damage to these structures, it is important
that antivenom is administered promptly, before any clinical manifestation of the symptoms.
Typical presynaptic neurotoxins will not cause fatal muscular paralysis with subsequent
elimination of respiratory muscles, but only affect cranial nerve muscles, triggering the
relevant symptoms and general muscle weakness. It is possible that the effect of these toxins
is also a factor in certain vegetative symptoms from envenoming by viperid snake (Viperidae)
venom.
Presynaptic neurotoxins do not form any major component of neurotoxins in the venoms
of coral and sea snakes, whilst in viperids these neurotoxins mostly present a single venom
component of neurotoxic importance. Certain exceptions exist, involving the Russels viper
(Daboia russelli), South African mountain adder (Bitis atropos), South American rattlesnake
(Crotalus durissus terrificus), and some of the Asian moccasins (Gloydius), as a certain
amount of postsynaptic -neurotoxin has been isolated from the venoms of these snakes as
well.
Fasciculins can be ranked among the neurotoxic components of snake venom that also
act presynaptically. These are acetylcholinesterase (AChE) inhibitors, thus increasing the
quantity of available ACh on a neuromuscular end-plate, which results in muscular
fasciculations; contractions like these do not seem to possess any paralyzing effect, although
they can potentiate the effect of certain presynaptic neurotoxins. These components are
contained in the venoms of some coral and sea snakes, including the black and green mamba
(Dendroaspis polylepis, D. viridis), but not the Jamesons mamba (D. jamesoni).
Presynaptic effects can be observed in dendrotoxins of the mamba (Dendroaspis sp),
although with use of a different kind of mechanism. By blocking potassium channels, these
substances cause a surplus of available ACh, permanent depolarization, elimination of a
neuromuscular end-plate and muscular paralysis. Their effect is boosted by the
anticholinesterase action of fasciculins.
 Snake Venoms 35

Enzymes with a Presynaptic Effect or Enzymes where Such Effect is Predominant -

Examples:
* Acanthoxin (AcTX), neurotoxic PLA2 isolated from the venom of the common death
adder (Acanthophis antarcticus).
* Agkistrodotoxin (AgkTX), neurotoxic PLA2 isolated from the venom of the Halys pit
viper (Agkistrodon halys).
* Ammodytin, neurotoxic PLA2 from the venom of the nose-horned viper
(Vipera ammodytes).
* Ammodytoxin (AmTX), neurotoxic and myotoxic PLA2 isolated from the venom of the
nose-horned viper (Vipera ammodytes) and Russels viper (Daboia russelli).
* Bungarotoxin (BgTX-), neurotoxic PLA2 from venoms of kraits (Bungarus sp.).
The toxin causes a presynaptic block of neuromuscular end-plates by inhibiting the release of
ACh on the neuromuscular end-plate.
* Caudoxin (Caudotoxin, CDX), neurotoxic PLA2 isolated from venoms of the Russels
viper (D. russelli) and Africas horned puff adder (Bitis caudalis).
* Crotoxin, a PLA2-containing protein complex; a substance with neurotoxic, hemolytic,
and necrotizing effects, affecting the release of ACh on the neuromuscular end-plate. Isolated
from the venom of the South American rattlesnake (Crotalus durissus terrificus).
* Daboiatoxin (DbTX), neurotoxic PLA2 isolated from the venom of the Russels viper
(Daboia russelli).
* Dendrotoxins (DTX), a series of toxins isolated from mamba (Dendroaspis sp.) venoms
in form of small protein molecules blocking voltage-controlled potassium channels in
neurons. The DTX I subtype of the black mamba (D. polylepis) belongs to the most efficient
venoms at all.
* Calciseptin, a highly efficient toxic neuropeptide, a selective blocker of L-type Ca2+
channels, isolated from the venom of the black mamba(D. polylepis).
* HTe and HTg toxins, neurotoxic PLA2 isolated from the venom of the mainland tiger
snake (Notechis scutatus).
* Mojave toxin (MoTX), neurotoxically acting PLA2 that exists in all neurotoxic
rattlesnakes of the Crotalus genus.
* Notexin (NoTX), neurotoxic PLA2 and anticoagulation PLA2 isolated from the venoms
of the Russels viper (Daboia russelli) and the mainland tiger snake (Notechis scutatus).
* Paradoxin (PDX), PLA2 with neurotoxic and coagulation effects isolated from venoms
of the coastal taipan (Oxyuranus scutellatus) and inland taipan (O. microlepidotus).
* Pseudexins (PsDX-A,-B,-C), a complex of isoenzymes of neurotoxic PLA2 isolated
from the venom of the red-bellied black snake (Pseudechis porphyriacus).
* Taipoxin (TaXn), a toxin with a strong neurotoxic PLA2-like and coagulation effect. It
prevents ACh to release from cholinergic nerve endings of the neuromuscular end-plate. The
toxin was isolated from the venom of the coastal taipan (Oxyuranus scutellatus).
* Textilotoxin (TeTX), a complex of toxins possessing a coagulation, hemodestruction
and thrombin-activating effect. Presynaptic neurotoxicity is also involved. Isolated from the
venom of the eastern brown snake (Pseudonaja textilis).
* Trimucrotoxin, neurotoxic and myotoxic PLA2 isolated from the venom of the brown-
spotted pit viper [Protobothrops (formerly Trimeresurus) mucrosquamatus].
36 Jiri Valenta

Postsynaptic Neurotoxins
Postsynaptic neurotoxins (-type) bind with high affinity to the -subunits of
neuromuscular end-plate nicotinic cholinergic receptors, where they competitively inhibit
ACh, through which they bring about a curare-like form of blocking and muscular paralysis
affecting striated muscles. The molecule of these neurotoxins is relatively small, which
facilitates the speed of penetration and distribution into the circulation following the bite. The
onset of the effect is more rapid compared to presynaptic toxins, which sometimes require
several minutes but often 30 minutes to 2 hours. The progress and lethality of the envenoming
is more severe due to a paralyzing effect on striated muscles, i.e. respiratory muscles. The
effect of postsynaptic neurotoxins is reversible and can be controlled by antitoxins, even in
cases of insufficient immunogenicity, which could be explained by molecular size. In
addition, a therapeutic effect can be reached by increasing the amount of ACh by
administering AChE inhibitors, such as neostigmin.
Biochemically, postsynaptic neurotoxins are classified in two groups according to
molecular size - short chain (60-62 amino acids) and long chain (70-74 amino acids) toxins.
Another type of toxin with postsynaptic action involves kappa neurotoxins that can block
acetylcholine receptors of neuronal transmission, which largely affects vegetative functions.
Postsynaptic neurotoxins make up the main functional part of venom in coral and sea
snakes. Only rarely are they found in small quantities in venoms of some viper and
rattlesnake species; see presynaptic neurotoxins.

Toxins with a Postsynaptic Effect or Toxines where Such Effect is Predominant -

Examples:
* Bungarotoxin (BgTX-), a neurotoxin from krait (Bungarus sp.) venoms. Causes
postsynaptic blocks of neuromuscular end-plates.
* Dendroaspin, a neurotoxin found in the venom of the Jamesons and green mamba
(Dendroaspis jamesoni and D. viridis, respectively).
* Erabutoxins (ErTX-A,-B,-C), postsynaptic nACh (nicotinic cholinergic receptor)
blockers isolated from the venom of Laticauda semifasciata, a sea krait species.
* Hannalgesin, a neurotoxin of the king cobra (Ophiophagus hannah) with analgesic
effects that can be blocked using Naloxon.
* -cobrotoxin (neurotoxin 3), an effective blocker of nicotinic ACh receptors on
neuromuscular end-plates. Isolated from the venom of the Indochinese spitting cobra (Naja
naja siamensis).

3.3.2.3. Venom Components with Effects on the Cardiovascular Apparatus

Substances affecting the cardiovascular apparatus comprise a relatively diverse range of
toxin and enzyme types, with varying target areas as well. Toxins decrease or conversely
increase vessel resistance, thus modifying systemic pressure, and affect heart function -
frequency, rhythm, myocardial contractility, and heart output.
Vasodilation is probably caused by both direct action of toxins on the vascular system
and the release of kinin-based hypotensive substances into the circulation, which result in
declining peripheral vessel resistance and hypotension, but in severe cases even circulation
collapse and shock. The decrease in pressure and the shock status is partially caused by,
amongst other things, damage to vascular epithelium at an endothelial level, endothelial
 Snake Venoms 37

junctions, and basal membrane, which is made manifest by extravasation of liquids, both at a
localized and systemic level. The mechanism, as well as a possible hemorrhaging, will greatly
potentiate the occurrence of circulatory failure including tissue and organ perfusion disorder,
with the symptomatology of capacity shock.
Since toxins damaging the integrity of vessel walls - hemorrhagins - affect at the same
time a number of other systems, they are covered by a separate chapter despite their crucial
role in potential fatal circulatory failure.
The venoms of burrowing asps (Atractaspis), contain sarafotoxins, substances increasing
vessel resistance and decreasing heart output. Other toxins from burrowing asp venom cause
coronary vasoconstriction, and ultimately bring on spasm, as well as changes in ECG
(electrocardiogram) in terms of ST-segment elevation and AV-blocking (disorder of the atro-
ventricular conduction in the heart), temporarily increasing myocardial contractility.
Specific substances affecting the heart occur as cardiotoxins in the venom of the cobra
(Naja). Similar toxins are contained in that of the Gabon and rhinoceros vipers (Bitis
gabonica and B. nasicornis, respectively). These toxins can cause rhythm and contractility
disorders, a temporary increase in coronary flow, with a subsequent loss in coronary and
systemic vessel resistance, and they can even cause direct damage to cardiac muscle.
Cardiotoxic action, in terms of decrease in myocardial contractility, constriction of coronary
flow, and decrease in systemic pressure, can be assigned to tumor necrosis factor (TNF) as
well as other cytokines released under envenoming by venoms of certain viperid species
(Viperidae), with examples including the asp viper (Vipera aspis).
Toxins, more particularly enzymes decreasing peripheral vessel resistance, thus systemic
pressure, are contained in the toxin range of the majority of viperids (Viperidae), which
specifically concerns Crotalinae snakes. Amongst others, these toxins were isolated from the
venom of Bitis snakes of Africa. This involves kallikrein-like enzymes, collectively referred
to as kinin or bradykinin releasing enzymes, which are obviously the most important cause of
hypotension occurrence beyond extravasation and hemorrhaging . Bradykinin stimulates
vascular endothelium to produce nitric oxide (NO), a substance that exerts significant
vasodilation activity via action on the cells of a vessel walls smooth muscles. The highest
values of bradykinin-releasing activity were found in the venoms of the Northern Pacific and
western diamond-backed rattlesnakes (Crotalus viridis or C. atrox, respectively), and the
Gabon (Bitis gabonica) and nose-horned vipers (Vipera ammodytes). In venoms of elapids,
kininogenases are only represented marginally or not at all. The highest level of activity has
been recorded in the venom of the Chinese cobra (Naja atra).
Except for the enzymes above, the participation of other peptides acting at other levels,
such as centrally, is presumed to occur.

Examples of Toxins and Enzymes with Effects on the Function of Heart and Vascular
Apparatus:
* Angiotensin converting enzyme inhibitors (ACE), present for instance in venoms of
lanceheads (Bothrops sp.). They can cause an acute hypotension by blocking conversion of
angiotensin I to angiotensin II, and by decreasing degradation of bradykinin that is cleaved by
ACE as well.
* Kallikrein-like kinin-releasing enzymes, for example a bradykinin potentiating factor,
are contained in venoms of certain vipers (Viperinae) and rattlesnakes (Crotalinae).
38 Jiri Valenta

* Cobrotoxins (Cbt), components of venoms of the cobra (Naja) and other coral snake
genera; they include a cardiotoxin with arrhythmogenic effects reducing myocardial
contractility.
* Sarafotoxins (Srt), vasoconstricting peptides increasing systemic vascular resistance
and reducing heart output. A part of venoms in burrowing asps (Atractaspididae).
* TaiCatoxin (taicatoxin, TCX); a complex of toxins blocking Ca2+ channels of excitable
membranes, for example in the heart. This toxin with a PLA2 activity is contained in the
venom of the coastal taipan (Oxyuranus scutellatus).
* HTe toxin that exists in the mainland tiger snake (Notechis scutatus) and black tiger
snake (N. ater), a protein with a PLA2 activity causing hypotension, etc.

3.3.2.4. Venom Components with Effects on the Vessel Wall

Vessel wall and function affecting toxins and enzymes are collectively termed
hemorrhagins. They cause endothelial damage in form of swelling or even desquamation, and
disorders to endothelial junctions. They could prove the reason for disruption of collagen
fibrils, damage to vessel basal membrane, and myonecrosis. The actions mentioned above
will result in vessel integrity disorders, largely manifesting themselves by extravasation in the
capillary area, i.e. leakage of liquids, ions, and later even plasmatic proteins and blood
elements outside the bloodstream. Clinical symptoms include edema that is mostly visible in
the hypodermis of the affected area and, in the case of increased activity or a higher quantity
of toxins, edema of the pulmonary interstitium with symptoms of acute pulmonary failure of
the ALI/ARDS type (acute lung injury / acute respiratory distress syndrome). A more severe
effect on vascular integrity will cause leakage of erythrocytes outside the bloodstream. In
cases of mild exposure, only local hemorrhaging occurs along with petechiae, ecchymoses,
and hemorrhagic vesicles, or combinations with the leakage of liquid, producing a
hemorrhagic edema in the body part affected. If exposure is higher, severe hemorrhaging is
manifest on mucous membranes and gums, in addition to near the bite wounds, whilst
bleeding into the gastrointestinal tract or brain will also occur.
In certain hemorrhagins, even direct hemocoagulation activities may occur that will
inhibit or conversely activate aggregation of blood platelets and possess a fibrinolytic effect.
The indirect impact of hemorrhagins on the hemocoagulation system involves endothelial
cell function disorders and disintegration, and exposure of or damage to the collagen and
basal membrane. For example, a tissue plasminogen activator (tPA) can be released, and
fibrinolysis increased. Over the acute phase of the action, hemorrhagins will not primarily
display procoagulation activities, nonetheless, as the envenomation proceeds, any
procoagulation and prothrombotic effect upon the abatement of increased fibrinolysis and
inhibiting action on platelets cannot be precluded due to damage to endothelium and sub-
endothelial structures.
Due to leakage of liquids from the vascular system and hemorrhaging, as well as by
stimulating endothelium to produce vasoactive mediators (NO, PGI2), hemorrhagins play a
great part in triggering hypotension, circulatory failure, and shock.
The majority of isolated hemorrhagins belong to a group of rather non-specific
proteolytic zinc-containing enzymes - Zn metalloproteases. They are usually classified as two
main groups according to molecular size and mechanism of effect. Typically, the first group
with a lower molecular weight (20-25 kDa) will have hemorrhagic and fibrinogen-degrading
 Snake Venoms 39

properties, while the other, possessing a larger protein molecule (50-90 kDa), will often have
desintegrin properties - it inhibits platelet aggregation.
Hemorrhagins are contained in the venom of most viperid snakes (Viperidae), burrowing
asps (Atractaspididae), as well as those of some Australian terrestrial elapid snakes.
Hemorrhagins isolated from various kinds of snake venoms are mostly termed on a basis
of specific hemorrhagic activity when applied intradermally in the black rat. Naturally, one
creature cannot fully express their systemic hemorrhagic effectiveness in the circulation as
experienced by diverse animal species, which is due to wide species-specific variability
concerning the representation of plasma protease inhibitors that exist in vertebrates. In most
cases, non-specific metalloproteases can be expected to act locally; however, they are
immediately inhibited in circulation by plasma inhibitors. That is why it is not fully clear as to
what extent hemorrhagins are responsible for symptomatology of diffusion microvascular
bleeding accompanied by heavy envenomation by the venom of viperids (Echis, Daboia,
Bothrops) or boigas (Dispholidus, Thelotornis). The auto-aggressive action of inflammation
mediators and, in particular, that of the coagulation enzymes like thrombin and plasmin, being
explosively attacked by specific venom proteinases, is likely to play a more important role in
this circumstance than the action of non-specific venom proteases.

Examples of Toxins Affecting the Vascular Wall:

* Ac1 5, AaH I-III; arrays of hemorrhagic metalloproteases from the venom of the
Chinese moccasin (Deinagkistrodon acutus).
* BaH 4, a hemorrhagic metalloproteinase isolated from the venom of Bothrops atrox
asper (B. atrox).
* Bothropasin, a hemorrhagic metalloproteinase from the venom of the jararaca
(Bothrops jararaca).
* Crotalotoxin, a toxin with hemorrhagic, myolytic, fibrinolytic and neurotoxic properties
isolated from the venom of Crotalus durissus vegrandis.
* Hemorrhagic factors (HF), metalloproteases from venoms of the Israeli mole viper
(Atractaspis engaddensis), jararaca (Bothrops jararaca) and brown spotted pit viper
[Protobothrops (formerly Trimeresurus) mucrosquamatus].
* HP IV, a hemorrhagic metalloproteinase with a fibrinolytic activity isolated from the
venom of the timber rattlesnake (Crotalus horridus).
* HR I, II, arrays of hemorrhagic metalloproteinases with fibrinolytic activities isolated
from venoms of the habu [Protobothrops (formerly Trimeresurus) flavoviridis] and the
common bamboo viper (T. gramineus).
* HT a, b, c, d, e, f, g, 1, 2, 3, hemorrhagic metalloproteinases isolated from venoms of
the western diamond-backed rattlesnake and red-diamond rattlesnake (Crotalus atrox and C.
ruber, respectively), and also from those of the mainland tiger snake (Notechis scutatusi) and
the black tiger snake (N. ater).
* ICPP (increasing capillary permeability protein), a protein isolated from the venom of
the Levantine viper (Macrovipera lebetina) with hemorrhagic properties.
* Jararhagin, a metalloproteinase with a hemorrhagic effects and anti-aggregation as
well as fibrinolytic properties isolated from the venom of the jararaca (Bothrops jararaca).
* Moojeni protease A, a metalloproteinase from the venom of the Brazilian lancehead
(Bothrops moojeni).
40 Jiri Valenta

* Mutalysin II, a hemorrhagic metalloproteinase isolated from the venom of the South
American bushmaster (Lachesis muta).
* Mucrotoxin A, one of the hemorrhagic metalloproteinases from the venom of the brown
spotted pit viper [Protobothrops (formerly Trimeresurus) mucrosquamatus].
* Proteinase H, a metalloproteinase from the venom of the eastern diamond-backed
rattlesnake (Crotalus adamanteus).
* Rhodostoxin (RhTX), a hemorrhagic toxin isolated from the venom of the Malayan pit
viper (Calloselasma rhodostoma).

3.3.2.5. Venom Components with Effects on Hemocoagulation

Snake venoms contain a number of toxins and enzymes affecting the function of the
hemocoagulation system - hemostasis. They interfere with the majority of processes in the
plasma coagulation system (PCS), moreover, they have an impact on the functioning of
platelets (PLT) as well as that of endothelium. The damage to endothelial and sub-endothelial
function and morphology, which has an essential impact on hemocoagulation disregulation, is
mentioned in the previous chapter covering hemorrhagins. The PCS and PLT functions can be
affected in terms of both procoagulation and anticoagulation. The outcome is pre-determined
specifically by the type of the toxin, but also by the level of exposure or pathophysiologic
changes depending on the duration since the beginning of an envenoming. For such reasons,
splitting the hemocoagulation-affecting toxins into groups according to the targeted point of
their effect may prove more acceptable than by eventual effect.
Clinically, the effect of hemocoagulation toxins in humans will largely be manifest as
hemorrhaging, even though in a hunted animal, a number of components will cause
widespread acute thrombotization, which is solely pre-determined by the quantity of toxins
related to the size of the prey. Again, disregulation of hemocoagulation proceeds subject to
the dose and effectiveness of the venom, from mere laboratory abnormities like
hypofibrinogenemia, prolonged PT (prothrombin time), APTT (activated partial thrombin
time), TT (thrombin time), and RT (reptilase time), and an increase in FDP (fibrin degrading
products) as far reaching as profuse and unmanageable bleeding from traumas, mucous
membranes and into organs, which in a number of cases will eventually result in death and
largely caused by DIC-like disorders with a great portion of hyperfibrinolysis. Toxins with
hemocoagulation activity are probably responsible for the majority of fatal cases of
envenomation by snake venoms around the world, largely those of Echis and Daboia snakes.
Hypercoagulation and thrombotic symptoms of envenoming will first manifest
themselves in laboratory findings by shortening coagulation periods, decreased AT
(antithrombin III) activity, and an increase in D-dim (D-dimer fibrin degradation product) to
high pathologic values. Even clinical symptoms of thrombotization or microthrombotization,
such as in bloodstream of the brain, mesenteric and coronary vessels, are nothing exceptional.
Hemocoagulation toxins are found in most venomous snakes, typically boigas
(Dispholidus and Thelotornis), but also vipers (Viperinae) of the Atheris, Bitis, Daboia,
Echis, and Macrovipera genera, and Crotalinae members, e.g. Bothrops, Lachesis,
Agkistrodon, Crotalus, and Trimeresurus genera. They are also inherent in the venom of
Australian terrestrial elapids, sea snakes and sea kraits, as well as that of some Naja cobras.
Hemostasis as such is determined by the action of toxins on diverse structures of the
hemocoagulation system.
 Snake Venoms 41

Venom Components with Effects on Platelets

The impact on the function of PLT is mostly determined by the action of the toxin on
either the surface activating structures of platelets or von Willebrands factor (vWF).
Inhibition of platelet aggregation is caused by enzymes of PLA2, fibrinogenase, nucleotidase,
ADPase (adenosine diphosphatase), and L-amino-acid-oxidase types and non-enzymatic
toxins. A number of enzymes, largely these of PLA2 type, have a pro-aggregating and
agglutinating effect on platelets as well, in addition to non-enzymatically acting components.
A considerable quantity of venom components determining the function of PLT has been
isolated, which largely belong to viperids (Viperidae).
Naturally, changes in the function, i.e. adherence of platelets, can be also triggered or
potentiated by activation at the site of damage on the vessel wall and exposure of collagen to
the basal membrane, both at a localized and systemic level. In laboratory findings, such a
status will be manifest by a higher or lower level of thrombocytopenia.

Examples of Enzymes and Toxins Affecting Platelets:

* PLT aggregation enzymatic inhibitors, isolated from venoms of the Halys pit viper
(Gloydius halys), Russels viper (Daboia russelli), asp viper (Vipera aspis), Palestine viper
(Macrovipera palestinae), eastern diamond-backed rattlesnake (Crotalus adamanteus),
Chinese moccasin (Deinagkistrodon acutus), Asian pit viper (Calloselasma rhodostoma),
brown spotted pit viper [Protobothrops (formerly Trimeresurus) mucrosquamatus], common
bamboo viper (T. gramineus), and black-necked spitting cobra (Naja nigricollis).
* Applaggin, a protein PLT inhibitor from the venom of the western cottonmouth
(Agkistrodon piscivorus).
* Arietin, bitistatin, a protein PLT inhibitor from the venom of the African puff adder
(Bitis arietans).
* Cardiotoxin (CTX), a protein PLT inhibitor from the venom of the black-necked
spitting cobra (Naja nigricollis).
* Carinatin and echistatin, peptide PLT inhibitors from the venom of the saw-scaled
viper (Echis carinatus).
* Desintegrin, a common name for antagonists of surface glycoprotein PLT receptors
preventing platelet activation, adhesion and aggregation (arietin, bitistatin, gabonin,
jaracetin, etc.).
* Lebetins, PLT aggregation inhibitors from the venom of the Levantine viper (Vipera
lebetina).
* Enzymatic PLT aggregation activators, isolated from venoms of the saw-scaled viper
(Echis carinatus), timber rattlesnake (Crotalus horridus), common lancehead (Bothrops
atrox), southern copperhead (Agkistrodon contortrix) and brown spotted pit viper
[Protobothrops (formerly Trimeresurus) mucrosquamatus].
* Aggregoserpentin, a protein PLT aggregation activator isolated from venoms of the
brown spotted pit viper [Protobothrops (formerly Trimeresurus) mucrosquamatus], common
bamboo viper (T. gramineus), and Asian pit viper (Calloselasma rhodostoma).
* Bitiscetin; evokes PLT agglutination through binding to vWF. Isolated from the venom
of the African puff adder (Bitis arietans).
* Convulxin, a protein PLT aggregation activator isolated from the venom of the South
American rattlesnake (Crotalus durissus).
42 Jiri Valenta

* Mamushigin, a platelet glycoprotein causing PLT aggregation, obtained from the

mamushi (Gloydius blomhoffii).
* Triwaglerin, a protein PLT aggregation activator isolated from the venom of the
Waglers palm viper (Trimeresurus wagleri or Tropidolaemus wagleri).

Venom Components with Effects on the Contact Path of Hemocoagulation

Activation.
Viperid snake (Viperidae) venoms contain kallikrein-like proteases that may activate
FXII, thus the contact pathway of the hemocoagulation system.

Venom Components Activating Prothrombin

The end result of PCS stimulation with an increase in thrombin activity is caused by
either activation of coagulation factors, mostly FV and FX, or direct intervention on the
prothrombin molecule and its modification to become an active thrombin-like molecule. Such
an action has a procoagulation effect with eventual consumption and exhaustion of the
hemocoagulation system and clinical DIC-like bleeding symptoms.
The FV and FX activators have been isolated from the venom of the Russels viper
(Daboia russelli), Levantine viper (Macrovipera lebetina), desert horned viper (Cerastes
cerastes), and other species.
A metalloproteinase entitled ecarin, from the venom of the saw-scaled viper (Echis
carinatus), modifies prothrombin into an enzymatically active and physiologically non-
inhibitive meisothrombin. A similar kind of toxicity is a feature of the South American
lanceheads (Bothrops sp.), as well as some colubrids (Colubridae) - the African boomslang
(Dispholidus typus) and Thelotornis kirtlandii, and the tiger grooved-neck keelback
(Rhabdophis tigrinus), an opistoglyphous snake species.
Other types of thrombin-activating enzymes include serine proteases, which function due
to the participation of phospholipids, and Ca2+, such as oscutatin, derived from the venom of
the coastal taipan (Oxyuranus scutellatus), the procoagulation protein from the venom of asp
vipers (Vipera aspis), etc.
Again, the third activator group are serine proteases, like notecarin from the venom of the
mainland tiger snake (Notechis scutatus), an Australian snake. These enzymes operate under
the presence of FV, phospholipids and Ca2+ ions.
The thrombin activity that occurs, based on the action of the serine protease types above,
can be inhibited by the heparin-AT complex.

Other Examples of Prothrombin-Activating Enzymes and Toxins:

* Afaacytin, a proteinase (, -fibrinogenase) that activates FX and other FF
(hemocoagulation factors). Isolated from the venom of the desert horned viper (Cerastes
cerastes).
* Carinactivase (CA-1), a toxin activating prothrombin depending on Ca2+ isolated from
the Romans saw-scaled vipers (Echis leucogaster) venom. Similar enzymes are found in
venoms of Daboia and Cerastes genera and other Echis species, Asian pit vipers
(Calloselasma) and lanceheads (Bothrops), where they are accompanied by the FX activator.*
Ecarin, prothrombin activator, a metalloproteinase isolated from Echis venoms.
 Snake Venoms 43

* Multactivase, a Ca2+ dependant prothrombin activator from the venom of Echis

multisquamatus.
* Textarin, a toxin activating prothrombin in the presence of phospholipids, FV and Ca2+.
Isolated from venoms of Australian snake species - the eastern brown snake (Pseudonaja
textilis) and the Demansia genus.
* VLFVA and VLFXA, FV and FX enzyme activators from the venom of the Levantine
viper (Macrovipera lebetina).
* VRV-V and VRV-X, FV and FX enzyme activators from the venom of the Russels viper
(Daboia russelli).

Venom Components Converting Fibrinogen to Fibrin

The term thrombin-like substances is lent to serine protease-like snake venom enzymes
that cleave fibrinopeptides - mostly FPA (fibrinopeptide A), from FBG (fibrinogen)
molecules, hence causing fibrinogen conversion to fibrin. It is interesting that the sequence
homology of these enzymes with thrombin is often a little bit lower than that of trypsin or
kallikrein. Therefore, the enzymes resemble thrombin, especially in terms of their fibrinogen-
converting activity. However, compared to thrombin, the substances above often lack other
thrombin properties like platelet activation, stimulation of endothelium, activation of FV,
FVIII and FXIII, stimulation of leucocytes, and others. A systemic conversion of fibrinogen
results in plasmin activation and reactive hyperfibrinolysis. Intravenous application of
purified FPA-cleaving enzymes, i.e. batroxobin from the common lancehead (Bothrops atrox)
has been tested clinically. In humans, it results in afibrinogenemia without systemic
endothelial damage and developed multi-organ disfunction. Naturally, afibrinogenemia is
associated with symptoms of hemorrhaging even from minor traumas, as well as the erosion
of mucous membranes.
In addition, certain enzymes that preferentially cleave FPB can probably induce
endothelial damage. The activity of such enzymes can be described as of procoagulative type
- generally, it cannot be influenced by physiological thrombin inhibitors. It may eventually
result in clinical symptoms like those of the DIC syndrome, with hypercoagulation,
microangiopathic hemolysis, and subsequent bleeding. The enzymes are contained in the
venom range in viperids (Viperidae), which largely relates to the Crotalinae subfamily
members, but is even visible in the African boomslang (Dispholidus typus) - a colubrid snake.

Examples of Thrombin-Like Enzymes Converting Fibrinogen to Fibrin (Fibrinogen-

Converting Enzymes):
* Acutin, an FBG-converting enzyme from the venom of Chinese moccasin
(Deinagkistrodon acutus).
* Batroxobin (BaXb), an FBG-converting enzyme cleaving FPA from FBG. Obtained
from the venom of the common lancehead (Bothrops atrox).
* Bilineobin, a thrombin-like proteinase isolated from the venom of the cantil
(Agkistrodon bilineatus).
* Cerastobin, an FBG-converting enzyme from the venom of the desert horned viper
(Cerastes cerastes).
* Clotase, an FBG-converting enzyme from the venom of the South American
bushmaster (Lachesis muta).
44 Jiri Valenta

* Crotalase (CrTA), an FBG-converting enzyme from the venom of the eastern diamond-
backed rattlesnake (Crotalus adamanteus).
* Flavoxobin, an FBG-converting enzyme cleaving FPA, isolated from the venom of the
brown spotted pit viper [Protobothrops (formerly Trimeresurus) mucrosquamatus].
* Gabonase, an FBG-converting enzyme cleaving FPA as well as FPB, isolated from the
venom of the Gabon viper (Bitis gabonica).

Venom Components Degrading Fibrinogen and Fibrin

Fibrinolytic and fibrinogenolytic activities of snake venoms stem from the enzymatic
action of proteinases on fibrinogen or fibrin. Depending on the primary point of effect on
fibrin and fibrinogen chains, -fibrinogenase and -fibrinogenase are differentiated. The
clinical symptomatology response to these substances involves increased bleeding from
wounds and symptomatology of hypofibrinogemia or even afibrinogenemia with FDP
elevation. Unlike fibrinogen-converting enzymes, the fibrinolytic and fibrinogenolytic
enzymes often present proteases with low specificity. While FBG and non-stabilized fibrin
are cleaved by a wide range of snake venom proteases, any fibrinolytic activity towards
stabilized fibrin or thrombus is displayed by a few of them.
Fibrinolytic and fibrinogenolytic proteases are inherent in the venom of numerous
viperids (Viperidae), as well as some elapids (Elapidae).

Examples of Fibrinogen and Fibrin Degrading Enzymes:

* Afaacytin, and -fibrinogenase that activates FX and other factors at the same time.
Isolated from the venom of the desert horned viper (Cerastes cerastes).
* Ancrod, an FBG-cleaving serine proteinase from the venom of the Asian pit viper
(Calloselasma rhodostoma).
* Atroxase, a fibrinolytic and fibrinogenolytic enzyme from the venom of the western
diamond-backed rattlesnake (Crotalus atrox).
* Fibrolase, a metalloproteinase with a fibrinolytic and fibrinogenolytic activity, obtained
from the venom of the southern copperhead (Agkistrodon contortrix).
* Lebetase, a metalloproteinase with a fibrinolytic and fibrinogenolytic activity, obtained
from the venom of the Levantine viper (Vipera lebetina).
* Proteinase F-1, an enzyme with a fibrinolytic and fibrinogenolytic activity, obtained
from the venom of the African black-necked spitting cobra (Naja nigricollis).
* VLAF, fibrinogenase, an FBG-cleaving serine proteinase, isolated from the venom of
the Levantine viper (Vipera lebetina).

Venom Components Inactivating Antithrombin and Other Serpins

Certain enzymes are capable of cleaving AT or other plasma inhibitors of serine
proteases - serpins. Such serine proteinase - CR serpinase - was isolated from the venom of
the common night adder (Causus rhombeatus). Even though it does not possess any thrombin
or other procoagulation activity as such, this enzyme features a procoagulation action through
destroying the thrombin inhibitor.
 Snake Venoms 45

C Protein Activating Venom Components

A direct C protein activator was found in the venom of the southern copperhead
(Agkistrodon contortrix) as well as in venoms of other rattlesnakes. Once activated, the C
protein will inhibit thrombin physiologically; once eliminated, procoagulation status occurs as
a result.

Venom Components Affecting Endothelium and the Vessel Wall

Action on endothelium and the vessel wall is inseparable from the hemocoagulation and
hemostasis area. Nevertheless, the toxins and enzymes attacking endothelium and vessel
walls possess other pathophysiological activities, causing them to be described as
hemorrhagins under chapter 3. 3. 2. 4 Venom components with effects on the vessel wall.

3.3.2.6 Venom Components Affecting the Complement

Influencing the complement by snake venom components can proceed in terms of both
activation and degradation. The venom of the cobra genus (Naja sp.) contains the so-called
cobra venom factor (CVF), which is a glycoprotein that locally activates C3 and C5
complement elements. Thus, a systemic activation of the complement via an alternative route
results in hemolysis, endothelial damage and activation of other inflammatory mechanisms.
The subsequent increase in vascular permeability will not only cause edema, hypotension,
hypoperfusion as far reaching as distribution shock, but is also likely to facilitate the entry of
toxins into a victims circulation. However, complement elements are inactivated by
proteolytic enzymes largely contained in viperid (Viperidae) venom.

3.3.2.7. Venom Components Possessing a Myotoxic Activity

Substances destroying muscle cells are collectively termed myotoxins. They are
represented by two types of toxins: firstly, this involves the basic proteins of lower molecular
weight displaying no enzymatic activities - such as found the in venom of rattlesnakes
(Crotalus). The second group consists of larger proteins with the molecular weight of 12-16
kDa and enzymatic activities of PLA2 type. Myotoxins cause irreversible damage to muscular
tissue as extreme as myonecrosis. In addition to rhabdomyolysis, enzymatic myotoxins can
simultaneously exert other activities resulting from their nature. They could attack a cell
membrane and act neurotoxically, cardiotoxically, and hemolytically, moreover, they have the
ability to affect hemocoagulation and pose a risk of triggering other locally destructive
activities.
The amount of myoglobin released through the action of myotoxins may cause or
potentiate an occurrence of renal failure, especially oligoanuria. In addition, a considerable
quantity of potassium is released during the destruction of muscle cells, resulting in
hyperkalemia which may cause detriment to myocardial function.
Myotoxins are found in the venom of many viperid snakes (Viperidae); as regards the
Viperinae subfamily, this namely involves the Russels viper (Daboia russelli), while for the
Crotalinae subfamily one example is the South American rattlesnake (Crotalus durissus
terrificus). They are also present in the venom of some elapids (Elapidae), chiefly the
Hydrophiinae subfamily, e.g. Australian terrestrial elapid snakes, as well as marine snakes -
sea snakes and sea kraits.
46 Jiri Valenta

Examples of Toxins and Enzymes Possessing Myotoxic Activities:

* BAM, an enzymatic myotoxin contained in the venom of the common lancehead
(Bothrops asper).
* CAM, a low molecular myotoxin contained in the venom of the eastern diamond-
backed rattlesnake (Crotalus adamanteus).
* Crotamine, a low molecular myotoxin contained in the venom of the South American
rattlesnake (Crotalus durissus terrificus).
* Crotoxin A, B and C, enzymatic myotoxins contained in the venom of the South
American rattlesnake (Crotalus durissus terrificus).
* Myotoxin VI:5, an enzymatic myotoxin of the venom of the common sea snake
(Enhydrina schistosa).
* Notexin, an enzymatic myotoxin of the venom of the mainland tiger snake (Notechis
scutatus).
* Taipoxin , and , enzymatic myotoxins of PLA2 type in the venom of the coastal
taipan (Oxyuranus scutellatus).
* Trimucrotoxin, an enzymatic myotoxin of PLA2 activity type, with a parallel neurotoxic
effect. Isolated from the venom of the brown-spotted pit viper [Protobothrops (formerly
Trimeresurus) mucrosquamatus].

3.3.2.8. Venom Components Affecting the Kidneys

Any isolated effects of certain toxins on renal tissues, i.e. specific nephrotoxicity, have
not been explicitly documented so far, although supposedly so by some authors. Nevertheless,
the action of a number of substances of largely enzymatic type results in damage to renal
functions and the onset of acute renal failure of predominantly the oliguric type.
Firstly, pre-renal elements are responsible for affecting renal functions, like systemic
hypotension and hypoperfusion of the kidneys caused by vasodilation, extravasation, loss of
liquids through diarrhea, vomiting and hemorrhaging. The effective components of kidney-
damaging venoms include vasodilation kininogens, ACE inhibitors, hemorrhagins and
hemocoagulation-affecting substances. The occurrence of this type of renal failure can be
further assisted by insufficient or late compensation of the circulating volume, as well as
insufficient blood pressure regulation.
Severe myoglobinemia and myoglobinuria, as a result of muscular tissue destruction by
the action of myotoxin, is another cause for renal failure. Myotoxins cause nephrons capable
of obstructing and disabling, especially in circumstances of insufficient blood flow through
glomeruli and poor urine flow through tubules. In addition, phospholipases convert lecithin to
nephrotoxic lysolecithin. Moreover, the hemolysis induced by the venom is a significant
factor in developing renal failure.
A large quantity of microthrombi obturating blood flow through the glomeruli may occur
due to the action of procoagulation components in venom, especially fibrinogen-conversion
enzymes and prothrombin activators.
In addition, a destructive effect brought about by enzymes acting locally on tissues of the
kidneys, glomeruli, and tubules cannot be precluded. Acute renal tubular necrosis can be
caused by the direct action of specific nephrotoxins.
As a result of action of the particular components mentioned above, or more frequently
through their interaction, acute renal failure develops, which is reversible in most cases.
 Snake Venoms 47

However, even irreversible failure may occur if treatment is inadequate or exposure to the
venom too high; in some cases, this can be accompanied by the onset of cortex necrosis.
The substances affecting renal functions and tissue are mostly found in venom from
Viperinae and Crotalinae snakes, but also some elapids (Elapidae).

3.3.2.9. Allergenizing Venom Components

When discussing systemic symptoms of envenoming by snake venom, allergic responses
following a bite are worthy of mention. These reactions are manifest through developments of
skin changes, redness and urticaria, angioneurotic edema in the cranial region, bronchospasms
resembling an asthma attack, and even anaphylactic shock.
The main reason for such complications is the entry of extraneous high molecular
substances, largely glycoproteids and polysaccharides into the circulation. In addition, the
phenomenon of cross reactivity between snake venom components and other allergens is also
a factor for such responses developing as well. For instance, it seems that patients with an
anaphylactic reaction to the bite by European vipers Vipera berus and V. aspis are, likewise,
allergic to stings by Hymenoptera insects like bees, wasps and hornets, and that these
symptoms are mediated through IgE antigens. Thus, it cannot be precluded that exposure to
the poison following a sting by hymenoptera may cause similar sensitization to that of snakes.
An acute anaphylactic reaction following a snakebite, even though not specific and toxic,
may pose a serious threat to a victim due to the speed of the onset and severity of symptoms,
especially if associated with symptoms of hypotension and shock relating to envenoming.

3.3.2.10. Venom Components with Various Activitiesa and Non-Protein Components

Some of the symptoms not included in the groups of effects triggered by snake venom
specified above, such as headaches and dizziness, nausea, vomiting, diarrhea, etc., may be
caused by other unidentified protein or non-protein components.
Other substances contained in snake venom, such as lectins, growth factors of neural
cells, polypeptide phospholipase and proteinase inhibitors, as well as other non-protein
components like amino acids, biogenic amines, fatty substances, yellow riboflavin, simpler
organic acids and ions, do not have a specific pathological effect in the envenomation of
humans. Such substances may function to support toxin activities or to protect a snake venom
gland, or are just by-products of the venom gland metabolism.

REFERENCES
ALLOATTI, G., GATTULLO, D., DALLA VALLE, R., et al. The haemodynamic effect of
Bitis nasicornis (Rhinoceros Horned Viper) venom. Gen Pharmacol, 1991, 22, No. 1, pp.
203206.
GANAIKABAHU, B., PUSHPARAJAN, K., et al. Myonecrosis due to Russells Viper bites
in Sri Lanka. Am J Trop Med Hyg, 1994, 50, No. 5, pp. 597601.
GOLD, BS. Neostigmine for the treatment of neurotoxicity following envenomation by the
Asiatic Cobra. Ann Emerg Med, 1996, 28, No. 1, pp. 8789.
GOLD, BS., PYLE, P. Successful treatment of neurotoxic King Cobra envenomation in
Myrtle Beach, South Carolina. Ann Emerg Med, 1998, 32, No. 6, p. 736738.
48 Jiri Valenta

HRDINA, V., HRDINA, R., JAHODAR, L., et al. Prirodi toxiny a jedy. Praha : Galen,
Karolinum, 2004, pp. 174237. (in Czech)
CHIPPAUX, JP., GOYFFON, M. Venoms, antivenoms and immunotherapy. Toxicon, 1998,
36, No. 6, pp. 823846.
JANSSEN, M., MEIER, J., FREYVOGEL, TA. Purification and charakterization of
antithrombin III inactivating enzyme from the venom of the African Night Adder (Causus
rhombeatus). Toxicon, 1992, 30, No. 9, pp. 985999.
KHADWAL, A., BHARTI, B., PODDAR, B., et al. Persistent coagulopathy in snake bite.
Indian J Pediatr, 2003, 70, No. 5, pp. 439441.
KOMORI Y., NIKAI T., SUGIHARAH. Isolation and characterisation of procoagulant from
the venom of Vipera aspis aspis. Int J Biochem, 1993, 25, No. 5, pp. 761767.
KORNALIK, F. Prothrombin converting-and fibrinolytic effects of ecarin. Czech Med, 1985,
8, No. 1, p. 5154. (in Czech)
KORNALIK, F. The influence of snake venom enzymes on blood coagulation. Pharmacol
Ther, 1985, 29, No. 3, pp. 353405. (in Czech)
KORNALIK, F. Toxins affecting blood coagulation and fibrinolysis. In SHIER, WT., MEBS,
D. (Eds.), Handbook of Toxinology. New York : Marcel Dekker, 1990, pp. 683759.
LEE, SY., LEE, CY., CHEN, YM., et al. Coronary vasospasm as the primary cause of death
due to the venom of the Burrowing Asp, Atractaspis engaddensis. Toxicon, 1986, 24, No.
3, pp. 285291.
MARSH, NA., WHALER, BC. The Gaboon Viper (Bitis gabonica): its biology, venom
components and toxinology. Toxicon, 1984, 22, No. 5, pp. 669694.
MEBS, D., KORNALIK, F. Intraspecific variation in content of a basic toxin in Eastern
Diamondback Rattlesnake (Crotalus adamanteus) venom. Toxicon, 1984, 22, No. 5, p.
831833.
MEIER, J., STOCKER, KF. Biology and distribution of venomous snakes of medical
importance and the composition of snake venoms. In MEIER, J., WHITE, J. (Eds),
Handbook of clinical toxicology of animal venoms and poisons. Boca Raton : CRC Press,
1995, pp. 364412.
OSHIMA, G., SATO-OHMORI, T., SUZUKI, T. Proteinase, arginineester hydrolase and
kinin releasing enzyme in snake venoms. Toxicon, 1969, 7, No. 3, pp. 229233.
PHILLIPS, RE., THEAKSTON, RD., WARRELL, DA. Paralysis, rhabdomyolysis and
haemolysis caused by bites of Russells Viper (Vipera russelli pulchella) in Sri Lanka:
failure of Indian (Haffkine) antivenom. Q J Med, 1988, 68, No. 257, pp. 691715.
REIMERS, AR., WEBER, M., MULLER, UR. Are anaphylactic reactions to snake bite
immunoglobulin E-mediated? Clin Exp Allergy, 2000, 30, No. 2, pp. 276282.
SEKOGUCHI, S., NIKAI, T., SUZUKI, Y., et al. Kinin-releasing enzyme from the venom of
Bitis arietans (Puff Adder). Biochim Biophys Acta, 1986, 884, No. 3, pp. 502509.
STCKLIN, R., CRETTON, G. The ultimate database on venomous animals, snakes. CD-
rom, Geneva : Atheris Laboratories, 1998.
SZOLD, O., BEN-ABRAHAM, R., FROLKIS, I., et al. Tumor necrosis factor as a mediator
of cardiac toxicity following snake envenomation. Crit Care Med, 2003, 31, No. 5, pp.
14491453.
TAKASAKI, C., TAMIYA, N., BDOLAH, A., et al. Sarafotoxins S6: several isotoxins from
Atractaspis engaddensis (Burroving Asp) venom that affects the heart. Toxicon, 1988, 26,
No. 6, pp. 543548.
 Snake Venoms 49

THEAKSTON, RD., WARRELL, DA., GRIFFITHS, E. Report of WHO workshop on

standardization and control of antivenoms. Toxicon, 2003, 41, No. 5, pp. 541557.
WATT, G., MEADE, BD., THEAKSTON, RD., et al. Comparison of Tensilon and
antivenom for the treatment of Cobra-bite paralysis. Trans R Soc Trop Med Hyg, 1989,
83, p. 570573.
WHITE, J., WARRELL, D., EDDLESTON, M., et al. Clinical toxinology where are we
now? J Toxicol Clin Toxicol, 2003, 41, No. 3, pp. 263276.
WOLLBERG, Z., SHABO-SHINA, R., INTRATOR, N., et al. A novel cardiotoxic
polypeptide from the venom of Atractaspis engaddensis (Burroving Asp): cardiac effects
in mice and isolated rat and human heart preparations. Toxicon, 1988, 26, No. 6, pp. 523
534.
Chapter 4

SNAKE ANTIVENOMS
4.1. HISTORY
The first immunization using snake venom to demonstrate a boost in immunity was
performed by Henry Sewall in 1887, by applying increased doses of venom from the
massassauga (Sistrurus catenatus) to a pigeon, which subsequently survived exposure to six
times the lethal dose. Then, in 1894, Phisalix and Bernard demonstrated the antivenomous
activity of blood in animals immunized by heat-treated venom from the asp viper (Vipera
aspis). Later in the same and the following year, effectiveness of serum obtained from
animals immunized with cobra venom against subsequent envenomation was proven by
Albert Calmette, who in 1895 was the first to prepare and administer a horse antivenom to a
man envenomed by a cobras venom.
The first horse antivenom produced commercially was again the work of Calmett - it was
produced for use in Vietnam in 1898. At the cusp of the 19th and 20th centuries, production
followed in the USA (McFarland, 1899), Australia (Tidwell, 1902), Brazil (Vital Brasil,
1905), and Japan (Ishizaka, 1907).
In the subsequent years, chiefly horse antivenoms were produced commercially.
Although these were never - and are still not - used successfully as preventive vaccines
against the effects of snake venom, their position as a specific therapeutic element in treating
snakebite symptoms is unique.

4.2. IMMUNOGENICITY OF SNAKE VENOMS

In terms of composition and chemical properties, snake venoms and their components
show a higher or lower level of immunogenicity in inducing antigens to develop. This kind of
property is used when manufacturing antivenoms against the effects of snake venom.
Although snake venom toxins and enzymes are principally immunogenic, humans
repeatedly exposed to snake venom will not be protected by the antigens developed. Any
slight immunity increase via neutralizing a clinically important amount of toxins is
insufficient. For example, Peter Gruber, a popular American snake hunter also known as
Rattlesnake Pete, was bitten about thirty times without becoming immune. There is also the
exceptional case of an Australian snake dealer with an allergy to horse antivenom, which was
triggered following repeated snakebites and subsequent administration of antivenoms.
52 Jiri Valenta

Lacking the possibility of specific treatment in case of further envenomation, the man was
successively immunized using venom from the mainland tiger snake (Notechis scutatus) at
his own request. This vaccination provided him with immunity for four months, during
which a snakebite by a highly venomous tiger snake exhibited only a minimal localized
response (Wiener, 1960). However, repeated exposures to a venom will, in most cases, tend
to result in hypersusceptibility with allergic symptoms. Nevertheless, indigenous people in
Mexico and India are used to stabbing themselves with snake fangs, believing it will increase
their immunity to snakebites, but this may be a dangerous habit with venom from certain
snakes, such as Echis snakes. Several highly efficient venom components, e.g. prothrombin
activators, are not very immunogenic; as a result, they are not neutralized by the antigens
developed and can cause a serious reaction.
Differences in the immunogenicity of specific toxin and enzymatic venom components
are determined by the size and type of the molecule. A number of protein toxins and enzymes
belong to glycoproteins, in which immunogenicity is determined by the nature of the sugar
component. A rule of thumb is that smaller and low-glycosylated molecules, such as those of
certain neurotoxins or myotoxins, possess lower immunogenicity, i.e. the capability of
inducing antigens to be produced against toxins.

4.3. PRODUCTION, COMPOSITION AND TYPES OF ANTIVENOM

Antivenom production is based on immunizing the animal selected by repeated
progressive doses of venom and subsequently collecting and treating the hyperimmune serum.
Various animals are used for laboratory and research purposes, for example the mouse, rabbit,
ass, goat, cow, llama, etc. Experimentally, IgY antigens have been obtained from the yolks of
immunized hens as well (Thalley, Carroll, 1990; Kiem, 2000). However, commercial
production is limited only to horse and sheep antivenoms. Animals are immunized using fresh
venom, with the resultant hyperimmune serum being subject to further treatment and
purification.
If venom from a single snake species is used for animal immunization, the resulting
serum is referred to as a monovalent or monospecific antivenom. Meanwhile, polyvalent or
polyspecific antivenom is produced by immunization using venom from multiple snake
species, which typically involves those inhabiting the territory for which the antivenom is
designed.
Effective antivenom components include antigens of IgG type and its fractions.
Antivenoms containing a whole IgG molecule are produced by precipitation of the serum IgG
fraction by ammonium sulphate or capryl acid. Antivenoms, where the F (ab)2 fragment is
used as the effective antigen, are prepared by cleaving the Fc fragment from the whole IgG
molecule using pepsin under pH 2 and subsequent precipitation, which is again performed
using ammonium sulphate or capryl acid. By cleaving the IgG molecule using papain under
pH 7-8, an antivenom with small Fab fragments is obtained. The final product is then
pasteurized.
In principle, only healthy animals are used for immunization. Any presence of an
infectious agent contagious to humans is eliminated by chemical treatment of the serum using
pepsin, capryl acid, pH 2, pasteurization, etc. However, the procedures recommended are not
 Snake Antivenoms 53

fully maintained by every producer, which may affect product effectiveness in addition to the
number and severity of side-effects.
Antivenoms are supplied in the form of solution or lyophilized. When stored in a dark
place under temperatures of 4 oC to 8oC, the liquid form will remain stable for approximately
5 years depending on type of stabilization, and the lyophilized form much longer. Naturally,
expiry dates are shorter as instructed by manufacturers. Higher temperatures will
proportionally reduce the content of effective antigens. Over a certain period of time,
antivenoms are capable of being stored and used even in an extreme tropical climate. They
can still remain effective for several months at temperatures of 20 oC to 37oC if stored in the
dark.

4.4. ANTIVENOM EFFICIENCY

As indicated by studies, the neutralization capacities determined in a laboratory, i.e. the
immunological properties of antigens as IgG and F(ab)2 and Fab fragments, are generally
comparable. However, differences may be insisted on for clinical use, which are determined
normally by molecular size, i.e. penetration capacity, as well as distribution velocity and half-
time excretion. The absence of the Fc-fragment in the antivenoms of F(ab)2 and Fab types,
bringing about a certain probability of reducing an antivenoms side effects, presents another
difference.
The antigen of IgG type possesses the distribution volume of the plasma. Compartments
with better accessibility can be reached by the antigens within 6 hours, while deeper and less
accessible compartments are reached within 30 hours. These antigens are excreted by
immunity system cells with a general half-time of 60 to 190 hours.
Antivenoms containing F(ab)2 fragments have about double the distribution volume
compared to that of plasma. They can reach accessible compartments in as little as an hour,
while less accessible tissues are reached within some 6 hours. Their half-time in the body is
from 20 to 50 hours, and are excreted in the form of IgG through the immunity system cells.
Fab-containing antivenoms possess the most rapid distribution to extravascular areas and
the largest distribution volume. Their smaller molecules seem to have a greater affinity to
tissue than other types of antigens. The half-time of Fab is very low - about four hours; with
regard to molecular size, it is determined by elimination through glomerule filtration. Some
works indicate that Fab fragments are less efficient than entire IgG molecules or F(ab)2
fragments. Other disadvantages include a short half-time, more frequent instances of
antigenemia and the necessity for repeated administration due to the recurrence of symptoms.
In general, antigens have a dual function - preventive and curative. In the former,
antigens unbind available toxin molecules before they can attach to target receptors, whereas
in the latter, they are capable of eliminating existing bound molecules of toxins, e.g.
postsynaptically curare-form effective neurotoxins, from receptors.
Antigen-toxin complexes can persist in the body much longer than antigens are
maintained in the circulation. Fab-toxin complexes have been discovered 9 days following
administration of an antivenom. These complexes are progressively eliminated by immunity
system cells.
54 Jiri Valenta

Dissociation of such complexes prior to destruction by the immunity system results in an

increasing level of the toxin, this being one of the reasons for recurrent envenomation.
Another reason for this complication, which occurs quite frequently, involves the progressive
release of toxins and enzymes from tissue at the bitten site, and successive unbinding of all
present antigens. Typically, symptoms return in cases of coagulopathy within 2 to 14 days
upon administration of antivenom. The occurrence of repeated deterioration is often in
inverse proportion to the dose of the antivenom prescribed; it is more frequent upon
administration of antigens of the Fab type, as already mentioned, however, this is no
exception following treatment with antivenom containing whole molecules of IgG. To
neutralize some venom components with low immunogenicity - e.g. prothrombin activators,
certain neurotoxins and myotoxins - an extreme amount of antivenom, up to many dozens of
doses, may be necessary to eliminate the effects of such substances.
In certain cases, antivenom appears not to be fully working due to envenomation
symptoms not abating. If morphological damage to a tissue by a toxin, or more often by an
enzyme, occurs prior to antivenom being administered, the antigens cannot treat the
developed affection further. For instance, this involves local envenomation symptoms
including necrosis, renal failure, presynaptic neurotoxicity, myonecrosis, etc. The affliction
may be mitigated by prompt application of antivenom. Differences in the toxin range of
snakes can be another reason for decreased antivenom efficiency. In most cases, this involves
intra-species variability in venom composition. Another reason may be the variability in
components of venom in snakes belonging to the same species but sourced from different
areas; when the animal designed to produce the antivenom is immunized with the venom of a
snake from a region different to that where the antivenom is to be used. If the effectiveness of
the antivenom is clinically reduced and possible variability suspected, a useful solution would
be to try applying antivenom from a different producer or region, if such is available.
A completely different situation is presented by cross immune response, which happens
relatively often. It refers to the reactivity of an antivenom to a venom toxin or enzyme not
used to produce the same antivenom. This is caused by the relationship or likeness of toxic
component molecules in venoms of different species of snakes. The cross immune response
was found by Lamb in 1902. A rabbit antivenom to counteract venom from the Indian cobra
(Naja naja) also demonstrated activity against the venom of the Russels viper (Daboia
russelli).
The cross immune response exists between Asian and African cobras, except the Naja
nigricollis. The Egyptian polyvalent antivenom is effective against the Sub-Saharan cobras as
well except the Cape cobra (Naja nivea), and against the venom of the Gabon viper (Bitis
gabonica). The antivenom produced to counteract the venom of the western diamond-backed
rattlesnake (Crotalus atrox) will neutralize venoms of another five rattlesnakes, however,
with the exception of the South American rattlesnake (Crotalus durissus), due to the presence
of neurotoxic crotoxin.
Polyvalent antivenoms containing a component active against thrombin-like enzymes are
capable of neutralizing these activities in venoms of other snakes too, for example the Gabon
viper (Bitis gabonica), Chinese moccasin (Deinagkistrodon acutus), common lancehead
(Bothrops atrox), and the eastern diamond-backed rattlesnake (Crotalus adamanteus). The
venom of the western diamond-backed rattlesnake (Crotalus atrox) can be neutralized by
antivenom treating the venom of the Russels viper (Daboia russelli); the venoms of sea
snakes and sea kraits can be neutralized by antivenom against the coastal taipan (Oxyuranus
 Snake Antivenoms 55

scutellatus); and venoms of the Russels viper (Daboia russelli), monocellate cobra (Naja
kaouthia), and the western diamond-backed rattlesnake (Crotalus atrox) can be neutralized by
anticobratoxin. An important and practical finding is presented by the possibility of
neutralizing the kinin-releasing enzymes of venom from the rock viper (Vipera xanthina),
Levantine viper (Macrovipera lebetina), asp viper (Vipera aspis), and common viper (V.
berus) using a monospecific antivenom of the nose-horned viper (V. ammodytes) (Zagreb,
Croatia). The cross immune response also occurs, vice versa, between snakes of different
species: Vipera, Cerastes, or Bitis; with their antivenoms reacting against the components of
night adders (Causus). Immunity responses have even been found throughout both snake
antivenoms and the venoms of scorpions, bees and frogs, as well as in botulin.
The information above indicates that the specificity of monovalent or polyvalent
antivenoms manufactured commercially may not always be strictly limited to the venoms of
indicated use, especially if the antivenom for the species in question is not available or the
snake cannot be identified. Conversely, one must consider that in circumstances of cross
immune response (antivenom against venom A vs. venom B), the reciprocity of the effect
may not and often does not exist (antivenom against venom B vs. venom A) and any
prediction of response A is highly complicated.

4.5. SIDE-EFFECTS OF ANTIVENOMS

Anaphylactic side-effects of antivenoms are caused by proteins and other antigens in the
preparations that present extraneous matters to humans. Horse antivenoms show a higher rate
of occurrence of anaphylactic reactions than those of sheep. The incidence and severity of the
course will greatly differ depending on the type and producer.
Antivenoms containing whole IgG molecules seem to be responsible for the highest
percentage, up to 30% of hypersensitive responses. The incidence is apparently increased by
the presence of the Fc fragment in the molecule, and the capability of the fragment to activate
the complement. Incidence upon application of F(ab)2 fragment-containing antivenoms is
lower; 10% is typically presented. In this case, i.e. in the absence of Fc-fragments, any
complement activation is only possible through an alternative method. Finally, the lowest
response incidence, about 0.8%, exists in antigens of Fab-fragment type. In such a
circumstance, the complement is not activated at all.
Adverse responses may not necessarily be linked to the type of antigen but to method of
production. A higher protein content, the presence of non-IgG proteins and protein clusters,
pyrogens, endotoxin, and similar substances will result in an increase in the occurrence of
anaphylactic reactions by up to 80%. Conversely, perfectly purified preparations, although
they contain whole IgG molecules, show a low incidence of adverse responses. Nevertheless,
it remains fully accepted that eliminating the Fc-fragment will reduce the risk of side-
responses, especially severe ones, by preventing activation of the complement.
Generally, two types of anaphylactic reaction occur following administration of
antivenom: early and late.
56 Jiri Valenta

Early Anaphylactic Reactions

These involve an allergy to a serum administered repeatedly, in most cases a horse

antivenom. In the past, the serum might have been applied not only as an antivenom against
snake venom, but also as an antitetanic or antirabies serum. In some cases, the possibility of
occurrence of this response has also been reported without any previous contact, this being
termed an anaphylactoid reaction. Early reactions occur anywhere from the moment of
application and up to three hours later. Incidence is very wide - it will increase with the size
of the dose and speed of application, but decrease with the level of refinement and accuracy
of development the preparation undergoes, as mentioned above.
Furthermore, it becomes apparent, depending on the severity and speed of its onset, in the
form of itching and redness, the occurrence of widespread urticarial dermal efflorescence
(hives), nausea, vomiting, and higher temperatures. In addition, as many as 40% of patients
with such a reaction are affected by more adverse systemic symptoms: hypotension,
bronchospasm, and the occurrence of angiotic edema. The most severe symptoms materialize
as anaphylactic shock and Quinkes edema, obstructing upper respiratory airways. The rise in
temperature may not be allergic in nature, but a response to the presence of pyrogens in the
antivenom.
Therapy and prevention of allergic responses to antivenoms will not differ from
procedures for anaphylactic symptoms of other etiology; these are listed in chapter 5.3.2
Prevention and treatment of serum anaphylactic reactions.

Late Anaphylactic Reaction - A Serum Sickness

Serum sickness typically occurs after several days, although can take up to three weeks to
show itself, upon application of antivenom. Incidence is estimated at up to 75% and will rise
in direct proportion to the quantity of antivenom applied. It becomes manifest via heightened
temperatures, itching, and the occurrence of allergic dermal efflorescences, arthrodynia and
articular edema, swollen lymph nodes, nephropathy with albuminuria, and by encephalopathy
in some rare cases.
The serum sickness will abate spontaneously or following treatment using antihistaminics
and corticosteroids for a few days. For therapy of serum disease, see chapter 5.3.2 Prevention
and treatment of serum anaphylactic reactions.

REFERENCES
BOYER, LV., SEIFERT, SA., CLARK, RF., et al. Reccurent and persistant coagulopathy
following Pit Viper envenomation. Arch Intern Med, 1999, 159, No. 7, pp. 706710.
CLAUS, I., MEBS, D. Cross-neutralisation of thrombin-like enzyme in snake venoms by
polyvalent antivenoms. Toxicon, 1989, 27, No. 12, pp. 13971399.
CHIPPAUX, JP., GOYFFON, M. Venoms, antivenoms and immunotherapy. Toxicon, 1998,
36, No. 6, pp. 823846.
 Snake Antivenoms 57

ISMAIL, M., MEMISH, ZA. Venomous snakes of Saudi Arabia and the Middle East: a
keynote for travellers. Int J Antimikrob Agents, 2003, 21, pp. 164169.
JANSSEN, M., FREYVOGEL, TA., MEIER, J. Antigenic relationship between the venom of
the Night Adder Causus maculatus and venoms of other Viperids. Toxicon, 1990, 28, No.
8, pp. 975983.
Al-JOUFI, A., BAILEY, GS., REDDI, K., et al. Neutralization of kinin-releasing enzymes
from viperid venoms by antivenom IgG fragments. Toxicon, 1991, 29, No. 12, p. 1509
1511.
KHADWAL, A., BHARTI, B., PODDAR, B., et al. Persistent coagulopathy in snake bite.
Indian J Pediatr, 2003, 70, No. 5, pp. 439441.
KHOW, O., CHANHOME, L., OMORI-SATOH, T., et al. Effectiveness of Thai Cobra (Naja
kaouthia) antivenom against Sea Snake (Lapemis hardwickii) venom: verification by
affinity purified F(AB')2 fragments. J Nat Toxins, 2001, 10, No. 3, pp. 249253.
KIEM, TX. The production of Calloselasma rhodostoma antivenom (C.R.A.V.) from egg
yolk of hens immunized with venom: its application for treatment of snake bite patients
in Vietnam. Proceeding of the XIIIth World Congress of the Internetional Society of
Toxinology, Paris 2000.
KORNALIK, F., TABORSKA, E. Cross reactivity of mono- and polyvalent antivenoms with
Viperidae and Crotalidae snake venoms. Toxicon, 1989, 27, No. 10, pp. 11351142.
LALLOO, DG., THEAKSTON, RD. Snake antivenoms. J Toxicol Clin Toxicol, 2003, 41,
No. 3, pp. 227290.
LIPPS, BV., KHAN, AA. Antigenic cross reactivity among the venoms and toxins from
unrelated diverse sources. Toxicon, 2000, 38, pp. 973980.
MEIER, J., WHITE, J. (Eds). Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995, 752 pp.
MOROZ, CH., de VRIES, A., GOLDBLUM, N. Preparation of an antivenin against Vipera
palestinae venom with high antineurotic potency. Toxicon, 1966, 4, pp. 205208.
SEDDIK, SS., WANAS, S., HELMY MA., et al. Cross neutralisation of dangerous snake
venoms from Africa and Middle East using the VACSERA polyvalent antivenom.
Egyptian Organisation for Biological Products and Vaccines. J Nat Toxins, 2002, 11, No.
4, pp. 329335.
THALLEY, BS., CARROLL, SB. Rattlesnake and skorpion antivenoms from the egg yolks
of immunized hens. Biotechnology (NY), 1990, 8, No. 10, pp. 934938.
THEAKSTON, RD., WARRELL, DA., GRIFFITHS, E. Report of WHO workshop on
standardization and control of antivenoms. Toxicon, 2003, 41, No. 5, pp. 541557.
WIENER, S. Active immunization of man against the venom of the Australian Tiger Snake
(Notechis scutatus). Am J Trop Med Hyg, 1960, 9, pp. 284292.
Chapter 5

SNAKEBITE: THERAPY AND PREVENTION

5.1. PREVENTION
There are essentially two circumstances under which humans and snakes interact,
resulting in potential snakebites - keeping snakes and staying in the wild within the creatures
habitat. A rule of thumb relating to snakebites is that prevention is the best kind of therapy, as
in any other affliction and disorder.
When addressing snake ownership, one should bear in mind that the animals not only
prove a danger to their keepers, but pose a risk to others through handling and any chance of
escape. A poorly secured snake could threaten visitors, family members, partners and,
naturally, children. Closing and securing a terrarium in the presence of children should be an
automatic reaction. Venomous snakes should be handled only to the extent necessary for
successful breeding. Their adaptation and nature dictates that snakes are not designed for co-
existence with man, with any unreasonable contact being potentially traumatic for both sides.
Therefore, it is completely unacceptable to handle a snake in the presence of other individuals
and do so under the influence of alcohol, which frequently has the effect of making people
feel brave and inhibits reactions. Unfortunately, such situations often result in snakebites and
envenomation. Indeed, it is not unreasonable to compare some especially perilous venomous
snakes to an unlocked gun cabinet, which is not really overstating matters. Handling a gun is
subject to the obligation to avoid the influence of alcohol and other substances affecting ones
state of mind, much like driving a car. Therefore, the same rule should be adhered to when in
contact with venomous snakes.
The most frequent causes of snakebite when keeping venomous snakes involve activities
carried out in terrariums - cleaning, placing water, and the like. Any reliance on the snake
maintaining a quiet, peaceful position in an opposite corner of the terrarium is foolhardy, as
born witness to by many shamefaced snake holders. Feeding young snakes that refuse to eat
can be another reason. Experience and concentration is essential when performing such an
activity - nevertheless, injuries even occur amongst highly experienced keepers. However,
handling snakes to collect venom is not a frequent reason for envenomation, apparently due to
the immense professionalism of such practitioners.
Staying in countryside or the wild poses a threat in terms of actively being in the presence
of snakes, i.e. via catching or passive unconscious contact. Snake hunters are ordinarily so
skilled and experienced that their error free behavior in any situation can be presumed,
although this is not always the case. Sometimes, a great desire on their part can make a hunter
60 Jiri Valenta

reflexively grasp a disappearing snake by its body, even at a dangerous distance behind its
head. The end result is obvious, much like that of a reputable herpetologist who went to look
at a sleeping mamba. Let any such and similar situation serve as a warning to other owners
and hunters.
Staying outside in areas with an increased occurrence of dangerous venomous snakes
brings certain rules that are essential to follow. Clothing should include solid boots and long
trousers; in addition, a shirt with long sleeves is advisable. Within the habitats of snakes or on
a camp site, dropping litter is not recommended as rubbish attracts rodents, which in turn
brings snakes. When out walking in the country, a point of destination should always be born
in mind when conducting movements that cannot be interrupted, such as jumping over
obstacles like stones, walking over a tree trunk lying across the road and the like. Turning
over stones, poking hands into holes, under bark or into other places where it is unclear what
lies within them is not wise. If a snake can be seen, a safe distance should be kept for
observing or taking pictures, which may mean several meters for large snakes. If a snake is to
be captured, two or three individuals should be in attendance.
In 1991, the US Navy issued pre-emptive rules of behavior for travelers in terrain rich
with venomous snakes, summarized as follows:

Do not put your hands and feet in areas that cannot be fully inspected or before you
explore them
Do not lift up and turn over stones and fallen logs using your bare hands - use a stick
or your legs in solid footwear with well-protected ankles
Do not disturb snakes
Do not put a sleeping bag near rocks, stones, litter, and cave entrances
Do not sit down before you thoroughly inspect a site
Do not collect wood for a fire after dusk
Do not walk over a fallen tree before you see the other side. Step up onto it first
Do not visit places with increased occurrence of snakes without wearing suitable
clothes and boots
Do not handle freshly killed snakes
Do not crawl under fences where the grass is high or ground enclosed
Do not leave a trail to kill a snake. Thousands of people are bitten by venomous
snakes when trying to kill them without firstly knowing their habits and patterns of
behavior
Last, but not least, do not panic

There is more worthwhile advice to add for those venturing into the countryside. As
already mentioned, snakes cannot hear, so any noisy behavior in places where snakes are
presumed to range just makes for an amusing scene rather than acts as a form of prevention.
A heavy tread when walking and any thumping will cause the ground to vibrate, which is
registered by snakes and will encourage snakes to leave the location. The common fear of
snakes ranging around a dry area flooded by sun is a blatant untruth, as snakes resistance to
the sun is very low. However, spending a quiet night in the same location can be dangerous in
the hot summer months, because a number of snakes hunt at dusk or even at night if
temperatures are high during the day.
 Snakebite: Therapy and Prevention 61

As is indicated by analysis of causes for snakebites amongst children by the common

viper (Vipera berus) in the Czech and Slovak Republics (Dluhorucky et al., 2000), as well as
the authors experience, there is a general lack of awareness of the danger posed, in addition
to loss of inherited atavism relating to an unknown animal. Precautions to guard against this
should include instructing children about the potential threats that close contact with snakes
present to them. Naturally, any such guidance should not provoke any unnecessary fear and
animosity, as this can stay with a person for their entire lifetime.

5.2. FIRST AID

5.2.1. First Aid for Laypersons

The basic rule of first aid is to remain calm and rational. The chances of rapidly
occurring life-threatening symptoms are usually very low. Any excitement and movement
will worsen an envenomation. Above all, the person affected must be settled down and put
into a sitting or lying position.
If the snakebite occurs in the habitat of multiple venomous snake species, the snake
should be identified or at least described to facilitate later identification. The time of the
snakebite is also information of high importance.
The next thing to do is to call an emergency service. This should be done even in the case
of an adult lacking any post-bite symptoms due to possible subsequent development of a toxic
or allergic response. Of course, calling the emergency services is absolutely necessary if a
child is affected.
Immobilizing the affected person and the limb is essential for delaying the progress of
envenomation. Applying an ordinary constrictive tourniquet, in order to restrict return flow in
the venous system, is not recommended, as slowing down venom distribution from the bitten
site using a tourniquet has an uncertain result; in addition, this impacts upon damage to limb
tissue by blood stasis and facilitating the likelihood of edema.
Venom distribution from the bitten site on a limb can provably by retarded by a pressure
immobilization bandage - PI, according to Sutherland (Fig 5 and 6). PI will be fully indicated
in snakebites by dangerously neurotoxic snakes that do not possess any potent necrotizing
venom components, e.g. cobras, like the Indian cobra (Naja naja), king cobra (Ophiophagus
hannah), Philippine cobra (N. philippiensis) and other elapids - Micrurus, kraits - Bungarus,
mambas - Dendroaspis, as well as sea snakes and sea kraits. The safe use of PI with positive
results has also been proven with Australian terrestrial elapid snakes, which possess highly
effective venom. However, as regards bites by other snakes, including rattlesnakes, PI
application is recommended only in special cases when timely aid from emergency services is
not forthcoming, especially for children.
The pressure immobilization bandage is fitted by tightly strapping the affected limb with
a wide elastic bandage to the greatest extent possible: from the fingers up to the trunk.
Starting by bandaging above the bitten site towards its periphery and then back to the trunk is
ideal, although less comfortable for the patient. Such a procedure is recommended for a
shorter period of time. Should the bandage be in place for longer, wind it from fingers
towards the trunk. This method protects the venous system, meaning it will not cause even the
62 Jiri Valenta

least amount of venous stasis, whilst minimizing the risk of pushing the venom out into the
circulation system. Finger tips must be kept unrestricted to maintain continual intact
circulation in the limb so affected. The tightness of the bandage is often compared to that of
bandaging an injured ankle. If the limb is painful upon PI application, the bandage is most
probably too tight. The bandage can be placed over trousers or a shirt as well, as any limb
moving whilst uncovered is undesirable. Of course, the strict rules mentioned above apply
especially to bites by highly dangerous snakes, those possessing a potent neurotoxic
component of venom. Following the application of the bandage, the limb must be secured
well to avoid movement using a splint. The PI can remain in place for a number of hours as
required; venom release is distinctively restricted even three hours afterwards. Naturally, any
movement will greatly reduce the bandages positive benefit. The PI will lose its function if
too slack, sufficient immobilization of the limb is not assured, or the PI is applied once
venom is already in the circulation. The PI should not be removed before reaching the place
of final treatment or prior to antivenom being applied (Sutherland, 1979).

Figure 5. Pressure immobilization bandage for upper limbs (edited according to Sutherland, 1979).

Figure 6. Pressure immobilization bandage for lower limbs (edited according to Sutherland, 1979).
 Snakebite: Therapy and Prevention 63

If for some reason the PI cannot be applied in instances of apparent envenomation by a

mortally dangerous neurotoxin from coral snake (Elapidae) venom, an arterial tourniquet can
be applied to delay development of respiratory muscle paralysis. The device is placed above
the bitten site towards the trunk; it may not be possible to feel the pulse at the limbs
periphery upon applying the tourniquet. The applied tourniquet must be soft and elastic to
avoid damaging the skin and neurovascular bundles at the site of application; the device must
be released for 15 seconds every 30 minutes. The application period is limited to two hours.
Although this method can save lives in certain extreme situations, it always increases the
level of localized damage to affected tissue and could cause gangrene. Therefore, the
implications of using one should be seriously considered.
Compression techniques should be applied as soon as possible following a bite, as the
neurotoxins with a low molecular weight will expand relatively promptly from the bitten site
with frequent parallel increases in capillary permeability. If a pressure immobilization
bandage is not applied, the limb must be immobilized by applying a splint or at least by fixing
it to the trunk.
Any traditional and commonly known techniques of handling the bitten site, like cutting
it open, sucking the venom out by the mouth, burning, rinsing it with oxidizing agents,
phenol, permanganate, hydrogen peroxide and others, are ineffective and involve potential
risk, so are not recommended. Furthermore, the thinking behind electrical impulses or electric
shock treatment, sometimes mentioned in literature for laypersons, is unfounded and naive.
Sucking the wound using a Sawyer extractor, as recommended commercially in the US,
seems to be ineffective, but will not cause any additional major damage to the tissue
compared to other localized methods. When using the device, care should be taken to ensure
accurate application on the bite openings, as for large rattlesnakes, such as the western
diamond-backed rattlesnake (Crotalus atrox), the distance between the openings can be
greater than the size of the suction opening of the extractor.
In case of pain and developing edema, especially if the pressure immobilization bandage
has not been applied, the affected limb can be slightly elevated by a support.
If the emergency services are expected to arrive in good time, any increased supply of
liquids by drinking is not recommended. In instances of serious complications, a full stomach
may cause vomiting and subsequent aspiration of stomach content. Conversely, if the
emergency services are hard to reach in extreme conditions, drinking liquids cautiously that
are easy to absorb, such as slightly sweetened water, weak or herbal tea, etc., is possible,
particularly after a bite by a viperid snake (Viperidae). The well-known practice of drinking
coffee or alcohol cannot be generally considered as very helpful. In most cases, this is
dangerous and can make the course of envenomation much worse.
Any laypersons use of analgesics and sedatives is generally not advisable, unless the
situation is not extreme. If that is the case, sedatives of ordinary use or doses of sleeping pills
can be administered. Analgesics should be free of acetyl salicylic acid, especially following
envenomation by a venom containing hemocoagulation-affecting components.
If an eye is affected by venom from so-called spitting cobras (Naja and Hemachatus), the
first thing to do is to rinse the eye so as to dilute or remove the contact-effective venom. The
best way of doing this is to use a stream of clean water, eye-flushing preparations like boracic
acid, or milk. If none from the above are available, cleansing the eye with any non-toxic, non-
irritant and non-infectious liquid, such as soft drinks, is possible and beneficial.
64 Jiri Valenta

Transport into a health facility should be facilitated by the emergency service called out
or an available car. In less accessible places, a helicopter may be necessary. In extreme
situations, efforts should be made to transport the affected person, with a minimum of
physical exertion on their part, to a place where health or transport assistance is available.

5.2.2. Medicinal First Aid

The affected person should be first calmed down. Systemic administration of sedatives
can be beneficial, especially in cases of anxious or hysterical behavior, with parenteral
administration of benzodiazepines as the best option. Chlorpromazine with an anti-emetic
effect following envenomation by viperid (Viperidae) venom can also be an option. The
standard doses are 25 to 50 mg in adults, and 1 mg/kg of body weight in children. Any deep
sedation is generally not desirable; in the indicated cases of its use, the essential life functions
of the patient must be inspected and respiratory airways protected from aspiration of stomach
content. The same steps must be taken should impaired consciousness be caused by the
envenomation or resulting complications.
In the case of pain that can be extensive locally, analgesics are applied. Caution is
necessary when administering opioids to a patient after possible envenomation by neurotoxins
from a coral snake (Elapidae) in all situations where assisted pulmonary ventilation is
necessary but cannot be provided. Any reduction in a patients ventilation efforts may result
in manifestation of respiratory failure. On the grounds of inhibition of platelet function,
administering salicylates is contraindicated, especially when the snake venom contains
hemocoagulation-affecting components, as found in Echis and Macrovipera species,
Bothrops, Lachesis, and other snakes. Appropriate analgesics include paracetamol or non-
steroid antiphlogistics with an analgesic effect, such as ibuprofen.
To avoid an allergic response to snake venom components and the onset of angioneurotic
edema, parenteral administration of corticosteroids is possible - hydrocortisone in a dose of 2
to 4 mg/kg IV (intravenously) or methylprednisolone IV in an equivalent dose. This treatment
can be supplemented with antihistaminics. Even though any positive effect of the preventive
measures above cannot be guaranteed, the patients potential responses should be eased.
Shortly following a snakebite, a pressure immobilization bandage (PI) should be applied
in the cases indicated, unless previously done so by the affected person, see chapter 5. 2. 1
First aid for laypersons. Using a PI when dealing with snake venom containing locally acting
cytotoxins and proteolytic enzymes is controversial. Under such circumstances a more severe
localized affection, especially necroses, is likely to occur due to prolonged action by enzymes
at the bite, as well as decreased perfusion of the tissue if edema develops under the bandage.
Nevertheless, the benefits of a PI have been proved experimentally after envenomation by the
eastern diamond-backed rattlesnake (Crotalus adamanteus), in addition to clinical tests on
snakebites by the Russels viper (Daboia russelli). In the cases above, a PI remained in place
for up to 7 hours without any increased incidence of necroses. Furthermore, venom release
from the bitten site following the PIs removal resulted in increased venom concentration in
the circulation, on average rising from 5 to 30 ng/ml. Despite lacking clinical data concerning
the benefits of PIs in relation to snakebites by European vipers, the effect of this method in
preventing more severe symptoms from snakebites, in cases of high venom doses, can be
 Snakebite: Therapy and Prevention 65

presumed positive. Certainly, putting on the bandage is advised if children are affected or a
delay in eventual treatment of the envenomation is expected.
If a PI has been applied by a layperson, the quality of performance and tightness should
be checked. The recommended pressure of the bandage is 40 to 70 mmHg (5.3-9.3 kPa) for
the upper limbs, and 55 to 70 mmHg (7.3-9.3 kPa) for the lower limbs. Fingers must be
perfused and appear normal; any ischemic painfulness in a limb indicates that the bandage is
too tight.
The method of bandaging has been developed with regard to the fact that venom largely
propagates from affected tissue into the circulation via lymphatic routes. The bandage will
limit lymphatic drainage and immobilize the limb. Therefore, the importance of this method
rests on compressing the lymph vessels in a wounded limb along the greatest section possible
and immobilization of the limb with a splint. The limbs immobility is very important to
eliminate the pumping action of muscles. Any compression without motional restraint is
ineffective, and is also true vice versa. If well-applied, compression will virtually inhibit the
venoms progress for hours without limiting oxygenation and venous drainage, which is a
problem associated with a tourniquet; naturally, sufficient blood flow through the limb, which
can be checked by perfusion of the finger tips, is a pre-condition.
If an arterial tourniquet has been applied by a non-expert following a bite by a mortally
venomous snake, such as a coral snake (Elapidae) with venom of serious neurotoxicity, it
must be removed, but only after application of a pressure immobilization bandage to the
affected limb.
Moreover, the bitten site is locally disinfected. In countries such as Australia, where the
venom can be identified using a kit should uncertainty exist concerning the snake species
involved, the bitten site is not wiped and disinfected so as to maintain traces of the venom
around the bite wounds.
To facilitate checking localized changes at the bite, a small hole can be cut out in the
pressure bandage applied for viewing purposes.
The bitten site cannot be subject to any of the traditional actions propagated, see chapter
5. 2. 1 First aid by a layperson.
If a patients vital functions, respiration, circulation, etc., are affected, securing or
supporting the same is a clear priority. Nevertheless, if an affliction of such a level occurs and
neither an acute anaphylactic reaction nor high exposure to neurotoxins are involved, the
symptoms of envenomation will become apparent in the order of dozens of minutes following
a snakebite.
An anaphylactic shock is subject to standard treatment methods. Epinephrine is
administered as follows: 0.3-0.5 ml IM (0.3-0.5 mg), 1:1000 dilution; 0.01 ml/kg of weight in
children IM (intramuscular); this is repeated as necessary every 5-15 minutes until the
circulation is stabilized; then volumotherapy is supplemented. Furthermore, corticosteroids
are administered: methylprednisolone 125 mg IV (1 mg/kg of weight in children), this is
repeated every 6 hours; in addition, antihistaminics are applied. Circulation collapse or shock
therapy must be accompanied by oxygen therapy.
Similarly, hypotension resulting from vasodilation and extravasation caused by toxins,
subsequent shock, and collapse of circulation, is followed by symptomatic treatment, i.e.
tonization of the vascular bloodstream by catecholamines and plasma expansion. In patients
under threat of a hemocoagulation disorder, alternative solutions based on dextrans are not
used due to their interference with platelet function.
66 Jiri Valenta

Symptomatic treatment is also employed within urgent medical aid in cases of a rhythm
and contractility disorder caused by cardiotoxin action. Any circulation affection treatment
always includes oxygen therapy.
In situations of apparent envenomation by neurotoxins, which will typically start with
paralysis of facial muscles, i.e. ptosis, ophtalmophlegia, dysarthria, and dysphagia, peroral
intake is contraindicated as a consequence of possible aspiration caused by loss of the
swallowing reflex. If respiratory failure is manifest, plus there is risk of aspiration, then
intubation and mechanical ventilation are an option. A patient thus affected might be fully
consciousness, therefore, adequate easing of their condition must be provided.
In cases of an eye being attacked by a spitting cobra (Naja and Hemachatus), see chapter
6. 3. 1. 5 Naja genus, the cobra and 6. 3. 1. 7 Other genera of African and Asian elapid snakes
(formerly under the name of the Bungarinae family), the eye is rinsed or the process repeated
if previously conducted by a non-expert. Clean water, a physiological saline solution, boracic
acid, or another similar eye-flushing preparation can be used. For intense burning pain,
application of a local anesthetic into a conjunctival sac is advisable. The analgesia will
eliminate the blepharospasm occurring, allowing for examination of the eyes, and help calm
the person affected. Epinephrin in the form of 0.1% drops may also be applied; dilution:
1:1000. See also chapter 5. 3. 3. 1 Localized damage.
Transport of the affected with suspected or apparent envenomation is carried out in a
lying position to the nearest health institution capable of handling severe systemic symptoms,
i.e. respiratory failure, severe hemostasis disorder, and circulatory failures. If doubts arise as
to envenomation having occurred and neither a local nor systemic response is manifest, plus
more than 24 hours has past since the attack, placing the patient within a standard department
for examination and observation suffices.
The case should be consulted with a toxinology centre as soon as the phase of urgent
medical aid has commenced to determine further steps, the need for potential hospitalization
at a dedicated centre, and in order to provide specific immunotherapy.

5.3. HOSPITAL TREATMENT

5.3.1. Specific Treatment - Immunotherapy

Specific therapy or immunotherapy (antivenom therapy) refers to the administration of

snake antivenom. If a monovalent antivenom is available and the snake species identified,
administration of the monovalent antivenom is preferable to a polyvalent antivenom. The
latter is, however, administered more often. In the home ranges of venomous snakes in the
wild, a species cannot be always identified with surety; in addition, where snakes are kept by
non-experts, monovalent antivenoms are frequently not available.
Administration of an antivenom will in some cases greatly reduce morbidity and
mortality. For example, following a snakebite by the saw-scaled viper (Echis carinatus),
lethality will decrease from 20% to 3%, while in envenomations by the South American
rattlesnake (Crotalus durissus terrificus), lethality will drop from 74% to 14%.
 Snakebite: Therapy and Prevention 67

5.3.1.1. Indications of Antivenom Administration

Application of antivenoms must be always considered properly due to their severe
potential side-effects. Generally, specific immunotherapy is indicated only in instances where
signs of systemic envenomation exist, or if a localized finding is extensive and progressing.
Localized indication schedules describing prodromes or early symptoms of systemic
envenomation are in place for certain types of envenomation with epidemiological relevance,
such as the Stockholm criteria (see Chart 4).

Chart 4. Stockholm criteria with indications for the use of antivenom

1. Hypotension and circulatory shock

2. Protracted severe gastrointestinal symptomatology
3. Mucous membrane edema with a risk of bronchial obstruction
4. Rapid extension of edema to an entire limb and the torso
5. Neurological symptomatology with depressed CNS and peripheral and central
paresis
6. In extreme cases of insufficient clinical signs:
Leukocytosis exceeding 15-20 x 109/l
Metabolic acidosis
Hemolysis
ECG changes
Hemocoagulation disorders

Gastrointestinal difficulties indicate early signs of systemic envenoming. They involve

nausea, vomiting, abdominal pain, and diarrhea, occurring very frequently in envenomations
by Crotalinae subfamily members and vipers (Viperinae). Slight symptoms of this type in a
healthy adult person would not constitute a direct indication to administer an antivenom.
However, for children such a situation must be considered more seriously, as the amount of
venom is greater in proportion to the weight of the child, and could reach a level of risk as a
result.
Another set of symptoms involves circulation being affected with signs of reduced
systemic pressure, progressing in some cases to circulation collapse and shock.
Accompanying symptoms may involve incidence of hypotension, including possible
syncopes, and the patient turning pale and sweating. The indications for antivenom
administration also involve rhythm disorders and changes in ECG under circumstances of
envenomation by venom including a cardiotoxic component.
Envenoming by neurotoxins is initially manifest by slack facial muscles, including
eyelid ptosis, external ophtalmoplegia with diplopia, dysphagia, dysarthria, salivation, and
depression of the cheeks and corners of the mouth. Subsequently, on exposure to postsynaptic
paralyzing neurotoxins, a feeling of general muscular weakness occurs, with eventual
paralysis of respiratory muscles.
An indication for antivenom treatment should also emphasis a finding involving
hemocoagulation disorders, which are based only in the laboratory in the initial phase of
envenomation; clinical signs of hemocoagulation - mostly bleeding - are a definite indication
of these. Abnormities reported by the laboratory, indicating administration of antivenom,
include not only prolonged coagulation times, but also symptomatology involving
68 Jiri Valenta

hypercoagulation, plus fibrinogen and fibrin degradation with a significant increase in total
FDP or D-dim and clinical or laboratory findings of hemolysis.
Envenoming by myotoxins, i.e. rhabdomyolysis, will be expressed by tension and pain in
the muscles, with later development of evident myoglobinuria. In this case, treatment with
antivenom is also indicated.
Administration of antivenom is also indicated in any case of impaired consciousness,
either qualitative or quantitative.
Damage to the kidneys will be mostly manifest by oliguria in later phases of
envenomation, as this is not an early indicator; however, the onset of prodromes, such as pain
in tapping the area above kidney, may indicate repetition of the dose of antivenom. If that is
the case, non-specific treatment will be more important, see chapter 5. 3. 3 Symptomatic
treatment.
From laboratory examinations, administration of antivenom is indicated by
leukocytosis above 20 x 109/l, elevation of AST, ALT, CK or other enzymes, and acidosis, in
addition to diagnosing hemocoagulation disorder.
Even though it is a well-known fact that antivenom therapy will, in most cases, neither
eliminate nor aid any local affliction already in place, administration of antivenom can be
indicated by severe local reactions as well, including sizeable edema, extensive ecchymoses
or vesicles of an area exceeding one half of the affected limb. In addition, it is necessary to
consider indications for administering, examples including the content of necrotizing
enzymes in the venom, or attack by a venom producing heavy edema in a narrow fascial
compartment, e.g. a finger, as well as development of local myonecrosis with a risk of
compartment syndrome. Possible neutralization of a local pool will depend on the rapidity of
antivenom penetration into the site of damage. The venom enzyme destructs the tissue
immediately, while any antivenom administered will always enter the given site after a delay.
Concerning penetration of the site of localized damage, the molecular size of the antigen - the
type of the antivenom - will probably not play an important role in microvascular damage at
the affected site. A large localized affliction can indirectly indicate the quantity and effect of
certain venom components of a largely enzymatic nature, as well as possible systemic damage
in future, which is another reason reinforcing it as an indication for administering antivenom.
In some cases, the positive effect of treatment will be determined by a short period
between the bite and application of antivenom. Timely antivenom therapy and neutralization
of certain venom components may prevent irreversible damage of attacked structures. This is
true not only in a number of enzymes, but also toxins, including presynaptic neurotoxic PLA2,
myotoxic enzymes and nephrotoxins causing renal failure, thrombin-like components
activating processes ending with microthrombosis occurring, endothelial damage, and other
consequences, or even enzymes destruction of tissues attacked at a greater distance around
the bitten site as a result of their propagation. For any efforts to influence a localized
affliction, administration of antivenom within 1 to 2 hours following a snakebite is essential.
Therefore, indication of antivenom administration should be deduced quickly, although
always based on the presence of systemic envenomation symptoms or extensive localized
affection.
If for some reason prompt antivenom therapy is not available, late administration of
antivenom is indicated provided treatment criteria are met, which will weaken the
effectiveness of venom components flushed out of the bitten site and unbind the toxins
temporarily, acting on specific receptors like postsynaptic neurotoxins, cardiotoxins, and
 Snakebite: Therapy and Prevention 69

others. Late administration of antivenom has proven effective 2 days after envenomation by
marine sea snakes, but even longer following the start of coagulopathy with envenomation by
Crotalinae snakes and viperines (Viperinae). Thus, any further delay between the snakebite
and the possibility of antivenom administration should not be excluded from subsequent
treatment.
Repeated administration of antivenom is indicated if signs of systemic envenomation
persist or when symptoms reoccur, which is typically recorded in venom components
affecting hemocoagulation and in other cases of related symptomatology, such as in
envenoming by Echis and Daboia snakes, rattlesnakes (Crotalus), Asian (Trimeresurus) or
Malayan (Calloselasma) pit vipers; other examples include the Indian krait (Bungarus
caeruleus), Indian cobra (Naja naja), etc. Returning symptoms will mostly manifest within 1
to 7 days following administration of antivenom, however, weaker symptomatology may
appear even after 10 to 14 days.
The recurrence of envenomation symptoms is probably due to two things: the first is
continued release of venom from the pool at the bite, while the second is the dissociation of
the antigen-toxin complex and faster antitoxin clearance. The return of recurrent
envenomation symptoms is in indirect proportion to the dose of the antivenom applied; in
addition, it is more frequent following use of antivenom containing antigens with a shorter
half-life, such as the Fab-fragment. When utilizing such antivenoms, repeated administration
is taken into account due to the effective half-time of such substances probably lasting less
then 12 hours. Of course, recurrence can still occur even if an antivenom is applied containing
a whole IgG molecule with a half-time that may exceed as many as 150 hours.

5.3.1.2. Contraindication of Antivenom Administration

The contraindication for administering venom comes in the form of an allergic reaction to
the animal serum involved, usually a horse serum. An absolute contra indicator as regards
horse serum can be considered a severe response in anamnesis following application of either
antitetanic or antirabies serum. Should an allergy be apparent to horse antivenom, a sheep
antivenom can be administered if available. Naturally, such a contraindication is not to be
considered in cases of severe life-threatening envenomation. The antivenom can be applied
upon a vital indication following prophylactic antihistaminic preparation, and under the
condition the patients safety is ensured should anaphylactic complications appear, see
chapter 5.3.2 Prevention and treatment of serum anaphylactic reactions.
Furthermore, a relative contraindication is the occurrence of another type of allergy or a
polyvalent form. In such case, the practicalities of antivenom therapy or non-specific
treatment should be thought over, depending on the envenomations progress, options for
symptomatic treatment, and the level of a patients sensitization.
A similar consideration is needed for patients that have undergone repeated exposure to a
horse antivenom. This circumstance cannot be termed as a contraindication; indeed, it just
highlights the necessity for rational consideration of the potential disadvantages of
administration and presumed immunotherapeutic effects. In instances of more severe
envenomation, the administering of antivenom will be fully indicated, although antihistaminic
premedication is a priority.
A relative contraindication may occur if a layperson or paramedic has given someone a
dose of antivenom. It should only be administered in extreme situations, e.g. following a bite
by a mortally venomous snake, and if prompt and adequate medical aid is otherwise
70 Jiri Valenta

unavailable. The decision to do it must be preceded by the process of weighing up the risk of
envenomation symptoms - such as imminent paralyzing neurotoxicity - against potential
severe anaphylactic shock that cannot be resolved on the spot.

5.3.1.3 Dosage and Method of Antivenom Administration

The dose of antivenom that can unbind venom enzymes and toxins depends on the
definite quantity of them in accessible compartments. Estimating the appropriate antivenom
quantity to a certain degree is possible based on the snakes species, the speed of the onset,
the severity of envenomation symptomatology, as well as the relevance of localized findings
in some cases. In instances of bites by snakes not near the top of an imaginary hierarchy of
mortality, e.g. Vipera and Cerastes snakes, Asian pit vipers (Trimeresurus), Crotalus
rattlesnakes, Agkistrodon and Gloydius snakes, kraits - Bungarus, Micrurus coral snakes, and
a number of other taxons, only one of two vials of the related antivenom can be applied to
begin with. In heavy envenomations caused by a mortally venomous snake like the large
cobras - Naja and Ophiophagus, mambas - Dendroaspis, taipans - Oxyuranus, tiger snakes -
Notechis or large Bothrops and Lachesis snakes, the initial amount required increases to three
and more vials, with subsequent repetition if antivenom effectiveness is low or symptoms
return. The overall amount of antivenom applied is not limited in the course of heavy
envenomations and may result in dozens of vials.
Even though intramuscular and localized administration is recommended by many
manufacturers, it is obvious that antivenoms are practically ineffective when delivered in this
form. Rapid intravenous delivery is the cause of the highest incidence of anaphylactic
reactions. The most convenient method of antivenom application is intravenous infusion of
diluted antivenom, preferably in 500 ml of electrolyte solution or 5% dextrose. The incidence
of anaphylactic reaction generally equals that of intramuscular administration and its
effectiveness in application is equivalent to that of intravenous administration. The
recommended infusion velocity should not exceed 4 ml of undiluted serum per minute;
however, instillation of the entire vial in 30 to 60 minutes is much more appropriate.
Dermal or conjunctival tests prior to applying antivenom will not always predict the
occurrence of early anaphylactic reaction or serum sickness later and are not recommended in
professional literature. Nevertheless, carrying them out remains a facultative practice and will
be dependant on a physicians approach or the methods of a medical workplace.
In extreme conditions - see the contraindication of antivenom administration section
above - the range of options available may involve intramuscular application of antivenom,
depending on the situation and equipment at disposal. However, considering the reduced
effectiveness of this method and that of delivering it very slowly intravenously, a greater risk
is posed of an acute allergic response occurring or even anaphylactic shock.

5.3.2. Prevention and Treatment of Serum Anaphylactic Reactions

In preventing an anaphylactic reaction, the application of epinephrine prior to antivenom

treatment has proven effective. The substance is administered subcutaneously, with a dosage
of 0.25 ml (i.e. 0.25 mg of epinephrine) and dilution of 1:1000 (0.1%). Administered in this
manner, epinephrine will greatly reduce the chances of early anaphylactic reaction. During
the patients preparation process, corticosteroids can also be used, with doses corresponding
 Snakebite: Therapy and Prevention 71

to between 2-4 mg of hydrocortisone/kg of weight, while use of the sedative first-generation

H1-receptor-antagonists like promethasine seems to be ineffective.
Early anaphylaxis therapy does not differ from that of the same response in different
etiology. In the case of minor symptoms like dermal manifestation, nausea, temperature, etc.,
intravenous application of corticosteroids at a dosage corresponding to 2-4 mg of
hydrocortisone - potentially in combination with an antihistaminic - will be sufficient. In
severe systemic reactions, including hypotension, circulation collapse, and anaphylactic
shock, vasopressor treatment is indicated using 0.3-0.5 ml of epinephrine (0.3-0.5 mg), at a
dilution of 1:1000 (0.1%), IM, with repeated doses as necessary, as are volumotherapy and
the application of corticosteroids and antihistaminics, see chapter 5. 2. 2 Medical first aid.
The treatment should include giving antihistaminics, H1-receptor-antagonists (for instance
chlorpheniramine maleate from the alkylamine group, dosage 10 mg per adult, 0.2 mg/kg of
body weight per child). Circulation collapse or shock therapy must be accompanied by
oxygen therapy. Any instance of bronchospasm as well as angioneurotic facial edema will
require the application of corticosteroids. Should respiratory failure appear due to a
bronchospasm or obstruction of the respiratory pathways caused by edema, tracheal
intubation and mechanical ventilation is indicated.
Positive results have been achieved from corticosteroid treatment for late anaphylactic
reaction - serum sickness, which can be treated, for instance, by prednisolone 5 mg PO every
6 hours over a period of 5-7 days. This can be supplemented by antihistaminics, especially if
there is pruritic affection. Symptomatology will abate in 2-4 days, many times even
spontaneously.

5.3.3. Clinical Symptoms of Envenomation and Symptomatic Treatment

5.3.3.1. Local Damage

Localized envenomation symptoms involve bite marks, pain, changes in the color of skin
at and around the bitten site, development of petechiae, ecchymoses, vesicles and
hemorrhagic efflorescences, as well as necrosis of affected structures and edema, the intensity
of which may go as far as to cause ischemic damage to tissue through a perfusion disorder.
The depth of the fang bite may vary depending on fang size and how effectively the
snake makes the bite. There are mostly two wounds, however, bite marks of just a single fang
or more fangs in a row on a single side are not unheard of due to a snake growing new ones.
Following a rapid fang stroke, only scratches of a varied length and depth can be evident on
the skin, although even these may be affected by envenomation, just as the same is not
precluded by a lack of bite marks. The small wounds including edges can be hemorrhagic,
may show slight bleeding or can be a livid color, including the areas around them. If only a
minimal quantity of locally acting components is present, there are no traces of these
symptoms at the site of bite. A localized allergic response may cause urticarial
symptomatology at the bitten site.
The pain experienced at and around a wound can be high in snakebites by the majority of
species, such as viperids (Viperidae), low or even negligible in some snakes like the cobra
(Naja), whilst locally reduced sensitivity to pain occurs in the case of snakebites by certain
elapids (Elapidae). Pain typically appears immediately at the bitten site, progressing together
with edema as far as the regional lymph nodes or even further. It persists on average between
72 Jiri Valenta

a week and 10 days, with its intensity dependant on snake composition, quantity and degree
of tissue damage. The overall painfulness of muscles caused by exposure to myotoxins, e.g.
the Russels viper (Daboia russelli), is considered a systemic envenomation symptom.
For giving analgesics, the principles apply as provided in chapter 5. 2. 2 Medical first aid.
Should more severe pain be experienced, application of opiate analgesics is indicated.
However, deep pharmacological analgesia is not always desirable as it may obscure the
occurrence of ischemic pain should flow occlusion evolve. In addition, the pains intensity
indicates the progress or regression of the localized affection.
Dermal efflorescence appears around the affected site depending on the content of
hemorrhagins and hemocoagulation-affecting components, indicating capillary affection and
cutaneous or sub-cutaneous bleeding. Developed redness, petechiae and ecchymoses, as well
as the bitten site, will not require any localized treatment.
The make-up and nature of proteolytic enzymes in the venom will cause more serious
damage to affected tissue, including the development of vesicles and even bullae, mostly
perfused, and the occurrence of early necrosis in skin or even deeper structures. Any bullae
and necrosis should be carefully removed surgically, the beds of which it is necessary to
repeatedly clean gently, especially if hemorrhagic. Bullae and most necrosis will be limited to
the surface structures of skin; the bed is usually vital and reparable after the hemorrhagic
layer is removed. If deeper structures are affected, careful debridement should be repeated as
necessary. The tissue healing process will take many days according to the level of damage.
For instance, in the case of necrosis caused by the Agkistrodon and Crotalus snakes, tissue
will recover in 14 to 77 days, with a mean period of 45 days. Cases of more extensive dermal
necrosis are solved through transplantation of skin.
Edema can be simple, without hemorrhaging, affecting only a part of the limb or
localized around the bite wound, with an intensity that will not prevent perfusion of tissues.
Such edema will not require any other intervention beyond mild cooling and the light
elevation of a limb. Hemorrhagic edema, often accompanied by hemorrhagic dermal
efflorescences, can be more extensive and intense. In such instances, immobilization of an
arm and routine monitoring of the intensity is necessary due to potential perfusion decrease
and ischemization of relevant tissues. Any potential cooling must be exercised very gently;
elevation of the arm will be limited by a possible decrease in perfusion pressure due to
hydrostatic causes. Heavier forms of edema can move from limbs to the trunk and even to the
other side of body.
The most severe form of localized affection involves intense edema preventing tissue
perfusion by developing compartment syndrome. Without any effective action, this will
inevitably result in deep necrosis and possibly amputation. Under circumstances of such a
threat, careful monitoring of blood flow through the limb is of the utmost importance, but
measuring or monitoring of pressure in each compartment affected is much better. The
pressure in tissue should not exceed 45 mmHg (60 cm H2O). If pressure values increase and
perfusion fails, fasciotomy is fully justified, of course, only if administration of antivenom
precedes this and changes in hemocoagulation are stabilized. Preventive execution of
fasciotomy is not indicated, any deep and not fully justified surgical action on damaged
structures may conversely induce a higher level of subsequent affection in the structures.
The duration of the edemas persistence will depend on the amount and composition of
venom; the acute phase will mostly abate within 10 days. Sometimes, in efforts or other loads
 Snakebite: Therapy and Prevention 73

on the tissue, edema as well as increased pain or other sensory or motional abnormities can be
reversible where periods may vary.
Gangrene is a serious but infrequent complication in localized damage. It develops as a
result of localized venom effects and tissue ischemia due to limited perfusion. Pre-emptive
measures involve a protective approach to the affected tissue and avoiding limb ischemization
- efforts to stabilize or minimize the severe edema and fasciotomy or rational anticoagulation
therapy in thromboembolic complications, where indicated. If occurrence of gangrene is
suspected, application of an anti-gangrene serum is indicated.
Apparent lymphadenopathy - an ailment affecting lymphatic tissue is brought on by
venom spreading from the bitten site. It is manifest through not only potential affection of
regional lymph vessels, but also more usually through the swelling of related lymph nodes.
Giving antibiotics to prevent localized infection is not always fully justified, even though
it is recommended by some authors. In South America, with early infection incidence of over
10%, it is obviously of greater importance than in Europe, where the occurrence of
phlegmons or abscesses at and around the bitten site is rather exceptional. Naturally, if
localized infection is suspected or even manifest, administration of antibiotics will be fully
indicated, as well as surgical drainage, where indicated. If the bacterial agent is unknown,
antibiotics well capable of penetrating tissue and boasting a wide spectrum of effects, e.g.
anaerobic flora, should be administered, examples being bactericide aminopenicillins
containing a -lactamase inhibitor, possibly supplemented by metronidasole; in
contraindications, bacteriostatic clindamycine should be applied.
The provision of antitetanic prevention is fully indicated.
Tissue at the bitten site and surrounding it can often be seriously damaged by the venom
components acting locally. The level and time of reparation depends on the medical approach
taken in dealing with such tissue. Any approach of unjustified intensity and invasiveness may,
in some cases, potentiate the developed affection iatrogenically. If there is no indication for
medical action, any handling of the area of localized changes will be contraindicated. Any
well-founded actions should be exercised very gently, with regard to potential traumatization
of the tissue around the site.
The definition of localized damage includes the eye being affected by the venom of
spitting cobras, see chapter 5. 2. 2 Medical first aid. Any corneal and conjunctival contact
with the venom is very painful. The enzymatic destruction of surface corneal and conjunctival
layers will cause corneal ulceration and severe conjunctival inflammation. As a complication,
inflammation of the iris (anterior uveitis) is brought on. Ultimately, the damage can even
result in permanent blindness. The rinsing procedure specified in the framework of first aid,
see chapter 5.2.2 Medicinal first aid, should be followed by repeatedly instilling the affected
eye using local anesthetics, antibiotics and corticoids to eliminate pain and avoid infection,
corneal defects and the onset of post-inflammation changes. Any treatment should proceed
under the surveillance of an optical specialist.

5.3.3.2. Absence of Symptoms, Envenomation Prodromes

In a number of cases, a snakebite will not cause clinical symptoms of envenomation, or
the affection is limited to localized signs. The former is as a result of a warning defensive bite
with no venom discharged - a dry bite. This occurs more often from solenoglyphous viperids
(Viperidae) - in as many as 50% of attacks - than elapids (Elapidae), see chapter 1. 4 The
venom apparatus in snakes. However, since the development of symptoms of envenomation
74 Jiri Valenta

or onset of complications can be delayed by several hours, observing the patient for a day is
useful. Whilst hospitalized, the following is tested as completely as possible in a laboratory
on a routine basis: hemocoagulation (PT, APTT, TT, FBG, FDP, D-dim, AT, PLT), blood
count, basic biochemical examination including hepatic tests (bilirubin, ALT, AST, GMT),
renal function (urea - U, creatinine), or possibly other special analytes (myoglobin, available
hemoglobin, etc.). If no clinical symptoms of envenomation occur within 24 hours and a
second laboratory examination proves negative, the patient can be discharged.
If envenomation is limited to localized symptoms, it is likely only to be an envenoming
by a small quantity of venom with largely localized effects, which mostly occurs following a
snakebite by lesser rattlesnakes (Crotalinae) or viperines (Viperinae) of a less dangerous
type. Under such circumstances, a patient is treated according to the damage sustained and its
intensity. If the case requires no further intervention by a hospital, the patient is discharged
home or placed in the care of a hospital ward following 24-hour observation in case of
repeated negative or minor laboratory findings (see above). Nevertheless, a check-up or the
provision of antitetanic prevention is required for both of the above.
Early prodromes of envenomation are largely of the gastrointestinal type: nausea and
vomiting - happening soon after the incident in many cases - pain in the epigastrium or
hypogastrium, and diarrhea. Affection of the central nerve system, CNS, is another case of
non-specific symptomatology. It can be exhibited by cranial pain, languor and vertigo, but
rarely by lightheadedness or syncopes, and loss of consciousness. If the effect on the CNS is
more severe or persists, the reason must be found and resolved, e.g. hypotension or possible
bleeding into the CNS. Increased body temperature may be involved, as well as shivering and
feverishness, plus there will be profuse sweating and leukocytosis discovered by laboratory
testing. Responses within the vegetative reactions may be affected in a non-specific manner.
Thirst, sinus tachycardia and hypertension that could occur in early phase of
envenomation should be assigned to the previously specified affection of the vascular system
with extravasation, or diagnosed as a psychosomatic reaction by the victim.
Treatment of the prodromal symptomatology comprises sedation and antiemetic therapy;
chlorpromazine at a dosage of 25-50 mg per adult and 1 mg/kg of body weight per child is
usually found as effective due to its strong antiemetic effect, sedative quality, and vegetative
system stabilizing properties.
The above-mentioned signs of non-specific symptomatology point to specific antivenom
therapy being required in most cases, and often precede other symptoms of systemic
envenomation. Prodromes usually abate within several hours, but have been known to persist
for 48 hours.

5.3.3.3. Affection of Nerve Tissue and Neuromuscular Connections

Neurotoxicity symptoms in their mildest form are almost indeterminable clinically,
involving the impact of a low quantity of presynaptically acting neurotoxic PLA2 from the
venom of some viperine snakes (Viperinae), examples being the European viper species,
Vipera ammodytes and V. aspis. However, extreme symptoms are exhibited as fatal
respiratory muscle paralysis largely caused by the curare-like effect of postsynaptically acting
neurotoxins or, most severely, their combination with potent neurotoxic PLA2 from the
venom of elapids (Elapidae).
The effect of the larger quantity of presynaptically acting neurotoxins of PLA2 type
contained in the venom of certain viperid snakes (Viperidae), like the Russels snake (Daboia
 Snakebite: Therapy and Prevention 75

russelli siamensis) or the South American rattlesnake (Crotalus durissus), can be clearly
discerned clinically. If fully developed, it is principally manifest in the area of the cranial
nerves not only through ptosis, ophtalmophlegia with double or fuzzy vision, dysphagia with
increased salivation, dysarthria, a variable degree of visible facial muscle paralysis, but also
through general muscular weakness. However, such apparent neurological symptomatology
in envenomation by viperid snakes (Viperidae) is rather rare, plus paralysis of the respiratory
muscles never occurs.
Any enzymatic damage to nerve endings by PLA2 is largely irreversible; symptomatic
treatment does not exist and would be unnecessary. Any further propagation of nerve ending
damage can be only prevented by immunologically unbinding neurotoxic PLA2 through early
administration of a relevant antivenom.
Paralysis of striated muscles is characteristic for venom neurotoxicity by elapid snakes
(Elapidae). Curare-like neurotoxins with postsynaptic effects, sometimes combined with
highly effective presynaptically acting enzymes, are capable of invoking paralysis of
respiratory muscles and fatal respiratory failure. The paralysis affecting the striated muscles
proceeds craniocaudally, preceded by cranial nerve affection symptoms described in the
previous section. Affliction by a venom possessing a substantial quantity of neurotoxins can
cause fatal paralysis in just minutes, although it usually takes several dozen minutes, but up to
10 hours is not unheard of. In a number of cases, consciousness is not affected, with
suffocation occurring whilst the victim is fully lucid.
Symptomatic treatment of such a status involves securing the patients respiratory
airways using tracheal intubation and mechanical ventilation. The postsynaptic curare-like
action of neurotoxins can be diminished or eliminated by acetylcholinesterase inhibitors. To
test the inhibitors efficiency, 10 mg of edrophonium chloride can be administered to an adult
patient. If positive, the victims status is greatly improved, peaking after five minutes and
then abating. Atropine sulphate, 0.5 mg for an adult patient, can be used as premedication to
block the muscarinic effect. If the test proves effective, treatment can continue via applying
neostigmine methylsulphate, a long-term cholinesterase inhibitor, at a dosage of 0.5 mg per
adult IV or SC every 20 minutes.
The procedure above has been corroborated following envenomation by the neurotoxins
of Asian cobra species: Naja naja, N. kaouthia, and N. philippiensis. However, it seems
ineffective when envenoming has occurred by neurotoxins combined with a fatal component
of presynaptically acting enzymes, as found in the venom of mambas (Dendroaspis sp.),
kraits (Bungarus sp.), Australian tiger snakes (Notechis sp.), taipan (Oxyuranus), and other
snakes. Successful symptomatic treatment should not be considered an alternative to applying
antivenom, but rather a useful complement to specific immunotherapy, which must be
administered in every case, unless contraindicated.

5.3.3.4. Rhythm and Cardiac Output Disorders

Heart function can be directly affected by the action of specific cardiotoxins, typically
inherent in venoms of the cobra (Naja) and Gabon and rhinoceros vipers, Bitis gabonica or B.
nasicornis, respectively. The effect of toxins on the conduction apparatus will be displayed in
the form of rhythm disorders in terms of tachycardia or bradycardia including AV-blocks,
plus the occurrence of non-physiological rhythms and extrasystoles. Myocardial affection
results in reduced myocardial contractility, i.e. cardiac output, which potentiates circulation
76 Jiri Valenta

collapse in the presence of both vasodilation and extravasation. Subsequently, the temporary
increase in coronary flow brought on by vasodilation can collapse due to loss of vessel tone
Specific effects wrought by cardiotoxins may be controlled by administering antivenom,
nevertheless, if the disorder is more severe and antivenom is not available or contraindicated,
symptomatic treatment by anti-arrhytmics is justified depending on the particular
circumstances, including the support of myocardial contractility using catecholamines, see
chapter 5. 3. 3. 5 Hypotension and shock.
Arterial vascular resistance, including that of coronary arteries, is increased by the
specific effect of sarafotoxins of Atractaspididae snakes. This will result in systemic
hypertension and myocardial ischemia with the relevant ECG changes. If that is the case,
vascular resistance and systemic pressure should be reduced with additional support of the
coronary flow through vasodilation therapy using nitrates.

5.3.3.5. Hypotension and Shock

Decreasing blood pressure in envenomation by snakes may have multiple causes. Aside
from hypotension, brought on by an anaphylactic reaction, see chapter 5. 2. 2 Medical first
aid, an early cause for vasodilatation is the release of bradykinin and, obviously, certain
venom components acting directly on the vessel wall or vasoregulation centre. Kininogens are
venom components in viperid snakes (Viperidae), such as the snakes of Bitis, Vipera and
Macrovipera genera, rattlesnakes (Crotalus), Australian terrestrial species, and other snakes,
see chapter 3. 3. 2. 3 Venom components with effects on the cardiovascular apparatus.
Extravasation is another reason for this, either discernable at a varied systemic level or
locally or severely, and is typically caused by hemorrhagins or other enzymes, resulting in
reduced intravascular volume. Enzymes acting this way are contained in venoms of a number
of viperids (Viperidae), such as the Macrovipera snakes, Bothrops and Lachesis snakes,
Crotalus species, Asian pit vipers (Trimeresurus), and others, see chapter 3.3.2.4. Venom
components with effects on the vessel wall. In addition, potential bleeding is another factor in
reduced vascular volume as well. Naturally, the effects of both accumulate in some cases.
Severe hypotension may result in circulation collapse, and even in the shock, preceded
by loss to adequate perfusion of tissues. In certain cases of envenomation, hemodynamic
disorder can be potentiated by reduced myocardial contractility.
In cases of slight systemic pressure decrease, a mild increase in intravascular volume
through the infusion of crystalloids is sufficient. If the hypotension is more severe, additional
application of colloids infusions that can be maintained in the circulation over longer periods
will be useful. Should hemocoagulation be affected in terms of diminished hemostasis,
dextran preparations further dimming platelet function must not be applied. Albumine
presents a superior means of compensation for volume. Administering at least 10 ml/kg of
body weight of fresh frozen plasma (FFP) will provide for not only volumoexpansion, but
also a certain level of normalization of potential DIC-like hemocoagulation disorder. Thus,
applying the plasma will be the most helpful solution in cases of hypotension in the presence
of a hemostasis disorder. By replenishing circulating volume or moderately increasing it,
blood pressure can be stabilized in most cases, especially when an antivenom is administered
at the same time. Moreover, increased diuresis induced by volume will also prevent renal
failure from emerging.
If hypotension continues despite volume therapy, or circulation collapse and shock are
intimated, administering vasopressoric catecholamines as an intravenous infusion is justified.
 Snakebite: Therapy and Prevention 77

For a patient weighing 70 kg, a medium dose of norepinephrine, i.e. 0.1 g/kg/min is
achieved by diluting 4 mg in 50 ml of volume and applied at a speed of 5 ml per hour. The
treatment will require continual monitoring of blood pressure and prompt infusion speed
control depending on the actual situation. Measuring venous pressure is useful, even in
instances of higher volumotherapy.
If envenomation has been caused by venom in which cardiotoxic myocardial contractility
-reducing components - can be expected, see chapter 5. 3. 3. 4 Rhythm and heart output
disorders, the giving of catecholamines with a -mimetic effect, e.g. dobutamine with a mean
dosage of 5 g/kg/min, is justified in serious cases.
Circulatory failure therapy includes oxygen therapy, along with mechanical ventilation
accompanied by comprehensive intensive care if severe shock associated with organ
hypoperfusion develops.

5.3.3.6. Hemocoagulation Disorders

Hemocoagulation disregulation or disorder is caused by various kinds of intervention by
venom components in the plasma coagulation system as well as platelet, endothelial and sub-
endothelial function. Lighter disorders will be exhibited only via laboratory findings, while
those more severe mostly manifest themselves through clinical signs of increased
hemorrhage through to unmanageable bleeding from wounds, mucous membrane tissue, the
nose, mouth, gums and conjunctiva, and up to bleeding into the organs - GIT, brain, body
cavities, and hematuria. However, the influence may also be of a procoagulative nature,
involving the developing of microembolization or thromboembolism in the early or late phase
of the affliction.
Activating the hemocoagulation system results in a DIC-like consumption disorder. As
this progresses, for instance, following envenomation by the venom of Echis snakes,
especially in collaboration with hemorrhagins, a certain degree of multiple organ dysfunction
syndrome (MODS) occurs, which is most frequently associated with pulmonary tissue of the
ALI/ARDS type being affected and oliguric renal failure. One of the reasons for this
development is the presence of microthrombotization and interstitial edema when capillary
integrity is damaged; symptoms include varied levels of respiratory distress syndrome, anuria,
elevation of bilirubin and hepatic enzymes, etc.
Hemocoagulation-affecting venom components are found in the majority of viperids
(Viperidae), principally the Echis and Daboia snakes, Bothrops and Lachesis snakes, and
certain Crotalus species. For other taxons, hemocoagulation is affected by the venoms of sea
snakes and sea kraits, in addition to certain Australian terrestrial elapids and the Naja cobra
genus, see chapter 3. 3. 2. 5 Venom components with effects on hemocoagulation.
Symptomatic treatment of hemorrhage is applied if antivenom administration is
contraindicated or unavailable either temporarily or long-term, or merely to provide support
for the primary treatment by antivenom. The priority of symptomatic treatment increases
following envenomation by prothrombin activator-containing venoms that possess poor
antigenicity, where specific immunotherapy may fail in some cases. The treatment must be
based on laboratory results for the given disorder and presumed type of affection. In the later
phases of developed DIC-like consumption disorder, which may already proceed as circulus
vitiosus of pathophysiological mechanisms without the cooperation of venom components,
symptomatic treatment is an option for managing status.
78 Jiri Valenta

In the case of changes in hemocoagulation examination, the test must be repeated after a
certain interval. In early phases, if any further development of the disorder is expected after at
least four hours and in the phases of abatement and convalescence, a period of 12-24 hours
until results normalize is sufficient.
Prolongation of PT, APTT and TT is usually the rule for the majority of PCS affection
types. If the prolongation is not extreme, no further treatment is required. However, parallel
RT prolongation means, together with high FDP levels, the presence of fibrin-soluble
complexes in the circulation. These indicate increased fibrinogenolytic and fibrinolytic
activity caused by hyperactivation of plasminogen or the presence of proteases of a similar
activity contained in the snake venom. Consequently, the parallel presence of a high D-dim
titer means a probability of widespread thrombin or thrombin-like activity with intravascular
development of stabilized fibrin-polymer complexes - a DIC-like consumption disorder. Both
types of affection will result in hypofibrinogenemia or even afibrinogenemia. In the initial
stages of the DIC-like disorder, AT activity may not be reduced. This is brought about by a
fundamental AT non-inhibitive enzyme with a thrombin-like activity, such as meisothrombin,
on the development of the disorder.
Any changes to platelet function that may cooperate in the affection in a number of cases
can be made evident through thromboelastographic blood examination - TEG.
Examining platelets using flow cytometry, as well as determining the activity of
coagulation factors, tPA, PAI, FPA, PF1.2, TAT, vWF, and other hemocoagulation laboratory
parameters, would be worthwhile for diagnosing the affection, however, it is not a routine
procedure at health facilities.
If hypofibrinogenemia or defibrination occurs with values decreased near zero and the
patient is not bleeding, applying a fibrinogen concentrate is not recommended. Replenishing
its quantity in the circulation without eliminating the cause for the defibrination will result in
a rise in FDP titer and fibrin-soluble complexes with possible consequent bleeding. If the
patient is bleeding, fibrinogen is replenished to the level of at least 0.5-1.0 g/l using
fibrinogen concentrates or fresh-frozen plasma that simultaneously contains coagulation
factors and inhibitors; the amount should be 10-20 ml/kg of weight. Administration of
hemocoagulation factor concentrates is indicated if a critical drop in the factors is found, with
indications including persistent obstinated bleeding. Relative contraindication of the
application is exhibited by an early phase of a DIC-like disorder with high D-dim values.
If AT activity has decreased due to insufficient production, consumption, or degradation
by proteases contained in venoms, substitution is recommended.
Heparin treatment in hemocoagulation disorders is recommended in cases of DIC-like
disorder following a snakebite by the Echis, Daboia, and Macrovipera snakes, as it will have
a pre-emptive effect should fibrin formations develop. In addition, it seems to reduce the
incidence of thrombocytopenia and DIC, but even hypotension and acute renal failure.
According to the work of Paul et al., 2003, with doses of 5,000 units and a further 2,500 units
every 8 hours, the treatment will reduce, in parallel with antivenom being administered, the
mortality of persons envenomed by the saw-scaled viper (Echis carinatus) and the Russels
viper (Daboia russelli) from 26% to 19%. Of course, these results are not highly significant.
Nevertheless, heparin therapy in terms of severe acute progress of DIC with associated
bleeding is not fully indicated. Inhibition of thrombin activity is not always determined by the
presence of the AT-heparin complex, consequently, heparin administration may not be
helpful if the cause lies elsewhere. However, where a previously existent DIC syndrome has
 Snakebite: Therapy and Prevention 79

been diagnosed and its status has been stabilized, i.e. bleeding has stopped, mini-
heparinization using UFH (non-fractionated heparin), or more preferably a prophylactic dose
of LMWH (low molecular heparin), is recommended until laboratory tests are fully
normalized.
Applying antifibrinolytics, such as tranexam acid, can be effective if bleeding has been
caused by increased plasminogen activation. Nevertheless, this concurrently results in
blocking the physiological destruction of microembolizations that might develop, preventing
recanalization of relevant sections, thereby potentiating the occurrence of organ failure as part
of the DIC-like disorder.
It is recommended to substitute platelets if bleeding still continues, in decline under
20,000-50,000/mm3, while the same action in erythrocytes should be taken in case of decrease
in Hct, i.e. hematocrite - erythrocyte concentration, below 25% to 30%.

5.3.3.7. Affection of Muscles

In general, snake venom substances with myotoxic effects consist of two types of
components: non-enzymatic toxins and enzymes of PLA2 type; their effect is often associated
with additional destructive activities; see chapter 3.3.2.7 Venom components possessing a
myotoxic activity.
Myotoxic venom components are present in most viperids (Viperidae), Australian
terrestrial elapid snakes and some sea snake species. For instance, a clinically relevant portion
of myotoxins is in the venom of the Russels viper (Daboia russelli), Levantine viper
(Macrovipera lebetina), South American rattlesnake (Crotalus durissus), rattlesnakes
(Crotalus sp.), lanceheads (Bothrops sp.), and Asian pit vipers (Trimeresurus sp.); as regards
elapids, this concerns the mainland tiger snake (Notechis scutatus) and the coastal taipan
(Oxyuranus scutellatus). Inherent in many snakes is a certain quantity of myotoxic
components, therefore, rhabdomyolysis and its consequences should be considered every time
envenomation occurs with a venom containing a high rate of enzyme activities.
The action of myotoxic components causes striated muscle cells to be destroyed, a
process called rhabdomyolysis, which results in minor or even major myonecrosis. Muscular
destruction is accompanied by muscular pain, such as in envenomations by the Russels viper
(Daboia russelli). Myoglobin and kalium ions are released into circulation. A higher amount
of myoglobin will cause obstruction in the area of glomerular capillaries and renal tubules,
especially if hemolysis proceeds concurrently, thus free hemoglobin is involved, presenting a
predisposition for renal insufficiency through to acute renal failure.
Hyperkalemia resulting from surplus kalium via intracellular deposits released, together
with oliguria, may eventually cause arrhythmia, which may even give rise to circulation
blockage in a non-treated person.
One elementary form of treatment tackling exposure to a high amount of myotoxins
involves antivenom therapy. Enzyme neutralization and the prevention of continued
destruction is only possible by an antigen, as well as for presynaptically acting enzyme
neurotoxins. Accordingly, an antivenom should be given as soon as possible whenever a
major proportion of myotoxins in the venom is expected.
Symptomatic treatment of status is limited to an adequate parenteral supply of liquids to
prevent a decrease in perfusion pressure in glomerules and facilitate production of a sufficient
quantity of primary urine. The importance of effective infusion therapy will be emphasized by
80 Jiri Valenta

hypotension developing through the action of relevant venom components, which especially
concerns envenomation by viperids (Viperidae).
Hyperkalemia may temporarily be stabilized by intravenous application of calcium in the
form of gluconate or chloride, or by using an ion exchanger and peroral and rectal application
of polystyrene sulphonic acid salts. If diuresis continues, it should be supported by a diuretics,
such as furosemid.

5.3.3.8. Renal Failure

Acute renal failure, mostly of the oliguric type, occurs via envenomation by snake
venoms through the action of several mechanisms. These include myoglobinuria and
hemoglobinuria, see chapter 5. 3. 3. 7 Affection of muscles and decreased perfusion pressure
and glomerule blood flow in hypotension due to vasodilatation and reduced intravasal volume
through extravasation or hemorrhage, plus chapter 5. 3. 3. 5 Hypotension and shock. Acute
renal failure may also be triggered due to glomerular perfusion obstruction by microthrombi
in instances of DIC-like hemocoagulation disorder associated with insufficient fibrinolysis.
The final specific cause presented is primary nephrotoxicity: direct damage of renal tissue -
glomerules and tubules - by enzymatic venom components. This type of mechanism has been
disputed by some authors, as venom components with a specific action on renal tissues
remain to be evidenced. However, they cannot be definitely precluded, see chapter 3. 3. 2. 8
Venom components affecting the kidneys.
Affection of renal function can be expected namely following envenomation by viperine
(Viperinae) and crotaline (Crotalinae) snakes. Nevertheless, renal damage cannot be
precluded even after envenomation by other snakes. The risk of occurrence can be estimated
according to the clinical progress of envenomation.
A key preventative action in renal failure following a snakebite is to secure adequate
perfusion pressure and sufficient renal blood flow. If systemic pressure cannot be sustained
by increasing intravascular volume, vasopressoric therapy is indicated, see chapter 5. 3. 3. 5
Hypotension and shock. As regards the necessity to maintain sufficient renal blood flow,
catecholamines are indicated if the condition of the circulation so allows, but not before
intravasculer volume is increased. Urgent vasopressoric treatment is at all times supported by
sufficient volume compensation, especially when liquids from the vessel bloodstream are
being lost through widespread extravasation into edema or through bleeding.
Again, any myoglobinuria and hemoglobinuria will require increased intravascular
volume and enhanced production of primary urine to reduce such molecules building up in
renal tubules.
The application of heparin is recommended, i.e. just to avoid or at least reduce the
development of fibrin formations and microthrombosis, including those decreasing
glomerular perfusion and contributing towards emergent renal failure, see chapter 5. 3. 3. 6
Hemocoagulation disorders.
Once renal failure has occurred, treatment does not differ from that of failure based on a
different etiology. If increasing vessel volume and application of diuretics proves insufficient
to ensure adequate diuresis and satisfactory urea and creatinine values in the serum, either one
of the continual renal replacement therapy (CRRT) methods - hemofiltration or hemodialysis,
or intermittent hemodialysis is indicated depending on a patients status and requirements
plus the capabilities of the health facility. Execution of (C)RRT in cases of severe activation
of DIC-like hemocoagulation disorder, such as by Echis snakes, may be frequently
 Snakebite: Therapy and Prevention 81

complicated by coagula formed in the (C)RRT system, even if adequate heparinization is

employed and heparinized hemofilters are used. If that is so, the regional citrate
anticoagulation method is a suitable option according to the experience of the authors
workplace.
The majority of cases of acute renal failure will have a reversible course. Nevertheless,
severe envenomation with complications or inadequate treatment may ultimately result in
irreversible damage and chronical renal failure could emerge.

5.3.4. Plasmaferesis Therapy

Plasmaferesis can be a satisfactory alternative to specific therapy by antivenoms

whenever an antivenom is not available, or in the case of insufficient clinical effect of a
usable dose. The method can be applied even when the affected individual suffers from an
allergy to the antivenom. In the authors experience, using this method is helpful typically in
envenomation involving more severe symptoms of hemocoagulation disorder. Its
effectiveness can be found through both laboratory examination and clinically, for instance,
by reducing PT and APTT.
Plasmaferesis can be combined with the administration of antivenom when recurrence of
symptoms occur. In such cases, the application of antivenom should alternate plasmaferesis
following recurrence of symptoms or serious laboratory findings. In severe cases, the method
must be applied repeatedly subject to the progress of envenomation and as required. The
benefits of plasmaferesis include an absence or at least reduced incidence of serum sickness
caused by high doses of antivenoms, although the disadvantages include a necessary technical
background for the same and the high cost in certain regions.

5.4. CONVALESCENCE FOLLOWING ENVENOMING

The acute phase of common localized affection - edema - will mostly abate within 10
days. The time necessary for sufficient epithelization in instances of dermal damage, bullae,
and surface dermal necrosis will be longer. Often such damage heals without any visible
scarring unless the skin is affected by necrosis at full depth. Deep dermal necrosis to a large
extent may require transplantation of skin following cleaning of the wound bed. Gross
damage to deep tissue structures, muscles and nerves may result in permanent deformations
including disorder of motional functions of the affected part of limb. In many cases, even
slightly affected tissue suffers from a certain sensation or painful symptoms over longer
periods in the order of months or years.
Convalescence following passed system envenomation depends on the severity of the
process and degree of tissue damage. The severe action of proteolytic enzymes may even
cause irreversible affection of certain systems, such as muscles, nerve endings, kidney, lungs,
etc., which may become evident on the function or possible morphological reconstruction of
such systems. Rehabilitation and convalescent care is symptomatic and will be implicated by
the type and level of affection.
82 Jiri Valenta

Envenomation by the majority of Viperinae and Crotalinae species is associated with

affection as far reaching as partial desquamation of endothelium and activation of
hemocoagulation processes at various levels. This will result, following completion of an
acute phase, in persistent activation of the system and prothrombotic status of the patient,
which is visible in most cases only through an increased amount of the final product formed
throughout the hemocoagulation in process - D-dim. Such a status may pose a predisposition
to thromboembolic complications occurring and should be rectified through application of
low molecular heparins, as well as in patients at risk of deep venous thrombosis, until the
cause abates, i.e. until hemocoagulation tests have been fully normalized.

REFERENCES
ALLOATTI, G., GATTULLO, D., DALLA VALLE, R., et al. The haemodynamic effect of
Bitis nasicornis (Rhinoceros Horned Viper) venom. Gen Pharmacol, 1991, 22, No. 1, pp.
203206.
AMSTUTZ, P., MOYO, JS. Disseminated intravascular coagulations. Cah Anesthesiol, 1996,
44, No. 3, pp. 219228.
AN, Y., YANG, N., ZHU, X. Management of coagulation dysfunction in critically surgical
patient. Zhonghua Wai Ke Za Zhi, 1996, 34, No. 6, pp. 348351.
BLAYLOCK, RS. Pressure immobilisation for snakebite in southern Africa remains
speculative. S Afr Med J, 1994, 84, No. 12, pp. 826827.
BOYER, LV., SEIFERT, SA., CLARK, RF., et al. Reccurent and persistant coagulopathy
following Pit Viper Envenomation. Arch Intern Med, 1999, 159, No. 7, pp. 706710.
COWLES, RA., COLLETTI, LM. Presentation and treatment of venomous snakebites at a
Nothern Academic Medical Center. Am Surg, 2003, 68, No. 5, pp. 445449.
DART, RC., GUSTAFSON, RA. Failure of electric shock treatment for Rattlesnake
envenomation. Ann Emerg Med, 1991, 20, No. 6, p. 659661.
DASSANAYAKE, AS., KARUNANAYAKE, P., KASTURIRATNE, KT., et al. Safety of
subcutaneous adrenalin as prophylaxis against acute adverse reaction to anti-venom
serum in snakebite. Ceylon Med J, 2002, 47, No. 2, pp. 4849.
ELLIS, AK., DAY, JH. Diagnosis and management of anaphylaxis. Can Med Ass J, 2003,
169, No. 4, pp. 307311.
GERMAN, BT., HACK, JB., BREWER, KL., et al. Pressure-immobilization bandages delay
toxicity in a porcine model of Eastern Coral Snake (Micrurus fulvius fulvius)
envenomation. Ann Emerg Med, 2005, 45, No. 6, pp. 603608.
GOLD, BS. Neostigmine for the treatment of neurotoxicity following envenomation by the
Asiatic Cobra. Ann Emerg Med, 1996, 28, No. 1, pp. 8789.
HABIB, AG., GEBI, UI., ONYEMELUKWE, GC. Snake bite in Nigeria. Afr J Med Sci,
2001, 30, pp. 171178.
HOWARTH, DM., SOUTHEE, AE., WHYTE, IM. Lymphatic flow rates and first-aid in
simulated peripheral snake envenomation. Med J Austr, 1994, 161, No. 1112, pp. 695
700.
HOWE, NR., MEISENHEIMER, JL. Jr. Electric shock does not save snakebitten rats. Ann
Emerg Med, 1988, 17, No. 3, pp. 254256.
 Snakebite: Therapy and Prevention 83

ISMAIL, M., MEMISH, ZA. Venomous snakes of Saudi Arabia and the Middle East: a
keynote for travellers. Int J of Antimikrob Agents, 2003, 21, pp. 164169.
JOHNSON, EK., KARDONG, KV., MACKESSY, SP. Electric shocks are ineffective in
treatment of lethal effect of Rattlesnake envenomation in mice. Toxicon, 1987, 25, No.
12, pp. 13471349.
JOLY, LM., SERMET, A., TURAK, B., SAMAMA, CM. Massive haemorrhage after dorsal
decompressive laminectomy. Ann Fr Anesth Reanim, 2005, 24, No. 10, pp. 12781281.
KORNALIK, F., VORLOVA, Z. Non-specific therapy of a hemorrhagic diathesis after a bite
by a zouny Bothrops asper (Barba Amarilla): a case report. Toxicon, 1990, 28, No. 12,
pp. 14971501.
LALLOO, DG., THEAKSTON, RD. Snake antivenoms. J Toxicol Clin Toxicol, 2003, 41,
No. 3, pp. 227290.
LEE, SY., LEE, CY., CHEN, YM., et al. Coronary vasospasm as the primary cause of death
due to the venom of the burrowing asp, Atractaspis engaddensis. Toxicon, 1986, 24, No.
3, pp. 285291.
LI, QB., HUANG, GW., KINJOH, K., et al. Hematological studies on DIC-like findings
observed in patients with snakebite in south China. Toxicon, 2001, 39, No. 7, pp. 943
948.
MARSH, NA., WHALER, BC. The Gaboon Viper (Bitis gabonica): its biology, venom
components and toxinology. Toxicon, 1984, 22, No. 5, pp. 669694.
MCKINNEY, PE. Out-of-hospital and interhospital management of crotaline snakebite. Ann
Emerg Med, 2001, 37, No. 2, pp. 168174.
MEIER, J., WHITE, J. (Eds). Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995, 752 pp.
POCHANUGOOL, C., WILDDE, H., BHANGANADA, K., et al. Venomous snakebite in
Thailand II: clinical experience. Mil Med, 1998, 163, No. 5, pp. 318323.
PREMAWARDHENA, AP., De SILVA, CE., FONSEKA, MM., et al. Low dose
subcutaneous adrenalin to prevent acute adverse reactions to antivenom serum in people
bitten by snakes: randomised, placebo controlled trial. Br Med J, 1999, 318, No. 7190,
pp. 14511452.
PAUL, V., PRAHLAD, KA., EARALI, J., et al. Trial of heparin in viper bites. J Assoc
Physicians India, 2003, 51, pp. 163166.
SPILLER, HA., BOSSE, GM. Prospective study of morbidity associated with snakebite
envenomation. J Toxicol Clin Toxicol, 2003, 41, No. 2, pp. 125130.
STEWARD, CJ. Snaker bite in Australia: first aid and envenomation management. Accid
Emerg Nurs, 2003, 11, No. 2, pp. 106111.
SUTHERLAND, SK. First aid for snakebite in Australia. Published by the Commonwealth
Serum Laboratories Parkville 3052, 1979.
SUTHERLAND, SK. The pressure immobilisacion technique. Med J Aust, 1994, 161, pp.
700701.
SUTHERLAND, SK. Treatment of snake bite. Aust Fam Physisian, 1990, 19, No. 1, pp. 21,
2442.
SUTHERLAND, SK., COULTER, AR. Early management of bites by Eastern Diamondback
Rattlesnake (Crotalus adamanteus): studies in monkeys (Macaa fascicularis). Am J Trop
Med Hyg, 1981, 30, No. 2, pp. 497500.
84 Jiri Valenta

SUTHERLAND, SK., COULTER, AR., HARTUS, RD. Rationalisation of first-aid measures

for Elapid Snakebite. Lancet, 1979, 1, No. 8109, pp. 183185.
SUTHERLAND, SK., NOLCH, G. Dangerous Australian animals. Flemington : Hyland
House Publishing, Australia, 2000.
THEAKSTON, RD., WARRELL, DA., GRIFFITHS, E. Report of WHO workshop on
standardization and control of antivenoms. Toxicon, 2003, 41, No. 5, pp. 541557.
VALENTA, J., SIMAK, J. Intoxikace zivocisnymi jedy. In POKORNY, J. (Ed.), Urgentni
medicina. Praha : Galen, 2004, pp. 258265 (in Czech).
WHITE, J., WARRELL, D., EDDLESTON, M., et al. Clinical toxinology where are we
now? J Toxicol Clin Toxicol, 2003, 41, No. 3, pp. 263276.
WARRELL, DA. Bites of Venomous Snakes. N Engl J Med, 2002, 347, No. 22, pp. 1804
1805.
WATT, G., MEADE, BD., THEAKSTON, RD, et al. Comparison of Tensilon and antivenom
for the treatment of Cobra-bite paralysis. Trans R Soc Trop Med Hyg, 1989, 83, pp. 570
573.
WATT, G., THEAKSTON, RD., HAYES, CG., et al. Positive response to edrophonium in
patients with neurotoxic envenoming by Cobras (Naja naja philippiensis). N Engl J Med,
1986, 315, No. 23, pp. 14441448.
WINKEL, KD., HAWDON, GM., LEVICK, N. Pressure immobilisation for neurotoxic snake
bites. Ann Emerg Med, 1999, 34, No. 2, pp. 294295.
WOLLBERG, Z., SHABO-SHINA, R., INTRATOR, N., et al. A novel cardiotoxic
polypeptide from the venom of Atractaspis engaddensis (Burroving Asp): cardiac effects
in mice and isolated rat and human heart preparations. Toxicon, 1988, 26, No. 6, pp. 523
534.
ZAMUDIO, KR., HARDY, DL. Sr., MARTINS, M., et al. Fang tip spread, puncture distance,
and suction for snake bite. Toxicon, 2000, 38, No. 5, pp. 723728.
Chapter 6

ENVENOMING AND SNAKEBITE TREATMENT IN

SPECIFIC SNAKE GROUPS

6.1. FAMILY: COLUBRIDAE, COLUBRIDS

The Colubridae family contains as many as 2,500 snake species classified into a number
of sub-families, and recently into 305 genera, with only some of them ranked as venomous
snakes.
The saliva gland in these snakes has modified into the venomous Duvernoys gland,
featuring a collecting duct that opens near enlarged grooved rear fangs. Due to the structure of
their venom apparatus, such creatures are termed opistoglyphous snakes; see chapter 1. 4 The
venom apparatus in snakes. Signs of envenoming in humans can be induced by as few as 30
species, with only five being capable of delivering a fatal course. The majority of the
remainder only possess islets of Duvernoys gland tissue beside the roots of teeth, which are
not enlarged and lack grooves. This means they have no injecting mechanism and cannot be
considered venomous animals, even though they are still capable of releasing a certain
amount of venom into a victim after a bite. In such cases, envenoming is typically
coincidental in nature; an example being a snakebite suffered by a frog taxidermist from the
western hog-nosed snake (Heterodon nasicus) the creature reacting to the smell of frogs
(Rehak, 1990). However, an exceptional local response after a snakebite by a non-venomous
colubrid snake may even occur in humans. In the Czech Republic, two such events have been
described, involving bites from the smooth snake (Coronella austriaca) (Rehak, 1992).
The venomousness of opistoglyphous snakes has always been underestimated;
nonetheless, several species may cause severe envenomation, which could potentially prove
fatal. For instance, two globally leading herpetologists died following bites by opistoglyphous
colubrid snakes: Karl P. Schmidt (1890-1957), who was bitten by an African boomslang
(Dispholidus typus) and Robert Mertens (1894-1975), bitten by a twig snake species
(Thelotornis kirtlandii).
This chapter is going to provide more details on two groups of snakes: firstly, it will
describe the five genera of the Colubrinae subfamily most important in terms of toxinology -
Boiga, Dispholidus, Malpolon, and Thelotornis, formerly entitled Boiginae, a subfamily that
was once considered separate but later disputed. The Natricinae subfamily, more specifically,
Rhabdophis genus, makes up the second group.
86 Jiri Valenta

As for other venomous and potentially venomous colubrids, only certain members are
listed in brief below due to the extreme number of genera, their disputable classification as
subfamilies, and the relatively low level of risk they pose.

6.1.1. Rhabdophis Genus

Species: The tiger grooved-neck keelback (Rhabdophis tigrinus), the cause of

envenomation described in Japan, and the red-necked keelback (Rhabdophis subminiatus),
with cases of envenoming described from European and North American captive collections,
can be deemed the most significant species in terms of epidemiology of the 17 comprising
this colubrid genus.
Other names: FR: Serpent tigrer dAsie; JAP: Yamakagashi (R. tigrinus). In native
languages: Ular Picung, Ular Lampeh (R. subminiatus).
Description: Medium bodied colubrids that mostly grow to 100 cm, but rarely to 150 cm,
they tend to possess large rear fangs placed in the anterior part of the upper jaw. They were
considered non-venomous for a long time and used to be sold and kept as such.
Home range and habitat: The localities inhabited by R. subminiatus mostly concern the
rather humid or wet and largely forested areas of NE India, S China, Hainan, the former
Indochinese region (Vietnam, Laos, Cambodia), the Malayan Peninsula, and Indonesia, while
the R. tigrinus resides in identical habitats in the territories of China, Hainan, Taiwan, Korea,
Russia, and Japan.
Toxins: The Duvernoys gland venoms of R. subminiatus and R. tigrinus are relatively
effective, with LD50 for mice equalling 6.5 mg/kg or 0.26 mg/kg of body weight respectively.
They contain a prothrombin-activator similar to ecarin in the saw-scaled viper (Echis
carinatus). An FX activator is also possibly present. The process of C protein activation,
increased fibrinolysis, and FBG degradation in envenoming are unlikely to be caused by
direct action of the venom components; they tend to develop as pathophysiological results of
thrombin activity at a systemic level and tPA impact.
Local symptoms of envenoming: Slight non-painful edema and bleeding from the bitten
site can be followed by ecchymoses and petechiae developing around the affected area. More
rarely, larger hematoms may appear.
Systemic symptoms of envenoming: Prodromes, like headache, nausea, and vomiting, will
commence anywhere between 30 minutes to several hours after a bite, resulting in fainting
more occasionally. Moreover, hemocoagulation disorder of the DIC type evolves with
symptoms apparent via laboratory testing, though these may take the form of clinical
symptoms in more severe envenomations. Bleeding from incisions, small traumas and gums,
epistaxis and perfused dermal efflorescences arise, followed by possible hematuria and
hematemesis with resulting enterorrhage. The symptoms of bleeding can persist as long as
five days, while changes in laboratory findings can be recorded for up to 40 days. Despite the
DIC syndrome caused by the envenoming, signs of tissue and organ damage resulting in
multiple organ dysfunction syndrome (MODS) are typically not present, although renal
failure may follow in rare cases.
Laboratory findings: Signs of DIC in progress are typically marked, i.e. decreased
fibrinogen levels, extending as far as afibrinogenemia, increased FDP concentration (D-dim),
thrombocytopenia, microangiopathic hemolysis, reduced AT activity, decreased levels of
 Envenoming and Snakebite Treatment in Specific Snake Groups 87

other coagulation factors and increased fibrinolytic activity. Nevertheless, AT activity may
remain intact, primarily as the envenoming begins. The ecarin-like prothrombin-activator will
trigger a precursor to a form of thrombin that cannot be inhibited physiologically -
meisothrombin, hence AT is not reduced. Neutrophilic leukocytosis is a factor in this and a
number of other envenomations.
Mortality: Two cases following a bite from the tiger grooved-neck keelback, R. tigrinus,
have been described in Japan. The first involved a 61-year-old man who died on day 62 with
the symptomatology of pulmonary edema in the course of hemodialysis, with tubular necrosis
and renal atrophy eventually discovered, while the second was a case of a 14-year old boy
who died from fatal intracerebral hemorrhage.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Antivenom is not available. Symptomatic treatment as the hemocoagulation
disorder develops should be based upon an estimated or examined degree of fibrinolysis and
the progress of DIC present. Antifibrinolytics that are adequate for certain levels of
fibrinolysis may, when applied in the procoagulation stage of DIC, block the physiological
destruction of microthrombi developed, which can potentiate the resulting hypoperfusive
failure of organs, such as renal failure. Under such circumstances, and should the patient not
be bleeding, anticoagulation therapy is preferable, i.e. miniheparinisation in normal AT
activity may be helpful. Sufficient hydration of the patient will be necessary to prevent renal
failure.

6.1.2 .Boiga Genus

Species: Of the 30 Boiga genus members, the spectacular mangrove snake (Boiga
dendrophila) is probably the best-known species. Aside from this, the brown tree snake
(Boiga irregularis), Sri Lankan cat snake (Boiga ceylonensis), and Forstens cat snake (Boiga
forsteni) seem species affording more significant epidemiological relevance.
Other names: Cat snake. FR: Serpent ratier brun (B. irregularis). FR: Serpent darbre,
Serpent des paltuviers, Serpent ratier des mangroves; in native languages: Ularburong (B.
dendrophila).
Description: Slender tree snakes up to 200 cm long, with distinctive eyes and of largely
nocturnal activity. They are strong swimmers.
Home range and habitat: The majority of the species range in forests and mangroves
throughout India including Nepal, Sri Lanka, the former Indochinese region, Malaysia,
Indonesia and the Philippines. New Guinea, N and W Australia and more recently also the
Island of Guam, home of the brown tree snake (B. irregularis) and the place where the genus
has been introduced. B. blandingi and the Fischers cat snake (B. pulverulenta) dwell amongst
the vegetation in central and western African territories.
Toxins: These are products of Duvernoys gland. In certain species (B. irregularis), the
venom contains the component of bungarotoxin-like postsynaptic neurotoxins and
acetylcholinesterase. As regards locally acting enzymes, the venoms include a percentage of
phospholipases and components displaying hemolytic activity; neither prothrombin activators
nor thrombin-like components are present.
Local symptoms of envenoming: These are limited to small dermal efflorescences, e.g.
vesicles with discoloration and the development of light edemas.
88 Jiri Valenta

Systemic symptoms of envenoming: Despite the non-complicated process of

envenomation described above, which applies even to children, snakebites should not be
underestimated. Changes in sensory perception may be triggered as well as lethargy, fatigue
and clinically insignificant symptoms of cranial nerve dysfunction, such as ptosis of eyelids.
Two cases of respiratory difficulties in children have been described several hours following
a snakebite (Fritts et al., 1990).
Laboratory findings: Not available.
Mortality: Not recorded.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. No antivenom is available. Mechanical ventilation may be required for small
children exposed to a high dose of venom in very special cases.

6.1.3. Dispholidus Genus

Species: The genus includes a single species, the African boomslang (Dispholidus typus).
Other names: Common African tree snake; FR: Serpent darbre du Cap.
Description: A slender-bodied arboreal and diurnal snake that can grow up to 200 cm. It
possesses rear fangs at eye level and boasts large eyes with round pupils. Resembling a
distant relative of the mamba, these snakes can be easily confused in the wild. The boomslang
is hard to discern from moderately venomous colubrids of the Thrasops genus. Following a
bite, the snake will hang down and chew prey. As a result of its toxicity, which is often
belittled, plus the poor availability of antivenom, the boomslang could be looked upon as a
time bomb in a non-experts terrarium.
Home range and habitat: Boomslangs reside open bushland and savannah woodland
almost throughout Sub-Saharan Africa from Senegal as far as Somalia and the Republic of
South Africa. If hemocoagulation symptoms appear following a bite from an unidentified
snake to the south of the home range of the African Echis saw-scaled vipers, the chances are
high that it is one from D. typus.
Toxins: The venom is highly effective - LD50 for mice IV amounts to 0.07 mg/kg of body
weight. An enzymatic prothrombin-activator is one of the main venom components;
nevertheless, prothrombin is primarily converted to a form of thrombin which is impossible to
inhibit physiologically - meisothrombin; see chapter 6. 1. 1 Rhabdophis genus. This will
result in the hemocoagulation disorder of the DIC type, but direct activation of FX and other
hemostasis elements is also possible. In addition, the action of toxins will activate
complement via alternative route.
Local symptoms of envenoming: Mostly reduced to a minimum, typically, light edema
develops, which in size and pain may increase in special cases. Incision will result in
bleeding, with other possible local changes associated with the hemostasis disorder, such as
petechiae, ecchymoses, perfused bullae, and smaller hematoms.
Systemic symptoms of envenoming: Mostly these begin as prodromes like nausea,
vomiting, abdominal, and cranial pain, and feelings of anxiety. The hemostasis disorder of the
DIC type, with symptoms such as bleeding from wounds, gums, nose and rectum, hematuria,
hematemesis and enterorrhage, will develop almost immediately but more frequently within a
few hours, exceptionally occurring after 48 hours. Rarely, intracerebral hemorrhage may
follow as well. At the same time, there is a risk of developing microthrombus deposits and
 Envenoming and Snakebite Treatment in Specific Snake Groups 89

their resultant obstructive action on the microcirculation, which may be co-responsible in

fatal renal failure with acute tubular necrosis.
Laboratory findings: Hemocoagulation tests indicate a disorder of the DIC type.
Coagulation times are prolonged or blood does not coagulate at all. Hypofibrinogenemia,
extending as far as afibrinogenemia and thrombocytopenia, increased FDP (D-dim) levels and
signs of microangiopathic hemolysis arise.
Mortality: Fatal courses of envenoming have been described, with several accompanied
by renal failure.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Administration of antivenom is indicated in cases of systemic envenoming
with clinical symptoms including light prodromes, as well as more significant laboratory
findings resulting from hemocoagulation examination.
Applicable antivenom: SAIMR BOOMSLANG ANTIVENOM, SAIMR, the Republic of
South Africa. Administration can prove effective in a later phase of envenomation too, even
after 32 hours of bleeding.
In case of symptomatic treatment, rules for therapy of consumption disorder of the DIC
type apply, i.e. supportive administration of fresh frozen plasma, at a dosage of 10-20 ml/kg,
and application of AT if its activity is reduced. Substitution of platelets and erythrocytes is
utilized should there be a significant decrease - see chapter 5. 3. 3. 6 Hemocoagulation
disorders. Heparin therapy has been subject to discussion (du Toit, 1980). Most probably, it
may worth considering as an option to prevent further development of microthrombosis in an
activated field once bleeding has fully stopped.
A patient can be discharged for home treatment 24 hours following abatement of all
systemic symptoms and significant laboratory tests. Any persisting laboratory
symptomatology of moderate prothrombotic activity should be resolved by pre-emptive
miniheparinisation, see chapter 5.4 Convalescence following envenoming.

6.1.4. Malpolon Genus

Species: In terms of epidemiology, the European Montpellier snake (Malpolon

monspessulanus) is of greater significance than the African false cobra (Malpolon moilensis).
Other names: FR: Couleuvre de Montpellier; DE: Europische Eidechsenatter (M.
monspessulanus). Moila Snake; FR: Couleuvre de Moila (M. moilensis).
Description: Growing up to 200 cm long, these are diurnal and relatively heavy bodied
snakes with large eyes and round pupils. Some will lift the anterior part of their body when
threatened, expanding their neck like cobras, such as M. moilensis.
Home range and habitat: M. monspessulanus resides in the diverse, largely dry and
shrubby habitats and semi deserts of Portugal, Spain, French coastal areas, NW Italy,
Slovenia, Croatian coasts, Herzegovina, Montenegro, Albania, Greek coastland, part of
Bulgaria, Turkey, specific Caucasian regions, and part of the western coast of the Caspian
Sea. As for Africa, this snake is found along the African northern coast from Morocco to
Egypt and N Sudan, in the Middle East (Jordan and Israel), Iraq, and Saudi Arabia. M.
moilensis is found in part of central West Africa, N Africa, and the Middle East.
Toxins: The Duvernoys gland venom contains a small but clinically recordable quantity
of neurotoxic components and enzymes causing local damage to tissue, as well as
90 Jiri Valenta

hemocoagulation-affecting components causing intrapulmonary hemorrhaging in mice,

although the quantity is insignificant for humans. The venom does not seem to contain
proteolytic and hemorrhagic enzymes and has no procoagulation effect. LD50 for mice
amounts to 6.5 mg/kg of body weight.
Local symptoms of envenoming: The wound is painful; edema will develop - rather large
in many cases - as well as lymphangitis and lymphadenitis. The changes on the skin do not
heal very easily. Local symptoms of paresthesia or even paresis of the affected limb may
follow.
Systemic symptoms of envenoming: Incidence of envenoming following a bite amounts to
15%. Common prodromes can be followed by affection of cranial nerves and eyelid ptosis, as
well as by a sense of muscular weakness in, for example, respiratory muscles, plus dyspnea,
and dysphagia in severe envenomations. Neurological symptoms will abate within 48 hours.
Laboratory findings: No specific changes.
Mortality: Not specified.
Therapy: For first aid and general rules of treatment, see Chapter 5 Snakebite: Therapy
and prevention. No antivenom is available. Mechanical ventilation may be required for small
children exposed to a high dose of venom in very special cases.

6.1.5. Thelotornis Genus

Species: The genus encompasses 3 species: the bird snake (Thelotornis capensis)
including 3 subspecies, the forest vine snake (Thelotornis kirtlandii) and the Usambara vine
snake (Thelotornis usambaricus).
Other names: Twig snake, vine snake; FR: Serpent liane du Cap (T. capensis). FR:
Serpent liane de Kirtland (T. kirtlandii).
Description: Very slender arboreal diurnal snakes up to 200 cm long, often highly
colored, with elongated heads, large eyes and horizontal pupils.
Home range and habitat: Arboreous and shrubwood savannahs (T. capensis) and
rainforests (T. kirtlandii) of Sub-Saharan E Africa, and the zone extending from S Angola to
the eastern coast.
Toxins: The venom resembles that of the African boomslang (Dispholidus typus), with
LD50 for mice IV 1.23 mg/kg of body weight. It contains the activator of prothrombin and
FX, the action of which accelerates fibrinolysis.
Local symptoms of envenoming: Local changes are not very distinctive; edema will be
mostly small, incision wounds will bleed. Additional local symptoms of the hemostasis
disorder are possible.
Systemic symptoms of envenoming: Bites will mostly pose no threat to humans;
nevertheless, the risk should not be underestimated. Cases of snakebite with DIC symptoms,
including lethal ones, have been described. The progress is identical to that of envenoming by
the African boomslang (D. typus), see Chapter 6. 1. 3 Dispholidus genus.
Laboratory findings: Probably identical to those described under chapter 6.1.3
Dispholidus genus.
Mortality: Lethal cases of envenoming have been described, including the death of Prof
Robert Mertens in 1975, the founder of modern herpetology. The courses of symptoms of
 Envenoming and Snakebite Treatment in Specific Snake Groups 91

fatal envenomation were similar to those of envenoming by the African boomslang (D.
typus).
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. No specific antivenom is available. The antivenom against the venom of the
African boomslang (D. typus) is not effective, no cross immune response exists. In terms of
symptomatic treatment, rules for therapy of DIC will apply, i.e. supportive administration of
fresh frozen plasma, application of AT if its activity is reduced, and substitution of platelets
and erythrocytes in case of significant decrease; see chapter 5. 3. 3. 6 Hemocoagulation
disorders.
A patient can be discharged for home treatment 24 hours following abatement of all
systemic symptoms and significant laboratory findings. Any persisting laboratory
symptomatology of moderate prothrombotic activity should be resolved by pre-emptive
miniheparinization, see Chapter 5.4 Convalescence following envenoming.

6.1.6. Some other Genera of Venomous Colubrid Snakes

Ahaetulla - formerly Dryophis, vine snakes, common green snakes, long-nosed whip
snakes. Extremely slender arboreal snakes up to 200 cm long that possess rear fangs; they are
found in the forests and tree plantations of India, Sri Lanka, China and SE Asia.
Amplorhinus, many-spotted snakes. Small snakes of largely green color up to 60 cm long
with rear fangs and aggressive behavior found in rather humid habitats throughout S Africa.
Arrhyton. Small snakes with rear fangs found in the Caribbean Islands.
Balanophis. Small snakes with rear fangs that dwell in fallen leaves in Sri Lankan forests.
Calamodontophis. Small snakes with rear fangs from Brazil.
Cerberus. Medium-sized aquatic snakes with rear fangs. Found in mangroves and other
wetlands and river mouths throughout SE Asia, Indonesia, New Guinea and N Australia.
Chrysopelea, flying snakes. Relatively long and slender-bodied arboreal snakes with rear
fangs that can flatten and expand their body and move by means of gliding jumps from one
tree to another. Found in the forests and tree plantations of India, Sri Lanka, Burma,
Malaysia, S China, Philippines and Indonesia.
Clelia, mussuranas. Large snakes with mostly nocturnal activity found in the forests of
Central and S America. In envenomings described, local edemas and ecchymoses were
involved without hemocoagulation effects.
Coluber, racers. Only two species are considered moderately venomous: the spotted whip
snake (Coluber ravergieri), and the braid snake (Coluber rhodorachis). These are medium-
sized or large slender-bodied and quite aggressive snakes with large round eyes. Both species
are found rather on the ground and in low vegetation in the territory from the Middle East as
far as Mongolia and a part of China.
In terms of taxonomy, Coluber is a genus of collective nature that is in the process of
splitting into a number of separate genera, meaning that according to the latest knowledge, the
species mentioned above will be classified as Hemorrhois ravergieri and Platyceps
rhodorachis.
Coniophanes, black-striped snakes. Small terrestrial snakes with rear fangs found in the
southern part of North America, Central and South America.
92 Jiri Valenta

Conophis, ES: Guarda camino. Medium-sized snakes growing up to 100 cm, with rear
fangs, diurnal activity and relatively effective venoms. Found in the dry forests and coastal
regions of Central America. Local symptoms of envenoming, pain at the bitten site and edema
have been described.
Crotaphopeltis. Medium-sized ranivorous snakes with rear fangs; they range in the moist
and swamp areas of S and W part of Africa.
Dipsadoboa. Small slender-bodied arboreal snakes with rear fangs found in Africa.
Dromophis. Relatively long and slender-bodied snakes found in African humid areas and
rainforests.
Elapomorphus. Small slender-bodied snakes that feature a small head and eyes, and boast
mainly longitudinal stripes. They are mostly nocturnal burrowing snakes found in the forests
of S America.
Enhydris, water snakes. Small up to medium-sized aquatic snakes up to 100 cm long,
with a quite robust body. They are found in the water reservoirs, swamps and brooks of India,
China, SE Asia, New Guinea and N Australia.
Eteirodipsas, Malagasy cat-eyed snakes. A monotypical genus of the Madagascar
colubrids.
Ficimia, hooknosed snakes. Small colubrids with rear fangs found in diverse American
arid habitats from S Texas as far as Honduras.
Fordonia. A monotypic genus containing a single species, the crab-eating water snake
(Fordonia leucobalia). A small colubrid dwelling in the mangroves and swamps of SE Asian
as far as N Australian coasts.
Heterodon. Small to medium-sized snakes 40 to 120 cm long that feature a robust body
and relatively effective venoms containing a postsynaptic neurotoxin. They are not
aggressive; when in danger, they will flatten their neck like cobras or play dead. They are
mostly found in the grassy localities, both humid and arid, as well as sandy deserts of North
America.
Homalopsis, water snakes. Medium-sized aquatic snakes with rear fangs. Their venom,
relatively ineffective, contains hemorrhagic components. The water snakes are found in the
freshwaters and brackish waters of India, Burma, the former Indochinese region and SE Asia.
Ialtris. Medium-sized and slender-bodied snakes with rear fangs found in Haiti and
Dominican Republic.
Imantodes. Medium-sized and extremely slender-bodied snakes with large eyes that can
grow up to 1 m. They possess rear fangs and nocturnal hunting habits. They are found in the
forests of Central and S America.
Ithycyphus. Arboreal snakes that can grow up to 150 cm, with rear fangs. Found in the
forest areas of Madagascar.
Langaha. Long and extremely slender-bodied arboreal snakes with rear fangs and a
flattened and prominent snout. They are active in the morning and found in Madagascar
rainforests.
Leimadophis. Formerly, this genus encompassed a wide range of species that have been
more recently classified under different genera like Antillophis, Arrhyton, Dromicus, Liophis,
Philodryas, Saphenophis and Umbrivaga. Lesser colubrids with rear fangs found in the
rainforests of Central and S America.
Leptodeira. Lesser and slender-bodied snakes with rear fangs found on the ground and in
the lower stands of warm American areas from Texas to Paraguay.
 Envenoming and Snakebite Treatment in Specific Snake Groups 93

Leptophis, parrot snakes. Long slender-bodied snakes with rear fangs found in trees as
well as other sites of the warmer regions of C and S America.
Liophis. A genus with a wide range of colubrid snakes of diverse size with rear fangs and
diurnal activity. Certain species are classified into a separate Lygophis genus. Found in varied
habitats throughout Central and South America including the Caribbean.
Lygophis see Liophis.
Macropisthodon. Medium-sized ranivorous snakes with rear fangs resembling
copperheads that range in identical areas. Found in the fields and grassy localities of India, Sri
Lanka, S China and a part of SE Asia.
Macroprotodon. A small nocturnal snake with rear fangs found in dry and rocky places
throughout SW Europe, N Africa and a part of the Middle East.
Madagascarophis. Terrestrial snakes with a more robust body and rear fangs found in the
bushland of Madagascar. M. meridionalis snakebite is reported to have caused bruising,
vesicles, and occasionally even cases of necrosis.
Masticophis. Long and slender-bodied diurnal snakes found in the deserts, beaches and
open woodlands of North and Central America and in the north of South America.
Myron. A monotypic species of small nocturnal snakes about 40 cm long found in the
swamps and mangroves of N Australia and New Guinea. No envenoming has been reported;
nevertheless, the venom is considered potentially dangerous.
Oxybelis, vine snakes. Relatively aggressive long and slender-bodied arboreal snakes
with rear fangs found in the forest habitats of N and S America from Texas as far as Bolivia
and Peru.
Oxyrhopus. Medium-sized, slender-bodied and largely nocturnal terrestrial snakes found
in America from Mexico to Peru.
Philodryas, green snakes. Slender-bodied arboreal reptiles of mostly green color. They
feature large eyes, round pupil and rear fangs; they are diurnal snakes up to 150 cm long
found in the forests of S America. Symptoms described following a snakebite by P. baroni
include local pain, edema with a peak in 24 hours that will recede after 48 hours,
lymphadenitis without regional nodes enlarged, development of dermal ecchymoses and
perfused bite wounds, without signs of systemic envenoming. Components showing a
procoagulation action have been evidenced in the venom. The hemorrhagic activity of the
venom can be neutralized using an antivenom against Bothrops snakes.
Philothamnus. Slender-bodied diurnal snakes of mostly green color. They feature large
eyes, round pupil and rear fangs that can grow up to 130 cm. Found near the water surfaces,
in humid woodland, and even in savannahs of W, E, and S Africa. Despite the content of
effective procoagulation components in the venom of P. natalensis, more severe
envenomings have not been described.
Psammophis. A number of slender-bodied diurnal snakes that possess rear fangs; they
can grow up to 200 cm. Usually found in rather arid and open terrains and plantations of
Africa, the Middle East and a part of Central Asia, W China, Burma and Thailand.
Psammophylax, Afrikaans: Skaapsteker (a sheep killer). Slender-bodied snakes about 100
cm long with rear fangs and relatively effective venoms found in the bushland of S Africa.
These snakes are neither considered dangerous to humans nor to the sheep, despite their
name.
Pseudoboa. Medium-sized nocturnal terrestrial snakes with rear fangs found in the
rainforests of S America.
94 Jiri Valenta

Ptychophis. Small ranivorous and piscivorous semi aquatic snakes with rear fangs that
pose a potential threat to a human as well. Found in Brazilian wetlands.
Pythonodipsas. Up to 60 cm long snakes that possess large rear fangs; they are active at
night and found in the rocky deserts of Namibia and Angola.
Siphlophis. Small up to medium-sized arboreal snakes with rear fangs and nocturnal
activity found in the forests of Central and S America.
Spalerosophis. Over 100 cm long snakes found in the deserts and bushland of N Africa
and the Middle East.
Stenorrhina. Medium-sized slender-bodied snakes with rear fangs found in the forests
and grassy areas of America from Mexico to Ecuador. A single Stenorrhina freminvillei
snakebite that has been described was accompanied by local pain and edema without any
systemic reactions.
Tachymenis. Small snakes with rear fangs found in the arid regions of NW South
America.
Tantilla, centipede snakes. Small and slender-bodied snakes, the smallest members of the
venomous snake group. Found in diverse terrains throughout America from central USA as
far as Argentina.
Telescopus, formerly Tarbophis. A range of species that comprise 80 to 130 cm long
medium-sized snakes boasting dark cross stripes, with rear fangs and nocturnal life. Found
mostly in the arid and rocky localities in Africa, the Balkan, and the neighboring regions of
Asia and Asia Minor.
Thamnodynastes. Small up to medium-sized terrestrial as well as arboreal snakes that
feature a more robust body, rear fangs and largely nocturnal activity found in the forests of S
America.
Thamnophis. A range of species that include lesser or medium-sized diurnal snakes found
on humid sites throughout North and Central America.
Thrasops. Large arboreal colubrids that dwell in the forests of tropical Africa.
Trimorphodon. Medium-sized and slender-bodied snakes up to 100 cm long with rear
fangs found in arid up to rocky and shrubby places throughout North and Central America.
Waglerophis. Medium-sized and quite robust ranivorous snakes with long rear fangs
found on rather humid sites in the forests of South America.
Xenochrophis, painted keelbacks. Medium-sized colubrid snakes that can grow even
more than 100 cm; they possess rear fangs. Found on humid localities and near water surfaces
from Afghanistan through S Asia as far as Indonesia.
Xenodon. Medium-sized or even large ranivorous snakes with a rather robust body, rear
fangs and aggressive behavior. Found in the humid forests and rainforests as well as near the
water surfaces of America from Mexico as far as Argentina.

Toxins: For the majority of opistoglyphous colubrids, a lack of information on venom

exists at laboratory and clinical level. Latest knowledge indicates that they primarily include
neurotoxins, largely of a postsynaptic type, and hemocoagulation-affecting components,
mostly in terms of prothrombin activation and development of the disorder of the DIC type.
One of these groups of toxins is present in practically all the venoms of the colubrids listed
above. Nevertheless, the concentration is typically so low that any clinical symptomatology of
a serious disorder will frequently not develop.
 Envenoming and Snakebite Treatment in Specific Snake Groups 95

Local symptoms of envenoming: Slight local damage can be expected such as

insignificant edema and signs of inflammation, as well as erythema or paleness, temporary
local bleeding, pain and burning, or conversely desensitization or even stiffness around the
bitten site. In certain species, for instance Homalopsis, venom with hemorrhagic activity is
found, meaning the bitten site can be subject to hemorrhagic changes. Snakebites can be
accompanied by lymphadenitis either including or excluding lymphangitis.
Systemic symptoms of envenoming: Symptoms of systemic envenoming, if any, will be
limited to prodromes, i.e. nausea, vomiting, abdominal and cranial pain, and shivering. In
cases of more severe envenoming, depending on the content of venom components, minor
signs of bleeding, such as in Philothamnus, or signs of languor and muscular pain can arise,
such as in Heterodon and Telescopus.
For most of the genera listed above, envenomation has never been described due to the
rarity and insignificant courses of the same, so they do not pose any major threat to humans.
Nevertheless, snakebites should not be underestimated, reasons for this being simply the lack
of information on specific cases as well as the potential for more severe or unexpected
courses.
Laboratory findings: Leukocytosis can be expected; as for envenoming by a venom
containing hemocoagulation-affecting components, in most cases a low level of consumption
coagulopathy may follow.
Mortality: No lethal cases following a bite by the snakes of the genera listed above have
been described.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Should rare symptoms of systemic envenoming be forthcoming, observation
will be helpful; supportive symptomatic treatment will be necessary only in special cases.
A patient can be discharged for home treatment 24 hours following abatement of all
possible symptoms and more significant laboratory findings.

REFERENCES
ATKINSON, PM., BRADLOW, BA., WHITE, JA., et al. Clinical features of Twig Snake
(Thelotornis capensis) envenoming. S Afr Med J, 1980, 58, No. 25, pp. 1007-1011.
BROADERS, M., RYAN, MF. Enzymatic properties of the Duvernoys secretion of
Blandings Tree Snake (Boiga blandingi) and of the Mangrove Snake (Boiga
dendrophila). Toxicon, 1997, 35, No. 7, pp. 1143-1148.
COOK, DG. A case of envenoming by the neotropical Colubrid Snake, Stenorrhina
freminvillei. Toxicon, 1984, 22, No. 5, pp. 823-827.
FAN, HW., CARDOSO, JL. Clinical toxicology of snake bites in South America. In MEIER,
J., WHITE, J. (Eds), Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995, pp. 667-688.
FITZSIMONS, DC., SMITH, HM. Another rear-fanged South African snake lethal to
humans. Herpetologova, 1958, 14, pp. 198-202.
FRITTS, TH., McCOID, MJ., HADDOCK, RL. Risk to infant on Guam from bites of the
Brown Tree Snake (Boiga irregularis). Am J Trop Med Hyg, 1990, 42, No. 6, pp. 607-
611.
96 Jiri Valenta

GERBER, JD., ADENDORFF, HP. Boomslang (Dispholidus typus) bite: case report. A Afr J,
1980, 57, No. 17, pp. 710-711.
GONZALES, D. Epidemiological and clinical aspects of certain venomous animals in Spain.
Toxicon, 1982, 20, p. 925.
GUILLIN, MC., BEZEAUD, A., MENACHE, D. The mechanism of activation of human
prothrombin by an activator isolated from Dispholidus typus venom. Biochim Biophys
Acta, 1978, 537, No. 1, pp. 160-168.
GUTIRREZ, JM. Clinical toxicology of snakebite in Central America. In MEIER, J.,
WHITE, J. (Eds), Handbook of clinical toxicology of animal venoms and poisons. Boca
Raton : CRC Press, 1995.
De HAAN, CC. Sense-organ-like parietal pits found in Psammophiini (Serpentes,
Colubridae). CR Biol, 2003, 326, No. 3, pp. 287-293.
HAYES, WK., LAVIN-MURCIO, P., KARDONG, KV. Delivery of Duvernoys secretion
into prey by the Brown Tree Snake, Boiga irregularis (Serpentes: Colubridae). Toxicon,
1993, 31, No. 7, pp. 881-887.
HILL, RE., MACKESSY, SP. Characterization of venom (Duvernoys secretion) from twelve
species of Colubrid Snakes and partial sequence of four venom proteins. Toxicon, 2000,
38, No. 12, pp. 1663-1687.
HOFFMANN, JJ., VIJGEN, M., SMEETS, RE., et al. Haemostatic effects in vivo after
snakebite by the Red-necked Keelback (Rhabdophis subminiatus). Blood Coagul
Fibrinolysis, 1992, 3, No. 4, pp. 461-464.
HUTTON, RA., WARRELL, DA. Action of snake venom components on the haemostatic
system. Blood Rev, 1993, 7, No. 3, pp. 176-189.
ISMAIL, M., MEMISH, ZA. Venomous snakes of Saudi Arabia and the Middle East: a
keynote for travellers. Int J of Antimikrob Agents, 2003, 21, pp. 164-169.
KORNALIK F, TABORSKA E. Procoagulant and defibrinating potency of the venom gland
extract of Thelotornis kirtlandi. Thromb Res, 1978, 12, No. 6, pp. 991-1001.
KUCH, U., JESBERGER, U. Human envenoming from the bite of the South American
Colubrid Snake species Phylodrias baroni Berg, 1895. The Snake, 1993, 25, p. 63.
LI, QB., HUANG, GW., KINJOH, K., et al. Hematological studies on DIC-like findings
observed in patients with snakebite in south China. Toxicon, 2001, 39, No. 7, pp. 943-
948.
LUMSDEN, NG., FRY, BG., MANJUNATHA KINI, R., et al. In vitro neuromuscular
activity of Colubrid venoms: clinical and evolutionary implications. Toxicon, 2004, 43,
No. 7, pp. 819-827.
MEIER, J., WHITE, J. (Eds). Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995, 752 pp.
MITTLEMAN, MB., GORIS, RC. Death caused by the bite of the Japanese Colubrid Snake
Rhabdophis tigrinus (Boie) (Reptilia, Serpentes, Colubridae). J Herpetol, 1978, 12, No.
1, pp. 109-111.
OGAWA, H., SAWAI, Y. Fatal bite of the Yamakagashi (Rhabdophis tigrinus). The Snake,
1986, 18, pp. 53-54.
PERSSON, H. Clinical toxicology of snakebite in Europe. In MEIER, J., WHITE, J. (Eds),
Handbook of clinical toxicology of animal venoms and poisons. Boca Raton : CRC Press,
1995.
 Envenoming and Snakebite Treatment in Specific Snake Groups 97

REHAK, I. Reprodukcni biologie hada Heterodon nasicus. Akvarium terarium, 1990, 33, .
8, pp. 30-32. (in Czech)
REHAK, I. Distribution, ecology and variability of snakes in Czechoslovakia. In KORSOS,
Z., KISS, I. (Eds.), Proc. Sixth Ord. Gen. Meet. Budapest : S.E.H., 1991, 1992, pp. 383-
388.
REHAK, I. Serpentes - Hadi, Hady. In BARU, V., OLIVA, O. (Eds.), Plazi - Reptilia. Praha
: Academia, Praha, 1992, pp. 106-172. (in Czech)
ROSENBERG, HI., BDOLAH, A., KOCHVA, E. Lethal factors and enzymes in the secretion
from Duvernoys gland of three Colubrid Snakes. J Exp Zool, 1985, 233, No. 1, pp. 5-14.
ROSENBERG, HI., KINAMON, S., KOCHVA, E., et al. The secretion of Duvernoys gland
of Malpolon monspessulanus induced haemorrhage in the lung of mice. Toxicon, 1992,
30, No. 8, pp. 920-924.
SEOW, E., KUPERAN, P., GOH, SK., et al. Morbidity after a bite from a non-venomous
Pet Snake. Singapore Med J, 2000, 41, No. 1, pp. 34-35.
SMEETS, RE., PELMAN, PG., HOFFMANN, JJ., et al. Severe coagulopathy after a bite
from a harmless snake (Rhabdophis subminiatus). J Intern Med, 1991, 230, No. 4, pp.
351-354.
Du TOIT, DM. Boomslang (Dispholidus typus) bite. A case report and a rewiew of diagnosis
and management. S Afr Med J, 1980, 57, No. 13, pp. 507-510.
STCKLIN, R., CRETTON, G. The ultimate database on venomous animals, snakes. CD-
rom, Geneva : Atheris Laboratories, 1998.
WARRELL, DA. Clinical toxicology of snakebite in Africa and the Middle East / Arabian
Peninsula. In MEIER, J., WHITE, J. (Eds), Handbook of clinical toxicology of animal
venoms and poisons. Boca Raton : CRC Press, 1995.
WARRELL, DA. Clinical toxicology of snakebite in Asia. In MEIER, J., WHITE, J. (Eds),
Handbook of clinical toxicology of animal venoms and poisons. Boca Raton : CRC Press,
1995, pp. 493-594.
WEINSTEIN, SA., KARDONG, KV. Properties of Duvernoys secretion from
opistoglyphous and aglyphous Colubrid Snakes. Toxicon, 1994, 32, No. 10, pp. 1161-
1185.
ZOTZ, RB., MEBS, D., HIRCHE, H., PAAR, D. Hemostatic changes due to the venom gland
extract of the Red-necked Keelback Snake (Rhabdophis subminiatus). Toxicon, 1991, 29,
No. 12, pp. 1501-1508.

6.2. FAMILY: ATRACTASPIDIDAE

This does not comprise a particularly extensive snake group, and is one which was
formerly classified into other families due to the diversity of fang configuration. It has since
been split into two subfamilies with approximately 10 genera and 70 species.
Members of this family, which was considered somewhat mysterious until very recently,
mostly burrow underground in dens and tunnels. This has resulted in adaptation to their
robust bodies and oval-shaped heads. The fangs are placed in either an anterior or posterior
position.
98 Jiri Valenta

If placed at the front, they are capable of being folded and moved - even to the sides - and
can be used even if the mouth is closed (Atractaspidinae). If stationary, they are placed in
either the front or rear (Aparallactinae).
The snakes of this family are largely found in Africa, with only a single species
(Atractaspis engaddensis) ranging in the Middle East.
Bites or side stabbing by members of certain genera with large fangs and powerful venom
can be dangerous, while other family members are harmless to humans.

6.2.1. Subfamily: Atractaspidinae

6.2.1.1. Atractaspis Genus

Species: Western forest mole viper (Atractaspis atterina), Battersbys mole viper
(Atractaspis battersbyi), southern or Bibrons burrowing asp (Atractaspis bibronii),
Boulengers mole viper (Atractaspis boulengeri), mole viper (Atractaspis coalescens),
Eastern Congo burrowing asp (Atractaspis congica), fat mole viper (Atractaspis corpulenta),
Bocages mole viper (Atractaspis dahomeyensis), Duerdens or beaked burrowing asp
(Atractaspis duerdeni), Israeli mole viper (Atractaspis engaddensis), Engdahls mole viper
(Atractaspis engdahli), false mole viper (Atractaspis fallax), variable mole viper (Atractaspis
irregularis), white mole viper (Atractaspis leucomelas), small-scaled burrowing asp
(Atractaspis microlepidota), Sahelian burrowing asp (Atractaspis micropholis), Atractaspis
phillipsi, reticulate mole viper (Atractaspis reticulata), and Scorteccis mole viper
(Atractaspis scortecii), including numerous subspecies. Out of the species above, only A.
atterina, A. bibronii, A. corpulenta, A. dahomeyensis, A. engaddensis, A. irregularis, and A.
microlepidota present some danger for a human. Members of other species are incapable of
posing any threat to man, either for their size or the small quantity of venom.
Other names: Burrowing asp or vipers, side-stabbing snakes, stiletto snakes; FR:
Atractaspid (Atractaspis sp.). HE: Saraf En Gedi (A. engaddensis).
Description: Small to medium-sized and mostly slender bodied with a maximum length
of 110 cm (A. microlepidota), these snakes feature an oval-shaped and highly flexible head
shaped for digging, an indistinct neck and small eyes. As regards coloring, dark tints prevail
on the top - black, or black and gray or brown, with the underside being pale or even white.
The upper jaw, i.e. the maxilla, is extremely reduced, with embedded hollow front fangs.
Their venom glands are extremely long and resemble those of coral snakes. The specialty of
burrowing asps is to pop out their relatively long fangs to the side of the jaws with the mouth
almost closed and to bite employing a lateral strike, which is made possible especially by the
flexibility of the jaws. The reason for this action is the necessity to hunt in narrow tunnels
created by rodents, lizards, and other animals dwelling underground. This specific kind of bite
is significant for humans when holding the creature behind its neck, as it may stab the hand
with repeated lateral strikes of its highly mobile head.
Home range and habitat: The Atractaspis species inhabit a major portion of Africa: the
western part (A. dahomeyensis, A. corpulenta), the south-west and central part (A. aterrima),
to the east, the territory from and including Ethiopia as far as the southern part of the
continent - Namibia, Botswana, and north of the Republic of South Africa (A. bibronii). NE
Egypt, Sinai, Israel, and Palestine (A. engaddensis) make up another part of their home range.
A zone throughout Africa from Mauritania to Kenya is home to A. irregularis, which is found
 Envenoming and Snakebite Treatment in Specific Snake Groups 99

in forests, in addition to A. microlepidota, the savannah-dwelling species that proves the most
dangerous to humans. Burrowing species prevail, their incidence particularly increasing after
rainfall in the territory of human settlements. They hunt at dusk and during the night.
Toxins: Characteristic toxins include sarafotoxin isolated from the venom of A.
engaddensis; it is cardiotoxic, causing hypertension, oscillation of systemic pressure, and in
certain phases also increased inotropy due to vasoconstriction, or even coronary vasospasm.
As a result, changes in ST-segment and T wave, prolongation of PR-interval, AV-block, and
cardiac failure can occur and are evident from ECG results due to myocardial ischemia. Toxin
is effective especially in vertebrates, chiefly mammals; it resembles mammal endothelin in its
composition and effects. Concerning other components, the venom contains mainly
hemorrhagic and proteolytic enzymes.
The quantity of venom is low - a maximum of 9.6 g of dry matter was obtained from A.
engaddensis - nevertheless, the venom features a relatively high toxicity, with LD50 IV for
mice starting from 0.075 mg/kg of body weight in A. engaddensis, and over 3 mg/kg of body
weight in A. micropholis. Immunogenicity of venom components is very low - a minimum
reaction has been achieved with the antivenoms available.
Local symptoms of envenoming: The bite wound immediately generates a varying level of
discomfort - from moderate through to intense severe and stabbing pain - that can be
accompanied by tingling and feelings of stiffness. Bleeding from the bitten site will persist.
Very early on, within an hour at longest, a localized edema will appear with regional
lymphadenopathy and palpable pain propagating into nodes. The bitten site is often
surrounded by a decolorized area or, conversely, erythema. This can continue with blisters
developing of hemorrhagic or suppurating content and dermal necrosis. The necrosis is likely
to be caused by ischemia generated by the edema in the areas of tight compartments on
fingers. Any potential abscesses under the skin are bacteriologically sterile and materialize
based on direct action by the venom. The edema will peak within 24 to 48 hours and start to
recede after 48 to 60 hours, typically disappearing within 4 to 7 days. Changes in the tone of
skin and increased sensitivity at the affected site may well last for a number of months.
Systemic symptoms of envenoming: Systemic envenoming will manifest through
headaches, a dry mouth, increased temperatures, rhonchus, pain through eye motions,
paleness, increased sweating, nausea, vomiting, and water-based non-hemorrhagic diarrhea.
Gastrointestinal symptomatology may not be present in cases of envenoming by A. bibronii.
In rare instances, ophtalmoplegia, dysphagia, vertigo, muscle weakness, muscles
fasciculations, and deafness occur. More severe envenoming presents itself through varying
states of mind, including syncopes, tachycardia with a frequency as high as 130 beats per
minute, hypertension of up to 180/110 mmHg, feelings of dyspnea, and changes in ECG in
the shape of myocardial ischemia and AV-blocks. The most severe and fatal courses are
signified by circulatory collapse and cardiac failure (A. engaddensis). No major signs of
neurotoxicity are present, and hemocoagulation is seldom influenced to a greater extent.
Laboratory findings: Increased values in leukocytes (11 x 109/l) and platelets (600 x
9
10 /l) have been recorded; in terms of other results, elevated APTT and PT (A. bibronii, A.
engaddensis), alkaline phosphatases and liver enzymes (A. engaddensis) have been
determined.
Mortality: Very low - a few fatal cases have been recorded, for instance, in Sudan and
Nigeria following a bite from A. irregularis or A. microlepidota. An extreme case involved a
bite by A. engaddensis, when death of the affected person occurred after 45 minutes with
100 Jiri Valenta

symptomatology of respiratory and circulatory failure. A post mortem examination even

revealed abnormal histological results from the liver.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. No antivenom exists to counteract Atractaspis genus venoms and no cross-
immunity effects from antigens for venoms of other African snakes occur, e.g. SAIMR
Polyvalent Snake Antivenom, the Republic of South Africa.
Desirable local treatment methods include moderate cooling of the edema, limb elevation
and immobilization, plus gentle treatment of defects and possible necrectomy. In some cases,
drainage of large blisters and abscesses is necessary.
For eliminating pain, analgesics based on paracetamol or non-steroid antiphlogistics
usually prove sufficient.
Symptoms of systemic envenoming are resolved symptomatically. Antibiotic treatment
has no special indications; serious abscesses are typically primarily sterile. The most
significant symptom concerns cardiac function, which will probably become apparent due to
myocardial ischemia based on coronary spasms and a heavy increase in peripheral vessel
resistance. In terms of therapy, using nitrates can be an option in extreme cases, although the
procedure has not been verified clinically.
If symptoms do not materialize following a bite, patients should be observed for 24
hours. Following an envenoming, a patient can be discharged for home treatment after 24
hours once systemic symptoms recede.

6.2.2. Subfamily: Aparallactinae

Genera: Amblyodipsas, Aparallactus, Brachyophis, Chilorhinophis, Elapocalmus,
Elapotinus, Hypoptophis, Macrelaps, Micrelaps, Poecilopholis, Polemon, and Xenocalamus.
In addition, this list could include Homoroselaps, newly recognized as elapid snakes;
however, formerly placed among colubrids.
Description: The snakes classified under the Aparallactinae subfamily are close relatives
to the Atractaspis snakes described above, with whom they are typically confused. The way
they live is similar to Atractaspidinae. Some of them possess fixed grooved fangs located in
the anterior or posterior part of the upper jaw (Aparralactus, Macrelaps). Information is
patchy for many examples of these snakes. Even though they are venomous, they pose no
serious threat to humans with some exceptions.
Home range and habitat: The subfamily covers African snakes ranging from Saharan
territories as far as the Republic of South Africa. They inhabit underground tunnels made in
soil, sand (Xenocalamus) or fallen leaves (Macrelaps). They are largely nocturnal creatures.
Toxins: A lack of information on toxins exists; a similar composition of venom to that of
the Atractaspis snakes described above can be expected.
Local symptoms of envenoming: Local affection is likely to be analogous to the
symptoms of snakebites by Atractaspis genus but lighter in form.
Systemic symptoms of envenoming: In some of the snake species, similar envenoming as
that already described under Atractaspis is possible. Nevertheless, nearly no systemic reaction
will be caused. Symptoms of unconsciousness and collapse following a snakebite from
Macrelaps microlepidotus have been reported in South Africa.
Laboratory findings: Not described.
 Envenoming and Snakebite Treatment in Specific Snake Groups 101

Mortality: A possibility of even a fatal course of envenoming by Macrelaps

microlepidotus is admitted.
Therapy: For symptoms of envenomation, therapy will follow the treatment described
under the chapter Atractaspis.

REFERENCES
ALKAN, ML., SUKENIK, S. Atrioventricular block in a case of snakebite inflicted by
Atractaspis engaddensis. Trans. R. Soc. Trop. Med. Hyg., 1975, 69, p. 166.
BLAYLOCK, RS. Snake bites at Triangle Hospital January 1975 to June 1981. Centr. Afr. J.
Med., 1982, 28, pp. 110.
BRITT, DP. Death following the bite of Burroving Viper. Nigerian Field, 1978, 43, pp. 41
42.
CORKILL, NL., IONDIES, CJP, PITMAN, CRS. Biting and poisoning by the Mole Viper of
the genus Atractaspis. Trans R. Soc. Trop. Med. Hyg., 1959, 53, pp. 95101.
CRANKO, JAW. A snakebite from a Burrowing Adder. Centr. Afr. J. Med., 1961, 7, pp.
215216.
CHRISTENSEN, PA.. Snakebite and the use of antivenom in Southern Africa. S. Afr. Med.
J., 1981, 59, pp. 934938.
ISMAIL, M., MEMISH, ZA. Venomous snakes of Saudi Arabia and the Middle East: a
keynote for travellers. Int. J. of Antimikrob. Agents, 2003, 21, pp. 164169.
KIRCHBERG, JS., DAVIDSON, TM. Envenomation by the Colubrid Snake Atractaspis
bibronii: a case report. Toxicon, 1991, 29, No. 3, pp. 379381.
KURNIK, D., HAVIV, Y., KOCHVA, E. A snake bite by the Burroving Asp, Atractaspis
engaddensis. Toxicon, 1999, 37, No. 1, pp. 223227.
LEE, SY., LEE, CY., CHEN, YM., et al. Coronary vasospasm as the primary cause of death
due to the venom of the Burrowing Asp, Atractaspis engaddensis. Toxicon, 1986, 24, No.
3, p. 285291.
MEIER, J., WHITE, J. (Eds). Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995, 752 pp.
OVADIA, M. Isolation and charakterisation of a hemorrhagic factor from the venom of the
snake Atractaspis engaddensis (Atractaspididae). Toxicon, 1987, 25, No. 6, pp. 621630.
STCKLIN, R., CRETTON, G. The ultimate database on venomous animals, snakes. CD-
rom, Geneva : Atheris Laboratories, 1998.
TILBURY, CR., BRANCH, WR. Observations on the bite of the Southern Burrowing Asp
(Atractaspis bibronii) in Natal. S. Afr. Med. J., 1989, pp. 327331.
VISSER, J., CHAPMAN, DS. Snakes and snakebite: venomous snakes and management of
snakebite in Southern Africa. Cape Town : Purnell, 1978, 152 pp.
WARRELL, DA. Clinical toxicology of snakebite in Africa and the Middle East / Arabien
Peninsula. In MEIER, J., WHITE, J. (Eds), Handbook of clinical toxicology of animal
venoms and poisons. Boca Raton : CRC Press, 1995, pp. 433492.
WARRELL, DA., ORMEROD, LD., DAVIDSON, NM. Bites by the Night Adder (Causus
maculatus) and Burrowing Vipers (genus Atractaspis) in Nigeria. Am. J. Trop. Med.
Hyg., 1976, 25, No. 3, pp. 51724.
102 Jiri Valenta

6.3. FAMILY: ELAPIDAE, ELAPID SNAKES

Elapid snakes (Elapidae) form an extensive family of venomous snakes, with opinions
differing on further subdivision depending on the author, in fact, multiple subfamilies are
often described. Decisive aspects for the current classification of elapid snakes include (1) as
yet unclear phyletic links between a number of Eurasian, African and American snakes -
therefore, these have been temporarily, until the classification issue is resolved, designated as
a single subfamily, Elapinae, containing some 17 genera with over 130 species; (2) in
addition, there is a well-founded relationship between Austropapuan elapids, sea snakes and
sea kraits; i.e. proteroglyphous aquatic snakes formerly placed under a separate Hydrophiidae
family. These snakes are now defined as a separate Hydrophiinae subfamily within the
Elapidae family, which contains about 43 genera and 165 species.
Elapids show some external morphological parallelism with colubrid snakes;
nevertheless, they differ from each other by the structure of the venom apparatus, this being
just one example. Shared features of the Elapidae family include fixed and non-swinging
fangs in the front section of the upper jaw (Proteroglypha), see chapter 1. 4 Venom apparatus
of snakes. In addition, the majority of elapid snakes typically possess a significant level of
effective neurotoxic venom components. In the wild, Elapidae family members inhabit
almost the entire home range of venomous snakes except in Europe, where many such species
are kept in captivity. Throughout their home range, certain coral snake family members are
considered some of the most perilous snakes and the most venomous animals to inhabit these
areas.

6.3.1. Subfamily: Elapinae

The recently recognized Elapinae subfamily consists of genera formerly classified as

Calliophinae, Bungarinae, Maticorinae, and Elapinae subfamilies. The former Bungarinae
family included 12 genera of venomous snakes that ranged almost throughout the whole of
Africa and a part of Asia, a zone that stretches from Central Asia across the Indian
subcontinent, S China and former Indochinese territory as far as the islands of the Philippines,
Indonesia and Malaysia. Indeed, included in their number are some of the most dangerous
snakes of all, such as representatives of the largest venomous snakes, the Asian king cobra
(Ophiophagus hannah), and the African black mamba (Dendroaspis polylepis). Elapid snakes
found throughout the American continent, formerly referred to as Elapinae, are another
important group in terms of toxinology, along with the numerous Micrurus genus. Another
two genera of this group, Leptomicrurus and Micruroides, merely include several snake
species that are rare or less significant for epidemiology.

6.3.1.1. Aspidelaps Genus, Shield Nosed Cobras

Species: South African coral snake (Aspidelaps lubricus), intermediate shield-nose snake
(Aspidelaps scutatus).
Description: Small to medium-sized snakes 45 to 75 cm in length of orange, salmon,
brownish or even reddish color with crossing black rings (A. lubricatus), or a darker random
 Envenoming and Snakebite Treatment in Specific Snake Groups 103

crosswise pattern and dark head (A. scutatus). They are active at night. When in danger, they
moderately spread the area of the neck like the cobra.
Other names: Western coral snake; FR: Serpent corail dAfrique du Sud, Serpent corail
du Cap (A. lubricus). Shield-nose cobra (A. scutatus).
Home range and habitat: These snakes reside in sandy and rocky arid habitats of
Namibia, Botswana, the Republic of South Africa, SE Zimbabwe and S Mozambique.
Toxins: The composition of venoms is not sufficiently known. The venoms largely
contain neurotoxins. Other components include PLA2, similar to the venoms of African cobras
of the Naja genus, as well as cytotoxic components generally.
Local symptoms of envenoming: The bitten site is painful with the development of
edema; lymphadenopathy occurs, including enlarged regional lymphatic nodes. Necrosis is
possible. Local changes abate very slowly.
Systemic symptoms of envenoming: If the quantity of venom is large or the victim is a
child, the neurotoxins may cause neurological symptomatology affecting cranial nerves and
precipitating feelings of languor, as well as even respiratory failure, in special cases, by
paralyzing the innervation of respiratory muscles.
Laboratory findings: Not described; leukocytosis is possible.
Mortality: Fatal cases are known (van Egmond, 1984; Warrell, 1995).
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Application of the pressure immobilization bandage is indicated, namely for
children and if any delay in definitive treatment is predicted. The bandage must not be
removed either before treatment by a health facility capable of dealing with serious symptoms
of muscular paralysis, or after systemic envenoming has been eliminated.
No antivenom is available, although a probability exists of cross-reactivity with the
venom of African cobras (Naja), at least for certain inherent components.
Painful edema will require a light elevation of the limb, immobilization and moderate
cooling. In cases of more severe affection, any subsequent larger necrosis may be solved by
necrectomy following demarcation. Severe symptoms of neurotoxicity, involving loss of the
ability to swallow, the cough reflex or apparent respiratory failure, will require airway
management and mechanical ventilation.
Following envenomation, a patient can be discharged for home treatment after 24 hours
once systemic symptoms recede. Any persisting local affection can be solved through
treatment as an outpatient.

6.3.1.2. Bungarus Genus, Kraits

Species: Of the twelve krait species, see chapter 7 List of venomous snakes, the most
common ones are the Indian krait (Bungarus caeruleus), blue krait (Bungarus candidus),
Ceylon krait (Bungarus ceylonicus), banded krait (Bungarus fasciatus), red-headed krait
(Bungarus flaviceps), many-banded krait (Bungarus multicinctus) and the Sind krait
(Bungarus sindanus).
From an epidemiologic viewpoint, the most significant species include the Indian krait
(Bungarus caeruleus), which is responsible for a number of fatal cases of snakebites in India,
the blue krait (Bungarus candidus), and many-banded krait (Bungarus multicinctus),
responsible for 8.4% of the total number of envenomings in S China.
Description: Snakes with large or medium-sized slender bodies. They grow to an average
length of 100 to 150 cm, with the maximum of 195 cm documented for the red-headed krait
104 Jiri Valenta

(Bungarus flaviceps). A deltoid-like or laterally compressed shape of body profile is typical

for these snakes. The color is dark, with typical paler or whitish rings. Kraits are active at
night; their behavior can be outlined as aggressive, with increased probability of strike, which
is why people resting at night are bitten. If disturbed during the day, they tend not to attack,
but rather keep their heads to the ground.
Other names: FR: Bongare (Bungarus). In native languages: Pama (B. fasciatus),
Sangchur, i.e. a stone breaker, Pee-un, i.e. a drinker (B. caeruleus).
Home range and habitat: They inhabit both open and dense woodland or scrubland,
mangrove stands and plantations - often near water - in the territory of SE Asia, from E
Afghanistan and Pakistan through India, Sri Lanka, the former Indochinese territory as far as
S China, including Taiwan and the Hainan islands, plus the islands of Malaysia and
Indonesia.
Toxins: Neurotoxins present the most dangerous and fatal component in krait (Bungarus)
venom, with -bungarotoxin - a potent postsynaptically acting toxin - presumably responsible
for the majority of fatal courses of envenoming. Candoxin is another type of postsynaptic
neurotoxin. The effect of both is reversible and can be well controlled by inhibiting
cholinesterase. However, the presence of -bungarotoxin, a neurotoxic presynaptically acting
PLA2 that causes irreversible damage and apoptosis of affected neurons, is probably
responsible for neurological affections that sometimes persist.
From the venom of B. multicinctus, polypeptidic cytotoxins/cardiotoxins have been
isolated, similar to the components found in Naja cobras, but without the necrotizing effect on
tissue.
The venoms of some kraits also contain myotoxically acting components, although at a
minor level. If any venom includes hemocoagulation-affecting components as well as general
cytotoxic enzymes, any such quantity is clinically negligible.
6 mg of dry matter of the venom of the Indian krait (B. caeruleus) is equivalent to a lethal
dose for a human being.
Local symptoms of envenoming: The bitten site often does not hurt - many times people
bitten whilst asleep do not sense any bite at all, but occasionally the site can be painful, with
rare cases of swollen regional lymph nodes, reddish coloring around the site or minor
bleeding from the bite wounds.
Systemic symptoms of envenoming: The absence of pain upon the snakebite and at the
bitten site can sometimes trigger intriguing situations. For example, a person so affected,
unaware of having been bitten when asleep, may not link developments to possible
envenoming by a krait, which in turn can result in assigning symptoms of paralysis in the area
of cranial and other nerves to acute idiopathic inflammatory polyneuropathy, cranial
polyneuritis, myasthenia gravis attack or other similar neurological affections.
More often, the clinical symptoms of envenoming initially become apparent through
prodromal symptoms such as nausea, vomiting, abdominal pain or feelings of discomfort in
the abdominal region, headaches, pain in the neck, thirst, languor, increased temperatures, and
anxiety. The onset of the symptoms occurs several minutes to several hours following a bite.
In most cases, neurotoxicity symptoms begin by affecting cranial nerves, with typical
signs including ptosis, ophtalmoplegia including oculomotoric paralysis, dysarthria,
dysphagia, difficulties with opening the mouth, a protruding tongue, increased salivation, and
facial as well as pseudobulbar paralysis. In up to three quarters of those affected, the process
is often accompanied by CNS affection, including alteration of consciousness, which is
 Envenoming and Snakebite Treatment in Specific Snake Groups 105

largely manifest through weariness, but also consciousness disorders. These present
themselves qualitatively, e.g. via lack of coordination, or via deep coma and anterograde
amnesia. In about a third to a half of those affected, clinically significant paralysis of
respiratory muscles occurs very early on, from as little as 30 minutes, but onset may
commence even after 7-12 hours, with airway management and mechanical ventilation
required. Presymptoms of this serious affection always include weakness in limbs, feelings of
tightness around the chest or general muscle weakness. Other symptoms triggered by the
action of neurotoxins can include influence of the vegetative system, largely in terms of
reduced activity of parasympathicus. This is manifest through mydriasis, hypertension,
tachycardia and paleness, but also through increased sweating, salivating and lacrimation.
The effect on respiratory muscles is reversible, largely abating within 4 days even
without treatment. Nevertheless, there have been cases of long-term residual affection of
motoric nerves (such as distal motoric neuropathy), as well as that of vegetative nerves (e.g.
dysfunction of oculomotoric muscles, difficulties with urinating, obstipation persisting over a
long time), which probably came to existence due to damage of related neurons by the action
of presynaptic neurotoxic enzymes.
Some envenomings, e.g. by B. caeruleus, may even involve rhabdomyolysis, which is
soon revealed through muscle pain; more severe myoglobinemia pre-determines renal failure.
Hemorrhaging has previously been described within the range of snakebites from the
banded krait (B. fasciatus). However, the venom of this snake probably lacks
hemocoagulation-affecting components; moreover, the species might be confused with other
snakes. The cardiotoxicity evident from experiments with dogs has not been described in
humans.
Laboratory findings: There is a shortage of findings through laboratory examinations,
with only neutrophilic leukocytosis frequent. Findings of hypokalemia and metabolic acidosis
are described. In cases of rhabdomyolysis, high serum levels of myoglobin and
myoglobinuria are present. Examination following a snakebite from B. fasciatus in China
produced the following laboratory findings, showing consumption coagulopathy that was,
however, disputed: FBG decreases and FDP increases, reduced AT activity, and decreased
2-antiplasmin.
Mortality: Mortality following snakebites from kraits is high. Out of 210 snakebites
recorded in Sri Lanka in 1996-1998, there were 16 fatal cases from envenomings treated,
equivalent to 7.6%. In southern China, the number of fatal cases is 10%. In non-treated
victims, a mortality rate of 77% and even 100% is recorded in India and Sri Lanka
respectively. The interval from a snakebite from B. candidus until death varies widely - from
3 to 288 hours, on average 96 hours. A report on death within 30 minutes following a bite has
been recorded in Java.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Immediate application of a pressure immobilization bandage is fully
indicated. The bandage should be kept on until arrival at a health facility capable of dealing
with potentially serious symptoms of muscular paralysis. If envenoming is proven, it is best
to remove the bandage once antivenom is applied, if this is available, or at least until the
administration of neostigmine, see below.
Any more effective antivenoms are available only against the venoms of B. fasciatus, B.
caeruleus and B. multicinctus.
106 Jiri Valenta

Bungarus fasciatus:
* ANTIVENIN POLYVALENT, Bio Farma, Indonesia;
* BANDED KRAIT ANTIVENIN, Thai Red Cross, Thailand;
* MONOVALENT KRAIT ANTIVENOM SERUM, Central Research Institute, India;
* POLYVALENT SNAKE ANTIVENOM SERUM, Central Research Institute, India.

Bungarus caeruleus:
* LYOPHILISED ANTI-SNAKE-VENOM SERUM Haffkine, India;
* MONOVALENT KRAIT ANTIVENOM SERUM Central Research Institute, India;
* POLYVALENT SNAKE ANTIVENOM SERUM Central Research Institute, India;
* SNAKE ANTIVENIN I.P. Haffkine, India.

Bungarus multicinctus:
* ANTIVENIN BUNGARUS MULTIC. AND NAJA NAJA ATRA Nat. Inst. Prev.
Med., Taiwan.

Polyvalent antivenoms, even though designed for B. caeruleus, prove insufficient when it
comes to reversing muscular paralysis or preventing later neurologic complications. No
antivenom against the venom of B. candidus exists; cross-immunity with antivenoms to
counteract that of other kraits is uncertain or does not exist.
Local findings to a minimum degree will not require any special treatment.
Symptomatic treatment in cases where antivenom is unavailable or not effective must be
capable of tackling the most serious symptom of muscular paralysis - dyspnea. This is
conducted by airway management using tracheal intubation and subsequent mechanical
ventilation. Such a procedure is essential as it brings the mortality rate of envenomings down
to a minimum. In addition, pharmacological inhibition of acetylcholinesterase using
edrophonium or neostigmine, at a dosage of 0.5-1.0 mg IV (10-15 /kg of body weight)
should follow premedication by 0.5 mg of atropine IV. Any late complications that arise due
to the action of neurotoxic enzymes can be controlled by timely administration of effective
antivenom, but not symptomatically. A sufficient supply of liquids reduces the probability of
renal failure if rhabdomyolysis is in progress.
Should treatment prove fully effective, the symptoms of envenoming will completely
abate within 6-14 days. However, minor neurological complications may persist over a period
of several years.
When there is a lack of symptoms following a bite, a patient should be observed for 24
hours. Following envenomation, the patient can be discharged for home treatment after 24
hours once all symptoms recede.

6.3.1.3. Calliophis, Hemibungarus and Maticora Genera, Asian Coral Snakes

Genera and species. The group of the genera mentioned above is sometimes divided into
separate subfamilies, Calliophinae and Maticorinae. The Calliophis genus includes the
Bibrons coral snake (Calliophis bibroni), spotted coral snake (Calliophis gracilis), and
Indian coral snake (Calliophis melanurus). The Hemibungarus genus members include
Hemibungarus calligaster, Japanese coral snake (Hemibungarus japonicus), Kellogs coral
snake (Hemibungarus kelloggi), and MacClellands coral snake (Hemibungarus
macclellandi). Some resources also list additional species or classify both species under a
 Envenoming and Snakebite Treatment in Specific Snake Groups 107

common one. The Maticora genus includes Maticora beddomei, blue Malaysian coral snake
(Maticora bivirgata), banded Malaysian coral snake (Maticora intestinalis), small-spotted
coral snake (Maticora maculiceps), and black coral snake (Maticora nigrescens). The
Maticora species and certain Hemibungarus species are by some authors newly placed in the
Calliophis genus.
Other names: Oriental coral snakes (Calliophis), barred coral snake (Hemibungarus
calligaster), long-glanded coral snake (Maticora). Beddomes coral snake (Maticora
beddomei). JA: Iwasaki-Wamon-Beni-Hebi (H. macclellandi), Hyan, Amami, Hai (H.
japonicus). Indonesia: Ular matahari (M. intestinalis).
Description: These are primarily small and slender bodied snakes 30-60 cm long, which
live underground (Calliophis, Hemibungarus) and above ground (Maticora) with largely
nocturnal activity. The largest members are the 90-cm-long H. maclellandi and the
spectacular M. bivirgata, with a maximum documented length of 185 cm. Maticora snakes
possess large venom glands that may comprise up to two thirds of their body.
Many species of the above genera above are quite rare or remain somewhat a mystery. It
is possible to describe them as shy and non-aggressive creatures with some exceptions.
Home range and habitat: Asian coral snakes inhabit lowlands as well as mountainous
forests, scrubland, and plantations in S and SE Asia - Nepal, India, Sri Lanka, former
Indochina, S China including Taiwan and the Hainan islands, S Japan, the Philippines,
Malaysia, and Indonesia. H. macclellandi has been known to reach an altitude of 4,000 m
above sea level in Nepal.
Toxins: The composition of their venoms is little known, but does contain a certain
quantity of largely postsynaptic neurotoxins, enzymes of the PLA2 type and general cytotoxic
substances. In some species, venoms are considered quite effective; nevertheless, only
exceptions are of potential threat to humans - C. bibroni, H. kellogi, H. macclellandi, and M.
bivirgata. Based on the composition of the venom of M. bivirgata, these snakes are believed
to be closely related to the Hemachatus and Naja genera.
Local symptoms of envenoming: Any local symptoms described only include pain and
edema. According to known or presumed venom composition, deeper affection of tissues, the
development of bullae or minor necrosis is possible in severe cases or following bites from
certain members of the genera, but usually only a clinically insignificant localized response
develops.
Systemic symptoms of envenoming: For the majority of incidents, no serious symptoms of
envenoming occur. Symptomatology is largely limited to less significant prodromes, such as
nausea, vomiting, abdominal pain and diarrhea. Nevertheless, cases of vertigo and dyspnea
have also been described, e.g. from M. intestinalis. The nature of the venom in some species
does not preclude clinical symptoms of neurotoxicity, such as affection of facial muscles
including ptosis, external ophtalmoplegia and dysarthria. More rarely, in especially serious
cases, even paralysis of swallowing and respiratory muscles with fatal consequences are
known relating to M. bivirgata and H. macclellandi.
Laboratory findings: Results of laboratory examinations are unknown. Any larger
primary changes cannot be expected, except for probably neutrophilic leukocytosis.
Mortality: Three fatal cases have been reported: a two-year-old child died 2 hours after a
snakebite from M. bivirgata (Harrison, 1957) - the same species might be the cause of death
for a man in Singapore 5 minutes following a bite (Lim-Leong-Keng et al., 1989). 8 hours
after a snakebite from a young specimen of H. macclellandi, an adult man died from
108 Jiri Valenta

respiratory muscular paralysis in Nepal (Kramer, 1977). The native people of Borneo have
handed down information on deaths following snakebites from Maticora snakes.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Following a bite, application of a pressure immobilization bandage is
indicated, which is not to be removed before arrival at a health facility or before more serious
symptoms of systemic envenoming can be ruled out. The bandage should not be kept on the
body longer than necessary due to the possibility of causing localized damage to tissues.
No specific antivenom is available. In the case of systemic symptoms following a
snakebite from C. bibroni, application of following antivenoms is recommended:

* MONOVALENT COBRA ANTIVENOM SERUM, Central Research Institute, India;

* POLYVALENT SNAKE ANTIVENOM SERUM, Central Research Institute, India.

As cross-immunity is also possible with the venom components of the remainder of

Asian elapids, other related antivenoms can be administered where strictly indicated, even in
the case of envenoming by other members of the genera mentioned above.
Local findings, if more significant, will require delicate handling because of pain and the
possibility of greater damage to tissues. Moderate elevation and cautious cooling is helpful.
In the instance of symptoms of systemic envenoming, observation or symptomatic
treatment depending on the type and severity of the affection is advisable, see chapter 5
Snakebite: Therapy and prevention. Extremely severe progress of a case may require airway
management using tracheal intubation and mechanical ventilation.
Should there be a lack of symptoms following a bite, a patient should be observed for 24
hours. Following envenomation, the patient can be discharged for home treatment after 24
hours once systemic symptoms recede.

6.3.1.4. Dendroaspis Genus, Mambas

Species: Eastern green mamba (Dendroaspis angusticeps), Jamesons mamba
(Dendroaspis jamesoni), black mamba (Dendroaspis polylepis), and western green mamba
(Dendroaspis viridis).
Description: Snakes of medium-size to large, they have extremely slender bodies and can
grow up to 150-250 cm, with the black mamba (D. polylepis) even capable of 250-350 cm.
The documented maximum figure of 425 cm for the black mamba makes this snake the
longest venomous snake in Africa and the second longest snake in the world. The black
mamba boasts coloring of an olive-brown to dark gray and has a light underside, the name
deriving from the black color inside its mouth. Other mambas are varying shades of green
including bright green. These snakes have a narrow head and large and distinctive eyes with
round pupils. They are arboreal animals, only the black mamba primarily lives a terrestrial
life in open bush country. All are active at night.
Mambas rank among the fastest snakes both as regards moving and striking when
disturbed. The speed and their short-tempered behavior make them highly dangerous
creatures. Anything intruding near a mambas shelter in a hollow tree or in the bush is likely
to be attacked. There have been stories of humans being bitten that find themselves in the
unfortunate position of between a snake and its nest. Mambas possess excellent vision and are
attracted by movement, meaning they can sometimes get into an unsafe distance from a
human. Mambas bite very swiftly and then promptly fall back, with strikes sometimes being
 Envenoming and Snakebite Treatment in Specific Snake Groups 109

repeated. In South Africa, the number of mamba snakebites peaks in spring - September to
February, then sharply decreases in the winter.
According to some, mambas compete with the African puff adder (Bitis arietans) and the
saw-scaled viper (Echis carinatus) for the dubious honor of supremacy in terms of mortality
from bites in Africa. However, the incidence of snakebites as well as the aggressiveness of
mambas is probably overstated.
Other names: FR, DE, AF: Mamba.
Home range and habitat: Mambas inhabit forests, savannah woodlands and bush as well
as tree plantations; the black mamba (D. polylepis) can also be found in open bushland and
semi deserts. Their home range includes E, S and Central Africa including Zanzibar Island;
from north to south mambas range through S Sudan to the Republic of South Africa, while
from west to east they are found from Ghana to Kenya. The western green mamba (D. viridis)
inhabits the humid forests of W Africa, in the zone from Senegal to Nigeria.
Toxins: The black mambas venom glands contain approximately 8-16 ml of liquid
venom. In the freshly hatched young, the amount is 1-2 ml of venom, which is sufficient
quantity to have a lethal effect on a human.
Primary venom components concern highly effective neurotoxins. Although curare-like
neurotoxins are not a feature of the mamba, their venom contains neurotoxically acting
nicotine acetylcholine receptor antagonists analogical to the postsynaptic neurotoxins of other
elapids (Elapidae) classified as , , and neurotoxins. Other neurotoxins are possibly
those boasting the greatest effectiveness: DTX dendrotoxins - peptides causing inhibition by
blocking voltage channeled by potassium for the re-polarization of neurons, thus causing
extension of the process.
This way, the substances support muscular paralysis, either at a central level or by
exhausting neuromuscular junctions by super-threshold stimulation. The effect of DTX is
very probably manifest on the vegetative nerves as well. A number of peptides isolated from
mambas venom potentiate neurotransmission in the CNS as well as in peripheral nerves.
They are limited only to the mambas venom outfit. The peptides, acting as muscarine
acetylcholine receptor ligands, may probably cause activation in the CNS. Fasciculins are
peptide acetylcholinesterase inhibitors increasing the intrasynaptic amount of acetylcholine,
which results in fasciculation of muscles. Dendroaspin natriuretic peptide DNP is a
polypeptide analogous to the human atrial natriuretic peptide; it is responsible for causing
diuresis through natriuresis and dilating the vessel bloodstream, which results in, among other
things, acceleration of venom distribution in the body of the victim. A certain proportion of
cardiotoxic components is also possible. The venom displays relatively high activity in terms
of hyaluronidases, which is also essential in facilitating propagation of venom components.
Hemolytic, hemorrhagic, and coagulation activities are almost lacking in mambas
venom.
Local symptoms of envenoming: A mambas (Dendroaspis) fangs are embedded in the
maxilla, i.e. the upper jaw, rather in the anterior part; they form the only maxillary teeth. In
the mandible, i.e. the lower jaw, there is a row of relatively massive non-venomous teeth.
This can provide a typical mamba bite pattern provided the attack is complete. Indeed, the
fangs may sometimes remain in the wound. Multiple bite wounds can be carried out
depending on the nature of the attack. The wound is not very distinctive and pain in form of
burning is quite low. Bleeding may occur from the bite wounds. Only minor redness tends to
110 Jiri Valenta

appear around the bitten site, followed by moderate localized edema. Localized pain,
inflammation, stiffening, and hypoesthesia, i.e. reduced sensitivity, will persist over a week.
Systemic symptoms of envenoming: Symptomatology, even highly serious, will often
manifest very early on - within ten minutes. This will mostly begin with prodromes like
nausea, vomiting, and abdominal pain. The envenoming process may continue with paleness,
goose pimples (cutis anserina), sweating - even profusely, irritation to the throat and a
potential cough, conjunctiva congestion (hyperemia), feelings of heat, photodysphoria and
more intense sensation of light, vertigo, ataxia (affection of coordination), somnolence and
languor, or conversely excitation and agitation through to loss of consciousness. Vascular and
cardiac symptoms can occur, from acral chills all the way up to circulatory collapse, including
peripheral vasoconstriction.
Neurological symptoms mostly start with cranial nerves being affected and muscular
fasciculations of limbs or a trembling sensation in the face or around the body. Muscular
dysfunctions are manifest as ptosis, ophtalmophlegia including unfocused, fuzzy or double
vision with non-reactive mydriasis and subsequent inability to move the eyelids and balls.
Dysphagia arises, sometimes including painful swallowing, and continues with paralysis of
soft palate and swallowing muscles accompanied by loss of the swallowing reflex and a risk
of aspiration of saliva or stomach content. Movements of the lower jaw and ability to lift the
head cease. The face takes on the look of a mask. Sensation in the area of affected nerves is
retained. A general sense of weakness through to loss of muscle strength in limbs occurs, as
does a urinating disorder or failure - sometimes even before respiratory muscles are affected.
Paralysis of respiratory muscles associated with possible affection of the respiratory centre
causes a decrease in respiratory frequency and respiratory failure. Respiratory failure results
in death if not adequately treated.
Laboratory findings: The results of laboratory examinations are not specific for
envenoming.
Mortality: In untreated cases, lethality is near 100%, whilst for envenomings that are
treated adequately and promptly, it can be almost zero (McNally, 1987; Warrell, 1995).
Among native populations in the home range of the snakes, mortality is expected to be very
high.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Immediate application of a pressure immobilization bandage is always fully
indicated. The bandage must not be removed before arrival at a health facility capable of
dealing with potentially serious symptoms of muscular paralysis. If envenoming is proven,
the bandage is preferably removed only after application of antivenom, if available, or
following one hour of observation without symptoms.
Applicable antivenoms:

* SAIMR POLYVALENT SNAKE ANTIVENOM, SAIMR, the Republic of South

Africa (D. polylepis, D. jamesoni, D. angusticeps, etc.);
* FAV-AFRIQUE, Aventis Pasteur, France (D. polylepis, D. jamesoni, D. viridis, etc.).

If the envenoming has already developed, a larger quantity of the antivenom should be
administered - up to 16-20 vials are recommended; the first 50 ml should be followed by
additional vials every 30-60 minutes until serious symptoms abate.
There is only a minimal local affection that will not require any special treatment.
 Envenoming and Snakebite Treatment in Specific Snake Groups 111

Swallowing and respiratory muscular paralysis will require airway management using
tracheal intubation and mechanical ventilation if manifested clinically with subsequent risk of
aspiration and respiratory failure. The same necessity arises in cases of a likely more serious
disorder of consciousness, where a risk of insufficient passability of airways or aspiration
may occur, principally for weakened swallowing and cough reflexes.
Nevertheless, consciousness is often retained even if muscular paralysis fully develops,
therefore, sedation of the patient is desirable in the course of therapy, including managed
ventilation.
Despite some recommendations, administration of cholinesterase inhibitors, like
edrophonium or neostigmine, is not indicated due to the possibility of potentiating the effects
of fasciculins.
Following successful therapy of the envenoming, the patient is detained another 12-24
hours in an intensive care unit and discharged during the following day for home treatment.

6.3.1.5. Naja Genus, Cobras

African species. Anchietas cobra (Naja anchietae), snouted cobra (Naja annulifera),
banded Egyptian cobra (Naja haje), Katian spitting cobra (Naja katiensis), black and white
cobra (Naja melanoleuca), Mozambique spitting cobra (Naja mossambica), black-necked
spitting cobra (Naja nigricollis), Cape cobra (Naja nivea), and Nubian spitting cobra (Naja
nubiae), African cobra (Naja pallida).
Asian species. Chinese cobra (Naja atra), monocellate cobra (Naja kaouthia), Indian
cobra (Naja naja), Central Asian cobra (Naja oxiana), Naja mandalayensis, Philippine cobra
(Naja philippiensis), Naja sagittifera, Peters cobra (Naja samarensis), Indochinese spitting
cobra (Naja siamensis), Indonesian cobra (Naja sputatrix), and golden spitting cobra (Naja
sumatrana).
Description: Cobras of the Naja genus are medium-sized snakes, with N. atra and N.
katiensis 100-130 cm long, N. kaouthia, N. annulifera and N. nivea about 200 cm long. The
length of 269 cm and weight of 3.2 kg for a N. melanoleuca is the documented record-
breaker. At the same time, this largest member of the genus is considered by some
herpetologists as the brainiest of all African elapid snakes. Cobras have a typical method of
deterrent or position of attack, whereby the anterior part of the body is lifted up and the ribs
expanded, forming a so-called hood, which makes the snake optically larger in front of an
intruder. The dorsal coloring is diverse, ranging from black and gray through to a creamy
brown or tones of red or yellow, including the typical speckled (N. atra, N. kaouthia or N.
naja) or banded (N. annulifera, N. melanoleuca or N. nigricollis) pattern of some species.
Cobras are relatively quick snakes, be it when moving or striking. Essentially, they are not
typically aggressive snakes, preferring to escape, as do most snakes; however, they can carry
out swift and targeted attacks if acutely threatened. These snakes are mostly night hunters, but
diurnal activity is not unusual, particularly for young individuals or when temperatures are
lower.
The structure of the venom apparatus, which features an open channel in the front part of
the fang, allows some cobra species to defend themselves by what appears to be spitting the
venom. In fact, this kind of action is not really spitting as the venom is discharged under
pressure by anterior openings in fangs, resulting in microscopic droplets being sprinkled over
a distance of approximately 2-4 m. This is dangerous if a face, or more particularly the eyes,
of an intruder become the target, which is the snakes intention. Amongst the African cobras,
112 Jiri Valenta

this ability is employed by N. katiensis, N. mossambica, N. nigricollis, and N. pallida;

whereas for the Asian cobras, this method is used by N. mandalayensis, N. philippiensis, N.
siamensis, N. sputatrix and N. sumatrana, and more rarely by N. atra and N. samarensis.
Other names: EN: Egyptian, Arabian, banded, brown, Angolan or snouted cobra (N. haje,
N. annulifera). Mali or West African spitting cobra (N. katiensis). Forest cobra, black and
white-lipped or black cobra (N. melanoleuca). EN: Mozambique spitting cobra; indigenous
language: mFezi (N. mossambica). EN: black, black-necked or spitting cobra (N. nigricollis).
Cape or yellow cobra (N. nivea). African or red spitting cobra (N. pallida). Chinese or Taiwan
cobra (N. atra). Monocellate, common, Thai cobra, Andaman cobra (N. sagittifera, N.
kaouthia). EN: Asian, Indian spectacled cobra (N. naja). Central Asian, Oxus cobra (N.
oxiana). Visayan, Peters cobra (N. samarensis). Indochinese, Indonesian, Malayan spitting
cobra (N. siamensis, N. sputatrix). Golden, equatorial spitting cobra (N. sumatrana). FR:
Cobra, Serpent lunetes (N. kaouthia).
Home range and habitat: In Africa, cobras (Naja) are found all across the continent
except the Sahara and several other inhospitable localities. They tend to prefer more arid
habitats, such as open savannahs, bush, open woodland and plantations, but always in close
proximity to water.

* Naja annulifera: grassy savannahs and bush, sometimes near water surfaces in SE
Africa, northwards to S Angola and northern Mozambique.
* Naja haje: savannahs, bush, open woodlands and plantations in N Africa from Morocco
to Egypt; in S Sahara from Senegal and Mauritania to Somalia; to the east as far as Uganda
and N Tanzania.
* Naja katiensis: dry savannahs in W Africa from Senegal as far as Central Nigeria and
W Cameroon.
* Naja melanoleuca: the woodland areas of W and Central Africa from Senegal to
Angola; eastward from Somalia to Zambia, as well as the islands of Zanzibar and So Tom.
* Naja mossambica: savannahs and bush in SE Africa from S Tanzania and Angola as far
as S Africa, as well as the islands of Zanzibar and Pemba.
* Naja nigricollis: bush and open woodlands in Sub-Saharan Africa from Senegal to SW
Somalia, and from E Africa to the west of the Republic of South Africa. Local occurrence
documented in Egypt as well (Rehak, Osborn, 1988).
* Naja nivea: arid areas of the western part of S Africa.
* Naja pallida: semi desert regions in NE Africa from S Egypt to NE Tanzania.

In Asia, the Naja genus cobras inhabit a vast area bordered by the eastern coast of the
Caspian Sea to the west, by Nepal and S China to the north, by Sri Lanka and Malaysia to the
south and by the Philippines to the east. They dwell in diverse habitats from arid and rocky
regions of Central Asia as far as muddy areas and humid forests of SE Asia.

* Naja atra: sparse vegetation including fields and plantations in SE China, NE Laos, N
Vietnam, Hainan, and Taiwan.
* Naja kaouthia: rather humid sites, in mountains they are found up to 1,600 m above sea
level in NE India, SE Nepal, Bangladesh and SW China; the range continues to the south
across the former territory of Indochina and Malaysian islands to the Andaman Islands.
 Envenoming and Snakebite Treatment in Specific Snake Groups 113

* Naja naja: grassy and rather farm areas including fields, and in the neighborhood of
settlement in E Pakistan, S Nepal, India, Sri Lanka and W Bangladesh. In the Himalaya, the
range can extend up to the altitude of 4,000 m above sea level.
* Naja oxiana: rather arid and rocky areas and localities with sparse vegetation in NE
Iran, S Turkmenistan, S Uzbekistan, W Tajikistan, Afghanistan, N Pakistan and N India.
* Naja philippiensis: forests of the islands of Luzon, Mindoro, Masbate and Marinduque,
the Philippines.
* Naja samarensis: forests of the islands of Bohol, Leyte, Mindanao, Samar and
Camiguin, the Philippines.
* Naja siamensis: rather humid habitats including rice fields and bamboo stands in
Thailand, Cambodia, S Vietnam, W Laos and E Burma.
* Naja sputatrix: rather humid habitats, swamps, rice fields and forest edges in Indonesia
the islands of Java, Bali, Lombok, Sumbawa, Komodo and Flores as far as Lomblen.
* Naja sumatrana: forests and jungles in S Thailand, Malaysia, Singapore, Sumatra and
Borneo as far as the Palawan Islands, the Philippines.

Toxins: The effectiveness of venom in the Naja genus, expressed as LD50 for mice,
differs among the individual species and is possibly determined by the content of neurotoxins.
The venom of N. philippiensis with LD50 for mice, 0.14 mg/kg of body weight, is probably
the most effective. Values already described for venoms of other species per kg of body
weight include 0.29 mg for N. naja, 0.49 mg for N. oxiana, 1.75 mg for N. haje, and 3.05 mg
for N. nigricollis.
Neurotoxins and necrotizing components principally comprise the clinically effective
venom substances. The proportional representation of these components determines the
possible process of envenoming, where either neurotoxic symptoms (N. philippiensis) prevail
or localized ones as extreme as excessive necrotic symptoms (N. nigricollis, N. mossambica).
Nevertheless, neither development of necrosis nor neurotoxic symptoms can be precluded
following a bite from any of the Naja cobras; essentially, the neurotoxic N. phillipiensis
produces necrosis in 8% of cases, while N. nigricollis and N. mossambica primarily cause
severe necrosis, although there is a low incidence of neurotoxic symptoms that pose a threat
to children in particular.
Neurotoxins are largely proteins that produce postsynaptic anti-depolarization blockages.
These -neurotoxins are presented in the form of molecules with both long and short chains,
see also chapter 3. 3. 2. 2 Venom components with neurotoxic activities. These are venom
components found in all cobras of the Naja genus, but they form a fundamental and clinically
significant proportion of the venoms in N. philippiensis, N. naja, N. atra, N. kaouthia, N.
sumatrana, N. haje, N. melanoleuca, N. nivea, and possibly N. oxiana. The venoms of some
cobras, e.g. N. atra, N. kaouthia and N. sumatrana, N. haje, N. melanoleuca, M. mossambica,
N. nigricollis, and N. nivea, also contain presynaptically acting neurotoxic PLA2. However,
the clinical effect of these substances on a human is minimal or does not become manifest (N.
nigricollis).
Even though the venoms of cobras of the Naja genus are generally lower in enzymes than
those of viperids (Viperidae), namely in locally effective proteinases, they contain cytotoxic
components causing serious localized damage - mostly necrosis. The necrotizing effect of the
venom can be explained by the function of polypeptidic cytotoxins, locally and myotoxically
114 Jiri Valenta

acting PLA2, complements of activating substances, hyaluronidase, and a number of other

venom components - largely enzymatic types.
Cardiotoxically acting substances - cardiotoxins - are components with the status of
polypeptidic cytotoxins and membrane toxins, which produce irreversible damage to
myocardial cells. Clinically, they can cause dysrhythmia, hypotension, and death.
The venoms contain components activating the complement via an alternative route: the
venom of the black-necked spitting cobra (N. nigricollis), contains PLA2 with an
anticoagulation effect and hemorrhagic enzymes.
Local symptoms of envenoming: The bitten site will mostly display only minor wounds -
at the beginning, any bite wound or scratching by an infant may not be noticeable at all. In the
majority of cases, the bite is accompanied by immediate pain, which persists for several days.
In some cases, severe pain may continue over the period of up to 10 days, e.g. N. sumatrana,
while in other cases, numbness may tend to occur at the bitten site, such as caused by N.
melanoleuca. Localized edema begins to develop 2-3 hours after the bite, typically peaking at
around day 2 or 3. The edema will mostly affect only the bitten limb, but severe advancing
edema may expand up to the torso, this is true except for a bite from N. philippiensis, which is
not usually accompanied by edema. Regional lymphadenopathy develops including a feeling
of strain or pain from enlarged regional lymph nodes.
Skin in the affected area darkens; peeling and sometimes ecchymoses can occur. By
approximately day 3, blisters start to form, frequently with red and yellow necrotic or blood
content. Additionally, necrosis develops in the skin, under the skin and in deeper tissues of
the affected area, reaching as far as the tendons. Despite this, serious damage to muscle tissue
and tendons is not a frequent occurrence. The process of tissue necrotization is accompanied
by a putrid smell. Thrombosis and microthromboses, which sometimes form at the site of
localized affection, can potentiate the extent of necrosis through perfusion disorders. Even
formation of a deep venous thrombosis in the affected limb has been described.
Approximately in a half of cases, the necrotic tissue is affected by secondary infection
involving generated phlegmons and fever. Bacteriological agents typically isolated include
Proteus rettgeri, P. morgani, Escherichia coli, Pseudomonas aeruginosa, Salmonela sp.,
Enterobacteriacae, and Staphylococcus aureus.
Tissue destruction requires long-term treatment and may result in scarring as well as
arthral damage as serious as ankylosis or limb deformation. The need to amputate is also
possible, plus relapses of the affection may be triggered. Severe local damage with the
development of excessive necrosis is typical for snakebites from the following African cobra
species: N. katiensis, N. mossambica, N. nigrocollis, and N. pallida; for Asian species this
concerns N. atra, N. kaouthia, and N. sumatrana. 40% of bites from the Chinese cobra (N.
atra) will result in necrosis, with persisting dysfunction of limbs in 10% of those affected.
Effect on eyes. Venom droplets impacting on an eye will be immediately followed by
severe pain, with subsequent blepharospasm, lacrimation, edema of the eyelid, fuzzy vision,
conjunctivitis, conjunctival chemosis, a white discharge and inflammatory affection of the
cornea - keratitis. Further developments, especially if treatment is inadequate, result in
generating corneal ulcerations, frontal uveitis and panophtalmitis with consequent blindness,
although attacks by Asian cobras do not result in such serious affection. Symptoms of
systemic envenoming do not arise in this way; in rare cases, venom may be transferred from
the conjunctival sac via lymph pathways to the distal parts of nervus facialis and thereby
affect the function of this nerve.
 Envenoming and Snakebite Treatment in Specific Snake Groups 115

Systemic symptoms of envenoming: Incidence of systemic envenoming following bites

from the cobras of the Naja genus vary according to author and species, ranging from very
low, i.e. 15% - 45% in the Malayan region (N. kaouthia, N. sputatrix, and N. sumatrana), up
to an extreme of 97% following a bite from N. philippiensis.
The process of envenoming mostly commences with the following prodromes: nausea,
vomiting, abdominal and cranial pain, hot skin and a sensation of the mouth being dry,
increased temperatures, salivation, redness or paleness to the face, sweating and vertigo.
These prodromal symptoms may soon be followed by symptoms of circulatory or neural
tissue affection, i.e. hypotension, reduced heartbeat, ataxia, and consciousness disorders, such
as restlessness, euphoria or disorientation, fatigue, somnolence, and potential loss of
consciousness; the latter of these symptoms can be also caused or potentiated by severe
hypotension leading up to a status of shock.
The main symptom of severe systemic envenoming in the majority of cobras of the Naja
genus involves that of neurotoxicity. Clinically significant affection of neuromuscular
junctions will become manifest especially with envenomings by N. philippiensis, whose
venom largely contains neurotoxins, with the proportion of neurotoxic symptoms to
development of necrosis being 14:1. As regards Asian cobras, this concerns N. naja and N.
kaouthia, where the neurotoxicity-necrosis rate is reversed: 1:3.7 (Davidson et al., 1995). In
Africa, neurotoxicity is presented namely due to a bite from N. haje, N. melanoleuca and N.
nivea. For the rest of cobra species, severe neurotoxic symptoms are less frequent or not
described despite the proven existence of neurotoxic components.
In the area of cranial nerves, neurotoxic symptoms mostly start with ptosis, external
ophtalmoplegia with dizziness or double vision, palatal and glossopharyngeal paralysis
including dysphagia, dysarthria and excessive salivation, and an inability to open the mouth
and stick out the tongue. Unilateral or bilateral auditory failure can also occur. The process
continues with weakness of neck muscles, meaning the head is not controllable and droops,
weakness of limbs including loss of reflexes and respiratory failure accompanied by shallow
diaphragmatic breathing when the respiratory muscles are weakened. Without any treatment,
death occurs due to respiratory failure associated with limited paralysis of striated muscles,
i.e. including respiratory muscles, and all this is in full consciousness. In some cases,
muscular fasciculations, spasms or tremors occur during the development of the neural
affection. The neurotoxic symptomatology typically continues to evolve through to
respiratory failure for duration of several hours. However, in the case of severe envenoming
by highly effective neurotoxic venom (N. philippiensis, N. melanoleuca, and N. kaouthia),
neuromuscular affection or the non-functioning of respiratory muscles is likely to occur 3-30
minutes following a bite. The commencement of neurotoxic symptoms after 24 hours in N.
philippiensis is the extreme reverse of this situation. Muscular paralysis mostly persists for 2-
3 days, but may do even more - for up to 14 days.
Envenomation by the majority of Naja cobras means that cardiotoxicity is not a major
clinical issue, although its progress involving severe hypotension and heart arrhythmias or
shock is possible. However, the effects of cardiotoxic components are largely limited to slight
hypotension and the presence of reversible abnormities in ECG with elevated ST-segment and
T wave inversion, which usually abate within a week, e.g. in N. naja.
An effect on hemocoagulation is not typical for envenomings by Naja cobras, but
sometimes it may occur following a bite from some African cobras, for instance N.
nigricollis; the incidence of which is about one third of those affected. The disorder is
116 Jiri Valenta

typically either that DIC-like or hemolytic, and is manifest as bleeding from the nose, gums,
and wounds. Even fatal subarachnoid hemorrhaging has occurred (Warrell, 1976).
Venom components in some cobras with largely cytotoxic venoms, like N. nigricollis,
may also cause hepatocellular affection with subsequent jaundice and elevated hepatic
enzymes.
Renal affection is rare and limited to proteinuria and microscopic hematuria. Any level of
potential hemolysis is clinically insignificant too.
Laboratory findings: Laboratory findings are not specific for envenomings. Leukocytosis
typically occurs - up to 30,000/mm3 (N. nigricollis). A decrease in Hct will accompany
hemorrhagic complications or hemolysis; decreased PLT and increased FDP may indicate
consumption coagulopathy. In patients envenomed by cytotoxic venom components (N.
nigricollis and N. atra) and displaying development of necrosis, hepatocellular affection
occurs with increased bilirubin, ALT and AST. Temporarily, urobilinogen in urine will be
found. Insignificant proteinuria, hemoglobinuria or microscopic hematuria also occur.
Mortality: Snakebites from the cobras of the Naja genus are believed to cause thousands
of deaths of people in Asia and Africa. Although such a statement as this is exaggerated,
envenomation by these snakes in their home range is epidemiologically significant,
accounting for something like 25% of fatalities of all cases of envenoming in Thailand. Out of
47 snakebites from N. sumatrana, two resulted in death. As regards the Chinese cobra (N.
atra) in China, responsible for a high incidence of cases, mortality is low - a mere 0.7%; in
Taiwan, fatal cases were recorded in 14% of all cases in 1904-1971. In the home range of the
Central Asian cobra (N. oxiana) of Iran and surrounding countries, from where information is
rather incomplete, mortality is expected to be caused by neurotoxicity (Warrell, 1995).
Mortality caused by the Indonesian cobra (N. sputatrix) is also presumed, most likely
affecting children. Numbers concerning mortality following bites from the Indian cobra (N.
naja) in India are very high, accounting for 50% - 70% of the victims being hospitalized,
which includes patients treated with antivenoms.
In Africa, fatalities after snakebites from the black and white cobra (N. melanoleuca) and
black-necked spitting cobra (N. nigricollis), with the development of pulmonary edema or
bleeding into the brain have been reported. A higher mortality has also been observed
following snakebites from the banded Egyptian cobra (N. haje). Out of 10 cases of
envenoming after a bite from N. nivea, only a single case proved fatal.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Although disputed due to potential deterioration to local damage, putting on a
pressure immobilization bandage is indicated following a bite from the majority of Naja
cobras, especially those with significant content of neurotoxins in their venom - N. haje, N.
melanoleuca, N. nivea, and Asian cobras of the Naja genus. The pressure immobilization
bandage may delay any severe neurological symptomatology by up to 30 hours. The bandage
is not recommended following bites from African spitting cobras with venoms that do not
show neurotoxicity clinically, but cause excessive necrosis (N. nigrocollis, N. mossambica).
In nearly a half (42%) of those envenomed by N. philippiensis, neurological symptoms
appeared due to neurotoxins released by removing the bandage. The bandage should not be
removed before arrival at a health facility capable of dealing with potentially serious
symptoms of muscular paralysis. If envenoming is proven, the bandage should be removed
only after application of antivenom, if such is available.
 Envenoming and Snakebite Treatment in Specific Snake Groups 117

Should no symptoms be displayed, the bandage may be removed following an hour of

observation. Any administration of opioid analgesics as a part of first aid is relatively
contraindicated as a result of loss of respiratory efforts and intensified respiratory failure
caused by developing paralysis. The patient must be observed and discharge from hospital is
possible following 24 hours of no symptomatic development.
The list below shows applicable antivenoms against venoms of African cobras of the
Naja genus.
Naja haje:

* ANTIREPT PASTEUR, Aventis Pasteur, France;

* FAV-AFRIQUE, Aventis Pasteur, France;
* FAVIREPT, Aventis Pasteur, France;
* IPSER AFRIQUE PASTEUR, Aventis Pasteur, France;
* SERUM ANTIVENIMEUX BITIS ECHIS NAJA PASTEUR, Pasteur Merieux,
France.
Other African Naja cobras:

* SAIMR POLYVALENT SNAKE ANTIVENOM, the Republic of South Africa;

* FAV-AFRIQUE, Aventis Pasteur, France.

If an envenoming has already commenced, a larger quantity of antivenom is

administered, with up to 10-20 vials recommended; the first 3 vials, i.e. 30 ml, should be
followed by additional doses every 30-60 minutes until the serious symptoms abate.
The list below shows applicable antivenoms against venoms of Asian cobras of the Naja
genus.
Naja atra:

* ANTIVENIN BUNGARUS MULTIC. AND NAJA NAJA ATRA, Nat. Inst. Prev.
Med., Taiwan.

Naja kaouthia:

* COBRA ANTIVENIN, Thai Red Cross, Thailand.

Naja naja:

* LYOPHILISED ANTI-SNAKE-VENOM SERUM Haffkine, India;

* MONOVALENT COBRA ANTIVENOM SERUM, Central Research Institute, India;
* POLYVALENT SNAKE ANTIVENOM SERUM, Central Research Institute, India;
* SNAKE ANTIVENIN I.P., Haffkine, India.

Naja sputatrix:

* COBRA ANTIVENIN, Thai Red Cross, Thailand.

* ANTIVENIN POLYVALENT, Bio Farma, Indonesia;
* NAJA NAJA SPUTATRIX, Twyford, Germany.
118 Jiri Valenta

Specific antivenoms for counteracting venoms of other Naja cobras are not available. If
necessary, some of the above-mentioned preparations can be used, preferably the polyvalent
forms effective against Naja naja.
Again, a higher quantity of the antivenom is applied - up to 100 ml, but even as much as
450-600 ml. Naturally, such high a dosage is associated with a higher incidence of allergic
reaction.
Respiratory insufficiency may occur even upon administration of adequate antivenom,
however, with a shorter period of persistence of the insufficiency. If antivenom is applied
only upon development of neurotoxic symptomatology, its effectiveness is reduced, in some
cases of affected tissues, e.g. N. nigricollis, no positive effect may become manifest.
Slight elevation and moderate cooling of the affected limb is desirable; pain should be
dimmed by analgesics. Any handling and treatment actions must be carried out delicately
with a view to avoiding a potentially high level of tissue damage. Development and
persistence of excessive edema may cause compartment syndrome to a certain extent; the
syndrome is subsequently co-responsible for forming and propagating necrosis. Measuring
compartment pressure is advisable; the values should not exceed 45 mmHg (6 kPa, 60 cm
H2O). Fasciotomy is indicated in the case of risk of closed tissue perfusion in any increase in
compartment pressure or any pulsation closure. Naturally, the points of tight compartments
and surroundings of finger joints are primarily exposed to the risk of necrosis forming.
The developed necrosis must be immediately removed surgically, which will reduce the
risk of more severe localized infection. Timely implantation of skin to the points of removed
necrosis will speed up the healing process. Any possible abscesses and fluctuating points are
incised, evacuated and drained. Even though prompt administration of a sufficient amount of
antivenom will neither prevent nor reduce the severity of any local tissue damage, it can
possibly reduce propagation of edema and thus the probability of compartment syndrome
with subsequent necessity for fasciotomy.
If at all possible, affected eyes should be rinsed with a stream of clean water, but more
preferably by a physiological saline solution. Milk is an alternative due to a possible link
between some venom components to its proteins. Pain can be eased by instillation of local
anesthetics into the conjunctival sac. Treatment of affected eyes - administration of
corticosteroids and antibiotics - should be managed by an eye specialist to minimize any
secondary damage of more seriousness.
Swallowing and respiratory muscular paralysis will require airway management using
tracheal intubation and mechanical ventilation if manifested clinically with a subsequent risk
of aspiration and respiratory failure. The same necessity will arise in cases of potentially more
serious consciousness disorders, where a risk of insufficient passability of airways or
aspiration may occur, namely in instances of diminished swallowing and cough reflexes.
Nevertheless, consciousness is typically retained even when muscular paralysis fully
develops. Therefore, sedation of the patient is desirable in the course of therapy, with
mechanical ventilation.
Symptomatic treatment must tackle the most serious symptom of muscular paralysis -
dyspnea, and this is carried out by airway management using tracheal intubation and
subsequent mechanical ventilation. This procedure is essential as it brings down the mortality
rate of envenomings to a minimum. In symptoms of neuromuscular paralysis, inhibition of
acetylcholinesterase using 10 mg of edrophonium IV (in children, 0.25 mg/kg of body
weight) is indicated to test the positivity of the effect. This is followed by administering
 Envenoming and Snakebite Treatment in Specific Snake Groups 119

neostigmine, at a dosage of 0.5-1.0 mg IV (10-15 /kg of body weight), with premedication

by atropine, 0.5 mg IV (50 /kg of body weight). The dose can be repeated following 30-60
minutes. Instead of individual doses in form of bolus, infusion can be applied following the
initial dose at a rate equal to a dose of neostigmine of 25 /kg/h. The procedure is indicated in
instances where antivenom is administered, as it will significantly reduce the period of
neuromuscular paralysis, which can persist for up to 7 days despite specific therapy. Muscular
paralysis and respiratory insufficiency will abate spontaneously over the course of time
without any further effects.
Any possible arrhythmias caused by cardiotoxins may recede following antivenom being
given or the same are treated symptomatically. Reduced pressure, including a possible state of
shock, will require volumoexpansion and vasopressoric treatment. In serious cases, a
contractility disorder is possible with the necessity of -mimetic support of the myocardium
using dobutamine.
Discharge of the patient is advisable only 24 hours after the symptoms of systemic
envenoming and more severe forms of localized damage have disappeared. Treatment of any
minor or regressing localized affections can be completed in form of outpatient therapy.

6.3.1.6. Ophiophagus Genus

Species: A monotypic genus containing a single species, the king cobra (Ophiophagus
hannah). The former subdivision to subspecies, i.e. O. h. borneensis, bungarus, elaps,
sinensis, vittata, brunnea and nordicus is not valid anymore.
Description: The king cobra (O. hannah), is the largest venomous snake. It can grow to
over 570 cm, the maximum being 600 cm although this has never been documented. Coloring
is shades of gray and brown through to olive, the throat and ventral part of the neck are
yellow. Sub-adult animals usually have darker bodies and light crossing stripes. A typical
feature is an upright fighting and defensive position of the anterior part of the body with a
spread hood. This way, a fully adult and well developed example can easily match the height
of a human. Any aggressiveness associated with these creatures is unfounded - bites are rare.
Of this low incidence affecting humans, the majority result from handling snakes or were
caused by the creatures becoming irritated. The king cobra is principally a diurnal animal,
hunting almost exclusively snakes and lizards. It will mostly bite the prey, holding it in its
mouth until immobilized or dead. A long-held bite may occur to a human as well.
Other names: FR: Cobra royal; other languages: Hamadryad.
Home range and habitat: The king cobra inhabits dense tropical forests, bamboo grooves,
mangroves, as well as plantations and open landscapes near water in the Indian Peninsula
from E Pakistan and Nepal to Sri Lanka, and almost the entire territory of SE Asia from
southern Chinese provinces - approximately to the 25th degree of northern latitude - including
the islands of Hainan and Taiwan as far as Malaysia, Indonesia and some of the Philippine
islands. In the Himalayas, their range can extend up to an elevation of 1,800 m above sea
level.
Toxins: The venom apparatus of the king cobra - the fangs and the venom gland - is
impressive and the amount of venom large, according to the size of the snake. The greatest
amount of venom collected was equal to 900 mg in dry weight. LD50 for mice amounts to
1.73 mg/kg of the body weight.
120 Jiri Valenta

The main effective components of the venom concern postsynaptic neurotoxins with a
high binding affinity to nicotine acetylcholine receptors. Out of a number of isoforms with a
long molecule, the neurotoxin identified as toxin b tends to be the most toxic example.
Other components include enzymes of PLA2 type acting as cardiotoxins. In a trial carried
out on mice, these caused the following ECG-abnormities: bradycardia, prolongation of the
PR-interval, extension of QRS-complex through to a complete AV-block.
In terms of hemocoagulation-affecting substances, the venom contains a serine protease
specifically activating X factor, which lacks a direct effect on prothrombin and FBG, PLA2
with inhibiting impact on PLT, lectin ophioluxin acting as a potent PLT-agonist (the first
toxin to be isolated from an elapid venom), enzymatic Hannahpep which causes
fibrino(geno)lysis, and others. Laboratory findings are described as consumption DIC-like
syndrome with decreased FBG, 2-antiplasmin and AT activity, and increased FDP;
nonetheless, envenoming has not been manifest by a more serious affection of
hemocoagulation clinically.
Furthermore, the venom contains components affecting the complement via an alternative
route as well as hemorrhagic substances, for instance hannahtoxin, which is a
metalloprotease.
Despite the large number of enzymatic components contained in the venom of the king
cobra (Ophiophagus) the cytotoxic and necrotizing components are less active than those of
Naja cobras.
Local symptoms of envenoming: Pain is felt at the bitten site very early on; edema is
mostly of medium size and affects only the given limb. However, excessive edema may
appear, spreading to the torso or to the neck via regional lymph nodes. Ecchymoses,
erythemas and bullae are formed in the course of further development of the local affection,
followed by necrosis of a minor size and extent from day 2 to 4, but only affecting some
individuals so envenomed. Proteus vulgaris has grown repeatedly from infected wounds..
Systemic symptoms of envenoming: The technique of the bite by the king cobra, with its
longer bite and method of venom delivery by chewing increases the likelihood of
envenomation. Based on the description of 35 snakebites, envenoming occurred in 33 cases,
with 2 lacking any symptoms, meaning the rate of envenoming is very high.
Symptoms of systemic envenomation commence with the following prodromes: nausea,
vomiting, abdominal and cranial pain, sweating, paleness to the skin and conjunctival
perfusion, which can be followed by haziness, hypotension as far reaching as circulatory
collapse and shock. Typically, hypotension is not severe in form and largely caused by
hypovolemia when edema occurs. Affection of the circulation is also possible, with
significant ECG changes and the onset of arrhythmia, including the slowing down or
accelerating of heart action. Clinically significant effects on hemocoagulation in the sense of
hemorrhaging are typically not involved in such envenomings.
Neurological symptomatology is the most serious. Developing in the order of minutes or
hours, it starts with a disorder of neuromuscular junctions of cranial nerves - ptosis, external
ophtalmophlegia including unfocused or double vision, increased salivation, dysphagia,
dysarthria, and facial muscle weakness, and follows as overall muscle weakness, loss of
reflexes and limited paralysis of striated muscles. As the affection develops, somnolence,
haziness, and other consciousness disorders may become associated; nonetheless,
consciousness is typically fully retained in terms of both quality and quantity. In over a half
of those affected, the envenoming process peaks within a few dozen minutes with non-
 Envenoming and Snakebite Treatment in Specific Snake Groups 121

functioning respiratory muscles and a certain period of shallow diaphragmatic breathing,

followed by respiratory failure.
Laboratory findings: Neutrophilic leukocytosis prevails in laboratory findings. Elevated
AST, ALT, CK, and LD (dehydrogenase lactate) is possible. Blood count including PLT
count is typically not affected, as are the hemocoagulation lab tests. The finding of DIC-like
consumption presented in the literature has been disputed, however, it cannot be definitely
precluded, primarily due to the possible syndrome occurring secondarily.
Mortality: The lethality of bites from the Ophiophagus cobra genus is high, ranging from
one third to a half of the affected persons according to resources, which might be close to
100% if left untreated. Neurotoxicity, in some cases with subsequent rapid death in the period
from a few minutes to 12 hours following a snakebite is the main cause.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Application of a pressure immobilization bandage is indicated due to the high
content of neurotoxins. The bandage can significantly help delay the onset of the neurotoxin
effects as long as it is not removed before arrival at health facility capable of dealing with
potentially serious symptoms of muscular paralysis. If envenoming is proven, the bandage
should be removed only after application of antivenom, if such is available. Should no
symptoms be apparent, the bandage is removed following an hour of the observation.
Any administration of opioid analgesics as a part of first aid is relatively contraindicated
as a result of loss of respiratory efforts and intensified respiratory failure caused by oncoming
paralysis. Every affected patient must be observed; discharge is possible only 24 hours after
no symptoms are displayed.
Applicable antivenoms:

* KING COBRA ANTIVENIN, Thai Red Cross, Thailand;

* MONOVALENT KING COBRA ANTIVENOM SERUM, Central Research Institute,
India;
* POLYVALENT SNAKE ANTIVENOM SERUM, Central Research Institute, India.

Usually a large quantity of antivenom is necessary: 15-20 or even more vials. The use of
1150 ml, i.e. 115 vials, seems to be the historical maximum. The initial 2-4 vials are followed
by an infusion of additional antivenom dissolved in physiological saline solution. Any
positive effect is typically recorded within several hours following application; analysis
carried out eleven hours upon administration of the antivenom did not detect any venom in
patients serum. Even though the muscular paralysis formed is reversible over the course of
time, any need for mechanical ventilation will be greatly reduced following specific therapy.
In spite of the fact that the venom of Ophiphagus does not show any significant level of
cross-immunity with the venoms of the Naja cobras, maybe only with those of N. oxiana and
N. kaouthia from Thailand, antivenom against venoms of cobras (Naja), death adders
(Acantophis sp.), tiger snakes (Notechis sp.) or sea snakes could be administered if no specific
antivenom is available.
Slight elevation of the affected limb is desirable; possible pain should be diminished by
analgesics. Moderate cooling is advisable. Any handling and treatment must be carried out
delicately with a view to further potential damage to tissues and the possible formation of
necrosis, especially at points of tight compartments, i.e. on fingers. The content of blisters and
bullae is exhausted in a sterile manner; microbiological examination of the content is
122 Jiri Valenta

advisable. Any emerging necrosis must be surgically removed, which will reduce the risk of
deterioration of status by a localized infection.
Swallowing and respiratory muscle paralysis brings a subsequent risk of aspiration of the
stomach content and respiratory failure and will require airway management using tracheal
intubation and mechanical ventilation. The same necessity will arise in cases of potentially
more serious disorders of consciousness, where a risk of insufficient passability of airways or
aspiration may occur, namely in case of diminished swallowing and cough reflexes.
Nevertheless, consciousness is typically often retained even when muscular paralysis fully
develops; therefore, sedation of the patient is desirable in the course of therapy, with managed
ventilation.
Symptomatic treatment must tackle the most serious symptom of muscular paralysis -
dyspnea, and this is managed by tracheal intubation and subsequent mechanical ventilation.
Acetylcholinesterase inhibitors, edrophonium and neostigmine, have been described as
inefficient. Nevertheless, due to the lack of experience with the therapy as well as the
presence of postsynaptic neurotoxins and absence of neurotoxins of the depolarization type
possessed by mambas (Dendroaspis), the treatment or its support by inhibiting
acetylcholinesterase is not contraindicated and is applicable.
Any possible hypotension caused by hypovolemia in cases of extravasation into edema
may be regulated by replenishing the circulating volume by infusions; rare and benign
arrhythmias can be corrected symptomatically if necessary.
Should a laboratory finding reveal a hemocoagulation imbalance, re-checks until the
status becomes stable will be sufficient; any rising clinical symptoms are rare and can be
corrected symptomatically as well; see 5.3.3.4, 5.3.3.5 and 5.3.3.6 in chapter 5.3.3 Clinical
symptoms of envenomation and symptomatic treatment.
Discharge of the patient is possible 24 hours after the symptomatology of the
envenoming has disappeared.

6.3.1.7. Other Genera of African and Asian Elapid Snakes of the Former Bungarinae
Subfamily
Boulengerina, water cobras. This genus includes the following species: the ringed water
cobra (Boulengerina annulata) and the Christys water cobra (Boulengerina christyi), FR:
Couleuvre annulaire.
These are robust snakes in tones of brown with lengths exceeding 200 cm, mostly
featuring a lighter crosswise pattern in the anterior part of the body.
With habitats strictly bound to water, these snakes live along coastal regions, in still
waters and streams of W and Central Africa.
No cases of envenoming have been registered, although stories of deaths amongst
fishermen on Lake Tanganyika and the River Ivindo in Gabon are spoken of.
Antivenom is not available.
Elapsoidea, venomous garter snakes. A genus containing eight garter snake species,
Elapsoidea sp. Note a possible confusion with the Thamnophis genus, also called garter
snakes. FR: Serpent jarretire.
The species of this genus range from small to medium-sized snakes, but exceptions can
reach 100 cm in length. They are largely active at night.
These garter snakes live underground, mostly in termite structures, in arid savannahs
(Elapsoidea sundevalli), sparse and grassy savannahs or savannah woodlands (Elapsoidea
 Envenoming and Snakebite Treatment in Specific Snake Groups 123

guentheri, Elapsoidea laticincta, Elapsoidea loveridgei, and Elapsoidea semiannulata), but

even in the mountainous forests (Elapsoidea nigra) of Sub-Saharan Africa.
Only rarely do bites occur and they will probably not prove significant; no fatalities have
been described.
Following a bite, there is localized pain, edema, and lymphadenopathy including enlarged
regional nodes.
Antivenom is not available.
Hemachatus. A monotypic genus including a single species - the rinkhals, Hemachatus
haemachatus; other names: ringhals, ring-necked spitting cobra; FR: Cobra cracheur
dAfrique du Sud.
Rinkhalses are snakes of a variable dark brown color, mostly featuring crosswise lighter
rings and a cross strip on the neck; they can grow up to 150 cm. They are classed among the
so-called spitting snakes.
These creatures inhabit grassy and sparse bush in S Zimbabwe and South Africa.
Their venom is relatively potent, even though not as venomous as that of the Naja cobras.
In addition, the glands contain only a small quantity of venom - approximately two human
lethal doses.
The progress of the envenoming, similar to that by Naja cobras, is less severe at both a
local and systemic level. Any venom hitting the eyes is not going to result in severe
permanent affection. Light localized edema and bruises come up at the bitten site. At a
systemic level, the envenoming will be manifest as somnolence, nausea, vomiting, vertigo,
and increased temperatures. Atrial fibrillation was recorded in an older female patient.
Neurotoxicity becomes apparent very rarely as diplopia, paralysis of the tongue, dysarthria,
weakness in the limbs, as well as temporary loss of consciousness and dyspnea to a certain
degree.
Fatalities are uncommon, but some have been described.
Homoroselaps. This genus includes the following species: the striped harlequin snake
(Homoroselaps dorsalis), and the spotted harlequin snake (Homoroselaps lacteus). FR:
Serpent arlequin. Formerly, they were typically placed among the colubrids (Colubridae) or
into the Atrastaspididae family.
Harlequins are snakes 30-60 cm long of a dark to black color, largely boasting a
longitudinal or crosswise pattern in pale to yellow hues; they are active at night.
These animals often reside in termite structures in bush and mountainous localities in
southern Africa.
A lack of information exists on these snakes; a bite is extremely rare.
Two cases have involved light or medium edema, locally increased hemorrhaging, 3-4
days of lymphadenopathy and headaches.
Antivenom is not available.
Paranaja. A monotypic genus consisting of a single species - the many-banded snake
(Paranaja multifasciata); other name: the burrowing cobra.
These cobras are under 80 cm long, being snakes of a brown hue with darker striping;
they dwell underground, but may also be arboreal, at least in part. They mostly range in the
forests of tropical W Africa. Their venom shows neurotoxic activity, although bites are rare.
None have been registered, nevertheless, knowledge has been handed down about the danger
they pose. Antivenom is not available.
124 Jiri Valenta

Pseudohaje. The genus contains the following species: the African tree cobra
(Pseudohaje goldii) and the hoodless cobra (Pseudohaje nigra). Other names: tree black
forest or Golds cobra (P. goldii).
Pseudohaje cobras are 150-200 cm long, grow to a maximum of 270 cm and are arboreal
snakes; they have a black slender body with a yellowish head and neck.
They are forest dwellers, seeking out watery environments, their home range is W to
Central Africa.
Nothing is known about the venom of these snakes. No snakebite has been registered, but
knowledge concerning their dangerousness and lethality has been handed down.
No specific antivenom is available; paraspecifically, SAIMR POLYVALENT SNAKE
ANTIVENOM produced in the Republic of South Africa can be used.
Walterinnesia. A monotypic genus with a single species - the desert cobra (Walterinnesia
aegyptia). Other names: black desert cobra or snake; FR: Cobra noir du dsert.
These are snakes of a dark brown to black hue growing to a size of 80-100 cm, and
resemble Naja cobras. These nocturnal snakes can be active even in very low temperatures
from 10 to 12 C. When disturbed, they do not stand upright, but tend to nestle against the
ground.
They reside in sandy and rocky habitats, but even in gardens and other irrigated
environments of their home range bordered by NE Egypt, W Iran, and N Saudi Arabia. Their
venom contains neurotoxins and any presence of specific cardiotoxins is uncertain.
A bite will probably not cause any serious affection. Symptoms include pain and edema
at the bitten site, a temperature which persists for several days, cranial pain, nausea, vomiting,
tachycardia, atrial extrasystoles, weakness, and discovery of leukocytosis. All of the persons
so affected recovered within several days without specific therapy. Nevertheless, lethal cases
have been spoken of, whilst two fatalities from Iraq remain unverified.
A monospecific antivenom is available upon request from the Department of Zoology,
Tel Aviv University, Israel.

Toxins: A lack of information on the venoms of the genera listed above exists due to their
low epidemiology relevance. For some of them, a certain level of neurotoxins is possible in
snakes like the Hemachatus, Paranaja, and Walterinnesia genera with fundamentally a
postsynaptic effect; nevertheless, their potency probably does not pose any significant threat
to humans. A similar status exists concerning cardiotoxic venom components (Hemachatus,
Walterinnesia), hemocoagulation-affecting components (Homoroselaps), and locally acting
cytotoxic enzymes (Elapsoidea, Hemachatus and Walterinnesia).
Local symptoms of envenoming: A snakebite is followed by pain, usually also by edema
to a minor extent and lymphadenopathy, including enlarged regional lymph nodes. In some
cases, bruising and increased hemorrhaging appears at the bitten site. More serious local
damage or destruction of tissue has not been described, although they are possible in extreme
cases.
Systemic symptoms of envenoming: The scope of systemic symptoms will be mostly
limited to nausea, vomiting, somnolence, vertigo, weakness, and increased temperatures.
Changes to the heart have been recorded, e.g. tachycardia, atrial extrasystolia, atrial
fibrillation (Hemachatus, Walterinnesia) as well as lighter neurotoxicity symptoms: diplopia,
paralysis of the tongue, dysarthria, weakness in the limbs, and a certain level of dyspnea
(Hemachatus). Temporary loss of consciousness has also been described.
 Envenoming and Snakebite Treatment in Specific Snake Groups 125

Laboratory findings: Except for recurrent leukocytosis, no changes in laboratory findings

are known.
Mortality: Cases of lethal snakebites are rare but documented in Hemachatus. As for
snakebites from the rest of the genera, no lethal cases are known; evidence of snake
identification was insufficient (Walterinnesia) or any deemed fatality is merely spoken of
(Boulengerina, Pseudohaje).
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Application of the pressure immobilization bandage is reasonable only
following a snakebite from the rinkhals (Hemachatus hemachatus) or the Boulengerina,
Paranaja, and Pseudohaje snakes due to the lack of data and possible content of neurotoxins,
plus if the victim is a child. The bandage should be removed only after arrival at health
facility capable of dealing with potentially serious symptoms of muscular paralysis.
Administration of antivenom, if such is available - see species-specific description - is
indicated only in the instance of more severe systemic symptoms.
Slight elevation of the affected limb is desirable; possible pain should be eased by
analgesics. Relief is achieved by moderate cooling. As deeper damage to tissues cannot be
fully precluded, namely in the points of tight compartments, any handling and treatment is
carried out delicately.
Eyes affected by a strike by the spitting cobra (Hemachatus) are rinsed with a stream of
clean water if possible, though a physiological saline solution is more preferable. Milk can be
used as well due to a possible link between some venom components and its proteins. Pain
can be smoothed by instillation of local anesthetics into the conjunctival sac. Treatment of
affected eyes - the administration of corticosteroids and antibiotics - should be managed by an
eye specialist to minimize any further serious secondary damage.
Any administration of opioid analgesics as a part of first aid is relatively contraindicated
because of loss of respiratory efforts and intensified, though rare, respiratory failure.
Other symptoms of systemic envenoming, including possible arrhythmia, are of lighter
nature and can be treated symptomatically where necessary - see chapter 5.3.3 Clinical
symptoms of envenomation and symptomatic treatment, and in most cases they abate
spontaneously.
Every affected patient must be observed. Discharge is advisable after 24 hours following
the absence of symptoms or once any systemic affection has abated.

6.3.1.8. Micrurus Genus, Coral Snakes

Species: The extensive Micrurus genus counts approximately some 60 species of coral
snakes (Micrurus), see chapter 7 List of venomous snakes. The number provided by resources
varies due to the unsettled system of classifying some species as subspecies and vice versa.
Instances of better known or epidemiologically more significant species include the eastern
coral snake (Micrurus fulvius) including several subspecies, painted coral snake (Micrurus
corallinus), Central American coral snake (Micrurus nigrocinctus), southern coral snake
(Micrurus frontalis), South American coral snake (Micrurus lemniscus), and aquatic coral
snake (Micrurus surinamensis).
Description: Coral snakes are small to medium-sized snakes, with some of them reaching
a length of over 100 cm (M. fulvius, M. lemniscatus, M.surinamensis). Their bodies boast
rings, mostly of black, red or yellow-white. Exceptionally, shades of blue and orange may
exist. The head, mouth and fangs are small. Coral snakes are largely active at night.
126 Jiri Valenta

They are fundamentally very shy and non-aggressive animals. Incidence of snakebites is
low, with fewer than 20-25 cases a year, most of which come from direct contact in the USA.
They are frequently confused with non-venomous king snakes (Lampropeltis), which can
successfully imitate the appearance of the eastern coral snake (Micrurus fulvius). Snakebites
are rare even in South America: in 1986-1990, 415 bites were recorded in Brazil, chiefly by
M. corallinus, M. lemniscatus, and M. frontalis. In the same country - the State of So Paulo,
110 bites by coral snakes were recorded in 1988-93, equivalent to 1% of all cases of attacks
by snakes. As a consequence of the small mouth and fangs, it is the fingers and adjacent parts
of the hand that are mostly affected. Any effective discharge of venom is determined by the
snake maintaining its bite and chewing.
Other names: EN: coral snake, eastern (Texas) coral snake (M. fasciatus); FR: Serpent
corail, ES and PT: Coralillo, Coralilla, Gargantilla (Central and South America).
Home range and habitat: The Micrurus snakes largely inhabit diverse types of
woodlands from rather arid pine, oak and denser broad-leaved forests in Central America and
southern North America, e.g. M. browni, M. diastema and M. fulvius, as far as the humid
forests of Central and South America, like M. alleni, M. annellatus, M. frontalis, M.
lemniscatus or M. nigrocinctus. Some species prefer rather arid and shrubby habitats, like M.
tschudii, M. frontalis and M. pyrrhus, while others seek the neighborhood of water, for
instance M. fulvius and M. multifasciatus. They can be found in farmed areas, for example M.
frontalis and M. mipartitus.
The home range covers a major part of the American continent, with North America
inhabited by M. fulvius including several subspecies dwelling the southern USA and NE
Mexico, and all other coral snakes ranging in Central and South America: Mexico is a home
range for some 13 species, e.g. M. bogerti, M. browni, M. diastema, M. elegans, M.
ephippifer and M. proximans, while regions to the south are inhabited by a whole range of
other species, such as M. dumerili, M. frontalis, M. lemniscatus, M. nigrocinctus and M.
tschudii.
Toxins: Coral snakes of the Micrurus genus do not possess a large venom apparatus,
hence the content of the venom gland and quantity of venom are low as well. A maximum
amount obtained from great coral snakes equals 20 mg of venom. Nonetheless, the venom has
great potency, with neurotoxins being its fundamental and most effective components. In the
majority of species, these are usually made up of -neurotoxins, i.e. proteins bound to
postsynaptic nicotine acetylcholine receptors that produce a postsynaptic anti-depolarization
block (M. frontalis, M. lemniscatus). At the same time, presynaptically acting neurotoxic
components are also found in some species, e.g. M. nigrocinctus. In South American coral
snakes (M. corallinus), this type of neurotoxin reduces the release of acetylcholine from nerve
endings of neuromuscular junctions. The neurotoxic effect can be also present in the
components discovered in the laboratory that display highly intense acetylcholinesterase
activity.
Other venom components, those merely described biochemically and experimentally in
most cases and seeming to lack any greater clinical relevance, include myotoxins and PLA2
with myotoxic effects capable of evoking muscle necrosis in mice. Components with
cardiotoxic, hemolytic and hemorrhagic effects have only ever been found in the laboratory
and that rarely, with M. averyi being the first ever case. The venom of coral snakes displays
only a minimal level of enzymatic and necrotizing activity with a low content of proteases
and somewhat higher level of phospholipases and hyaluronidases.
 Envenoming and Snakebite Treatment in Specific Snake Groups 127

Local symptoms of envenoming: As already mentioned, most bites take place on fingers
and the areas between them. Even in apparent envenomings, local findings are minimal - the
points of bite wound are typically diminutive, and in the majority of cases, a droplet of blood
can be discharged from them. Typically light edema comes up, but not always. The skin
around the bitten site can lose color or conversely turn slightly red. Rare paresthesia may
spread on the entire limb. Owing to the extremely low proteolytic and cytotoxic activity of
venom, despite a certain hemorrhagic activity found in M. fulvius fulvius, snakebites from
coral snakes of the Micrurus genus are not followed by any deeper tissue affection.
Administration of antibiotics is not indicated.
Systemic symptoms of envenoming: The degree of local symptoms is never equal to the
presence or quantity of venom injected, and using it to estimate the relevance of the systemic
envenoming is impossible. Nonetheless, some factors are useful for prediction purposes - the
presence of a bite wound, from which there is a possibility of a droplet of blood being
discharged, and a statement by the victim concerning the length and manner of the bite. This
may have lasted from just a few to several dozen seconds, plus the chewing method of snakes
could have been employed. All this indicates a high probability that systemic neurotoxic
symptoms will follow. However, any absence of such marks does not preclude envenomation,
although it may reduce its probability. The proportion of those envenomed in North America,
i.e. following a bite from the eastern coral snake (M. fulvius) ranges from 40% to 75% of
those affected.
Systemic envenoming is manifest through neurotoxic symptomatology largely within 2 to
6 hours, but it can take between 12 or even 24 hours following the snakebite. Prodromes of
envenoming have not been described. Serious muscular paralysis, including delayed onset of
the same, can appear relatively quickly and is difficult to control by specific therapy.
The first sign of neuromuscular affection symptoms is ptosis. Ophtalmophlegia will
follow accompanied by double or indistinct vision, dysarthria and dysphagia including
swallowing disorders, saliva accumulation and discharge from the mouth cavity. Facial
paralysis produces a myasthenic effect. Pupil non-reactivity, contraction or anisocoria is
typically present. The state can be accompanied by qualitative changes in consciousness -
somnolence, languor or euphoria, with further development involving general muscle
weakness, sometimes muscular fasciculations, loss of swallowing and cough reflexes, and
fatal paralysis of respiratory muscles. The symptoms of neurotoxicity will peak after 72
hours, and their acute phase abates after 5 to 7 days without any bearing on the application or
quantity of antivenom. The muscle weakness following an envenoming persists for 4 to 6
weeks.
The course of envenoming can be complicated by aspiration bronchopneumonia unless
the airways are managed using tracheal intubation.
The envenomation involves neither signs of cardiotoxicity, including arrhythmias, nor
hemocoagulation disorders.
Laboratory findings: CC and myoglobin values are typically increased in the serum.
Myoglobin may occur in urine as well, causing it darken. Leukocytosis is possible. In general,
laboratory findings are not typical for the envenoming.
Mortality: With no possibility of adequate treatment, the lethality of systemic
envenoming used to be very high in the past, but today, with forced pulmonary ventilation
and specific therapy, 3 fatalities were recorded from 415 snakebites described in Brazil during
1986-1990, with M. corallinus, M. lemniscatus, and M. frontalis co-responsible for the
128 Jiri Valenta

deaths. In the Brazilian state of So Paulo, no fatality from the 110 snakebites recorded
occurred between 1988 and 1993. The same goes for the 39 envenomings described in the
USA.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention.
Immediate application of a pressure immobilization bandage is fully indicated. The
bandage should not be removed before arrival at health facility capable of dealing with
potentially serious symptoms of muscular paralysis. If envenoming is proven, the bandage
should be removed only after application of antivenom or at least after administration of
neostigmine, see below.
Applicable antivenoms:

* ANTICORAL, Instituto Clodomiro Picado, Costa Rica (M. carinicauda - synonym M.

dumerilii, M. f. fulvius, M. nigrocinctus);
* ANTI-MIPARTITUS, Instituto Clodomiro Picado, Costa Rica (M. mipartitus);
* ANTIELAPIDICO, Instituto Butantan, Brazil (M. corallinus, M. frontalis);
* ANTIELAPIDICO, Lab. Vencofarma do Brasil, Brazil (M. corallinus, M. frontalis);
* ANTIVENIN (MICRURUS FULVIUS), Wyeth, USA (production closed).

Antivenom proves most effective if applied before the envenoming has fully developed.
Once severe symptoms of muscular paralysis appear, the period of necessity for mechanical
ventilation may not be reduced by applying the antivenom, even if a large quantity of 10 vials
is administered, and any application before paralysis sets in may not always have a pre-
emptive effect. Nevertheless, in cases of believed envenoming, see systemic symptoms of
envenoming, or systemic symptoms commence, application of antivenom is indicated with a
quantity of 3-6 vials; in Brazil, 10 vials are recommended. The time lapsed between the
snakebite, or more specifically the rise of symptoms and application of antivenom, is
important for further progress of the disease.
The specific antivenoms developed against coral snakes of the Micrurus genus do not
seem to be reversible; cross-immunity is probably poor. Nonetheless, antivenoms prepared to
counteract venoms of elapid snakes from the same hemisphere, i.e. northern antivenoms
against northern species and southern antivenoms against southern species, can be applied
when needed, as they show some level of immunogenic relationship. According to an
experiment carried out on mice, cross-immunity exists between the venom of the North
American eastern coral snakes (M. fulvius) and Mexican antivenom, or the antivenom for the
Australian mainland tiger snake (Notechis scutatus). As for venoms of some Central
American coral snakes, they are impossible to neutralize by any of the antivenoms available
at all.
A rather disguised and local finding that is usually only moderately painful will not
require any special care.
Application of an acetylcholinesterase inhibitor, edrophonium or neostigmine, may in
some cases result in reducing muscular paralysis. The Brazilian ministry of health
recommends for adult patients an application of 0.5 mg of neostigmine (approx. 10 g/kg of
body weight) in five doses at 30-minute periods, which is followed by a longer break and
repeated as necessary; each administration is premedicated with 0.6 mg (50 g/kg of body
weight) of atropine sulphate to neutralize the muscarine effect. Cases of reversed block only
 Envenoming and Snakebite Treatment in Specific Snake Groups 129

by inhibiting acetylcholinesterase are known from Brazil. However, in the case of snakebites
from M. nigrocinctus, such a procedure is ineffective, as the venom contains clinically a
distinctive proportion of presynaptic neurotoxins. The situation with coral snakes found in
Mexico is similar.
As regards symptomatic treatment, its application can be delayed or prove ineffective if
antivenom is unavailable. It must promptly manage any possible complications arising from
muscular paralysis, i.e. aspiration and respiratory failure, airway management using tracheal
intubation, and subsequent mechanical ventilation.
A sufficient supply of liquids will prevent any possible renal failure if a higher quantity
of myoglobin is released.
Heparin is not indicated.
A patient can be discharged 24 to 48 hours after abatement of symptoms of systemic
envenoming. Observation of an affected person with asymptomatic development should last
for approximately 24 hours.

6.3.1.9. Leptomicrurus and Micruroides Genera

Genera: The Leptomicrurus genus including four species and Micruroides, a monotypic
genus consisting of Micruroides euryxanthus.
Description: Small to medium-sized dark snakes that feature a light pattern
(Leptomicrurus) or color rings like the coral snakes of the Micrurus genus (Micruroides).
Epidemiological relevance of these snakes is very low (Micruroides) or insignificant.
Other names: EN: Arizona (Sonoran) coral snake; FR: Serpent corail dl Arizona
(Micruroides). EN: Thread coral snake; FR: Serpent corail fin (Leptomicrurus).
Home range and habitat: The Leptomicrurus snakes inhabit the forests of South
America; Micruroides euryxanthus dwells in rocky and stony habitats of Mexico and southern
USA.
Toxins: Insufficient information of venoms of the genera above is available. The
neurotoxic components contained will be probably similar to the neurotoxins found in
Micrurus snakes.
Local symptoms of envenoming: The bite wound is diminutive; the local pain is rather
low. Paresthesia, locally reduced sensation and muscle strength occur at the bitten site,
without any major progression. Other local alterations are typically absent (M. euryxanthus).
Systemic symptoms of envenoming: Not described except the envenoming by M.
euryxanthus. Nausea, light muscle weakness and possibly somnolence can be involved.
Accommodation and photophobia disorders have occurred. Primarily, a light form of
envenoming similar to that caused by venoms of Micrurus snakes can be expected.
Laboratory findings: Not known.
Mortality: Not specified.
Therapy: For first aid and general rules of treatment, see Chapter 5 Snakebite: Therapy
and prevention. Treatment is similar to that of snakebites from the coral snakes of the
Micrurus genus. Specific antivenoms are not available. In the case of a more severe
envenoming by E. micruroides, SORO ANTIELAPIDICO, Instituto Butantan, Brazil is an
applicable antivenom.
Cross-reactivity with venoms of Micrurus snakes is insufficient; antivenoms against
North American coral snakes are ineffective in case of envenoming by Micruroides.
130 Jiri Valenta

The patient can be discharged 24 hours after abatement of symptoms of systemic

envenoming. The same time applies to the observation of the affected person with symptom-
less development.

REFERENCES
Chapters 6.3.1.1 - 6.3.1.7:
BERNHEIM, A., LORENZETTI, E., LICHT, A. et al. Three cases of severe neurotoxicity
after Cobra bite (Naja kaouthia). Swiss Med Wkly, 2001, 131, pp. 227228.
BLAYLOCK, RS., LICHTMAN, AR., POTGIETER, PD. Clinical manifestation of Cape
Cobra (Naja nivea) bites. A report of 2 cases. S Afr Med J, 1985, 68, No. 5, pp. 342344.
BRITT, A., BURKHART, K. Naja naja Cobra bite. Am J Emerg Med, 1997, 15, No, 5, pp.
529531.
CISZOWSKI, K., HARTWICH, A. Envenoming by Malayan Cobra (Naja naja sputatrix)
case report. Przegl Lek, 2004, 6, No. 4, pp. 412416.
DAVIDSON, TM., SCHAFER, S., KILLFOIL, J. Cobras. Wilderness Environ Med, 1995, 6,
pp. 203219.
DU, XY., CLEMETSON, JM., NAVDAEV, A., et al. Ophioluxin, a convulxin-like C-type
lectin from Ophiophagus hannah (King Cobra) is a powerful platelet activator via
glycoprotein VI. J Biol Chem, 2002, 227, No. 38, pp. 3512435132.
Van EGMOND, KC. A fatal bite by the Shield-nose Snake (Aspidelaps scutatus). S Afr Med
J, 1984, 66, No. 19, p. 714.
FRIGG, C., SIEBER, T., PAGANONI, O., et al. Snakebite intoxication by Cobra venom.
Anaesthesist, 2001, 50, No. 11, pp. 856860.
GOLD, BS. Neostigmine for the treatment of neurotoxicity following envenomation by the
Asiatic Cobra. Ann Emerg Med, 1996, 28, No. 1, pp. 8789.
GOLD, BS., PYLE, P. Succesful treatment of neurotoxic King Cobra envenomation in Myrtle
Beach, South Carolina. Ann Emerg Med, 1988, 32, No. 6, pp. 736738.
GOMEZ, HF., DAVIS, M., PHILLIPS, S., et al. Human envenomation from a wandering
Garter Snake. Ann Emerg Med, 1994, 23, No. 5, pp. 11191122.
GOMES, A., DE, P. Hannahpep: a novel fibrinolytic peptide from the Indian King Cobra
(Ophiophagus hannah) venom. Biochem Biophys Res Commun, 1999, 266, No. 2, pp.
488491.
GRUSCHWITZ, MS., MAHLER, V., RUPPRECHT, M., et al. Snake bite by a poisonous
snake. Report of an unusual case. Hautarzt, 1994, 45, No. 5, pp. 330334.
HARRISON, JL. The bite of a blue Malaysian Coral Snake or Ular Matahari. Malayan
Nature Journal, 1957, 11, pp. 130132.
HILLIGAN, R. Black mamba bites: a report of 2 cases. S Afr Med J, 1987, 72, pp. 220221.
HODGSON, SP., DAVIDSON, TM. Biology and treatment of the Mamba snakebite.
Wilderness Environ Med, 1996, 2, pp. 133145.
HUANG, MZ., WANG, QC., LIU, GF. Effect of acidic phospholiopase A2 purified from
Ophiophagus hannah (King Cobra) venom on rat heart. Toxicon, 1993, 31, No. 5, pp.
627635.
 Envenoming and Snakebite Treatment in Specific Snake Groups 131

KANCHANAPONGKUL, J. Neurotoxic envenoming following bites by the Malayan Krait

(Bungarus candidus). J Med Assoc Thai, 2002, 85, No. 8, pp. 945948.
KARNCHANACHETANEE, C. King cobra bite. J Med Assoc Thai, 1994, 77, No. 12, pp.
646651.
KRAMER, R. Zur Schlangen Fauna von Nepal. Rev Suisse Zool, 1977, 84, No. 3, pp. 721
761.
KRENGEL, B., WALTON, J. A case of Mamba bite. S Afr Med J, 1967, 41, pp. 11501151.
KULARATNE, SA. Common Krait (Bungarus caeruleus) bite in Anuradhapura, Sri Lanka: a
prospectiv clinical study, 19961998. Postgrad Med J, 2002, 78, No. 919, pp. 276280.
LATIFI, M. Variation in yield and letality of venoms from Iranian snakes. Toxicon, 1984, 22,
No. 3, pp. 373380.
LAOTHONG, C., SITPRIJA, V. Decreased parasympathetic activities in Malayan Krait
(Bungarus candidus) envenoming. Toxicon, 2001, 39, No. 9, pp. 13531357.
LEE, WH., ZHANG, Y., WANG, WY., et al. Isolation and properties of a blood coagulation
factor X activator from the venom of King Cobra (Ophiophagus hannah). Toxicon, 1995,
33, No. 10, pp. 12631276.
LI, QB., HUANG, GW., KINJOH, K., et al. Hematological studies on DIC-like findings
observed in patients with snakebite in south China. Toxicon, 2001, 39, No. 7, pp. 943
948.
LIFSHITZ, M., MAIMON, N., LIVNAT, S. Walterinnesia aegypia envenomation in a 22-
year-old female: a case report. Toxicon, 2003, 41, No. 4, pp. 535537.
LIM-LEONG-KENG, F., LEE-TAT-MONG, M. Fascinated snakes of Southeast Asia an
introduction. Kuala Lumpur : Tropical Press, 1989.
MARKWALDER, K., KOLLER, M. Mamba bites. 2 case reports and observations on the
therapy of neurotoxic poisonous snake bites. Schweiz Rundsch Med Prax, 1987, 76, No.
46, pp. 12811284.
McNALLY, SL., REITZ, CL. Victims of snake bite. A 5-year study at Shongwe Hospital,
Kangwane, 19781982. S Afr Med J, 1987, 72, No. 12, pp. 855860.
MEIER, J., WHITE, J. (Eds). Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995, 752 pp.
NIRTHANAN, S., CHARPANTIER, E., GOPALAKRISHNAKONE, P., et al.
Neuromuscular effects of candoxin, a novel toxin from the venom of the Malayan Krait
(Bungarus candidus). Br J Pharmacol, 2003, 139, pp. 832844.
POCHANUGOOL, C., LIMTHONGKUL, S., SITPRIJA, V., et al. Managment of Cobra bite
by arteficial respiration and supportive therapy. J Med Assoc Thai, 1994, 77, No. 3, pp.
161164.
POCHANUGOOL, C., LIMTHONGKUL, S., WILDE, H. Management of Thai Cobra bites
with a single bolus of antivenin. Wilderness Environ Med, 1997, 8, No. 1, pp. 2023.
POCHANUGOOL, C., WILDE, H., JITAPUNKUL, S., et al. Spontaneus recovery from
severe neurotoxic envenoming by a Malayan Krait Bungarus candidus (Linnaeus) in
Thailand. Wilderness Environ Med, 1997, 8, No. 4, pp. 223225.
REID, HA. Cobra-bites. Br Med J, 1964, 2, p. 540545.
SAUNDERS, CR. Report of a Black Mamba bite of a medical colleague. Cent Afr J Med,
1980, 26, No. 6, pp. 121122.
SHARMA, SK., KOIRALA, S., DAHAL, G. Krait bite requiring high dose antivenom: a case
report. Southeast Asian J Trop Med Public Health, 2002, 33, No. 1, pp. 170171.
132 Jiri Valenta

SINGH, G., PANNU, HS., CHAWLA, PS., et al. Neuromuscular transmission failure due to
Common Krait (Bungarus caeruleus) envenomation. Muscle Nerve, 1999, 22, No. 12, pp.
16371643.
STCKLIN, R., CRETTON, G. The ultimate database on venomous animals, snakes. CD-
rom, Geneva : Atheris Laboratories, 1998.
TAKASAKI, C., YOSHIDA, H., SHIMAZU, T., et al. Studies on the venom components of
the Long-glanded Coral Snake, Maticora bivirgata. Toxicon, 1991, 29, No. 2, pp. 191
200.
TRISHNANANDA, M., OONSOMBAT, P., DUMAVIBHAT, B., et al. Clinical
manifestation of Cobra bite in the Thai farmer. Am J Trop Med Hyg, 1979, 28, No. 1, pp.
165166.
TUN-PE, AYE-AYE-MYINT, WARRELL, DA., et al. King Cobra (Ophiophagus hannah)
bites in Myanmar: venom antigen levels and development of venom antibodies. Toxicon,
1995, 33, No. 3, pp. 379382.
WARRELL, DA. Clinical toxicology of snakebite in Africa and the Middle East / Arabien
Peninsula. In MEIER, J., WHITE, J. (Eds), Handbook of clinical toxicology of animal
venoms and poisons. Boca Raton : CRC Press, 1995.
WARRELL, DA. Clinical toxicology of snakebite in Asia. In MEIER, J., WHITE, J. (Eds),
Handbook of clinical toxicology of animal venoms and poisons. Boca Raton : CRC Press,
1995.
WARRELL, DA., GREENWOOD, BM., DAVIDSON, NM., et al. Necrosis, haemorrhage
and complement depletion following bites by the Spitting Cobra (Naja nigricollis). Q J
Med, 1976, 45, No. 177, pp. 122.
WATT, G., MEADE, BD., THEAKSTON, RD., et al. Comparison of Tensilon and
antivenom for the treatment of Cobra-bite paralysis. Trans R Soc Trop Med Hyg, 1989,
83, pp. 570573.
WATT, G., PADRE, L., TUAZON, ML., et al. Bites by Philippine Cobra (Naja naja
philippinensis): prominent neurotoxicity with minimal local signs. Am J Trop Med Hyg,
1988, 39, No. 3, pp. 306311.
WATT, G., THEAKSTON, RD., HAYES, CG. Positive response to edrophonium in patients
with neurotoxic envenoming by Cobras (Naja naja philippiensis). N Engl J Med, 1986,
315, No. 23, pp. 14441448.
ZALTZMAN, M., RUMBAK, M., RABIE, M., et al. Neurotoxicity due to the bite of the
Shield-nose Snake (Aspidelaps scutatus). A case report. S Afr Med J, 1984, 66, No. 3, pp.
111112.

Chapters 6.3.1.8 - 6.3.1.9:

BARROS, AC., FERNANDES, DP., FERREIRA, LC., et al. Lokal effect induced by venoms
from species of genus Micrurus sp. (Coral Snakes). Toxicon, 1994, 32, No. 4, pp. 445
452.
FAN, HW., CARDOSO, JL. Clinical toxicology of snake bites in South America. In MEIER,
J., WHITE, J. (Eds), Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995.
GERMAN, BT., HACK, JB., BREWER, KL., et al. Efficiecy of a pressure-immobilization
bandage in delaying the onset of systemic toxicity in a porcine model of Eastern Coral
Snake (Micrurus fulvius) envenomation. Ann Emerg Med, 2004, 44, No. 4, pp. 90.
 Envenoming and Snakebite Treatment in Specific Snake Groups 133

GOMEZ, HF., DART, RC. Clinical toxicology of snakebite in North America. In MEIER, J.,
WHITE, J. (Eds), Handbook of clinical toxicology of animal venoms and poisons. Boca
Raton : CRC Press, 1995, pp. 619644.
GUTIRREZ, JM. Clinical toxicology of snakebite in Central America. In MEIER, J.,
WHITE, J. (Eds), Handbook of clinical toxicology of animal venoms and poisons. Boca
Raton : CRC Press, 1995.
KITCHENS, CS., van MIEROP, LH. Envenomation by the Eastern Coral Snake (Micrurus
fulvius fulvius). A study of 39 victims. JAMA, 1987, 258, No. 12, pp. 16151618.
LAMAR, WW. A new species of Slender Coralsnake from Colombia, and its clinal an
ontogenetic variation (Serpentes, Elapidae: Leptomicrurus). Rev Biol Trop, 2003, 51, No.
34, pp. 805810.
MEIER, J., WHITE, J. (Eds). Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995, 752 pp.
Nget-Hong Tan, Gnanajothy Ponnudrai. The biological properties of venoms of some
American Coral Snakes (genus Micrurus). Comparative Biochemistry and Physiology
Part B. Biochemistry and Molecular Biology 1992, 101, No. 3, pp. 471474.
PETTIGREW, LC., GLASS, JP. Neurologic complications of a Coral Snake bite. Neurology,
1985, 35, No. 4, pp. 589592.
RIBEIRO, LA., ALBUQUERQUE, MJ., De CAMPOS, VA., et al. Death caused by
venomous snakes in the State of Sao Paulo, evaluation of 43 cases from 1988 to 1993.
Rev Assoc Med Bras, 1998, 44, No. 4), pp. 312318.
De RODT, AR., PANIAGUA-SOLIS, JF., DOLAB, JA., et al. Effectiveness of two common
antivenoms for North, Central, South American Micrurus envenomations. J Toxicol Clin
Toxicol, 2004, 42, No. 2, pp. 171178.
ROSSO, JP., VARGAS-ROSSO, O., GUTIERREZ, JM., et al. Characterisation of -
neurotoxin and phospholipase A2 activities from Micrurus venom. Determination of the
amino sequence and receptor-binding ability of the major -neurotoxin from Micturus
nigrocinctus nigrocinctus. Eur J Biochem, 1996, 238, No. 1, pp. 231239.
RUSSEL, FE. Bites by the Sonoran Snake Micruroides euryxanthus. Toxicon, 1967, 5, No. 1,
pp. 3942.
SERAFIM, FG., REALI, M., CRUZ-HOFLING, MA, et al. Action of Micrurus dumerilii
carinicauda Coral Snake venom on the mammalian neuromuscular junction. Toxicon,
2002, 40, No. 2, pp. 167174.
STCKLIN, R., CRETTON, G. The ultimate database on venomous animals, snakes. CD-
rom, Geneva : Atheris Laboratories, 1998.
WISNIEWSKI, MS., HILL, RE., HAVEY, JM., et al. Australien Tiger Snake (Notechis
scutatus) and Mexican Coral Snake (Micrurus species) antivenoms prevent death from
United States Coral Snake (Micrurus fulvius fulvius) venom in a mouse model. J Toxicol
Clin Toxicol, 2003, 41, No. 1, pp. 710.

6.3.2. Subfamily: Hydrophiinae

The group of Hydrophiinae snakes is the second of two recently recognized subfamilies
of the elapid family (Elapidae). Formerly the group only comprised aquatic snakes - sea
snakes and sea kraits and was designated Hydrophiidae. The new Hydrophiinae subfamily
134 Jiri Valenta

contains, aside from aquatic sea snakes and sea kraits, terrestrial Austropapuan elapids -
snakes that were earlier categorized as a separate subfamily of taipans (Oxyuraninae). For
reasons of better presentation of texts and similarities in both former snake groups as regards
morphology and toxinology, the section below has been segmented in relation to historic
groups, i.e. the terrestrial snakes of Oxyuraninae, and aquatic snakes of Hydrophiidae.

6.3.2.1. Terrestrial Austropapuan Elapids (Formerly: Oxyuraninae Subfamily)

Once entitled Oxyuraninae, a taipan subfamily, this group comprises all members of the
elapid family (Elapidae) found in Australia, Tasmania, New Guinea, and other islands in the
vicinity. Even though snakes of some genera display a certain morphological resemblance to
those of other families, all members of this subfamily possess fixed anterior fangs that do not
swing. Examples of similarities between snakes include the Echiopsis genus or death adders
(Acanthophis) that resemble viperids (Viperidae) in appearance, the fang length in taipans
(Oxyuranus) can reach up to 1.3 cm, which is rather typical for viperids, etc. Incidentally,
Austropapuan elapids are proteroglyphous snakes, just like all elapids (Elapidae).
In terms of the seriousness of envenomation, eight genera, from which consequences of
envenoming are known, are described below from the total of 27 genera comprising the
group. The remaining varieties are briefly and generally addressed, although any possible
outcome from a potential envenoming are mentioned.

Acanthophis Genus, Death Adders

Species: Common death adder (Acanthophis antarcticus), Acanthophis hawkei,
Acanthophis laevis, northern death adder (Acanthophis praelongus), desert death adder
(Acanthophis pyrrhus), Acanthophis rugosus and Acanthophis wellsi.
Description: This snake rather resembles a viperid due to the shape of its head and the
thickset body of 40 to 90 cm long with a short tail. The tip of the tail is elongated and
terminates in a thorn. When moved, the thorn looks like a worm, thereby attracting prey. The
color range of the snake includes varied tints of brown and red-brown. The species is active at
dusk and night, but bites have even been recorded during the day.
Home range and habitat: Death adders mostly range in fairly arid and sandy areas with
sparse vegetation in southern and eastern (A. antarcticus) or central and western Australia (A.
pyrhus), as well as the damp tropical forests of N Australia, New Guinea and neighboring
islands (A. hawkei, A. laevis, A. praelongus, A. rugosus), where the most common venomous
snakes are found.
Toxins: Neurotoxins make up the most clinically important venom components. These
are largely of the postsynaptic type, however, amongst their number is presynaptically acting
PLA2. Other components with much less distinctive effects concern enzymes with
hemocoagulation effects, which in a human can be registered only in laboratory tests. These
tend to be anticoagulant and fibrino(geno)lytic in nature, affecting platelet function.
Proteinases and phospholipases (PLA2) are substances predominantly responsible for the
majority of the activities above. The venom does not contain components causing more
serious rhabdomyolysis, although some evidence of myotoxicity is obvious based on
increased CC in the plasma of the envenomated persons.
 Envenoming and Snakebite Treatment in Specific Snake Groups 135

Local symptoms of envenoming: The afflicted site almost lacks any edema; only
increased sensitivity and strain in lymphatic pathways will exist, in addition to enlarged
lymph nodes of the region in question. In general, local affliction is discreet in form.
Systemic symptoms of envenoming: The majority of persons bitten are typically
envenomed. Symptoms commence with the following prodromes: headache, languor,
abdominal pain, nausea, and vomiting; in rare cases, collapse may occur.
In nearly every envenomed individual, neurotoxicity symptoms below will manifest
clinically: ptosis, dysarthria, ophtalmophlegia with diplopia, dysphagia, and overall muscle
weakness. For about a quarter of those so afflicted, the status of pseudobulbar difficulties or
respiratory failure will require management of airways using intubation and mechanical
ventilation for a period of between 2 to 24 hours. Neurotoxicity symptoms with varied
intensity can persist for 72 hours; nevertheless, they tend to be fully reversible if adequate
treatment is applied, unlike in cases of envenoming by taipan venom.
A more serious clinical impact on hemocoagulation - increased hemorrhaging - occurs
very rarely and in a moderate form. In up to a third of those affected, ECG changes in terms
of T wave inversion and rare instances of brachycardia will occur, with a possible second
degree of AV-block as well. A single example of reversed renal failure has been described,
apparently due to myoglobinuria.
Laboratory findings: Hemocoagulation laboratory tests reveal moderate prolongation of
PT and APTT. A non-standard slight decrease in PLT occurs that persists for several days as
well as insignificant leukocytosis. Tests may sometimes display a clear increase in plasmin
activity. In general, results are ordinary and not very distinctive.
Mortality: 50% mortality of untreated persons was reported by Tidswell in 1906. Such a
rate seems exaggerated even for this period. In 1981-1991, only a single lethal case was
recorded in Australia, nonetheless, the need for mechanical ventilation in up to a quarter of
those envenomated may mean high potential mortality in cases with no therapy.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Immediate application of a pressure immobilization bandage is fully
indicated. The bandage should not be removed before arrival at a health facility capable of
dealing with any possible serious symptoms of muscular paralysis. If envenomation is
proven, the bandage should be removed only after application of antivenom or at least after
administration of neostigmine, see below.
Applicable antivenoms:

* DEATH ADDER ANTIVENOM, Commonwealth Serum Laboratories, Victoria,

Parkville, Australia (Acanthophis antarcticus, A. praelongus, A. pyrrhus);
* POLYVALENT SNAKE ANTIVENOM, Commonwealth Serum Laboratories,
Victoria, Parkville, Australia (Acanthophis antarcticus, etc.).

Local affection is rather indistinct and usually only moderately painful, so should not
require any special care.
Application of acetylcholinesterase inhibiting neostigmine, see below, will typically
result in even dramatic momentary improvement of muscular paralysis. Ultimately,
envenomation symptoms are typically fully controlled by the relevant antivenom.
Symptomatic treatment in instances where antivenom is unavailable or application is
delayed must address possible complications that arise due to muscular paralysis - aspiration
136 Jiri Valenta

and respiratory failure - by managing the airways using tracheal intubation and subsequent
mechanical ventilation. In addition, pharmacological inhibition of acetylcholinesterase using
neostigmine, at a dosage of 0.5-1.0 mg IV (10-15 /kg of body weight) with premedication
by 0.5 mg of atropine IV is advisable as well.
Sufficient supply of liquids will prevent any possible renal failure if a higher quantity of
myoglobin is released. In rare cases of possible increased hemorrhaging, either symptomatic
treatment is applicable or antifibrinolytics if a DIC-like disorder can be excluded. Heparin is
not indicated.
The patient can be discharged for home treatment after 24 hours once all systemic
symptoms recede.

Austrelaps Genus, Australian Copperheads

Species: Pygmy copperhead (Austrelaps labialis), highlands copperhead (Austrelaps
ramsayi), Australian copperhead (Austrelaps superbus).
Other names: Australian (Kangaroo Island or highland) copperhead (EN).
Description: In gray-black and shades of brown to red, these slender and small-headed
snakes feature relatively large eyes and round pupils. They can grow up to 75-130 cm, with a
maximum length of 170 cm. These snakes are mainly active during the day even if
temperatures drop somewhat at times when other snakes are hibernating. If daytime
temperatures are high, they become active at night as well. They are frequently found in
colonies with higher numbers of individuals.
Home range and habitat: Australian copperheads reside in damp, wet localities and
places near water in SE Australia, Tasmania, and neighboring islands (A. superbus and A.
labialis), as well as the mountain ranges of SE Australia (A. ramsay).
Toxins: Based on LD50 for mice, the venom can be rated about 12th in the hierarchy of
toxicity. Clinically, the powerful neurotoxins it contains are of maximum effectiveness.
Myotoxins are another important component. The hemolytic enzymes present are of PLB
type, those of PLA2-like (superbins) weaken hemostasis by inhibiting PLT function and
affecting the plasmatic coagulation system.
Local symptoms of envenoming: Changes at the bitten site are not major - in some cases,
edema and erythema appear.
Systemic symptoms of envenoming: At a systemic level, the envenoming manifests itself
as classic prodromes - nausea, vomiting, and headaches. Eventually, consciousness disorders
and muscular paralysis can occur. The latter becomes apparent via typical symptoms in facial
and swallowing muscles. In instances of severe envenomation, respiratory difficulties
requiring intubation and mechanical ventilation are rare but do occur.
The high levels of myoglobin and hemoglobin generated from severe rhabdomyolysis
and hemolysis can result in renal failure.
Laboratory findings: Myolysis and hemolysis are followed by increased levels of
plasmatic CC and myoglobin, in addition to free hemoglobin found in the serum and urine.
Mortality: Not described.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. The pressure immobilization bandage is fully indicated; it should only be
removed after arrival at health facility capable of dealing with potentially serious symptoms
of muscular paralysis.
 Envenoming and Snakebite Treatment in Specific Snake Groups 137

Applicable antivenoms:

* POLYVALENT SNAKE ANTIVENOM, Commonwealth Serum Laboratories,

Victoria, Parkville, Australia (Austrelaps ramsayi, Austrelaps superbus, etc.);
* TIGER SNAKE ANTIVENOM, Commonwealth Serum Laboratories, Victoria,
Parkville, Australia (Austrelaps superbus, and others).

The local affection will not require any special care.

If antivenom is not available, severe envenomation may require management of airways
and mechanical ventilation. Application of acetylcholinesterase inhibitors may well prove
effective; see chapter 5. 3. 3. 3 Affliction of nerve tissue and neuromuscular connections.
Symptomatic therapy should reflect the risk of renal failure by boosting the supply of
liquids with possible diuretic support. Hemocoagulation dysbalance will react positively to
the specific treatment; nevertheless, a positive effect can also be expected from symptomatic
treatment based on the type of affliction.
The patient can be discharged for home treatment after 24 hours once all systemic
symptoms recede.

Hoplocephalus Genus
Species: Pale-headed snake (Hoplocephalus bitorquatus), broad-headed snake
(Hoplocephalus bungaroides) and Stephens banded snake (Hoplocephalus stephensi).
Description: Gray to black or brownish snakes with a distinctive head, lighter ventral
section, and whitish or yellowish pattern, they can grow up to 45-75 cm, the maximum length
being 100 cm. They are shy, predominantly nocturnal creatures - when threatened, they carry
out a swift strike without warning.
Home range and habitat: Found in E Australia in humid forests and coastal woodlands,
neighboring inland forests of the arid eucalyptus variety (H. bitorquatus and H. stephensi),
and sandy or rocky areas (H. bungaroides).
Toxins: The venom is quite effective and can be fatal for a human. Fortunately, the
production of venom in this snake group is only low. It contains powerful neurotoxins,
enzymes with hemocoagulation effects (largely in terms of prothrombin activation, like
hopsarin D, resembling the human FXa by structure and function), and myotoxins causing
rhabdomyolysis. The effect of cardiotoxic components has also been described (Chew et al.,
2003).
Local symptoms of envenoming: The edema that comes up at the bitten site is typically
lesser or medium in nature; the area around the site is erythematous. Lymphadenopathy
occurs, the limb is painful. Local signs of a hemostasis disorder may be present, e.g. bruises,
intradermal bleeding, or direct hematoms.
Systemic symptoms of envenoming: Systemic envenomation mostly commences with
headaches, plus nausea and vomiting may set in early with gastrointestinal hemorrhaging -
hematemesis. In the envenomed person, neurotoxicity symptoms appear very soon, leading up
to respiratory failure and, later, vertigo or even collapse.
A DIC-like hemocoagulation disorder of the DIC type occurs, which usually becomes
clinically manifest as increased hemorrhaging, such as epistaxis, hematuria, and other
symptoms. Procoagulative, i.e. (micro)thrombotic, complications are likely to arise.
138 Jiri Valenta

The nature of the venom makes renal failure possible under the high levels of myoglobin
due to rhabdomyolysis in progress, which will also be manifest as muscular pain. Naturally,
the impact of neurotoxins is not the key factor in systemic envenoming, nor are neurotoxicity
symptoms. It is the effect on hemocoagulation mentioned above that remains the most serious
symptom.
Arrhythmia has been described in the form of nodal bradycardia with numerous
supraventricular and ventricular extrasystoles, receding spontaneously after eight hours.
Laboratory findings: In envenoming by H. bungaroides, leukocytosis with a peak value
21 x 109/l was described. In hemocoagulation lab tests, a DIC-like disorder prevailed:
thrombocytopenia, defibrination showing decreased values (reaching less than 0.5 g/l),
prolongation of PT (INR 1.6), and APTT above 200. The D-dim level is above 20 mg/l (the
normal amount being less than 0.3 mg/l), but the AT level still remains intact. In the serum,
increased CC is typically found, i.e. 25.1 microcat/l (the normal amount being below 3.3
microcat/l). An increase in CRP to 59 mg/l was also recorded, the normal amount being less
than 7 mg/l.
Mortality: Fatalities have not been described. Nevertheless, the effectiveness of the
venom makes lethal progress of the envenoming possible.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Application of a pressure immobilization bandage is indicated.
The antivenom against the venom of tiger snakes (Notechis) is recommended for specific
immunotherapy.
Any local affection can be smoothed by a cool compress - ice should be avoided; in cases
of more intense pain, the limb is immobilized and elevated. Any large hematoms generated,
although this is rare, must be evacuated; the measure needs to be carried out only once the
coagulation disorder has abated.
In symptomatic therapy, the DIC-like hemocoagulation disorder can be treated by
applying 10-20 ml/kg of body weight of fresh frozen plasma, and AT, if its activity has
decreased; see also chapter 5. 3. 3. 6 Hemocoagulation disorders. Miniheparinization may
probably have a positive effect on persisting signs of hypercoagulation once hemorrhaging
has ceased, even though the merits of its application have been the subject of debate.
Increased supply of liquids will prevent renal failure. In cases of severe neurotoxicity
symptoms, intubation and mechanical ventilation might be necessary, though very rarely.
The patient can be discharged for home treatment after 24 hours following abatement of
systemic symptoms and more serious laboratory symptomatology.

Notechis Genus, Tiger Snakes

Species: The black tiger snake (Notechis ater) with a number of subspecies, and the
mainland tiger snake (Notechis scutatus).
Description: Thickset snakes 100-150 cm long, exceptionally up to 250 cm. They are of
dark color with possible lighter cross stripes. Largely active during the day and at dusk, they
can be active at night as well in hot periods. Cases of aggressive behavior are possible; when
threatened, the snake will spread its neck in a similar manner to cobras.
Home range and habitat: They mostly dwell in humid areas, forests and bushland,
sometimes more open spaces, but they still prefer environments neighboring water, including
coastal regions in SE and SW Australia, the surrounding islands and Tasmania.
 Envenoming and Snakebite Treatment in Specific Snake Groups 139

Toxins: Ranked fourth in an imaginary hierarchy of snake venom due to its effectiveness
on mice, its toxicity is always compared to that of taipans (Oxyuranus) (Sutherland et al.,
2000). As for the impact on humans, this venom is considered one of the most effective of all.
Fortunately, the quantity available in these snakes is only low.
From clinically relevant components, the venom contains both neurotoxic substances
with a postsynaptic effect and PLA2 with a presynaptic action. As for hemocoagulation
components, the venom contains prothrombin specifically activating proteinases, including D
group activators that are similar in function to human FXa (hopsarin-D).
Other venom compounds include myotoxins with significant effects and enzymes with
less noteworthy hemolytic effects.
Local symptoms of envenoming: Local affliction is minor, with a bite being typically hard
to discern. In some cases, venom droplets are evident at the bitten site. The wounds may
bleed. Lymphadenopathy sets in; lymphangitis and lymphadenitis are manifest as strain and
minor pain.
Systemic symptoms of envenoming: Systemic envenoming may become manifest very
early on, within five minutes. It is most likely to begin with the following prodromes:
headaches, nausea, and vomiting. Early hypotension is possible to occur.
Neurotoxicity is apparent due to hazy or double vision, facial and swallowing muscle
innervation disorders, and dysarthria, followed by overall muscle weakness leading up to
respiratory muscular paralysis, with which there is a risk of aspiration and respiratory failure
requiring management of airways and mechanical ventilation. Should no adequate specific
treatment be available, the development of this status may last for 5 hours.
Complications associated with a DIC-like hemocoagulation disorder may occur early-
after 30 minutes following a bite, although such progress is usually slower. As a result,
prothrombotic statuses arise with (micro)embolisms that trigger ischemia in tissues in the
coronary and pulmonary bloodstreams, as well as other bloodstreams. Exhaustion of the
coagulation system will manifest following the prior activation at a systemic level as
fundamentally increased hemorrhaging, in addition to the possibility of hemorrhage into
organs, e.g. the brain. As DIC proceeds, hemorrhaging will occur despite the application of
antivenom.
Hemodynamic disorders may set in - decreased heart output and pulse volume, plus
manifestation of heart failure with increased pulmonary vascular pressure. The changes
described above can be evidently associated with ischemization of myocardium and
pulmonary vessels by (micro)thrombi.
Myoglobinemia and myoglobinuria, together with less significant hemoglobinuria,
generated in the course of proceeding rhabdomyolysis and hemolysis, are a predisposition for
subsequent renal failure.
Laboratory findings: In hemocoagulation lab tests, symptomatology of consumption
coagulopathy will prevail as follows: prolonged PT and APTT, plus FBG depletion up to
afibrinogenemia and thrombocytopenia. Lab tests of VIII, IX, XI, and V factor levels
revealed a loss of over 50% in some cases; the presence of components inhibiting these
factors is also possible. Myoglobinemia is followed by the discovery of myoglobinuria.
Leucopenia has also been recorded.
Mortality: In the period 1981-1991, 4 fatalities were registered. Fatal cerebral
hemorrhaging in an eleven-year-old boy as well as several sudden deaths were described. As
140 Jiri Valenta

for the number of fatalities in Australia, envenoming by the mainland tiger snake (N.
scutatus) takes second place, with bites from brown snakes (Pseudonaja) in prime position.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Immediate application of a pressure immobilization bandage is fully
indicated; the bandage should only be removed upon arrival at a health facility capable of
dealing with systemic envenomation.
Satisfactory neutralization of venom components with neurotoxic and hemocoagulation
effects can be achieved via application of an antivenom, usually if delivered in time.
Any later administration may not fully combat presynaptically acting neurotoxic enzymes
and DIC-like hemocoagulation complications, if the same are already in progress.
Nonetheless, it is indicated in such cases as well.

* TIGER SNAKE ANTIVENOM, Commonwealth Serum Laboratories, Victoria,

Parkville, Australia (Notechis ater, Notechis scutatus, etc.);
* POLYVALENT SNAKE ANTIVENOM, Commonwealth Serum Laboratories,
Victoria, Parkville, Australia (Notechis scutatus, and other snakes);
SEA SNAKE ANTIVENOM, Commonwealth Serum Laboratories, Victoria, Parkville,
Australia (Notechis scutatus, and others).

A minimal local affliction will not require any special treatment.

Symptomatic therapy must primarily manage satisfactory ventilation and avoid possible
aspiration when any specific immunotherapy is absent or necessarily delayed and severe
systemic symptoms of neurotoxicity exist. If dysphagia and ventilatory insufficiency occur,
tracheal intubation and mechanical ventilation will be indicated.
Hemocoagulation dysbalance will require treatment according to the type of affection. A
procoagulative status as well as increased hemorrhaging can be treated by applying 10-20
ml/kg of body weight of fresh frozen plasma, and AT in instances of its decreased activity in
the serum; see also chapter 5. 3. 3. 6 Hemocoagulation disorders. The merits of administering
heparin have been debated. A positive effect of this substance is recorded in experiments on
dogs, but only when administered before an envenoming. Application in minute doses is
recommended in the period outside any clinically evident bleeding should there be signs of
hypercoagulation based on a hemocoagulation test.
Myoglobinuria and hemoglobinuria will require raising the supply of liquids to prevent
renal failure. Any further potential severe hemodynamic disorders must be treated
symptomatically as individually manifested. If any occur, myocardial ischemia markers
should be examined and any possible pulmonary embolism ruled out.
The patient can be discharged for home treatment after 24 hours following abatement of
all systemic symptoms and normalization of significant laboratory symptomatology.

Oxyuranus Genus, Taipan

Species: Inland taipan (Oxyuranus microlepidotus) and coastal taipan (Oxyuranus
scutellatus) including subspecies, the coastal taipan (O. s. scutellatus) and Papuan taipan (O.
s. canni).
Other names: EN: Western taipan, fierce snake, small-scaled snake; scientific:
Parademandsia microlepidota (O. microlepidotus). EN: Australian (New Guinea) taipan (O.
scutellatus).
 Envenoming and Snakebite Treatment in Specific Snake Groups 141

Description: Medium-sized, large or robust snakes up to 300 cm long, although 335 cm is

possible in O. scutellatus, predominantly in hues of brown and light-bellied. The head is
elongated; eyes are large with round pupils. Taipans are active in the day and at dusk, and in
hot weather at night. Fangs are up to 1.3 cm long and larger than those of other coral snakes
(O. scutellatus).
Home range and habitat: Taipans inhabit arid areas and sparse bush of the central part of
eastern inland Australia (O. microlepidotus); humid forests plus arid areas with sparse
vegetation along northern coastal Australia (O. scutellatus scutellatus), and the southern coast
of Papua-New Guinea (O. scutellatus canni).
Toxins: The venom of the coastal taipan (O. scutellatus) is considered the third most
effective in the world. A lethal dose for humans is approximately 5 mg of dry matter of
venom; the mean quantity in the venom gland as usually specified is 120 mg of dry matter,
with the maximum being 400 mg (Sutherland 1990, 2000). The inland taipan (O.
microlepidotus) is probably the most venomous snake. The minimum specified LD50 for mice
is a mere 0.01 mg/kg of live weight; the mean quantity of the venom discharged when biting
is 17.3 mg. This produces an envenoming capacity equal to LD50 for 1,730 kg of mice,
making it the record holder amongst venomous snakes (Morrison, 1983-4).
The venom primarily contains neurotoxins, with the major part formed by PLA2 with
presynaptic effects, and a lesser proportion of postsynaptic neurotoxins. The neurotoxic
components found in taipan venom are recognized by some authors as being the most
effective of all. PLA2 with presynaptic neurotoxicity and a powerful procoagulative effect is
formed from substances termed taipoxin (O. scutellatus) or paradoxin (O. microlepidotus).
The venom components can activate prothrombin to thrombin, with FXa- and FVa-like
protein complexes and PLA2 with coagulation effects, in addition to the previously mentioned
components of taipoxin and paradoxin.
Taicatoxin, which blocks calcium channels of excitable membranes and may trigger
arrhythmia, is another complex of venom components.
In addition, the venom also display myotoxic and a low fibrinolytic activity, causes
aggregation and activation of platelets, and possesses insignificant hemorrhagic properties.
Local symptoms of envenoming: Bites are not painful, and might even go ignored.
However, bleeding may occur. Lymphangitis and lymphadenitis are typically present, often
with strain or even feelings of pain in 93% of snakebites. Nevertheless, such local signs may
not necessarily mean a systemic envenomation has taken place.
Systemic symptoms of envenoming: The majority of taipan snakebites, over 80% of cases,
are accompanied by a systemic envenomation. The process will typically begin with the
following prodromes: headaches, nausea, vomiting, and bellyache.
The main affection symptoms concern manifestations of neurotoxicity and hemostasis
disorder. Neuromuscular transmission disorders will appear in up to 85% of those concerned,
usually beginning with ptosis, followed by ophtalmophlegia and double vision, facial muscle
paralysis, pseudo-bulbar paralysis including dysarthria and dysphagia, and overall muscle
weakness. In over 40% of cases of envenoming, paralysis of respiratory muscles occurs as
well, with tracheal intubation and mechanical ventilation proving necessary.
Hemocoagulation disorders occur in the majority of affected persons, with over 90% of
displaying at least laboratory symptomatology of coagulopathy, in nearly 80% non-
coagulability of blood is found, and 35% - 50% show clinical signs of hemorrhaging - most
frequently from the gums and nose - as well as hematuria and hemorrhagic diarrhea.
142 Jiri Valenta

Bradycardia, possibly continuing through to AV-block with ECG changes in terms of T

wave inversion, occur in the majority of those affected. Envenomation may be accompanied
by periods of unconsciousness and hypertension. Any rhabdomyolysis in progress may even
lead to secondary renal failure.
Laboratory findings: The prevailing laboratory result from the envenoming is
hemocoagulation system disorder. The basic lab tests show prolonged PT and APTT,
thrombocytopenia and hypo- or even afibrinogenemia occurring, and a highly distinct
elevation in FDP levels, including that of D-dim, is found. A more detailed test will reveal
signs of activated fibrinolysis, with the discovery of plasminogen and 2-antiplasmin, as well
as reduced activity of FV, VIII, IX, XII, and XIII. A clear decrease in C protein level occurs.
Nevertheless, AT activity is typically not significantly affected. A triple increase in the level
of von Willebrands factor indicates endothelial activation and damage.
In biochemical laboratory tests, myoglobin is typically found in the serum and urine, with
troponin level elevation present in about 8% of the patients.
Mortality: The historic mortality rate of 80% caused by taipan snakebites seems to be
overstated - such a percentage would correspond to the occurrence of systemic envenomation
following the bite. However, the severe symptoms of envenoming experienced by most
victims can result in fatal courses unless adequate therapy is provided. The venoms potency
may cause death very early on, in terms of minutes, especially in children repeatedly bitten.
In 1981-1991, there were two cases of death in Australia. In the group of 166 patients
bitten by the Papuan taipan (O. scutellatus canni), lethality occurred in 4.3% of those
envenomed. This relatively low level of mortality can be ascribed to prompt and adequate
treatment, especially the opportunity to receive mechanical ventilation.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Immediate application of a pressure immobilization bandage is fully
indicated. The bandage should not be removed before arrival at a health facility capable of
dealing with serious systemic symptoms. If envenoming is proven, the bandage should be
removed upon application of antivenom, or at least once the possibility of symptomatic
treatment, principally mechanical ventilation, has been safeguarded.
Timely administration of appropriate antivenom, at best a species-specific one, will
reduce the seriousness and period of neurotoxicity manifestation, namely by influencing
PLA2 with presynaptic effects.
Repeated application of antivenom, even for longer periods following the snakebite, will
also have a positive effect. However, if antiserum application is delayed, neuromuscular
affliction will persist. The specific immunotherapy necessary regulates the symptoms of
hemocoagulation disorder relatively effectively.
Applicable antivenoms:

* TAIPAN ANTIVENOM, Commonwealth Serum Laboratories,Victoria, Parkville,

Australia (Oxyuranus microlepidotus, Oxyuranus scutellatus);
* POLYVALENT SNAKE ANTIVENOM, Commonwealth Serum Laboratories,
Victoria, Parkville, Australia (Oxyuranus microlepidotus, Oxyuranus scutellatus, etc.).

The minimal local affliction should not require any special treatment. In cases of painful
lymphadenopathy, the limb can be elevated and moderately cooled.
 Envenoming and Snakebite Treatment in Specific Snake Groups 143

If paralysis of swallowing and respiratory muscles is manifest, with a risk of aspiration

and clinical signs of respiratory failure, airway management using tracheal intubation and
subsequent mechanical ventilation is necessary without delay.
Any persisting DIC-like coagulopathy found can be corrected by applying fresh frozen
plasma, 10-20 ml/kg of body weight. AT substitution is indicated by reduced AT activity.
Any cases of a more intensive hemocoagulation disorder must be treated symptomatically in a
complex manner; see chapter 5. 3. 3. 6 Hemocoagulation disorders. Heparin may be an
effective option to help neutralize increased thrombin activity and the resulting prothrombotic
status. However, application of heparin in instances of envenoming by taipan venom is
considered to have a reduced effect and will be contraindicated whilst patients are bleeding.
Nevertheless, miniheparinization by unfractionated heparin (UFH) or low LMWH doses can
prove both pre-emptive and protective if subsequent complications occur due to persisting
prothrombotic changes following endothelial damage within the preceding coagulation
disorder.
The patient can be discharged for home treatment after 24 hours following abatement of
all systemic symptoms and normalization of significant laboratory findings.

Pseudechis Genus, Black Snakes

Species: Mulga snake (Pseudechis australis), spotted mulga snake (Pseudechis buttleri),
Colletts snake (Pseudechis colletti), blue-bellied black snake (Pseudechis guttatus), Papuan
black snake (Pseudechis papuanus), red-bellied black snake (Pseudechis porphyriacus).
Other names: EN: king brown snake, black snake (P. australis).
Description: Robust snakes, they tend to grow to 120-200 cm, with the maximum of 275
cm recorded for P. australis. When threatened, they spread their necks in the manner of
cobras (Naja). These snakes are active during the day and at dusk in colder periods; a very
high increase in temperatures during the day makes them active at night.
P. australis can be extremely aggressive when provoked. Strikes can be repeated, with
the snake chewing as it bites.
Home range and habitat: The snakes of this genus range in diverse habitats almost
throughout Australia and New Guinea (P. papuanus), from semi desert regions, arid, rocky
and hilly landscapes, as well as dense or even tropical forests (P. australis, P. guttatus), and
swampy areas (P. porphyriacus).
Toxins: The venom is not of extreme danger; it contains neurotoxins plus components of
hemorrhagic, myotoxic and hemolytic type and those of general cytotoxicity. Myotoxicity is
caused by mulgatoxin of great potency. The venoms components affect hemocoagulation by
activating prothrombin.
In 1986, herpetologist John Cann obtained an extreme quantity of venom from P.
australis, a 250 cm long snake - 2.5 ml of liquid venom containing 1,350 mg of dry matter,
this being at a time when the previous historic maximum of venom had been obtained from a
king cobra (Ophiophagus hannah): 900 mg of dry matter.
Local symptoms of envenoming: Even though local damage is presented as the most
significant affliction triggered by Austropapuan terrestrial elapid snakes, in most cases it is
limited to edema with lymphadenitis and lymphangitis, including feelings of strain and
medium pain in the limb and lymph nodes. However, the bite wound may drip; in the
minority of cases, even subdermal abscesses may form due to tissue damage and
decomposition rather than from the results of infection.
144 Jiri Valenta

Systemic symptoms of envenoming: The process of envenoming will typically commence

with the following prodromes: nausea, vomiting, headaches, and bellyache. Following a
snakebite from the Papuan black snake (P. papuanus), the neurotoxicity manifest is
registered, although rarely with the need for mechanical ventilation, unlike cases of
snakebites from the mulga snake (P. australis) and red-bellied black snake (P. porphyriacus),
where almost no clinical symptoms of acute neurotoxicity have been recorded. Exceptions
include instances of loss of the senses of smell and taste for up to several months and a
number of cases of epilepsia following envenoming by the red-bellied black snake (P.
porphyriacus).
The process of envenomation typically includes hemocoagulation effects accompanied by
spontaneous hemorrhaging and hematuria in more difficult cases.
Even though a serious effect triggered by myotoxins and hemolysis is not typical for
envenoming, rhabdomyolysis may still occur, especially in instances involving delayed
administration of antivenom following a bite from the mulga snake (P. australis). Symptoms
of renal dysfunction are also possible.
Laboratory findings: Hemocoagulation analysis shows prolonged PT and APTT,
hypofibrinogenemia, thrombocytopenia, FDP elevation, activated fibrinolysis, and depletion
of hemocoagulation factors; even a high elevation of CC and myoglobin in the serum and
myoglobinuria can be present.
Mortality: Since 1981, no fatality related to an attack by a Pseudechis snake has been
registered in Australia and probably elsewhere.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Immediate application of a pressure immobilization bandage is indicated; the
bandage should be removed only upon arrival at a health facility capable of dealing with
systemic envenomation.
Administration of appropriate antivenom is indicated where a reaction at a systemic level
occurs, as with other cases of envenoming.
Applicable antivenoms:

* BLACK SNAKE ANTIVENOM, Commonwealth Serum Laboratories, Victoria,

Parkville, Australia (Pseudechis australis, Pseudechis butleri, Pseudechis colletti, Pseudechis
guttatus, Pseudechis papuanus, Pseudechis porphyriacus);
* POLYVALENT SNAKE ANTIVENOM, Commonwealth Serum Laboratories,
Victoria, Parkville, Australia (Pseudechis australis, Pseudechis papuanus, etc.);
* TIGER SNAKE ANTIVENOM, Commonwealth Serum Laboratories, Victoria,
Parkville, Australia (Pseudechis colletti, Pseudechis guttatus, Pseudechis porphyriacus, and
other snakes);
* SEA SNAKE ANTIVENOM, Commonwealth Serum Laboratories, Victoria, Parkville,
Australia (Pseudechis porphyriacus, etc.).

As the venom of Pseudechis snakes displays cross-immunity with the venom components
of tiger snakes (Notechis), a minor amount of this antivenom can be applied as an alternative.
However, cross-immunity with Pseudonaja snakes does not exist.
Due to a greater chance of local affliction of tissue at the bitten site, it is recommended to
remove the pressure immobilization bandage as soon as possible. Of course, this should not
take place before the necessary treatment is available or a systemic envenomation is ruled out.
 Envenoming and Snakebite Treatment in Specific Snake Groups 145

Special care and attention should be paid to the local affliction due to the likelihood of
causing pain and potentially damaging tissue; the afflicted limb needs to be immobilized,
elevated, mildly cooled, and possible subsequent trauma avoided. Abscesses at the bitten site,
if any, should be drained with care. Antibiotics are indicated if infectious etiology or
secondary local infection is suspected.
Rare cases of clinical symptoms of profound muscular paralysis will require management
of airways and mechanical ventilation.
A potentially persisting hemocoagulation disorder can be treated symptomatically; a high
myoglobin level in cases of rhabdomyolysis will require an increased supply of liquids in
order to guard against renal failure.
A patient can be discharged for home treatment after 24 hours following abatement of all
systemic symptoms and normalization of significant laboratory findings.

Pseudonaja Genus, Brown Snakes

Species: Dugite (Pseudonaja affinis), speckled brown snake (Pseudonaja guttata),
peninsula brown snake (Pseudonaja inframaculata), Ingrams brown snake (Pseudonaja
ingrami), ringed brown snake (Pseudonaja modesta), gwardar (Pseudonaja nuchalis), eastern
brown snake (Pseudonaja textilis); with the most significant and dangerous species being P.
textilis, P. affinis and P. nuchalis.
Other names: EN: Brown snake, dugit (P. affinis). Gwardar (P. nuchalis). Common or
eastern brown snake (P. textilis).
Description: Largely slender bodied snakes that range from 50 to 150 cm in length; the
largest species, i.e. P. affinis and P. textilis, can grow up to 150-200 cm, with P. textilis
capable of reaching even 240 cm. They are mostly diurnal animals; nocturnal activity in hot
periods is possible, but rare. P. affinis is a more short-tempered and lively species than the
rest of the genus, which increases the level of risk of this snake.
Home range and habitat: Brown snakes reside in quite arid and open land, including the
scrub and open bush of Australia; the most perilous (P. textilis) can even be found in humid
localities in the eastern half of Australia, and Papua-New Guinea.
Toxins: The venom of P. textilis possesses potency of toxin about ten times higher than
that of other Pseudonaja snakes, with LD50 for mice SC of 0.053 mg/kg of body weight,
placing this species second in the chart of most effective snake venom.
The components responsible for such high and rapid fatality of envenoming in a human
are probably those termed cardiotoxins by some authors, causing dramatic circulatory
collapse.
The venom contains effective neurotoxic components of largely presynaptic action, as
well as compounds with hemocoagulation effects, mostly by potent activation of prothrombin
with a resulting DIC-like consumption disorder.
The presence of primarily nephrotoxic venom components is also possible. The effects of
myolytic, hemolytic, and general cytotoxic enzymes are limited or not evident at all.
Local symptoms of envenoming: The bite, the area around it, and the limb are typically
not painful. In some cases, bleeding from the bitten site and local formation of bruises may
occur. The generation of moderate edema and lymphadenopathy is possible.
Systemic symptoms of envenoming: The process of envenoming normally commences
with the following prodromes: nausea, vomiting, and headaches. Typically, neurotoxicity
becomes apparent very early on, largely within 30 minutes, by afflicting facial muscles with
146 Jiri Valenta

ptosis, ophtalmophlegia with double or hazy vision, and dysarthria. More serious signs of
neurotoxicity are rare.
In acute and fatal cases of envenoming, severe circulatory collapse with hypotension and
possible circulatory failure typically occur very soon, possibly caused by rapid intravascular
coagulation in the coronary stream with myocardial ischemia, or deep hypotension for other
cardiodepressive reasons.
In the majority of envenomings, a hemocoagulation disorder of the consumptive type
prevails, largely with clinical signs of hemorrhaging, but even featuring (micro)thrombotic
complications.
Renal failure, possibly with signs of acute tubular necrosis, occurs in up to 5% of those
envenomated, which means the highest incidence among the terrestrial Austropapuan elapid
snakes.
Laboratory findings: Hemocoagulation tests will typically reveal consumption
coagulopathy with prolonged PT and APTT, hypofibrinogenemia, thrombocytopenia, and
elevated FDP including D-dim.
Mortality: Bites by the eastern brown snake (P. textilis) are responsible for the largest
proportion of fatalities caused by all such instances in Australia; 11 cases were recorded in
1981-1991. In some cases of envenoming by Pseudonaja snakes, sudden and unexpected
death has occurred very soon, in just 35 to 90 minutes, following circulatory collapse and
cardiac arrest with minimal changes found in the post mortem report. Other fatalities have
been caused by endocranial hemorrhaging. Such facts make Pseudonaja snakes the most
dangerous in the Austro-Papuan region.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Immediate application of a pressure immobilization bandage is fully
indicated; the bandage should be removed only upon arrival at a health facility capable of
dealing with systemic envenomation, either after antivenom is applied or once envenoming is
ruled out. If envenoming is proven, the bandage should be removed once an antivenom is
applied, or at least when there is a possibility of symptomatic treatment being provided.
Considering the potential seriousness of the envenomation process, administration of a
relevant antivenom is indicated as soon as is possible if systemic symptoms occur.
Applicable antivenoms:

* BROWN SNAKE ANTIVENOM, Commonwealth Serum Laboratories, Victoria,

Parkville, Australia (Pseudonaja affinis, Psedonaja nuchalis, Pseudonaja textilis);
* POLYVALENT SNAKE ANTIVENOM, Commonwealth Serum Laboratories,
Victoria, Parkville, Australia (Pseudonaja affinis, Psedonaja nuchalis, etc.).

The local affliction is insignificant and will not require any special care.
The most dangerous signs of a severe envenoming are cardiac collapse with hypotension
and potential circulatory failure. Hypotension requires intensive care without delay so as to
strive to maintain hemodynamics by either increasing intravenous volume or supportive
treatment by means of catecholamines. The latter involves application of either norepinephrin
or medicine for -mimetic support of myocardium, depending on the symptoms present.
As cardiodepressive symptomatology can be caused by myocardial ischemia via
(micro)embolisms within the activation of thrombin at a systemic level, there is a theoretical
option of heparinization for a threatened patient. However, the utilization of heparin is
 Envenoming and Snakebite Treatment in Specific Snake Groups 147

contraindicated due to hemorrhagic complications of the envenoming. Nevertheless, evident

myocardial ischemization found with corresponding biochemical and hemocoagulation
laboratory results and absent clinical signs of hemorrhaging allow for use of heparin when
there is a vital indication.
The DIC-like consumption disorder in progress can be treated symptomatically by
applying fresh frozen plasma (10-20 ml/kg) and AT, if its activity has been critically reduced.
In cases of more intensive consumption disorder and hemorrhaging, see chapter 5. 3. 3. 6
Hemocoagulation disorders.
Any threat of possible renal failure will require the sufficient supply of liquids, even
though such instances are typically not caused by myoglobinuria but microembolisms in
progress in the renal vascular system. Therefore, in order to prevent this consumption
coagulopathy needs to be monitored.
The patient can be discharged for home treatment after 24 hours following abatement of
all systemic symptoms and normalization of significant laboratory findings.

Tropidechis Genus
Species: Rough-scaled snake (Tropidechis carinatus), Tropidechis sadlieri.
Other names: EN: Clarence river snake (T. carinatus).
Description: These are snakes that can grow up to 60-70 cm, and rarely up to 100 cm.
They feature large eyes and round pupils; their color is brown through to a gray-green with
dark discontinuous stripes on the dorsal section of the body, the belly is pale in tone. They are
mostly active during the day, but also at night if daytime temperatures are high. Their
aggressive nature raises the potential danger they pose.
Home range and habitat: This group of snakes inhabits damp tropical forests, but is also
found in the neighborhoods of settlements, gardens, parks, and golf clubs in the territory
comprising the central and northern part of the coast and surrounding inland areas of Eastern
Australia.
Toxins: These snakes produce a relatively high quantity of venom that possesses
neurotoxic activities - both presynaptic and postsynaptic - as well as myotoxic and hemolytic
components. In addition, it contains compounds with hemocoagulation effects, amongst them
trocarin, a group D prothrombin activator, comparable with FXa in humans in terms of both
structure and function.
Local symptoms of envenoming: Local changes are not very distinctive, with possible
minor edema surrounded by erythema, painful lymphadenopathy, and bruising.
Systemic symptoms of envenoming: At a systemic level, the envenoming will be manifest
through prodromal headaches and nausea; temporary loss of consciousness can occur very
rapidly. A risk of muscular paralysis may require intubation and mechanical ventilation.
When inadequate treatment is given, the rhabdomyolysis and hemolysis present will result in
renal failure. Hemocoagulation disorders are possible following prothrombin activation,
although they have not been clinically described.
Laboratory findings: Hemoglobinuria and myoglobinuria.
Mortality: Even though no fatalities have been described, the nature of the venom can
cause fatalities in humans.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Immediate application of a pressure immobilization bandage is indicated; the
148 Jiri Valenta

bandage should be removed only upon arrival at a health facility capable of dealing with
systemic envenomation.
Applicable antivenoms:

* TIGER SNAKE ANTIVENOM, Commonwealth Serum Laboratories, Victoria,

Parkville, Australia (Tropidechis carinatus, etc.);
* SEA SNAKE ANTIVENOM, Commonwealth Serum Laboratories, Victoria, Parkville,
Australia (Tropidechis carinatus, and others).

The minor localized affliction will not require any special care.
Muscular paralysis can be successfully controlled through specific treatment, though
mechanical ventilation may be necessary for a definite period of time. Hemocoagulation
disorders may be treated symptomatically; heparinization using a small dosage can have a
positive effect on persisting signs of hypercoagulation once hemorrhaging has abated, even
though its application has been disputed. Increasing the supply of liquids could prevent renal
failure.
The patient can be discharged for home treatment after 24 hours following abatement of
all systemic symptoms and normalization of significant laboratory findings.

Other Species of Austropapuan Terrestrial Coral Snakes (A Former Oxyuraninae

Subfamily)
Aspidomorphus. Not very large snakes up to 70 cm long, with brownish to brown-black
color, ranging in New Guinea and the surrounding islands.
Cacophis, dwarf-crowned snakes. Small to medium-sized and non-aggressive snakes 25-
70 cm long, with brownish, reddish and steel-gray color and largely nocturnal activity that
inhabit forest localities in coastal E Australia.
Demansia. Medium-sized or even robust, these extremely slender snakes with large eyes
can grow up to 200 cm in some species. They reside in diverse habitats of predominantly
western and northern Australian regions.
Snakebites will in most cases cause only a localized and not very painful edema and livid
color of skin at the bitten site. Arrhythmias in terms of stroke irregularities have been
described as a part of systemic envenoming.
Denisonia. Robust, but not very large snakes, less than 50 cm long, with a short tail and
nocturnal activity found in NE Australia.
Even though their venom contains mainly neurotoxins, these snakes are not dangerous;
envenomation will probably take place without coagulation defects.
Drysdalia. Not very large snakes, less than 75 cm long, with a robust body; they are
mostly active at night. They inhabit the SE, S, and SW coasts of Australia including
surrounding inland territories. The venom probably contains chiefly myotoxins causing
rhabdomyolysis, but is not considered dangerous.
Echiopsis. Not very large but thickset snakes, less than 60 cm long, with a short tail. They
are largely nocturnal animals ranging in grassy and shrubby territories in the southern part of
W Australia and its southern coastland including surrounding inland territories.
Clinically, envenomings resemble those caused by the death adders (Acanthophis).
Snakebites generate edema and coagulation defects, which could qualify these animals as
potential dangerous snakes.
 Envenoming and Snakebite Treatment in Specific Snake Groups 149

Elapognathus. Small brownish snakes less than 50 cm long with a thickset body found in
SW Australia.
Furina. Small and slender gray-black snakes less than 50 cm long, predominantly active
at night. They mostly reside in rather arid habitats of SE Australia; one of the species even
ranges across the continent except the southern part, and also New Guinea and surrounding
islands.
Glyphodon. Dark brown to black snakes with the length less than 90 cm; they are
nocturnal animals found in the eastern part of the Cape York Peninsula.
Locally, envenomation will manifest with erythema and pain around the bitten site; at a
systemic level, pain in epigastrium, nausea, vomiting and aqueous diarrhea occur. There is no
effect on hemocoagulation. Envenomation is not considered dangerous; however, the venom
is impossible to neutralize by any available antivenom.
Recently, members of the genus are classified under the Furina and Cacophis genera.
Hemiaspis. Not very large snakes - about 50 cm long, with maximum of 90 cm. Their
dorsal part is grayish, olive or brownish, but populations with dark to black color, i.e.
melanotic ones, exist as well. On hot days, these largely diurnal snakes can be also active at
dusk. They mostly range in humid habitats in E Australia.
The snakebite is typically followed by distinctive pain at the bitten site; edema and
lymphadenopathy occur, as well as benign laboratory signs of consumption coagulopathy.
Loveridgelaps. A monotypic genus containing the Solomons small-eyed snake
(Loveridgelaps elapoides), also referred to as the orange-banded snake. It is a relatively rare
species that can grow 80-100 cm, but exceptionally even 150 cm long. It is active at dusk and
in the night. The body of this snake boasts wide cross stripes, with light up to orange and
black color; its head is light as well. This species dwells near waters in the tropical forests of
the Solomon Islands.
Snakebites have not been registered; they can be potentially dangerous. Antivenom is not
available.
Micropechis. Medium to large size, these surface or also burrowing snakes can grow as
much as 150 cm, with the maximum of 200 cm. They feature variable coloring with a ring-
like pattern in the rear part of the body. They are predominantly nocturnal snakes, and inhabit
the tropical forests and swamp areas of New Guinea and the Aru Archipelago.
The course of envenoming can be potentially grievous or even fatal.
Ogmodon. A small burrowing snake of brownish color found in the Fiji Archipelago.
Parapistocalamus. A monotypic genus with a single species - Hedigers or also
Bougainville snake (Parapistocalamus hedigeri). This species can achieve the length of 40-60
cm; it features dark up to black color with a light belly and cross stripe on its head. It is a
burrowing nocturnal species that dwell in the forests of Papua-New Guinea and the Solomon
Islands.
Paroplocephalus: see Suta below.
Rhinoplocephalus, synonym: Unechis. Small and slender nocturnal snakes with the
maximal length of 50 cm. Found in SW, SE, E and N Australia and the southern part of
Papua-New Guinea. No evidence for snakebites exists.
Salomonelaps. Medium-sized snakes that grow up to 100 cm. They are active in the night
and range in the forest areas of the Solomon Islands. No evidence for snakebites exists.
150 Jiri Valenta

Simoselaps. Small short-tailed burrowing snakes with variable patterns of rings along the
body. They are primarily night hunters and range in diverse habitats of W and SE Australia.
This snake genus is not considered dangerous.
Suta. Small snakes with chiefly nocturnal activities. The majority of them feature black
spots on their head. They inhabit diverse habitats of a greater part of Australian continent.
Toxicity of their venoms is only low.
Toxicocalamus. Small snakes that range in the island regions of Indonesia, New Guinea
and Papua-New Guinea.
Vermicella. Not very sized snakes that can achieve a maximum of 30 cm; the young are a
mere 17 cm long. They are found on diverse localities across the most of the Australian
territory.
Effects of envenoming may include temporary hypotension. The course of envenoming is
benign, with no indication for application of antivenom. The local affliction is typically
insignificant.

Toxins: The venom of the genera listed above is not very dangerous to humans, as a
consequence of limited potency or the small amount available. Fundamentally, they are likely
to consist of neurotoxins, components with hemocoagulation effects, myotoxins, plus
hemolytic and cytotoxic enzymes that form mixtures of varied proportions, just as in other
snakes of the Oxyuraninae subfamily.
Local symptoms of envenoming: Snakebites from a majority of the genera above will be
restricted to less significant local symptoms, such as pain, minor edema, erythema, and
lymphadenopathy.
Systemic symptoms of envenoming: If at all described, the symptoms of systemic
envenoming are typically not serious; they will be limited to headaches, nausea, vomiting,
possibly pain in the epigastrium, and diarrhea. Nevertheless, a more grievous course is also
possible, namely in children, with possible manifestations of neurotoxicity, myotoxicity,
hemocoagulation disorders, and renal failure.
Laboratory findings: The results of laboratory tests will correspond to the type of toxin
loads and affection levels; changes will not be probably significant.
Mortality: Even though fatalities in snakebites from the genera above have not been
described, severe cases of envenoming are still possible.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Although envenoming by the above snakes will not be dangerous to a human
in most cases, application of a pressure immobilization bandage in cases of snakebite can be
recommended; the bandage should not be removed before arrival at a health facility or after
any systemic affliction has been ruled out. In case of signs of systemic envenoming,
symptomatic therapy is advisable based on the type of affliction; see chapter 5. 3. 3. Clinical
symptoms of envenomation and symptomatic treatment.
The patient can be discharged for home treatment after 24 hours following abatement of
all possible symptoms and normalization of potentially more significant laboratory findings.
 Envenoming and Snakebite Treatment in Specific Snake Groups 151

REFERENCES
FATOVICH, DM., HITCHCOCK, T, WHITE, J. Mild snake envenomation. Emerg Med
(Fremantle), 2002, 14, pp. 8588.
CHEW, MS., GUTTORMSEN, AB., METZSCH, C., et al. Exotic snake bite: a challenge for
the Scandinavian anaesthesiologist? Acta Anaest Scand, 2003, 47, No. 2, p. 226.
ISBISTER, GK., DAWSON, AH., WHYTE, IM. Two cases of bites by the Black-bellied
Swamp Snake (Hemiaspis signata). Toxicon, 2002, 40, No. 3, pp. 317319.
JELINEK, GA., BREHENY, FX. Ten years of snake bites at Fremantle Hospital. Med J Aust,
1990, 153, No. 1112, pp. 658661.
LALOO, D., TREVETT, A., BLACK, J., et al. Neurotoxicity and haemostatic disturbances in
patients envenomed by the Papuan Black Snake (Pseudechis papuanus). Toxicon, 1994,
32, No. 8, pp. 927936.
LALOO, DG., TREVETT, AJ., BLACK, J., et al. Neurotoxicity, anticoagulant activity and
evidence of rhabdomyolysis in patients bitten by Death Adders (Acanthophis sp.) in
southern Papua New Guinea. Q J Med, 1996, 89, p. 2535.
LALOO, DG., TREVETT, AJ., KORINHONA, A., et al. Snake bites by the Papuaa Taipan
(Oxyuranus scutellatus canni): paralysis, haemostatic and elektrocardiografic
abnormalities, and effect of antivenom. Am J Trop Med Hyg, 1995, 52, No. 6, pp. 525
531.
LALOO, DG., TREVETT, AJ., NWOKOLO, N., et al. Electrocardiografic abnormalities in
patients bitten by Taipans (Oxyuranus scutellatus canni) and other Elapid snakes in
Papua New Guinea. Trans R Soc Trop Med Hyg, 1997, 91, No. 1, pp. 5356.
LALOO, DG., TREVETT, AJ., OWENS, D., et al. Coagulopathy following bites by the
Papuan Taipan (Oxyuranus scutellatus canni). Blood Coagulation and Fibrinolysis, 1995,
6, No. 1, pp. 6572.
MEIER, J., WHITE, J. (Eds). Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995, 752 pp.
MORRISON, J., PEARN, J., COVACEVICH, J., et al. Studies on the venom of Oxyuranus
microlepidotus. J Toxicol Clin Toxicol, 198384, 21, No. 3, pp. 373385.
PATTEN, BR., PEARN, JH., DEBUSE, P., et al. Prolonged intensive therapy after snake
bite. A probable case of envenomation by the rough-scaled snake. Med J Aust, 1985, 142,
No. 8, pp. 467469.
RAO, VS., JOSEPH, JS., KINI, RM. Group D prothrombin activators from snake venom are
structural homologues of mammalian blood coagulation factor Xa. Biochem J, 2003, 369,
No. 3, pp. 635642.
RAO, VS., KINI, RM. Pseutarin C, a protrombin activator from Pseudonaja textilis venom:
its structural and functional similarity to mammalian coagulation factor Xa-Va complex.
Tromb Haemost, 2002, 88, No. 4, pp. 611619.
SOUTHERN, DA., CALLANAN, VI., GORDON, GS. Severe envenomation by the Taipan
(Oxyutanus scutellatus). Med J Aust, 1996, 165, No. 1112, pp. 662664.
STCKLIN, R., CRETTON, G. The ultimate database on venomous animals, snakes. CD-
rom, Geneva : Atheris Laboratories, 1998.
152 Jiri Valenta

SUBBURAJU, S., KINI, RM. Isolation and purification of superbins I and II from Austrelaps
superbus (copperhead) snake venom and their anticoagulant and antiplatelet effects.
Toxicon, 1997, 35, No. 8, pp. 12391250.
SUTHERLAND, SK. Death from snake bite in Australia, 19811991. Med J Aust, 1992, 157,
No. 1112, p. 740746.
SUTHERLAND, SK. First aid for snakebite in Australia. Published by the Commonwealth
Serum Laboratories Parkville 3052, 1979.
SUTHERLAND, SK. Treatment of snake bite. Australien Family Physisian, 1990, 19, No. 1,
pp. 2141.
SUTHERLAND, SK., NOLCH, G. Dangerous australian animals. Flemington : Hyland
House Publishing, Australia, 2000.
TIBBALLS, J. The cardiovascular, coagulation and haematological effects of Tiger Snake
(Notechis scutatus) venom. Anaesth Intensive Care, 1998, 26, No. 5, pp. 529535.
TIBBALLS, J. The cardiovascular, coagulation and haematological effects of Tiger Snake
(Notechis scutatus) prothrombin activator and investigation of release of vasoactive
substances. Anaesth Intensive Care, 1998, 26, No. 5, pp. 536547.
TIBBALLS, J., HENNING, RD., SUTHERLAND, SK., et al. Fatal cerebral haemorrhage
after Tiger Snake (Notechis scutatus) envenomation. Med J Aust, 1991, 154, No. 4, pp.
275276.
TIDSWELL, F. Researches on Australien venoms, snake-bite, snake-venoms and antivenene:
the poison of the Platypus, the poison of the Red-Spoted Spider. Sydney : NSW
Department of Public Health, 1906.
TREVETT, AJ., LALOO, DG., NWOKOLO, NC., et al. The efficacy of antivenom in the
treatment of bites by the Papuan Taipan (Oxyuranus scutellatus canni). Trans R Soc Trop
Med Hyg, 1995, 89, No. 3, pp. 322325.

6.3.2.2. Aquatic Genera of The Hydrophiinae Subfamily (A Former Hydrophiidae

Family)
Genera and species. Consisting of over 50 species of snakes that dwell in tropical and
subtropical seas, this group covers multiple genera of sea snakes and the Laticauda genus of
sea kraits.
Members include the Aipysurus genus, Stokes seasnake (Astrotia stokesii), Disteira
snakes, turtle-headed seasnakes (Emydocephalus), Enhydrina seasnakes with the
representatives being for example the common seasnake (Enhydrina schistosa), Ephalophis
and Hydrelaps snakes, Hydrophis and Kerilia genera, Kolpophis, Lapemis, Parahydrophis,
Pelamis, Thalassophina (Praescutata) and Thalassophis sea snakes; for a list of species, see
chapter 7 List of venomous snakes.
The sea krait subfamily (Laticaudinae) comprises five species of these snakes, for
example the common sea krait (Laticauda laticauda) or Laticauda semifasciata; for other
species, see chapter 7 List of venomous snakes.
Other names: FR: Serpent de mer, JAP: Umi-Hebi (sea snakes and sea kraits).
Description: Sea snakes number almost 50 species of small-headed marine varieties,
featuring a robust flattened tail and body lengths from 50 to 170 cm, the latter being the
elegant sea snake (Hydrophis elegans), the largest Australian sea snake species. Some well-
built animals of certain varieties may even grow up to 300 cm. Sea snakes vary in color; they
are often darker, sometimes boasting crosswise stripes. The body is of a typical type, with a
 Envenoming and Snakebite Treatment in Specific Snake Groups 153

vertically flattened tail adapted to fast swimming and a small head. The nostrils feature flap
valves and the lung to the right is enlarged, this elongation up to the tail base forms an air
reservoir allowing the creatures to remain submerged. These snakes are good divers - some of
them are even capable of reaching depths of 100 m; nevertheless, they must always go back
up to breathe. The venom apparatus consists of two venom glands, and 2-4 usually small and
thin fixed fangs with channels placed in the anterior part of the maxilla, hence they are
deemed proteroglyphous snakes.
The subfamily and genus of sea kraits (Laticauda) covers five members of semi
terrestrial aquatic snakes approximately 100 cm long, reaching a maximum of 150 cm. In
terms of body and venom apparatus structure they resemble sea snakes, but they boast more
distinctive patterns of crosswise stripes, mostly in hues of yellow, blue, creamy white, and
dark to black colors.
The composition of potent venoms of either snake subfamily brings to mind that of
Austropapuan terrestrial elapid snakes (formerly Oxyuraninae), close relatives of marine
varieties that are likely to have evolved from these snakes.
Sea snakes and sea kraits are not aggressive in nature - the victims of their bites are
usually fishermen, in whose nets the snakes can get snarled. According to White (1995), there
is such a high number of these snakes in certain localities that a single fisherman using a
conventional net for fishing can encounter up to 100 snakes daily. In the 1950s, 150
envenomed fishermen were registered in 10% of Malayan villages to Reid (1975). The
presumed annual incidence throughout Malaysia fluctuates around 1,500 cases, and the global
number of bites suffered by fisherman from marine snakes is estimated as 15,000-75,000,
with a fatality of several percent; the common seasnake (Enhydrina schistosa) being
responsible for more than a half of bites. In addition, E. schistosa is held accountable for the
majority of serious envenomings and fatalities. Other representatives typically referred to as
highly dangerous include Hydrophis cyanocinctus and Lapemis hardwickii. Aside from
snakebites caused to fishermens hands while removing a snake from the net, or to a leg from
the bottom of the boat, snake attacks also occur when a snake is stepped on in shallow water
or handled, such as in an aquarium. Snakebites through swimming and diving are extremely
rare. Marine snakes do accompany divers sometimes, although they will not attack them, even
though cases of seeking out physical contact have occurred. Moreover, the fangs of the snake
tend not to be sufficiently robust and long enough to gnaw through diving suits, but
exceptions do exist, such as Aipysurus laevis and Astrotia stokesii with fangs of over 5 mm
long.
Home range and habitat: Sea snakes predominantly inhabit coastal regions and coral
reefs in the Indian and Pacific Ocean. Their home range is delimited by the entire eastern
African shore to the west, the coasts of the northern part of Australia to the south, the
southern and coastal regions of Korea (the Yellow Sea and South China Sea) and the
Philippine Sea to the north, and the western coasts of Central America and upper South
America. The maximum concentration of such snakes is probably in the coral reefs of the
Australian northern coast. One of the species, the pelagic sea snake (Pelamis platurus), can be
considered an ocean wanderer, as groups cross the entire sea snake home range. Concerns
have been raised about this snake passing through the Panama Canal and subsequently
settling in the Caribbean.
Sea kraits (Laticauda) inhabit SE Asia including certain islands of this region; they are
rarely found in coastal N and E Australia. They dwell in reef areas, along the shore, in sludgy
154 Jiri Valenta

estuaries, etc. Unlike sea snakes, sea kraits sometimes leave the water either for drinking or
laying eggs. They can reside in water in caves along the coast or in lakes inland, for instance,
on Te-Nggano, one of the Solomon Islands.
Toxins: The venoms of sea snakes and sea kraits are considered highly efficient, largely
due to their extreme neurotoxic potency. The most dangerous species is likely to be the
common sea snake (Enhydrina schistosa), which possesses about 8-15 mg of dry matter of
venom with toxicity equal to LD50 0.04 mg/kg of mice IP (intra peritoneam, within the
peritoneal cavity); this is an extremely high value comparable only to that of taipan venom.
With regard to human weight, this snake is capable of delivering approximately three or four
lethal doses. However, in the relatively abundant pelagic sea snake (Pelamis platurus) with
almost comparable venom toxicity, 0.09 mg/kg of mice IV, the available quantity of dry
matter of venom is a mere 0.25 mg and bites from this snake are usually described as benign
(White, 1995).
The basic venom components comprise neurotoxins and myotoxins of variable mutual
proportion. As for playing a part in suspected muscular paralyses, myotoxic muscle affliction
is probably responsible, while for certain members of the group, for instance, the Stokes
seasnake (Astrotia stokesi) and the yellow sea snake (Hydrophis spiralis), the venoms have
neurotoxic effects without any clinical evidence of myotoxicity.
In nearly all cases, neurotoxins of the aquatic Hydrophiinae snakes are those with
postsynaptic effects of type bound to -subunits of nicotine cholinergic receptors of
neuromuscular end-plates, which predominantly come from the small-molecule neurotoxin
group. Exceptionally, the venom may contain neurotoxins with presynaptic effects as well,
such as PLA2 isolated from the venom of Laticauda semifasciata.
Myotoxins are mainly members of the PLA2-type enzyme group. In general, they form
hyaline necrosis in striated muscles. They attack fibrils in diverse muscles and at varied
intensity, with several per cent of cells afflicted, even resulting in total destruction of muscle.
Local symptoms of envenoming: Bites from marine snakes are usually not painful,
although very rare cases of sharp pain (Hydrophis spiralis) or subsequent increased sensitivity
lasting several days (Pelamis platurus) have been described. The bite marks are difficult to
discern or are diminutive; however, small bites of other teeth - non-venomous ones - are
sometimes evident, including those based in the mandible. The brittle and mostly very tiny
fangs may be detained in the wound and covered by surface layers of the skin, so easily
missed. Following a snakebite, edema will not form, except in rare exceptions (P. platurus);
there is only some extent of lymphadenopathy with increased regional lymph nodes.
Occurrence of a livid area around the bitten site is possible.
Waterborne injuries with more distinctive local affection, such as easily discernable
stabs, edema, skin reactions, etc., are typically caused by other marine wildlife, either fish or
invertebrates.
Systemic symptoms of envenoming: Approximately 80% cases of bites from marine
snakes will either proceed without any symptoms of envenoming, or any affliction is only
minor. Of the remaining 20% of cases of more severe affliction, about 40% were fatalities
when untreated, but today the number of mortalities has almost dropped to zero owing to the
possibility of treatment by antivenoms (Reid, 1975).
Systemic symptoms of envenoming commence with sensations of being cold or frozen,
anxiety, languor and sleepiness, restlessness or euphoria, headaches, increased body
temperatures, clammy and sticky sweating, thirst, and reduced heartbeat. Classic envenoming
 Envenoming and Snakebite Treatment in Specific Snake Groups 155

prodromes may arise too, such as nausea, vomiting, abdominal pain, and convulsion.
Although frequent and described in this kind of state, the feelings of fear and anxiety may not
always indicate a systemic envenoming, but merely a general mental response to a snakebite.
Initial symptomatology can sometimes occur very quickly following an attack, primarily in a
serious envenoming, but a delay in onset of 2-4 hours is possible.
Neurotoxicity begins to manifest depending on the quantity and effectiveness of toxins,
extending from several minutes to a number of hours, the average being 0.5 to 3.5 hours. It
develops conventionally, with cranial nerves being the initial region afflicted, with following
ptosis, mydriasis with a poor response to light exposure, and external ophtalmophlegia with
diplopia or blurred vision. Subsequent vision disorders are indications of a highly severe
envenoming. The affection continues with dysarthria, dysphagia including discharge of saliva
difficult to control, inability to stick out the tongue, and a swallowing and cough disorder. A
risk of regurgitation of stomach content and its aspiration into the lungs arises. Spasticity of
certain groups of muscles, such as pseudotrismus of jaw muscles is presented; however, such
a state is more probably caused by myotoxins rather than by a neurotoxic affection. Limited
muscular paralysis is then transferred to the neck and back muscles disenabling the individual
from sitting; tendon reflexes are reduced or disappear. Disabled respiratory muscles pose a
fatal risk; clinically, this starts with accelerated shallow breathing and is followed by
respiratory failure with cyanosis, hypoxic syncope, and possible death. Naturally, pain in the
respiratory muscles damaged by rhabdomyolysis can be co-responsible for the affliction of
the muscles. Paralysis of limb muscles does not usually occur.
Myotoxicity will mostly start to manifest as feelings of muscle strain or stiffness within
30 mins to 4 hours. Myalgia arises following pain developing in muscles under passive
extension. In cases of severe envenoming, muscle pain becomes apparent within two hours
following a bite. In some cases, the signs of myolysis can be the first or even only symptom
of a systemic affliction. The effect on muscles is complemented by blocked transmission on
neuromuscular end plates, thus potentiating a functional disorder of striated muscles. The
fibrils will mostly regenerate 1-2 weeks following the damage a biopsy carried out 6
months afterwards showed only minor changes in the muscular structure (White, 1995).
Hyperkalemia and myoglobinuria are integral parts of the myolysis.
Hyperkalemia becomes manifest as changes in ECG in terms of a prominent T wave,
prolonged QRS-complex or occurrence of ventricular arrhythmia, or even circulatory failure
in severe envenomings.
Myolysis and myoglobinuria result in oliguria and renal failure, principally if hydration
and production of primary urine is insufficient. Necrosis of distal tubules was found in some
fatalities involving renal failure.
In late phases of envenoming, hypertension and increased sweating was observed.
Laboratory findings: In rather poor laboratory results, increased CC, AST, kalemia and
myoglobin values in the serum can be registered, aside from common neutrophilic
leukocytosis. Myoglobinuria appears within approximately 3 to 6 hours. Changes
accompanying hyperkalemia are evident from ECG - a prominent T wave, QRS-complex
extension, or ventricular arrhythmia. In case of renal failure, serum urea and creatinine levels
will increase and kalemia will rise. No signs of coagulopathy or hemolysis are evident from
the lab tests.
156 Jiri Valenta

Mortality: In an early phase, lethality in case of envenoming by marine snakes is caused

by respiratory failure, while in the late phase, death is caused by complications due to oliguric
renal failure.
The analysis of 101 treated snakebites in Malaysia during 1957-1964, as carried out by
Reid, found 8 fatal cases, with the common sea snake (Enhydrina schistosa) responsible for
seven of them. At a time before the advent of antivenom treatment and mechanical
ventilation, generally prior to 1961, presumed lethality in Malaysia was 10% of those
attacked (Reid, 1975). Lethality following a snakebite from the pelagic sea snake (Pelamis
platurus) has not been sufficiently evidenced, but is presumed according to tradition in
India, Costa Rica, Panama and Columbia.
Admitting the speculated incidence of 15,000-75,000 snakebites and the current mortality
of 1-5% of this number, an approximate prediction of annual global lethality is probably in
the region of 150-3,700 cases.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Immediate application of a pressure immobilization bandage based on
research by Sutherland is fully indicated. The bandage should not be removed before arrival
at a health facility capable of dealing with potentially serious symptoms of muscular
paralysis. If envenoming is proven, the bandage should not be removed before application of
antivenom or at least administration of neostigmine, see below.
Applicable antivenoms:

SEA SNAKE ANTIVENOM, Commonwealth Serum Laboratories, Victoria, Parkville,

Australia.
If the preparation above is not available, the antivenom against the venom of the
mainland tiger snake (Notechis scutatus) is applicable (Sutherland et al., 2000): TIGER
SNAKE ANTIVENOM, Commonwealth Serum Laboratories, Victoria, Parkville, Australia.

Administration of antivenom is indicated whenever neurotoxic symptoms, clinical or

laboratory signs of myolysis occur. The quantity of the antivenom is determined by the level
of seriousness of envenoming, i.e. the severity of symptoms and the speed of their onset, with
approximate requirement of 1 to 10 vials.
The rather indistinct and generally pain-free localized affection will not require any
special care. Any inflammatory complications are rare. Pre-emptive administration of
antibiotics is not indicated.
As for the critical proportion of neurotoxins with postsynaptic effects, application of
acetylcholinesterase inhibiting neostigmine has proven useful in clinical manifestations of
neurotoxicity, especially when no antivenom is available; dosage: 0.5-1.0 mg IV (10-15
g/kg), with premedication of 0.5 mg of atropine IV. To eliminate neurotoxins, hemodialysis
can also be employed due to the small size of the molecules. Symptomatic treatment should
prevent any potential complications associated with possible muscular paralysis, such as
aspiration of stomach content and respiratory failure, by airway management using tracheal
intubation and subsequent mechanical ventilation.
Adequate hydration of the affected person is important when rhabdomyolysis is in
progress. Increasing the supply of liquids, ideally in the form of crystalloid infusion, will
provide for production of sufficient quantity of primary urine, thereby diluting the volume of
myoglobin, hence generating a pre-emptive effect on possible renal failure. Alkalinization of
 Envenoming and Snakebite Treatment in Specific Snake Groups 157

urine is likely to have a preventive effect as well. In cases of more serious myolysis, which is
indicated by a sharp increase in CC and myoglobinuria, ECG and kalemia monitoring is
essential. Efforts to control developing oliguria in a conservative manner are possible by
means of diuretics. Hyperkalemia, just like the previously formed oliguria, must be solved
through hemodialysis or hemofiltration.
Observation of those concerned for a least period of 24 hours is necessary in every case.
This is true despite the probability of systemic envenoming being minimal if there are no
symptoms of envenoming, including laboratory results, within 4 hours after a snakebite.
The patient can be discharged following systemic envenoming for home treatment after
24 hours once all systemic symptoms recede.

REFERENCES
AMARASEKERA, N., JAYAWARDENA, A., ARIYARATNAM, A., et al. Bite of sea snake
(Hydrophis spiralis): a case report from Sri Lanka. J Trop Med Hyg, 1994, 97, pp. 195
198.
FULDE, GW., SMITH, F. Sea snake envenomation at Bondi. Med J Aust, 1984, 141, No. 1,
pp. 4445.
WHITE, J. Clinical toxicology of sea snakebites. In MEIER, J., WHITE, J. (Eds), Handbook
of clinical toxicology of animal venoms and poisons. Boca Raton : CRC Press, 1995, pp.
159170.
REID, HA. Antivenom in sea-snake bit poisoning. Lancet, 1975, 1, No. 7907, pp. 622623.
REID, HA. Epidemiology and clinical aspects of the sea snake bites. In DUNSON, W.A.
(Ed.), The biology of the sea snakes. Baltimore : University Park Press, 1975, pp. 417
462.
REID, HA. Epidemiology of sea-snake bites. J Trop Med Hyg, 1975, 78, No. 5, pp. 106113.
SUTHERLAND, SK., NOLCH, G. Dangerous Australian animals. Flemington : Hyland
House Publishing, 2000, 201 pp.
RUAL, F. Les envenomations marines: Lexample de la Nouvelle-Caledonie. Medicine
Tropicale, 1999, 59, No. 3, pp. 287297.
SOLRZANO, A. A case of human bite by the Pelagic Sea Snake, Pelamis platurus
(Serpentes: Hydrophiidae). Rev. Biol. Trop, 1995, 43, No. 13, pp. 321322.
STCKLIN, R., CRETTON, G. The ultimate database on venomous animals, snakes. CD-
rom, Geneva : Atheris Laboratories, 1998.

6.4. FAMILY: VIPERIDAE, VIPERIDS

The viperid family (Viperidae) forms a relatively extensive group of venomous snakes
this classification now covers in excess of 30 genera, numbering over 220 species. It can be
subdivided into three subfamilies, with Causinae snakes discerned by some as a separate
entity. One of the subfamilies - Crotalinae snakes - was earlier classified as another family.
Viperidae snakes as a whole possess perfect venom apparatus - large erectile fangs with a
fully closed channel, and muscles capable of regulating the discharge of venom
158 Jiri Valenta

(Solenoglypha); see chapter 1. 4 Venom apparatus of snakes. Their body is mostly thickset
and rather short, whilst the triangular head is wide. The Crotalinae subfamily has one more
sensitive sensory organ - a pair of heat-sensing pits. In some crotaline snakes, like Crotalus
and Sistrurus, the tail includes a feature called a rattle; see chapter 1. 3 Snake morphology.
Viperid snakes (Viperidae) inhabit all continents except for Australia and, of course, the
Antarctic. Highly adaptive in terms of evolution, members of this group make up the
northern-most (the European viper, Vipera berus) and southern-most (the Patagonia
lancehead, Bothrops ammodytoides) venomous snakes in existence. In addition, they also
dwell at the highest elevation of all venomous snakes (the Himalayan pit viper, Gloydius
himalayanus). Snakes of some genera are much sought after by hobbyists as pets, such as
Crotalus snakes, nose-horned vipers (Vipera ammodytes), Asian pit vipers (Trimeresurus
spp.), and others.
The venoms of Viperidae snakes primarily contain enzymatic components with locally
destructive effects; in addition, they mostly attack vascular and hemocoagulation systems.
Neurotoxic components in viper venoms, if at all present, possess an enzymatic structure and
are mostly insignificant clinically.

6.4.1. Subfamily: Azemiopinae

Genera and species: This is a monotypic subfamily with a single genus, Azemiops, and a
single species, the Feas viper (Azemiops feae).
Other names: Vipre de Feae (FR).
Description: The Feas viper is an extremely rare and attractively looking snake up to 90
cm long. It rather resembles a colubrid or elapid. Coloring varies from dark blue to black,
with light - mostly yellowish - thin rings, and an orange head.
Home range and habitat: They reside in humid mountainous and sub-mountainous
forests in S China, Tibet, N Burma, and N Vietnam.
Toxins: The venom is relatively potent; LD50 in mice IV is 0.52 mg/kg (Warrell, 1995).
Activities correspond to the toxin composition in viperid snakes except for the absence of
procoagulative, anticoagulative, and myolytic enzymes.
Local symptoms of envenoming: Only a few cases of envenoming have been described.
At a local level, a snakebite will only manifest with pain and edema.
Systemic symptoms of envenoming: No systemic signs of envenoming are known. In
more severe cases, hypotension is possible with potential manifestation of vegetative
dystonia.
Laboratory findings: Not known; leukocytosis is possible.
Mortality: Mortality is neither described nor expected.
Therapy: Symptomatic treatment; antivenom is not available.

6.4.2 Subfamily: Viperinae

The Viperinae subfamily recently has been defined as covering approximately 13 genera
of some 65 species.
 Envenoming and Snakebite Treatment in Specific Snake Groups 159

The anatomy of viperine snakes is similar to that of most viperids (Viperidae); in

addition, they resemble the rest of the family in many ways. They have a thickset body,
largely with a broad distinctive head. Many of them feature dorsal serpentine or intermittent
patterns made of blurred spots. According to the structure and function of their venom
apparatus, featuring large erectile fangs embedded in maxilla, they may be ranked among
solenoglyphous snakes; see chapter 1. 4 Venom apparatus of snakes. With some exceptions,
they are surface foragers. The venom composition roughly corresponds to that of other
viperids - there is a significant proportion of enzymes that sometimes have important
destructive potency towards tissues, and in many cases also components afflicting
hemocoagulation and the vascular system. Although sometimes clinically evident, potential
neurotoxins form a less important component; they are always of an enzymatic nature with
presynaptic effects.
The members of the Viperinae subfamily inhabit a predominant part of European and
African regions and most of Asia. In the field of epidemiology of snake envenomings, they
play a major role across Africa, Europe, and certain Asian regions.

6.4.2.1. Adenorhinosa and Atheris Genera

Species: The Uzungwe mountain bush viper (Adenorhinos barbouri) is the only member
of the Adenorhinos genus; in addition, it has been recently reclassified under the Atheris
genus as Atheris barbouri. The bush viper genus (Atheris) contains 10 species with the rough-
scaled bush viper (Atheris squamiger) and the Great Lakes bush viper (Atheris nitschei) being
probably the best known representatives; for other members, see chapter 7 List of venomous
snakes. Two of the species above are now mostly classified as separate monotypic genera,
Montatheris and Proatheris, with the Kenya mountain viper (Montatheris hindi) and lowland
swamp viper (Proatheris superciliaris), respectively, being the only species.
Other names: FR: Vipre arboricole.
Description: The Atheris snakes are relatively slender viperines; they can grow up to 50-
75 cm, but only 40 cm in case of A. barbouri. The body color is typically in hues of brown,
olive or gray, through to gray/black, which is often combined with a light or yellowish pattern
(A. nitschei). Head and neck scales can in some species stick out and form small horns or
make the snake look hairy or spiny. The majority of these snakes possess a prehensile tail.
They are largely shrub or tree dwellers, ranging anywhere from ground level to the height of
about six meters; however, they can climb down and move along the surface as well. The rare
snakes of the Montatheris and Proatheris genus live only a terrestrial life. Mostly active at
dusk or at night, these snakes can hunt - or also bask - during the day in higher elevations
when lower temperatures allow.
Home range and habitat: Bush vipers dwell in shrub, reed, bamboo, and tree stands
including forests in diverse localities. Atheris snakes are predominantly found in Central-
western and Eastern Africa, with fragments of populations reaching Central Africa west of
Guinea-Bissau, to Kenya in the east and Malawi in the south. A. squamiger resides in SE
Nigeria up to NW Angola, Congo-Brazzaville as far as S Uganda, W Kenya, and Ghana. As
for the Adenorhinos bush vipers, S Tanzania is their home range.
Toxins: The venom of Atheris snakes is believed to be quite potent: LD50 for mice
amounts to 5 mg/kg SC. Among others, it contains components affecting the vascular system
in terms of vasodilation and endothelial damage, including hemorrhagic components and
160 Jiri Valenta

hemocoagulation-afflicting compounds, such as FBG-converting enzymes, an FV and Ca2+

dependant prothrombin activator, and enzymes that activate PLT aggregability, etc.
Local symptoms of envenoming: The bite can be very painful, with possible immediate
propagation as far as regional lymph nodes. The edema that generates at the bitten site is
typically rather localized and not very large, but is rarely quite sizeable. Petechiae, bruises or
even hemorrhagic blisters are formed, and regional lymphadenopathy occurs. Minor cases of
necrosis are likely to occur at the bitten site, as well as peripheral cyanosis probably caused
by tissue congestion and local hemorrhaging. The edema will, in most cases, disappear in two
days. Residual pain may persist for about a week to a month, even at the points of related
lymph nodes. A minor motional disorder at the bitten site can persist over a longer period.
Systemic symptoms of envenoming: All available clinical information on such
envenomings is rather limited and generally based on bites from Atheris squamiger. Recently,
two cases of envenoming by Proatheris superciliaris have been described (Valenta et al.
2008, Keyler 2008).
Early following the bite, envenoming is followed by nausea, vomiting, and diarrhea;
symptoms may be even more severe. Vertigo, vision disorders, shivering, fever, increased
sweating, hypertension, and pain when breathing occur. A bite from P. superciliaris has
caused renal function disorders with oliguric renal failure and thrombotic angiopathy.
Disorders of or reduced consciousness with respiratory difficulties can, very occasionally in
severe cases, result in the necessity for tracheal intubation and mechanical ventilation. Early
circulation collapse has also been described, as well as a serious hemocoagulation disorder
with hematemesis and a fatal course. Nevertheless, the majority of envenomings will be not
significant and should be of a benign type.
Laboratory findings: The blood count will reveal neutrophilic leukocytosis and
hemolysis. Hemocoagulation test records prolonged PT, APTT and TT, up to extreme levels;
FBG level is reduced, and FDP increased. AT activity - especially in early phases - is
typically not reduced; plasminogen concentration decreases with settlement within three days
have been described. Biochemical findings only reveal LD and CC level increases in serum of
minor significance, and proteinuria.
Mortality: Lethality of the snakebite is rare. A fatal case was described (Lanoie et
Branch, 1991) with production of massive edema, non-coagulable blood, hematemesis, and
death on day 5, under a hemorrhagic shock.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Limb immobilization and delicate local treatment is advisable with moderate
cooling and elevation if pain, edema, and congestion are present. Analgesics including opiates
and antiphlogistics, except ASA, can be administered in cases of profound pain; sedation is
also applicable.
No antivenom is available; Robinson et al. (2004) describe a positive effect from an
antivenom no longer available: NEAR MIDDLE EAST ANTIVENOM, Behringwerke,
Germany; with its range of effects including Cerastes, Echis, and Vipera snakes. Other
antivenom containing effects against the viperids mentioned above, especially those of the
Echis genus, may possess a certain level of effectiveness against the venoms of Adenorhinos
and Atheris snakes as well. To eliminate toxin components, plasmaferesis has been employed
too (Keyler 2008).
Any potential case of hypotension will require IV application of crystalloids or colloid
solutions. At the same time, an increased supply of liquids will work to prevent renal failure.
 Envenoming and Snakebite Treatment in Specific Snake Groups 161

The possible hemocoagulation disorder with hemorrhaging can be treated using an

administration of 10-20 ml of fresh frozen plasma per kg; application of AT if its activity is
reduced is advisable. For other treatment options in case of hemocoagulation disregulation,
see chapter 5. 3. 3. 6 Hemocoagulation disorders. Heparinization may prove useful, except for
the phase of bleeding: UFH, at a dosage of 70-200 units/kg (5,000-15,000 units/day per adult)
or a relevant pre-emptive dose of LMWH.
Most envenomings will take place without any more serious systemic symptoms and
abate the following day; in more severe cases, a normal status can be expected within a week.
The patient can be discharged for home treatment after 24 hours following abatement of
systemic symptoms and more serious laboratory symptomatology.

6.4.2.2. Bitis Genus, Puff Adders

Species: This snake genus contains approximately 14 species of African puff adders, with
the most significant representatives being the African puff adder (Bitis arietans), Gabon viper
(Bitis gabonica), and also the rhinoceros viper (Bitis nasicornis). For other members of this
genus, see chapter 7 List of venomous snakes.
Other names: FR: Vipre heurtande, Vipre hbraique (B. arietans); Vipre du Gabon (B.
gabonica). EN: Horned viper (B. nasicornis). Former names: Bitis lachesis (B. arietans).
Description: The lengths Bitis snakes grow to vary according to species, from 20 cm for
the Peringueyis adder (B. peringueyi) to 120-150 cm for the large and robust Gabon vipers
(B. gabonica), the record holder for the greatest documented length in viperids (205 cm). The
majority of these snakes are usually colored by a range of contrasting spots and stripes in
shades of brown, gray to silver, olive, green with lighter tints, and yellow to a creamy tone.
The Gabon viper (B. gabonica) is probably the snake with the most contrasting coloration,
which paradoxically presents a very effective way of mimicking leaves on the forest floor for
these snakes. Movements of the Bitis snakes, especially the robust and potent Gabon viper (B.
gabonica), is relatively slow, meaning an increased risk of unwanted contact with humans.
The Gabon viper is thought to be a calm and placid animal; allegedly, this snake tolerates
handling and is even termed a toy for Gabonese children. Nevertheless, the striking speed and
the record length of the fangs, a documented maximum being 5.5 cm, prompt a high level of
cautiousness when in contact with this spectacular snake. Sensing danger, the Gabon viper
will hiss loudly, puffing up its body. A subspecies, B. gabonica rhinoceros, alternatively now
designated a separate species, B. rhinoceros, features scales placed on the end of its snout that
elongate it into a distinctive horn. The rhinoceros viper (B. nasicornis) presents a similar, but
lesser member of the genus. The African puff adder (Bitis arietans) is probably Africas most
widespread dangerous venomous snake, and one reportedly with the greatest share of human
envenomings in Sub-Saharan Africa. This snake is apparently responsible for more bites and
fatalities in people and domestic cattle than all of the remaining African snakes together, the
reason for which might be the slow movement mentioned above. Snakebites from lesser
African Bitis vipers are not usually dangerous to adults. Other members of the genus are rare,
like the Angolan adder (Bitis heraldica) or still relatively unknown, e.g. the red adder (Bitis
rubida - Branch, 1997, the species discoverer).
Bitis vipers are largely nocturnal snakes; in colder periods of the year or in southern
regions, they like basking in the sun.
Home range and habitat: The African puff adder (B. arietans arietans) lives in the
savannahs of the Sub-Saharan region to S Africa, and the SW Arabian Peninsula,
162 Jiri Valenta

predominantly in the grassy sections of the bush. B. arietans somalica inhabits Somalia, SE
Ethiopia, and NE Kenya.
B. gabonica is found in woodland and forest localities in S Sudan, S Nigeria, Uganda,
Tanzania, Congo-Brazzaville, Gabon, Angola, central and S Zambia, E Zimbabwe,
Mozambique, and some of the western territory of the Republic of South Africa.
The rhinoceros viper (B. nasicornis) ranges in the woodland and primary forest habitats
in W Kenya, S Sudan, Rwanda, Burundi, S Uganda, the central part of Congo Brazzaville,
DRC, NW Angola, Gabon, Liberia, and S Guinea.
Toxins: Bitis snake venoms are far from the top of the list of effectiveness. LD100 of B.
arietans venom for SC administration in mice is 6 mg/kg, which is approximately thirty times
less than the effectiveness of toxins from sea snakes, taipans, or Indian cobras. Snakebite
incidence, morbidity, and mortality of envenoming vary subject to venom quantity, which in
B. arietans is theoretically sufficient to kill 4-5 persons, while in B. gabonica it can be up to 1
g of dry matter. In terms of their activities, the venoms of the African puff adders (Bitis)
predominantly affect the cardiovascular and hemocoagulation system; they also possess
hemorrhagic and destructive cytotoxic enzymes, such as proteinases, hyaluronidases,
hydrolases, phospholipases, etc.
The venom of B. arietans contains, amongst other commonly given enzymes, also
thrombolytic and fibrino(geno)lytic enzymes, bitistatin, a protein-like toxin inhibiting platelet
aggregation and prolonging hemocoagulation time, and kinin, which releases an enzyme
responsible for hypotension.
Compared to other species, B. gabonica features less effective venom, although a serious
envenoming can be still secured due to the quantity of venom in the venom apparatus of this
viper. The venom contains gabonase - an enzyme with a thrombin activity, and gabonine - an
anti-PLT peptide that inhibits PLT aggregation induced by collagen - plus thrombin, and
arachidon acid. The gabonase action brings about a DIC-like syndrome. The low FDP levels
mentioned by some papers are not typical for the process of the disorder and can be probably
caused by hindered immunodetection in partial cleavage of antigens by toxins. The activities
of toxins, hemorrhagins and the pathophysiological changes induced by these substances will
damage the capillary system with a clinical picture of pulmonary and GIT affection. The
venom lacks neurotoxins; however, it contains cardiotoxins responsible for arrhythmias and
myocardial contractility disorders with a reduced volume of heartbeat and heart output. In
addition, it reduces peripheral vascular resistance either locally, i.e. through the bradykinin
formations, or at a systemic level by its impact on vasomotoric centers. Furthermore, toxins
cause a metabolic alteration with reduced oxygen utilization, increased lactatemia, and
glycemia.
The venom composition of the rhinoceros viper (B. nasicornis) is very similar to that of
B. gabonica: it mainly contains cardiotoxins, hemocoagulation-affecting enzymes, and
proteinases damaging tissues. Local as well as systemic symptoms of envenoming correspond
to the symptomatology of envenoming by the B. gabonica venom, although they do not reach
its intensity due to venom quantity. The venoms components have an impact on activation of
hemocoagulation in both an internal and external manner; at the same time, they potentiate
the plasmin activity that is, however, inhibited when concentrations are larger. Similarly,
platelet adhesion, which is increased by a low toxin concentration, is inhibited by reduced
ADP-reactivity when toxin doses are higher.
 Envenoming and Snakebite Treatment in Specific Snake Groups 163

Local symptoms of envenoming: With regard to the size of fangs, marks of bites can be
evident at the bitten site as penetration by a single or two teeth, in rare cases also by three to
four teeth. Such duplicity can occur by the frequent presence of growing teeth behind the first
and functional fangs. Envenoming is also possible through merely a deep scratch by one or
two fangs. The bitten site is painful, lymphadenopathy occurs with enlarged regional lymph
nodes. The onset of edema production is relatively prompt; the edema is largely one of
hemorrhagic nature and can spread around the torso, irrespective of applying antivenom.
Even though its intensity will mostly not increase to the level required for compartment
syndrome to occur, edema of the carpal channel with depressed nervus medianus and
subsequent surgical release has been described (Wildi et al., 2001). Besides this, fasciotomy
has had to be carried out at the authors workplace due to a precipitous development of
compartment syndrome affecting a forearm. The presence of edema is typical in every
envenomed person, reaching a maximum within 1-2 days and persisting for 5 days up to 3
weeks. Blisters, petechiae, ecchymoses, and extensive bruises through to localized
hemorrhaging come up on the surface of the skin, with the subsequent spread of
erythrodermia around the body. Several cases feature necrosis that occurs following a few
days to a week; this can be superficial, but in some cases considerable and deep, with the
necessity for debridement and even amputation. Less frequently, thrombosis may take place
in the bloodstream of the affected region. Severe local reactions can follow in over a half of
bites.
Systemic symptoms of envenoming: Systemic symptoms of envenoming following a
snakebite from Bitis snakes, namely African puff adders (B. arietans), occur in less than half
of afflicted persons, including increased temperatures and fevers of over 40 oC, fatigue,
somnolence, nausea, vomiting, abdominal pain, and cold fevers with sweating. The symptoms
appear very early on, but in some cases may be delayed by a number of hours after a bite;
they will persist for a relatively long time - up to 8 days following an attack.
Affliction of the cardiovascular system will manifest itself via vasodilation, myocardial
depression with bradycardia or tachycardia, and may even result into circulation collapse and
shock. In case of envenoming by the Gabon viper (B. gabonica), which contains effective
cardiotoxins, cases of circulatory failure crop up soon after a bite and resulting in possible
unconsciousness. The effect of the cardiotoxins will be visible as tachycardia, severe
hypotension, prolonged QT-interval, T wave inversion and potential cardiac arrest.
Arrhythmias can persist for several days.
Coagulopathy, largely with clinical signs of increased hemorrhaging, is a serious aspect
of the systemic envenoming process. Perfusion of the tissue at and around the bitten site is
possible. If the progress of the hemostatic disorder is more severe, it is accompanied by
epistaxis, bleeding from mucous membranes, gastrointestinal, chest and pelvis hemorrhaging,
as well as hematuria. Even though certain signs indicate that coagulopathy will probably not
always be that resembling DIC (low FDP), there is endothelial damage, probably also directly
caused by toxins, with a clinical picture of extravasation from affected capillaries. The non-
DIC-coagulopathy does not preclude any future conversion into DIC via the commencement
of relevant pathophysiological mechanisms. Symptoms of microangiopathic hemolytic
anemia can be present. Endothelial and capillary damage as such is accompanied by a risk of
liquids and proteins being released into the pulmonary interstitium and subsequently
producing a shock to the lungs in the form of respiratory failure.
164 Jiri Valenta

A selective bond of the venom in the kidney associated with hematuria, hemoglobinuria,
or myoglobinuria make some patients predisposed to renal failure. Hepatorenal failure is also
known to occur.
Symptomatology may include a vague metabolic alteration with limited oxygen
utilization, increased glycemia, and high lactatemia.
Laboratory findings: The existence of neutrophilic leukocytosis presents a non-specific
test result. Hemocoagulation disorder is manifest via prolonged PT, APTT, and TT,
thrombocytopenia and decreased FBG. Increased levels of FDP are possible, including D-dim
in some cases, but normal FDP levels found are specified as well: 1.25-10 mg/l with standard
values from 10 to 40 mg/l (Warrell et al, 1975). Decreased AT, PC, FV, and FVIII activities
have also been determined. The presence of poikilocytes and schistocytes indicating
microangiopathic hemolysis is possible. Naturally, hemorrhaging is accompanied by
decreased Hb and Hct.
Biochemical lab tests typically show increased levels of bilirubin, AST, ALT, and LD.
Hyperglycemia and hyperlactatemia are determined - up to 8.9 mmol/l. Erythrocytes,
hemoglobin and myoglobin are found in urine.
Mortality: The mortality of snakebites from the African puff adder (B. arietans) is high,
equaling 2 out of every 10 envenomed persons, even if antivenom is applied. Death can occur
relatively early after a bite, with symptoms of circulatory failure or profound hemorrhaging.
In the late phase of the diseases, an envenomed person can die from the consequences of
gangrene, sepsis, and septic shock, i.e. multiple organ failure.
In case of the Gabon viper (B. gabonica), the mortality of any higher epidemiological
significance following a snakebite is rather unexpected due to the low incidence of attacks by
this snake. Nevertheless, any potential fatal envenoming after a successfully completed bite
by this species will not differ in terms of mortality of snakebite to that of B. arietans.
Fatalities due to any other member of the Bitis genus are not known, but cannot be ruled
out.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Limb immobilization and delicate local treatment is advisable, with moderate
cooling and elevation in case of pain, edema, and congestion. Analgesics including opiates
and antiphlogistics, except ASA, can be administered in case of intensive pain; sedation is
also applicable.
If a proven envenoming is manifested, such as by hemorrhaging, thrombocytopenia,
hypotension, bradycardia or other systemic symptoms, as well as edema enveloping over a
half of a limb, or should severe local changes take place, administration of antivenom is fully
indicated.
Applicable antivenoms:

* SAIMR POLYVALENT SNAKE ANTIVENOM, South African Institute for Medical

Research, the Republic of South Africa (Bitis arietans, Bitis gabonica, and others);
* ANTIREPT PASTEUR, Aventis Pasteur, France (Bitis lachesis-arietans, etc.);
* FAV-AFRIQUE, Aventis Pasteur, France (Bitis arietans, Bitis gabonica, etc.);
* FAVIREPT, Aventis Pasteur, France (Bitis arietans, etc.);
* SERUM ANTIVENIMEUX BITIS ECHIS NAJA PASTEUR, Pasteur Merieux, France
(Bitis gabonica, Bitis lachesis-arietans).
 Envenoming and Snakebite Treatment in Specific Snake Groups 165

In certain cases, if symptoms of envenoming persist, a higher number of vials must be

administered - up to 15. If applied early, immunotherapy may even reduce the development of
necrosis.
In local treatment, the necessity to delicately handle damaged tissue, which is often
perfused and tends to produce necrosis, is emphasized. When treating the affected parts with
bullae and necrosis, surface removal and early necrectomy is advisable; in rarer cases - if
gangrene sets in - amputation may be necessary.
Symptomatic treatment is subject to the status of the patient; circulation can be
maintained by increasing intravasal volume and applying catecholamines, or -
sympathomimetics and -sympathomimetics. In addition, boosting the supply of liquids will
be essential for satisfactory diuresis to be retained. Any onset of arrhythmia, especially when
persisting, must be solved symptomatically, which in extreme cases can even conducted by
temporary cardiostimulation.
In cases of hemorrhaging, recommendations include the application of fresh frozen
plasma, in a quantity from 10 to 20 ml/kg, or possibly AT if its activity has significantly
reduced. For further information, see chapter 5. 3. 3. 6 Hemocoagulation disorders. If
hemorrhaging continues due to increased fibrinolysis and any responsibility of DIC
symptomatology has been ruled out, antifibrinolytics can be applied. Miniheparinizing the
patient with a dose of 70-200 units UFH/kg/24 hours or an applicable pre-emptive dose of
LMWH is advisable when bleeding has been paused. Applying leeches (Lavonas et
Tomaszewski, 2002) is an intriguing form of therapy.
Respiratory insufficiency may even be a prompt for supportive mechanical ventilation;
renal failure will require the use of extra-corporeal methods of elimination.
The preventive use of antibiotics is not indicated, but essential in case of development of
inflammation from any bacteria found; this should even cover any potential anaerobic
infection.
The patient can be discharged for home treatment after 24 hours following abatement of
all systemic symptoms and normalization of significant laboratory findings; minor local
afflictions can be solved via outpatient treatment. Any persisting laboratory indications of
moderate prothrombotic activity should be managed by pre-emptive miniheparinization, see
chapter 5.4 Convalescence following envenoming.

6.4.2.3. Causus Genus, Night Adders

Species: Sometimes placed into a separate subfamily, Causinae, this genus consists of six
species including the night adder (Causus defilippi), green night adder (Causus resimus),
common night adder (Causus rhombeatus), etc.; see chapter 7. List of venomous snakes.
Other names: FR: Vipere nokturne.
Description: Night adders are relatively slender snakes that grow up to approximately 60-
70 cm. Their body is dorsally colored in shades of brown, gray, or green. They possess a large
venom gland, and can inject an enormous quantity of venom when striking successfully. They
are rather aggressive snakes; when attacking, they possess the ability to extend their necks
like cobras do, but do not lift the anterior part of their bodies. They are largely active at night,
which is also when the majority of bites occur.
Home range and habitat: Night adders inhabit rather humid as well as dry grassy parts of
bush or forests and environments around of rivers, wetlands, and fields. They usually stay on
166 Jiri Valenta

the ground, but sometimes are found in shrubs as well. Their home range involves E, SE,
Central, and W Africa to the south of the Sahara.
Toxins: The venom of night adders contains a number of predominantly enzymatic toxins
typical for viperid snakes, with hemocoagulation-afflicting compounds, numbering amongst
them procoagulative and anticoagulative enzymes which are probably the most significant
substances. In addition, the venom of C. rhombeatus possesses CR-serpinase, an enzyme that
can inactivate AT. The venom neither possesses its own thrombin-like activity nor induces
FBG. Furthermore, it contains a number of enzymes (proteinases, hyaluronidases, hydrolases,
and phospholipases) with principally less serious cytotoxic activities clinically.
Local symptoms of envenoming: Locally, envenoming by a night adder (Causus) becomes
manifest via pain, edema - mostly slight or medium, and lymphadenopathy with painful
enlargement of lymph nodes in the related area in some cases. Minor hemorrhaging from the
afflicted site is possible; necrosis is not formed.
Systemic symptoms of envenoming: Any systemic symptoms are mostly likely limited to
increased temperature. Signs of languor, somnolence, and the occurrence of hypotension with
tachycardia are less common. Cases of light hematuria settled spontaneously have been
described.
Laboratory findings: There is only minor neutrophilic leukocytosis shown;
hemocoagulation and biochemical values do not show any changes.
Mortality: Fatalities are not known.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention.
Limb immobilization and delicate local treatment is advisable, with moderate cooling and
elevation in case of any pain, edema, and congestion present.
No antivenom is available; a certain probability of cross-reactivity with some African
polyvalent antivenoms exists, although administration is not indicated. Symptoms of
envenoming will abate spontaneously.
Should systemic symptoms exist, symptomatic treatment is applied.
An increased supply of liquids to protect against renal perfusion is advisable for potential
hypotension in cases of severe envenoming, especially when hematuria occur at the same
time.
The patient can be discharged for home treatment after 24 hours once all systemic
symptoms recede.

6.4.2.4. Cerastes Genus, Desert Horned Vipers

Species: The Cerastes snake genus consists of three species, with the desert horned viper
(Cerastes cerastes) being the one best-known, plus the Arabian horned viper (Cerastes
gasperettii) and Sahara horned viper (Cerastes vipera).
Other names: EN: Sahara, African, Egyptian, desert, sand horned viper; FR: Vipre
cornue (C. cerastes). EN: Sahara hornless, common sand, Avicennas, Cleopatra, lesser
cerastes viper; FR: Vipre dAvicena (C. vipera).
Description: Cerastes vipers do not exceed 70 cm in length. Their color is a gray/brown
and tones of gray. The head is broad, with the desert horned and Arabian vipers boasting
horn-like projections above their eyes. They like hiding in the sand with only the head
protruding above the surface. When hidden, the snakes let humans pass by in close proximity.
However, should a person stop, the viper will escape fearing it has been discovered, thereby
 Envenoming and Snakebite Treatment in Specific Snake Groups 167

becoming of interest to the intruder. Sidewinders, they leave typical traces of their side
movements on loose sand. They are predominantly nocturnal snakes. Cerastes snakes are
much sought after by snake keepers, so bites from horned vipers are nothing rare.
Home range and habitat: These snakes typically reside in sandy and rocky regions of
Saharan Africa, from SE Morocco as far as Egypt, and the central parts of Mali, Niger, Chad,
and Somalia to the south. The home ranges of the desert horned viper (C. cerastes) and the
Arabian horned viper (C. gasperetti) extend across Israel and the Arabian Peninsula as far as
SW Iran.
Toxins: The venom of Cerastes snakes largely contains enzymatic compounds of
proteolytic activity that impact on the hemocoagulation system. The components of the
venom destroy, amongst other things, FBG molecules - afaacytin, cerastes F-4; they have
thrombin-like properties - cerastocytin - and activate FX and PLT aggregability. The results
of venom effects typically include localized destruction and a DIC-like hemocoagulation
disorder.
Local symptoms of envenoming: Local symptoms of envenoming are mostly limited to
formation of painful medium-sized, potentially hemorrhagic edema with lymphadenopathy
and swollen lymph nodes in the related area. The bite wounds often display slight
hemorrhaging. Petechiae and ecchymoses appear on the skin, with less frequent hemorrhagic
vesicles and minor areas of necrosis. In rare cases, serious affliction of deeper tissues and
muscles is possible with permanent deformities and persisting motional disorders, for
example, if fine structures of the arm are hit.
Systemic symptoms of envenoming: Envenoming by the Cerastes viper genus is typically
not serious, hence the bibliography does not provide very numerous records. Systemic
symptoms are largely not very distinctive or only manifest as minor discomfort, increased
temperature, nausea, or vertigo and vomiting. Nonetheless, this will not eliminate any effect
of procoagulative, anticoagulative, or platelet-aggregating venom components, which may be
clinically evidenced by hemorrhaging or the tendency for (micro)thrombi to develop,
predominantly on the bitten limb. Coagulation disorder typically resembles that of DIC;
clinically, mostly minor bleeding from stab and bite wounds is present. Cases of five-day
successful therapy of the DIC syndrome in a 3-year-old child and 18-year-old woman without
using an antivenom are described, as well as tachycardia, hypertension, and urine retention in
2-year-old and 4-year old children. Serious or fatal courses of envenoming are rare. However,
shock status with symptoms of pulmonary affliction and reversible oliguric renal failure with
necessary hemodialysis has been described from the authors workplace.
In the Czech Republic, 9 cases of bites from the desert horned viper (C. cerastes) have
been reported in the past 6 years, from which not one envenoming took place, in four cases
only a local response occurred, and there were four cases of systemic envenoming, with two
of them following a more intensive course: one of patients underwent shock status with
incipient respiratory insufficiency, while in the other, symptoms of DIC and hemolysis
occurred with subcapsular renal hematom, pancreatitis and oliguric renal failure, with
hemodialysis required. A relatively serious edema of the arm was complicated by phlegm.
Convalescence was approximately achieved within two months.
Laboratory findings: Hemocoagulation values show prolonged PT, APTT and TT; the
values of which are impossible to measure at the stage of developed envenoming. The FBG
level decreases, while that of FDP, including D-dim, goes up. The level of thrombocytopenia
168 Jiri Valenta

may not correspond to the significance of the consumption, as well as the potentially declined
AT activity. More grievous hemorrhaging is accompanied by reduced Hb and Hct.
Mortality: No fatalities are known, but still possible because of the nature of the venom,
especially in children and in case of insufficient treatment.
Therapy: Although in most instances of bites there is only a localized envenoming or a
low-level systemic response, giving first aid to the fullest possible extent is advisable, and
general rules of treatment apply; see chapter 5 Snakebite: Therapy and prevention.
Applying antivenom is indicated where a more significant systemic response occurs or if
a patients status is deteriorating, although this is only visible in laboratory results.
Applicable antivenoms:

* ANTIREPT PASTEUR, Aventis Pasteur, France (Cerastes cerastes, Cerastes vipera,

and other snakes);
* FAVIREPT, Aventis Pasteur, France (Cerastes cerastes, and others);
* POLYVALENT SNAKE ANTIVENOM, Saud Arabia (Cerastes, etc.).

Antivenom is also applicable if a significant local affliction is found, although neither

improvement of the affected tissue nor mitigation of the necrosis formed can be expected with
certainty.
The affected limb should be elevated, immobilized and moderately cooled;
administration of analgesics is advisable. If hemorrhagic bullae occur, their surface should be
removed and the bed treated; in rather rare cases of necrosis, early necrectomy is indicated.
If a DIC-like hemocoagulation disorder is found, administration of fresh frozen plasma is
applicable; the dosage being 10-20 ml/kg. For following steps of treatment based on the
significance of the symptomatology, see chapter 5. 3. 3. 6 Hemocoagulation disorders. If the
patient is not bleeding and an examination shows signs of increased thrombin activity and
consumption - a significant increase in D-dim - miniheparinization by pre-emptive doses of
UFH (Unfractionated Heparin) or LMWH is advisable.
The need for a sufficient supply of liquids to protect renal function applies. Any decrease
in systemic pressure will be firstly corrected by supplying liquids; catecholamines can be
applied only if this fails or critical hypotension occurs. Any other potential complications
should be solved according to symptomatology.
Discharge of the patient is possible after 24 hours following abatement of all clinical
symptoms and more significant laboratory abnormities. Any persisting laboratory
symptomatology of rather moderate prothrombotic activity should be managed by pre-
emptive miniheparinization, see chapter 5.4 Convalescence following envenoming.

6.4.2.5. Daboia Genus

Species: Daboia presents a monotypic genus consisting of the Russels viper (Daboia
russelli; formerly: Vipera russelli). This single species is subdivided into subspecies: Daboia
russelli russelli, formerly called the pulchella or nordicus subspecies, or also the western
form, and Daboia russelli siamensis, former also the formosensis, limitis or sublimitis
subspecies, or also the eastern form.
Other names: EN: Taiwan Russells viper; FR: Vipre de Russell; native names: Daboia,
Tic-Polonga.
 Envenoming and Snakebite Treatment in Specific Snake Groups 169

Description: The Russels viper (D. russelli) is a large and thickset snake achieving a
length of over 100 cm, with the greatest recorded length being 185 cm. Coloring is in the
form of brownish or brown/gray shades with three rows of oval spots featuring a dark or light
lining arranged lengthwise.
Daboia, as this animal is also called, is the snake with the highest epidemiological
significance in its home range of Sri Lanka, with the incidence of 400 bites per 100,000
residents a year and a high mortality rate, see below. Victims include 93% of farmers - rice
growers.
Home range and habitat: This viper can be found in almost any habitat except dense
forests, often in paddy fields. D. russelli russelli ranges in Pakistan, India, Bangladesh, and
Sri Lanka, and the home range for D. russelli siamensis is S China, Central and S Burma,
Central Thailand, Taiwan, and a part of Indonesia - E Java, and the islands of Komodo,
Flores, and Lomblen.
Toxins: The quantity of effective venom the Russels viper (D. russelli) can produce is
quite high, approximately up to 200 mg of dry matter. Naturally, the rule that not every bite
could cause an envenoming applies in this case, as with other snakes: 28% of the envenomed
were free of any clinical symptoms within one of the studies (Myint-Lwin et al., 1985). The
venom includes enzymes with a procoagulative action, e.g. activation of FV, FIX, and FX,
and those possessing a direct fibrino(geno)lytic activity, etc. The occurrence of DIC-like
coagulopathy results in a severe disorder of coagulum production with hemorrhaging and
endothelial damage. The venom of D. russelli siamensis possesses presynaptic neurotoxicity
as well, probably caused by PLA2 which cannot be controlled by anticholinesterase. In
addition, PLA2-like enzymes are responsible for myonecrosis to develop. Myoglobin,
microthrombi in glomerular capillary beds, and the likelihood of toxins with a direct action on
renal tubules cause renal damage including following tubular necrosis.
Local symptoms of envenoming: Pain is the initial sign of a snakebite, with subsequent
edema. The bite wounds may bleed. The pain present in the majority of those afflicted will
increase over time, and the sore edema spreads to related lymph nodes, and even to the torso
within hours. Regional lymph nodes become enlarged. The strain and pain in the limb will
mostly persist for 1-4 days. Petechiae, ecchymoses, and hemorrhagic blisters, and more
rarely, in some 2-9% of cases, necrosis are formed on the skin in the area of envenoming.
Local hemorrhaging occurs in about 30% of cases. Even though the severity of systemic
symptoms of envenoming will be largely equal to the extent of the edema, some patients with
systemic envenoming, about 6%, may exhibit merely minor local afflictions.
A higher proportion of afflicted persons, 14% - 77%, feature muscle pain caused by
myonecrosis that can be discerned as either local pain upon palpation, or even pain at a
systemic level that can persist for approximately 5-7 days regardless of early administration
of venom.
Systemic symptoms of envenoming: As with the majority of vipers, prodromal symptoms
of envenoming are displayed in form of nausea, vomiting, epigastric, and hypogastric pain,
diarrhea, or possibly the onset of angioneurotic edema. Hypotension with tachycardia and
circulation collapse in the early phase indicates a serious envenoming. In the late phase,
hypertension, probably due to renal damage, is possible to register.
The most typical symptom of envenoming by the venom of Daboia russelli is a DIC-like
hemocoagulation disorder in some 80% of the patients; in nearly a half of those envenomed
this will manifest with spontaneous hemorrhaging, while some will exhibit thrombocytopenia
170 Jiri Valenta

and signs of increased capillary permeability. Typical clinical symptoms are hematuria,
hemorrhaging from mucous membranes and gastrointestinal hemorrhaging, including
hematemesis and enterorrhage, as well as hemorrhaging into lungs, airways, from small
wounds, and nose and subconjunctival hemorrhaging. Damage to the capillary endothelium
will be displayed as facial edema - even after 12-50 hours, i.e. conjunctival chemosis; more
rarely, fluidothorax and ascites are formed. Coagulopathy and related symptomatology will
peak on days 1-3 and persist for about a week.
The procoagulative activity of toxins responsible for profound coagulopathy, at least to
some extent, will be co-responsible for another symptom of envenoming and cause for
mortality - renal failure. The causes for acute renal failure that can be present in nearly a half
of afflicted persons involve formation of fibrin deposits and microthrombi in the renal
capillary beds, a direct action of toxin on the renal tissue and myoglobinuria which will arise
based on necrosis of muscles. The renal perfusion disorder is boosted by hypotension due to
vasodilation, extravasation of liquids, and hypovolemia in instances of hemorrhaging. In
nearly 10% of patients, this results in tubular necrosis with persisting oliguria. Renal failure
occurs suddenly; in most of the patients, it is preceded and accompanied by a painful
palpation in the lumbar region. This type of failure presents a significant prodromal symptom
that can be utilized as an invaluable indication of future failure.
Further symptomatology of envenoming is based on presynaptic neurotoxicity.
Conduction in motoric nerves will slow down; nevertheless, the intensity of damage will not
increase to the level of paralysis of respiratory muscles. Clinically, this is manifest through
overall weakness, bilateral ptosis, external ophtalmoplegia, double or blurred vision,
dysphagia, dysarthria, and difficulties in opening the mouth. The onset of neurotoxicity that
presents a predominant and distinctive feature of Daboia russelli russelli venom, apparent in
nearly 80% of those affected, can be sometimes set in early - within an hour - but can occur
later, even 48 hours after the envenoming.
Pain, increased sensitivity, and strain in muscles all over the body are caused by
myonecrosis at a systemic level. This is typically assigned to the action of neuromyotoxic
PLA2 enzymes. Both neurological and myotoxic symptomatology will abate in about 5-7
days.
In some cases of systemic envenoming, cardiac damage with changes found in ECG lab
tests can be also registered.
Severe envenoming after a snakebite from the Russels viper is defined by the presence
of at least one afflicted system, be it the nerve system - ptosis, ophtalmoplegia, dysphagia,
etc.; circulation - hypotension, tachycardia, circulation collapse; hemocoagulation -
hemorrhaging and extravasation; or the kidneys - renal failure, tubular necrosis; in addition, a
consciousness disorder is also possible as part of a severe envenoming.
Laboratory findings: 70% - 90% of envenomings bring leukocytosis with a prevalence of
polymorphonuclear leukocytes, which can be further escalated due to a response following
administration of antivenom.
Hemocoagulation tests routinely reveal prolonged PT, APTT a TT and
hypofibrinogenemia; plus thrombocytopenia in a lesser number of cases. Reduced levels of
FV, FX, and APC found will also relate to the consumption disorder. High levels of FDP
including D-dim indicate, besides reduced levels of plasminogen and 2-antiplasmin, to
escalation of fibrinolysis. Increased levels of vWF are probably based on activation of the
hemocoagulation system.
 Envenoming and Snakebite Treatment in Specific Snake Groups 171

In the plasma, free hemoglobin and myoglobin can be discerned as an effect of hemolysis
and rhabdomyolysis. CC may be elevated only marginally. A reduced level of Hb and Hct is a
consequence of hemorrhaging or hemolysis; decreased albumin values correspond to
increased capillary permeability and proteinuria.
Proteinuria, myoglobinuria, hemoglobinuria, extending to hematuria, may be found in
urine; cylinders of erythrocytes and fibrin deposits can also be present.
In about a half of the concerned, myofibril separation and edema-borne fragmentation,
dilated capillaries, myonecrosis, and mononuclear infiltration can be documented by
histological laboratory tests.
Mortality: Mortality following a snakebite from the Russels viper (Daboia russelli) is
among the highest in terms of both epidemiology and percentage of deaths of those
envenomed. According to diverse resources and types of evaluation, mortality ranges from
1.25% to 8% of those attacked and can achieve 19% - 24% of those envenomed.
In Burma, mortality in 1930 exceeded 2,000 cases, which equals to 15.4 per 100,000
inhabitants, while in the 1980s it was over 1,000 persons, i.e. 3.3 fatal cases per 100,000
inhabitants; in Sri Lanka, mortality accounts for 5 cases per 100,000 inhabitants, which is
1.25% of all envenomed.
In almost every person who died there was oliguric renal failure with symptoms of or
estimated acute tubular necrosis. In some cases, the status was complicated by hypotension,
gastrointestinal hemorrhaging, lung and pleural cavities, subendocardial hemorrhaging, and
cerebral hemorrhaging. Death occurred within 15 hours to 7 days, with 2.5 hours in case of a
4-year child being an extreme figure.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Limb immobilization and gentle local treatment can be recommended, with
mild cooling and elevation in the case of any pain, edema and congestion present. Analgesics
including opiates and antiphlogistics, except ASA, may be administered in instances of
intense pain; sedation is also possible.
Antivenom is indicated where systemic symptoms exist.
Applicable antivenoms:

* RUSSELL'S VIPER ANTIVENIN, Thai Red Cross, Thailand (Daboia russelli

siamensis);
* LYOPHILISED ANTI-SNAKE-VENOM SERUM, Haffkine, India (Daboia russelli,
etc.);
* SNAKE ANTIVENIN I. P., Haffkine, India (Daboia russelli, and others).

Repeated application is recommended depending on a patients status; especially in cases

of severe envenoming, the maximum recommended dose can be exceeded. If the antivenom is
administered early, repeatedly and in high dosage, it will effectively influence recovery of
hemocoagulation in most cases; this could eliminate the disorder within 10 hours. Application
of antivenom, especially if not applied immediately, will mostly not have a pre-emptive effect
on renal failure and the onset of myonecrosis; the same applies to manifest neurotoxicity.
Any potential blisters and less probable necrosis are treated in an ordinary and gentle
manner once the coats of bullae have been removed and necrectomia carried out. If a rare
occurrence of compartment syndrome is suspected, monitoring the significance of the
syndromes development and that of tissue perfusion is essential. The correct forms of
172 Jiri Valenta

treatment include measuring pressure in the tissue, elevating the limb, administering manitol,
and, in extreme cases, fasciotomy; see chapter 5. 3. 3. 1 Local damage and 6. 4. 3. 3 Crotalus
and Sistrurus genera: rattlesnakes and ground rattlesnakes. The necessity for deeper
debridement is very rare, just as is the occurrence of phlegmon.
In case of hypotension, which is an initial and key symptom of circulatory affliction,
volumoexpansion and administration of catecholamines will be relevant. Experimental
application of Naloxon (0.2 mg/kg IV) as well as high doses of methylprednisolone (30
mg/kg/10 min) did not bring about any effect. At the same time, volumotherapy, with diuresis
still retained, is a proper form of avoiding renal failure.
A DIC-like hemostasis disorder, which is based on the level and phase of envenoming,
will manifest via either intensified procoagulative processes, production of fibrin deposits,
and microthrombi, namely evident in glomerular capillaries. In earlier phases or instances of
hemorrhaging due to eventual exhaustion of the hemostatic mechanism and non-regulated
fibrinolysis, it is typically easy to control by applying an antivenom. Nonetheless, as with the
DIC syndrome, modulating a coagulation activity that develops for other reasons is advisable
at the same time by administering fresh-frozen plasma (10-20 ml/kg) and AT, provided AT
activity has been already reduced; for further details see chapter 5. 3. 3. 6 Hemocoagulation
disorders. Despite the chances of escalated fibrinolysis occurring already, any
antifibrinolytics applied will pose the risk of aggravating renal failure by fixation of
glomerular microthrombosis, increasing the possibility of respiratory failure. Administering
5,000 units of heparin (70 units/kg) followed by 2,500 units (35 units/kg) after 8 hours,
accompanied by the administration of antivenom, insignificantly improved the course of the
DIC-like coagulation disorder in cases of envenomings by vipers. Thus, heparin can be
applied, outside of periods of bleeding, not only in an early phase of envenoming with a
manifested hemostasis disorder, but also in the phase of convalescence in order to manage
any persisting thrombophilia with potential (micro)thrombotic complications.
Renal failure is difficult to tackle via both specific and symptomatic therapy. To help
reduce the incidence, modulation of hemocoagulation activity with efforts to minimize the
occurrence of microthrombosis, the sufficient supply of liquids, and maintaining perfusion
pressure is applicable. In nearly a half of the envenomed, hemodialysis or an alternative
(C)RRT method is necessary.
Any neurological and myotoxic symptoms developed cannot be practically managed by
treatment, they will simply abate after some time. In patients with dysphagia, eliminating any
peroral intake will be essential to avoid aspiration. In instances of obstructed respiratory
airways due to paralysis of relevant muscles, the airways must be managed; if the disorder is
severe, even tracheal intubation with potential mechanical ventilation could be necessary.
The patient can be discharged for home treatment after 24 hours following abatement of
all systemic symptoms and normalization of significant laboratory results; minor local
affliction can be treated by means of outpatient treatment. Any persisting laboratory picture
indicating mild prothrombotic activity should be managed by pre-emptive miniheparinization;
see chapter 5.4 Convalescence following envenoming.

6.4.2.6. Echis Genus, Saw-Scaled Vipers

Species: Recently, there are 15-16 species and subspecies contained in the genus of saw-
scaled vipers (Echis), with taxonomy not yet normalized. The saw-scaled viper (Echis
carinatus) with its two but probably even more subspecies presents the best-known and most
 Envenoming and Snakebite Treatment in Specific Snake Groups 173

important species; other members of the genus include the Palestine saw-scaled viper (Echis
coloratus), Romans saw-scaled viper (Echis leucogaster), West African carpet viper (Echis
ocellatus), and Egyptian saw-scaled viper (Echis pyramidum). Even though names like Echis
multisquamatus, sochureki, hughesi, jogeri, megalocephalus etc. are sometimes ranked
among species, other resources present them as the subspecies of Echis carinatus or Echis
pyramidum - see chapter 7 List of venomous snakes; some may probably refer to local forms
only.
Other names: EN: Carpet viper, Indian little viper; FR: Echide carne. Other languages:
Afai, Phoorsa, Bankoraj (E. carinatus).
Description: Saw-scaled vipers (Echis) tend to be smaller snakes of lengths ranging 20-
30 cm (E. carinatus sinhaleyus) and 50-85 cm (E. coloratus, E. pyramidum), featuring a
triangular head and quite large eyes with vertical pupils. They are predominantly brown in
color, with relatively distinct dark and light spots that can be slightly yellow in hue, which
often blend together to form a compact pattern. They possess good motional skills, and as
such can be ranked among fast-moving and swift snakes. In general, they are considered
short-tempered creatures. When in danger, the saw-scaled viper coils up, rubbing its lateral
keel-like scales and producing a typical loud, dry sound that resembles that of a saw cutting
wood, which probably serves the same purpose as the warning sound emitted by rattlesnakes.
Echis snakes are one of the most significant types in terms of epidemiology, responsible
for the majority of fatal snakebites not only in their home range, where they are abundant -
even appearing near human settlements - but globally too. They can be expected to cause
injury and death to more people than any other snake. For example, victims in Nigeria occupy
10% of the beds in hospitals; in the savannah-like part of Nigeria alone, up to 23,000 people
reportedly die from snakebites by saw-scaled vipers. Reports of serious envenomations from
W, Central and N Africa, once attributed to the saw-scaled viper (E. carinatus), actually relate
in all likelihood largely to E. leucogaster and E. ocellatus, a member of the former E.
carinatus subspecies, as E. carinatus does not inhabit this area at all.
Echis genus snakes are mostly active at night, although they are also diurnal hunters in
colder localities or periods.
Home range and habitat: The saw-scaled viper (E. carinatus) resides in sandy and stony
or sparsely grassed habitats, which are generally arid and flat, in Central and S India, as well
as N and E Sri-Lanka. The Palestine saw-scaled viper (Echis coloratus) ranges in the
savannahs and stony areas of the Middle East, from E Egypt across Israel, Jordan, Lebanon,
and the W part of the Arabian Peninsula as far as Yemen. The same terrain is inhabited by E.
multisquamatus and E. sochureki in Central Asia from Azerbaijan and E Iran as far as
Pakistan and NW India. The Romans saw-scaled viper (Echis leucogaster) and the West
African carpet viper (Echis ocellatus) reside in savannahs and semi deserts, but even forest
boundaries in the Sub-Saharan region from Senegal as far as Sudan; whilst the Egyptian saw-
scaled viper (Echis pyramidum) inhabits similar territories in NE Africa from Algeria
throughout Egypt and as far as Somalia and Kenya.
Toxins: The toxin content in each of the genus members is similar within the range of
known and typical differences; a specialty being a light neurotoxic affliction (ptosis) caused
by E. pyramidum. Nevertheless, the course of envenomation and mortality indicate variability
in the level of severity. For instance, the course of an envenoming following a snakebite from
E. carinatus seems to be more dangerous than one by E. coloratus venom. However, one
cannot rely upon a benign course of envenoming occurring, so every case concerning a saw-
174 Jiri Valenta

scaled viper must be recognized and treated as one that could pose an immediate risk to life.
As regards E. carinatus venom, the LD50 for mice IV equals about 0.3 mg/kg (Latifi, 1984).
Enzymes and toxins with an essential impact on hemocoagulation make up the key
groups in the venom components in Echis snakes. The main effect of the venom is a
procoagulative one; with the ecarin enzyme responsible for direct activation of prothrombin
to a different type of thrombin - meisothrombin - which cannot be inhibited by AT-heparin
complex. Although this substance does not seem to possess its own coagulation activity,
ecarin is a potent prothrombin activator that is subsequently converted to -thrombin. Even a
small quantity of ecarin can result in a number of positive feedbacks that boost explosive
thrombin activation, enabling meisothrombin to freely propagate in the circulation without
any threat posed by inhibition. Thrombin converts FBG to fibrin, activates PLT and the
complement, and causes chemotactical action on leukocytes. Emerging fibrin formations may
be not fully stabilized and are promptly destroyed to form a large quantity of FDP; in some
cases this does not correspond with the level of D-dim found. Plasminogen activation
proceeds. A DIC-like consumption disorder and reactive fibrino(geno)lysis occur. This results
in afibrinogenemia, formation of thrombogenic and disintegrated intima due to damaged
endothelium and endothelial junctions, increased capillary permeability with symptoms of
hemorrhaging, and interstitial edema. Other venom components concern fibrino(geno)lytic
and fibrin-converting proteinases and echistatin, a desintegrin-like peptide which inhibits the
PLT aggregation activated by thrombin, epinephrine, collagen, or PAF. Such an activity of
echistatin can in some cases manifest via inadequate PLT participation in the consumption
coagulopathy in progress. However, this does not eliminate the effect of venom components
conversely causing increased PLT aggregability in parallel with formation of fibrin
microthrombosis, which are produced as a result of a thrombin activity at a systemic level.
The existing hemorrhagin-like substances participate in damaging vascular walls, including
basal membranes and extracellular structures, thereby aggravating prothrombotic activation,
intima disintegration, hemorrhaging, formation of fibrin deposits, and microthrombi.
The presence of presynaptic enzymatic neurotoxin is possible in some species, such as E.
pyramidum, but with no clinical importance.
The venoms of the Echis snakes, as with the majority of vipers, contain a range of
cytotoxic and destructive proteolytic enzymes, e.g. proteinases, hydrolases, hyaluronidases,
phospholipases, and other substances causing local damage to tissues including small
necrosis.
Cardiotoxic venom compounds must not be overlooked, even though arrhythmia can be a
result of fibrin deposits and microthrombi present in the myocardium and conduction system.
A lethal dose of dry venom for an adult is approximately 5 mg; when biting, the saw-
scaled viper (E. carinatus) can release up to 12 mg of venom. A certain but rather low
percentage of bites without envenoming, which are called dry bites, can occur in this genus as
with other venomous snakes. For instance, five cases out of 120 attacked persons proceeded
without symptoms of envenoming, including local signs. The shortest snake that actually
caused envenoming measured just 17.5 cm.
Local symptoms of envenoming: Bite marks ranging from scratching to multiple wounds,
are rather indistinct; indeed, cases have existed where these are not visible at all.
Consequently, vague bite marks from this diminutive viper will not preclude a possibility of
envenoming. In almost every case, the initial symptom of envenoming involves pain at the
bitten site with possible redness around the wound. For most victims, the pain will spread to
 Envenoming and Snakebite Treatment in Specific Snake Groups 175

regional lymph nodes. In most cases, a moderately intense edema typically occurs, which
extends over half of the limb and does not exceed beyond regional nodes. It usually persists
for one to two weeks. In some envenomed persons, the edema can be described as a mild and
localized one, disappearing as quickly as within 48 hours. The size of the edema does not
relate with the severity of systemic symptoms and cannot be used as a criterion for the
severity of envenoming.
Locally, most affected persons - up to 80% - will exhibit hemorrhaging and bruising.
Cases of blisters and lesser necrosis are rather rare - only present in 10-15%.
Infection complications, phlegmons, and abscesses are not frequent but still possible. In
rare cases, they can even extend to deeper structures including giving rise to osteomyelitis.
Systemic symptoms of envenoming: Typical prodromes of the envenoming include
nausea, vomiting, and abdominal pain, but only in a quarter of those affected. However, some
affected individuals do consume herbal mixtures boasting an emetic effect as a part of native
treatment procedures. Other early symptoms of systemic envenoming include headache,
shivering, increased temperature, and fatigue, extending to altered consciousness.
Nevertheless, even a highly severe envenoming may not be accompanied by the prodromes
listed above.
Hemocoagulation disorder - the DIC-like one in all cases - presents the most serious
manifestation of envenoming, occurring as it does in the majority of the envenomed. Clinical
symptoms of the hemostasis disorder can be registered within dozens of minutes up to 27
hours after the envenomation; in most cases, they will firstly manifest in hemocoagulation
laboratory tests with prolonged times, defibrination, and increased FDP. Clinically, these are
most often displayed in the form of bleeding from gums, mucous membranes, nose, small
wounds, and stabs, as well as under the skin, and into muscles and the retroperitoneum.
Subconjunctival and retroorbital hemorrhaging or hemorrhaging into retina also takes place.
The persons affected exhibit gastrointestinal hemorrhage, which is manifest via hematemesis
and enterorrhagia; furthermore, they suffer hematuria, pulmonary hemorrhage, genital tract
hemorrhage, and hemorrhoids. Intracerebral hemorrhage is also possible. Miscarriages occur
in pregnant women. The hemostasis disorder can persist for 10-14 days.
Nevertheless, every case of envenoming with consumption hemocoagulation disorder
may not be accompanied by hemorrhaging - oliguric renal failure due to the formation of
fibrin deposits and microthrombi in the glomerular system may be present early on,
potentiated by hemoglobinuria in the case of intravasal hemolysis, and hypovolemia in
instances of hemorrhaging and extravasation.
In late stages of more severe envenomings, dyspnea or even respiratory failure of
ALI/ARDS type is possible, including such a level of severity that requires mechanical
ventilation. The main reason for the complication above to occur is damage to pulmonary
capillary integrity in cases of DIC-syndrome, including extravasation of liquid into the
pulmonary interstitium, and symptoms of interstitial or even alveolar pulmonary edema, or
again possible formation of fibrin deposits and microthromboses in the pulmonary vascular
beds.
Hypotension following the envenoming mostly relates to the hemorrhaging or
extravasation in progress.
Dysrythmias related to ventricular extrasystoles with drop-outs in the sinus node, junction
rhythms with slight QRS-complexes or alternative junction or ventricular rhythms with wide
complexes have been recorded in some cases; even T wave inversion and changes in ST
176 Jiri Valenta

section have been described. As direct cardiotoxicity of Echis venoms is not known, although
it probably cannot be precluded, microthrombotization into the myocardium and temporary
myocardium ischemization might be involved.
Again, the recorded cases of reversible elevation of serum levels of hepatic enzymes,
which peak as late as day 12 of envenoming and quickly abate, might probably be caused by
hepatic tissue perfusion disorders due to microembolisms.
Neurotoxins present in rare cases in venoms of some species, e.g. E. pyramidum, can
cause a very light and benign affliction of cranial nerves, for instance, ptosis. No reports
concerning the presence of substances with neurotoxic actions in the venom of the saw-scaled
viper (E. carinatus) are available.
Laboratory findings: Hemocoagulation laboratory tests exhibit key changes as well as
early symptoms of systemic envenoming, with PT, APTT, and TT often prolonged to non-
measurable values, the FBG level has decreased sometimes to zero values; FDP levels,
including D-dim, typically increase. In some cases, D-fragment can also be present in form of
monomers rather than dimers if stabilization of the intravascular fibrin through the action of
FXIII does not take place. AT activity is typically not reduced; significant thrombocytopenia
may or may not be recorded. Certain coagulation factors, like FV, FVIII, FII, and FXIII,
exhibit reduced activity, while FX and FVII factors show normal values. Non-detectable PC
levels are found, probably due to their activation and consumption. A laboratory
hemocoagulation test is recommended every 6 hours until normalization is registered, and
subsequently on a daily basis according to status to check if toxin release continues or not.
Leukocytosis and anemization as a result of hemorrhaging and hemolysis can be found in
the blood count. Schistocytes, poikilocytes, and free hemoglobin can be detected as the
microangiopathic hemolytic syndrome proceeds.
Biochemical findings lack typical specialties. The increased levels of conjugated
bilirubin, ALT and AST probably relate to a hepatic parenchyme perfusion disorder. The
increased levels of non-conjugated bilirubin relate to hemorrhaging.
Oliguric renal failure is accompanied with increased urea, creatinine, and kalium in the
serum.
Urine, including residual urine, typically exhibits proteinuria and hemoglobinuria.
Mortality: Mortality is high; 7-20% of individuals without treatment probably die
(Warrell et al., 1977; Coppola et Hogan, 1992). Total mortality is very difficult to estimate;
victims without envenoming are not currently recorded, neither are certain fatal forms of
envenoming in places where help is not available. Under adequate specific treatment, lethality
described equates to nearly 3% from those affected. Intracerebral and profusive internal
hemorrhage - mostly of the gastrointestinal type - with subsequent hypovolemic shock are
considered the most frequent causes of death. Renal failure can be another; fatalities caused
by respiratory failure are also possible. For their definitively high mortality, saw-scaled vipers
(Echis) are probably the most significant venomous snakes worldwide in terms of
epidemiology.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Limb immobilization and gentle local treatment can be recommended, with
mild cooling and elevation in cases where pain, edema, and congestion are present.
Analgesics including opiates and antiphlogistics, except ASA, can be administered for intense
pain; sedation is also possible.
Antivenom is indicated where systemic symptoms exist.
 Envenoming and Snakebite Treatment in Specific Snake Groups 177

Applicable antivenoms:

* LYOPHILISED ANTI-SNAKE-VENOM SERUM Haffkine, India (Echis carinatus,

etc.);
* SNAKE ANTIVENIN I. P., Haffkine, India (Echis carinatus, and other snakes);
* IPSER AFRIQUE PASTEUR, Aventis Pasteur, France (Echis carinatus, etc.);
* ANTIREPT PASTEUR, Aventis Pasteur, France (Echis carinatus, Echis coloratus,
Echis pyramidum, and others);
* FAV-AFRIQUE, Aventis Pasteur, France (Echis leucogaster, Echis ocellatus, etc.);
* FAVI-REPT, Aventis Pasteur, France (Echis leucogaster, and other snakes);
* SERUM ANTIVENIMEUX BITIS ECHIS NAJA PASTEUR, Pasteur Merieux, France
(Echis carinatus, and others).
* SAIMR ECHIS ANTIVENOM, SAIMR, the Republic of South Africa (Echis
ocellatus);
* ANTI ECHIS COLORATUS, Felsenstein Medical Research, Israel (Echis coloratus);
* MONOVALENT SAW-SCALED VIPER ANTIVENOM, Central Research Institute,
India (Echis carinatus);
* POLYVALENT SNAKE ANTIVENOM SERUM, Central Research Institute, India
(Echis carinatus, etc.).

Application of antivenom is indicated in cases of symptoms of systemic envenoming -

both prodromal and specific, and when there is bleeding or early renal failure, but even in
instances of more significant laboratory findings. In addition, application of antivenom can be
indicated where local affliction is found, especially if localized hemorrhaging occurs and
laboratory hemocoagulation laboratory tests are impossible. In cases of envenomation by the
Palestine saw-scaled viper (E. coloratus), which is considered less dangerous, treatment by
antivenom is recommended only beyond a certain level of seriousness of systemic symptoms
of envenoming, for instance: hemorrhaging, existence of proteinuria, serum urea elevated
above 7 mol/l, PLT decrease below 100,000/mm3 or Hb decrease below 130 g/l (Benbassat
et Shalev, 1993).
The initial quantity of antivenom is subject to the severity of symptoms or laboratory
findings; a range of 2-4 vials is recommended. Hemostasis becomes normalized after 2-40
hours following the first vial of antivenom; however, many times the administration of
antivenom must be repeated after several dozen hours due to reoccurring venom component
effects, which are evident from laboratory results based on repeated prolonged PT and APTT,
as well as non-coagulable blood found or repeated hemorrhaging.
Antivenom treatment may not prove satisfactory, which is actually a rule of thumb for the
saw-scaled vipers (Echis) and maybe more than any other species. This is not only due to
species-specific antigenic variability in venom components within the Echis genus, but also to
differences between specimens of the same species from various regions. The immense
challenge faced when controlling prothrombin-activating components is another factor.
In case of unavailability, insufficient quantity, or low effectiveness of the antivenom,
venom components can be eliminated by plasmaferesis and by repeating the same if
applicable.
The effectiveness of treatment using an antivenom or plasmaferesis is evidenced by
reduced times in the hemocoagulation test results.
178 Jiri Valenta

Even though the local affliction, including formation of potential necrosis, cannot
probably be influenced by giving antivenom, it still can be used to indicate the level of
envenoming and prove of prognostic value due to systemic symptoms expected. The local
affliction is typically not serious; standard treatment procedures can be applied. Gentle limb
elevation is required due to pain and edema, as well as administration of analgesics; mild
cooling of the limb can bring subjective relief. In rare cases, necrectomy must be applied in
late phases, mostly to the maximum extent of 1-15 cm2, but rarely with subsequent
transplantation of skin.
Clinical but even more severe laboratory symptoms of hemocoagulation disorder will
also require application of symptomatic therapy in most cases. The procedure is almost the
same as that for treating the DIC-like hemostasis disorder for other reasons. AT substitution,
which is typically not required at least in the early phase of envenoming, presents a certain
kind of exception. Levels and activity of AT as such are usually not distinctively reduced;
meisothrombin cannot be inhibited via AT. Otherwise, standard therapy and substitution
methods apply. Administration of fresh frozen plasma, at a dosage of 10-20 ml/kg, might in
some cases help combat the hemocoagulation disorder; in addition, it presents a quality form
of compensation for lost volume, be it due to hemorrhaging or extravasation. Complementing
the specific therapy using antivenom with heparinization, with a single dose of 70 units/kg
followed by 35 units/kg after 8 hours or 100 units/kg over 24 hours continually IV, can have a
positive effect on the results of the treatment (Paul et al., 2003), although this has not been
confirmed by some research. However, in the period whilst patients bleed, the treatment
method described above can be controversial. In case of lighter progress without bleeding,
treatment using only heparin without an antivenom is recommended following a snakebite
from the Palestine saw-scaled viper (E. coloratus)(Gilton et al., 1989).
To prevent (micro)thrombotic complications and inhibition of thrombin activity as such,
administration of heparin, at a dosage of 70-200 units of UFH/kg over 24 hours, or a relevant
pre-emptive dose of LMWH is applicable once bleeding has stopped. Of course,
administration of the same is fully applicable if AT activity has decreased, which is possible
any time later, in cases of potential induction of DIC or for patients with reduced levels
already prior the disease. Application of concentrated FBG is not indicated in most cases. If
integrity of the patients vascular system has not been significantly affected by an accident or
necessary surgery, hemorrhaging should not occur even if FBG values are near zero, although
FDP levels can be increased by FBG administration, which would be contra-productive.
Thus, FBG application is indicated only exceptionally, as well as that of coagulation factor
concentrates, see chapter 5. 3. 3. 6 Hemocoagulation disorders. Naturally, hypotension and
profound hemorrhaging will require substitution to retain vessel volume and perfusion
pressure values; consequences of exsanguination present the main cause of mortality in this
case.
In this way, volumotherapy and vasopressure treatment become another integral part of
efforts to regulate hemostasis in cases of hemorrhaging. Increasing the supply of liquids -
infusion of electrolytes - will be one of the measures to prevent renal failure. Less remarkable
oliguria can be controlled by diuresis support using furosemide. If renal failure has already
occurred - frequently the oligoanuric type, hemodialysis or another (C)RRT method will be
required.
Oxygen therapy is indicated in cases of respiratory failure or decreased oxemia. Outside
simple administration of oxygen, a continual positive airway pressure system, or at least
 Envenoming and Snakebite Treatment in Specific Snake Groups 179

intermittent expiration against resistance in the rehabilitation period, can be applied. Any
diuretics given will reduce a patients intravasal volume as well as the quantity of
extravascular pulmonary water, and can improve the existing level of pulmonary affliction.
The risk of renal failure in cases of intravasal volume restriction should be considered at
all times.
Any further grievous forms of pulmonary damage will require managed ventilation.
The arrhythmia that has occurred and splanchnic or other types of hypoperfusion
affliction, based on hypotension, that have taken place in the course of hemorrhaging, or
based on microthrombosis, are solved symptomatically.
The patient can be discharged for home treatment after 24 hours following abatement of
all systemic symptoms and normalization of laboratory findings. Any persisting laboratory
results indicating mild prothrombotic activity should be managed by pre-emptive
miniheparinization; see chapter 5.4 Convalescence following envenoming.

6.4.2.7. Eristicophis and Pseudocerastes

Species: The Eristicophis and Pseudocerastes are monotypic genera including the
McMahons desert viper (Eristicophis macmahoni) and Persian horned viper (Pseudocerastes
persicus), respectively. As for the latter, Pseudocerastes persicus fieldi subspecies is
considered to be a separate species. The Pseudocerastes snakes were formerly classified
under the Daboia genus.
Other names: EN: Asian sand, Iranian horned, leaf-nosed viper; FR: Vipre de McMahon
(E. macmahoni). EN: Asiatic horned, Fields horned viper, false-horned viper; FR:
Pseudocraste de Perse, Vipre des sables Perse (P. persicus).
Description: The MacMahons viper (E. macmahoni) usually grows up to 60 cm, its
maximum length being 80 cm. This snake features a pronounced head, and is colored in tones
of light brown and darker spots.
The Persian horned viper (P. persicus) is a little bit larger, normally shorter than 85 cm,
although the maximum length is 100 cm. It is gray to brown in color with darker spots. Its
triangular head boasts small horns above the eyes. Both viperids are predominantly nocturnal
snakes. Bites by the MacMahons viper are very rare.
Home range and habitat: The MacMahons viper (E. macmahoni) resides in sandy and
sparsely vegetated stony areas in E Iran, S Afghanistan, and W Pakistan. The Persian horned
vipers (P. persicus) habitats include the desert and stony territories of Iran, S Afghanistan,
Pakistan, and N Oman for P. persicus persicus; whilst P. persicus fieldi is found in Iraq, N
Saud Arabia, Jordan, Israel, and the Sinai region of Egypt.
Toxins: The venom of the MacMahons viper (E. macmahoni) is considered highly
potent; it may cause serious envenomings, including fatalities. Aside from hemocoagulation-
afflicting components, locally acting enzymes, and other compounds presumed due to its
closeness with the Cerastes and Echis genera, the presence of enzymatic neurotoxins is also
possible.
The venom of the Persian horned viper (P. persicus) does not appear to possess such
effectiveness, with LD50 for mice IV fluctuating around 1 mg/kg (Latifi, 1984). It may well
exhibit procoagulative activity; neurotoxicity is probably determined by the presence of
PLA2,, which has been found in P. persicus fieldi; finally, the venom contains enzymatic
components that are only likely to produce local effects on humans.
180 Jiri Valenta

Local symptoms of envenoming: The bitten site and the developed edema - largely only
localized or medium-sized - are painful; lymphadenopathy occurs, including enlargement of
regional lymph nodes. Cases of small-sized necrosis are possible although not described.
Systemic symptoms of envenoming: Only local symptoms of envenoming have been
registered for a number of descriptions of snakebite from P. persicus. In cases of systemic
symptoms, a moderate affliction can be probably expected, roughly similar to that caused by
Cerastes snakes. A course of envenoming following snakebites by the MacMahons viper (E.
macmahoni) is described, involving abdominal pain, intestinal dystension, serosanguineous
discharge from urethra, dysphagia, and ptosis.
Laboratory findings: Not known; neutrophilic leukocytosis can be expected, or changes
in hemocoagulation laboratory tests.
Mortality: In two of five cases of envenoming by the MacMahons viper (E. macmahoni)
described, death occurred within several hours after the attack.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Limb immobilization and gentle local treatment can be recommended, with
mild cooling and elevation where pain, edema, and congestion are present. Analgesics
including opiates and antiphlogistics, except ASA, can be administered in instances of severe
pain; sedation is also possible.
Applicable antivenoms:

* Eristicophis macmahoni - no specific antivenom is available. In envenomings with

severe clinical manifestation, administration of antivenoms against Echis carinatus, Cerastes
cerastes, or Macrovipera lebetina can be tested for potential cross-reactivity of E.
macmahonii toxins with those of these viperids.
* Pseudocerastes persicus - ANTIREPT PASTEUR, Aventis Pasteur, France (Cerastes-
Pseudocerastes persicus, etc.). Monospecific antivenoms are manufactured in Iran. Again, if
the envenoming displays severe clinical symptoms and no antivenom is available,
administration of other antivenoms against Echis carinatus, Cerastes cerastes, and
Macrovipera lebetina can be tried for potential cross-reactivity of P. persicus toxins with
those of these viperid snakes.

Further treatment is symptomatic and based on the symptoms of envenoming; see chapter
5. 3. 3 Clinical symptoms of envenoming and symptomatic treatment.
Observation of patients is essential for 24 hours following a snakebite, even if no
symptoms are apparent.

6.4.2.8. Macrovipera Genus, Large Palearctic Vipers

Species: The Macrovipera genus comprises four species: the desert viper (Macrovipera
deserti), Levantine viper (Macrovipera lebetina), Moorish viper (Macrovipera mauritanica),
and Cyclades blunt-nosed viper (Macrovipera schweizeri).
Other names: EN: Leventin viper, bluntnose viper; FR: Vipre de Levant, viper minute;
AR: Tagerza; RU: gjurza (M. lebetina). EN: Desert Leventin viper; FR: Vipre du Sahara (M.
deserti). EN: Morocco viper; FR: Vipre de lAtlas (M. mauritanica). EN: Leventin viper;
FR: Vipre des Cyclades (M. schweizeri).
Description: The Macrovipera genus snakes are quite robust, lengths vary from 60-90 cm
(M. schweizeri) to 120-150 cm, and rarely up to 200 cm (M. lebetina). The Levantine viper is
 Envenoming and Snakebite Treatment in Specific Snake Groups 181

a viperine boasting a length that makes it one of the longest of the Viperinae subfamily.
Another example is Bitis arietans, which is equally impressive size wise as one of its
subspecies, M. lebetina obtusa (euphratica), can measure 200 cm, although a specimen in
Armenia reached an undocumented 218 cm. These viperids have triangular heads, large eyes
and vertical pupils. They are mostly gray to brown in hue, with spots varying from red
through green, yellow and darker shades, blurring into a lengthwise zigzag line or signs of
crosswise stripes. They are snakes of largely nocturnal activity, but can be found also during
the day following rain at night.
Home range and habitat: The desert viper (Macrovipera deserti) inhabits slopes covered
with forest in the mountains of NE Algeria, Tunisia, and NW Libya. The Levantine viper (M.
lebetina) including all of its subspecies, resides in stony and arid steppe localities in Cyprus,
Turkey, Lebanon, Syria, Israel, Jordan, Saudi Arabia, Kuwait, Iraq, Iran, Afghanistan,
Turkmenistan, Uzbekistan, Armenia, Pakistan, N India, and Kashmir.
The Moorish viper (M. mauritanica) can be found in steppe, stony and forested localities
in hills and mountains in NW Morocco, and on the coasts of Algeria and Tunisia.
Cyclades blunt-nosed viper (Macrovipera schweizeri) is an inhabitant of the Greek
islands of Kimolos, Milos, Polinos, and Siphnos.
Toxins: In terms of toxinology, the specifics of the species and subspecies only differ to
an ordinary extent; the key toxin groups are probably identical in all species and subspecies;
at a clinical level, the approach to envenoming can be generalized to either the Macrovipera
genus or M. lebetina.
The M. lebetina venom is highly potent, with LD50 for mice IV fluctuating at about 0.4
mg/kg (Latifi, 1984); based on MLD, which is 3 mg/kg of mice SC; its toxicity is comparable
to that of venoms from the common viper (Vipera berus), jararaca (Bothrops jararaca), or
Egyptian cobra (Naja haje). A well-built adult snake has a relatively large amount of venom
available. Some resources state that its bite can prove fatal even to a camel.
The venom contains components afflicting hemocoagulation in both a procoagulative and
anticoagulative manner. Procoagulation action can be assigned to FV and FX activators, to
name but two. These enzymes neither activate prothrombin nor participate in FBG
degradation. Fibrinogenases contained in the venom possess a potent proteolytic activity and
degrade the FBG -chain, thereby altering its clotting ability by thrombin. As for
anticoagulation components, these can involve lebetins, platelet activation inhibitors,
fibrino(geno)lytic and other serum proteinases. Some of the subspecies, such as M. lebetina
turanica, possess a FV inactivating protease. The venom contains a protein increasing
capillary permeability, myotoxic lebetin, cardiotoxin, and a number of others.
Local symptoms of envenoming: Immediately upon a bite, pain in the wound occurs, with
early onset of edema that can be large, often extending around the whole limb. The pain and
edema propagate to the relevant regional lymph nodes preceding lymphangitis and
lymphadenopathy, including enlargement of the relevant regional nodes. In some cases, the
edema may even spread to the torso. Ecchymoses, hemorrhagic vesicles, and local
hemorrhaging come up around the bitten site. Development of necrosis is frequent; even
extreme forms can be expected. Occurrence of compartment syndrome is possible.
Systemic symptoms of envenoming: Systemic affliction may arise soon after a bite. In
most cases, nausea, vomiting, epi- and hypogastric pain and diarrhea occur. The affected
person also begins to sweat. A rising sensation of thirst is the result of extravascular
hypovolemia, diarrhea, potential hemorrhaging, and a response of the vegetative system. A
182 Jiri Valenta

tendency towards hypotension with tachycardia appears in the circulation with circulation
collapse and shock possible in instances of no given treatment. ECG changes can be
registered. Some forms of sharp envenoming may even result in cardiac syncope and
circulatory failure.
Symptoms of a profound hemostasis disorder clearly indicate envenomation by the
Levantine viper (M. lebetina). Clinically, they largely manifest as hemorrhaging from
injuries, small wounds and stabs, as well as from mucous membranes and GIT, but also as
hematuria, etc. As the hemocoagulation disorder is in part the one resembling DIC and the
venom contains toxins directly destroying capillary integrity, extravasation of liquids occurs
and microthromboses develop. Potential renal failure is triggered by microthromboses, as
well as the persisting hypotension, insufficient perfusion of renal glomerules, free
hemoglobin and myoglobin in the serum, and apparently the direct action of some toxins on
kidney structure.
Laboratory findings: The examination of hemocoagulation in cases of more severe
envenomation is in accord with the disorder of the consumption coagulopathy type.
Hypofibrinogenemia exists due to both direct degradation of FBG and its consumption within
the syndrome in process. PT and APTT will prolong; the decline of platelets may not be
dramatic due to the toxic reduction of their function. An increased D-dim level does not
always correspond to a sharp increase in all FDP. The discrepancy is based on the direct
action of proteases on FBG cleavage. Declined AT activity can be registered even three hours
after an attack; the chance of schistocytes being found is possible. Microangiopathic
hemolysis is responsible for the free hemoglobin found.
Blood results typically reveal neutrophilic leukocytosis. Increased myoglobin levels can
be caused by the lytic action of myotoxic enzymes. Later on, renal failure becomes manifest
by an increase in serum urea and creatinine. In addition, potentially more severe splanchnic
area perfusion disorders within a shock, or the significant presence of microthromboses, will
result in elevation of transaminases or pancreatic amylase.
Mortality: The mortality rate for envenomings by the Levantine viper (M. lebetina) is
high; resources show an extreme 30% for non-treated persons, with even 50% being reported
for Iraq.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Limb immobilization and gentle local treatment can be recommended, with
mild cooling and elevation where pain, edema, and congestion are present. Analgesics
including opiates and antiphlogistics, except ASA, can be administered in cases of severe
pain; sedation is also possible.
Applicable antivenoms:

* FAVI-REPT, Aventis Pasteur, France (Macrovipera deserti, etc.);

* ANTIREPT PASTEUR, Aventis Pasteur, France (Vipera-Macrovipera lebetina, and
others);
* EUROPEAN VIPER VENOM ANTISERUM, Institute of Immunology, Croatia
(Macrovipera lebetina, and other snakes).

Administration of antivenom is indicated for symptoms of clinical signs of envenoming

at a systemic level, e.g. vomiting, abdominal pain, hypotension, arrhythmias, and any form of
increased hemorrhaging; but even in instances of more significant pathology findings via a
 Envenoming and Snakebite Treatment in Specific Snake Groups 183

laboratory hemocoagulation test, such as prolonged PT and APTT, hypofibrinogenemia, and

high FBG or D-dim levels.
Moderate cooling and elevation of the afflicted limb during therapy is suitable, as is
covering and treating any developing derma defects in accordance with common practice.
Demarcation of any necrosis formed should be supported; deeper ones will require careful
necrectomy and debridement. In cases of suspected compartment syndrome, measuring
pressure in tissue and timely fasciotomy, enforced by hypoperfusion, is advisable; see chapter
5. 3. 3. 1 Local damage. Development of deep necrosis with infection in the afflicted tissue
will require treatment using antibiotics impacting on anaerobic bacteria and of good
penetrating capacity; however, pre-emptive administration of antibiotics is not indicated.
The existing hypotension requires intravascular volume to be increased; if necessary,
sufficient systemic pressure must be managed using vasopressors.
Administration of fresh-frozen plasma, at an approximate quantity of 10-20 ml/kg, will
provide for increases in intravasal volume, as well as help to reduce the level of DIC-like
hemocoagulation dysregulation. If AT activity is reduced, boosting the AT-heparin inhibition
complex by AT substitution is advisable. Non-fractionated heparin can be applied to prevent
thrombophilia and production of (micro)thromboses if there is no serious hemorrhaging, this
at an approximate dosage of 70-200 units/kg over 24 hours (Barkagan et al., 1988).
If laboratory results do not exhibit production of (micro)thromboses and their destruction
based on the presence of high D-dim levels, plus significant hemorrhaging persists,
antifibrinolytic therapy may be helpful, by using tranexam acid or aprotinin for example.
In circumstances of extravasation of a liquid into pulmonary interstitium with the
possible formation of microthromboses, developing respiratory failure can be treated based on
severity using oxygen therapy, with continuous positive airway pressure (CPAP) or
mechanical ventilation as a last resort. Weakening the intensity of symptoms, i.e. decreasing
the quantity of water in the pulmonary tissue, can be sometimes achieved by reducing
intravasal volume through the support of diuresis. Nevertheless, maintaining sufficient
perfusion of kidneys due to impending renal failure is essential even if this kind of therapy is
employed. Thus, it is clear that treatment and prevention of pulmonary and renal failure will
require a slightly controversial approach, where evaluation of priorities in terms of protecting
and supporting organ functions is the physicians responsibility.
The patient can be discharged for home treatment after 24 hours following abatement of
all systemic symptoms and normalization of significant laboratory results. Any persisting
laboratory results indicating mild prothrombotic activity should be managed by pre-emptive
miniheparinization; see chapter 5.4 Convalescence following envenoming.

6.4.2.9. Vipera Genus, Palearctic or Eurasian Vipers

Species: The Vipera genus numbers over 20 species and dozens of subspecies. The best-
known species include the nosed-horn viper (Vipera ammodytes), asp viper (Vipera aspis),
common viper (Vipera berus), Latastes viper (Vipera latastei), Baskian viper (Vipera
seoanei) and meadow viper (Vipera ursini) as the most widespread species in Europe; for
Turkey and the Middle East, this involves the Palestinian viper (Vipera palestinae), Armenian
mountain viper (Vipera raddei), and rock viper (Vipera xanthina) that has been proposed to
be placed into a new separate genus as Montivipera xanthina. For other members of this
genus, see chapter 7 List of venomous snakes.
Other names: FR: Vipre; DE: Otter, Viper; SK: vretenica; RU: zmeja.
184 Jiri Valenta

Description: The members of the Vipera genus are snakes of a mean length ranging from
50 to 70 cm, with the meadow viper (V. ursinii) limited to 35 cm, whilst long robust snakes
extend up to 1m. The rock viper (V. xanthina) grows to a maximum of 120 cm and the
Palestinian viper (V. palestinae) 130 cm. Vipers possess typical, broad, triangular heads with
large eyes and vertical pupils. The color of their backs ranges from a gray/brown through to
brown, gray to gray/white, gray/black, and black. The spots on their back are mostly vague,
forming a typical longitudinal zigzag line, for instance for V. berus, V. latastei, V. palestinae,
and V. ursinii; although they may be distinctive, as seen on V. aspis, and V. xanthina. Black
melanotic forms are known, for example, in the common viper (V. berus), V. nikolskii, and
Baskian viper (Vipera seoanei); the back of the blackish V. kaznakovi exhibits two long pale
stripes. Vipers are surface foragers; they are active mainly at night, but come out during the
day in colder localities or periods.
Home range and habitat: In general, the Vipera genus members range in diverse habitats,
from sandy and stony deserts and semi deserts, e.g. V. latastei or V. palestinae, through to
mountain slopes, valleys and screes, for instance, V. aspis, V. raddei, V. ursinii, and V. berus,
open woodlands - V. ammodytes, V. ursinii; forest clearances - V. berus; forests - V. berus, V.
palestinae, and V. xanthina; humid places (V. seoanei, V. xanthina), and the outlying areas of
swamps and bogs (V. berus).
The home range of vipers (Vipera) includes Europe (V. ammodytes, V. aspis, V. berus, V.
latastei, V. nikolskii, V. seoanei, V. ursinii, and V. wagneri), Turkey, W and Central Asia and
the Middle East (V. albicornuta, V. barani, V. bornmuelleri, V. darevski, V. ebneri, V.
erivanensis, V. kaznakovi, V. latifii, V. lotievi, V. palestinae, V. pontica, V. raddei, and V.
xanthina) and N Africa (V. latastei, and V. monticola). The steppe viper (V. renardi) is found
in localities from NE Romania as far as China, the common viper (V. berus) reaches to the
Far East, N China, and Korea, and the range of V. berus sachalinensis is Russia as far as
Sakhalin Island (see figure 7).
Toxins: In the Vipera genus snakes, venoms are relatively potent, with effectiveness
parameters like LD50 and DLM in mice comparable to the most powerful venoms of Bothrops
or Naja and Hemachatus snakes. LD50 for mice IV of the V. xanthina venom is about 0.4
mg/kg (Latifi, 1984). Naturally, only a small quantity of venom is available in the majority of
these vipers due to their size, which does not correspond to a lethal dose for a healthy adult.
Naturally, this does not apply to the large members of the genus - the Palestinian, Armenian
mountain viper, and rock viper (V. palestinae, V. raddei and V. xanthina).
In terms of toxin and enzyme structure, the venom does not fundamentally differ from
those of other Viperinae snakes. The venom of most Vipera species contains hemorrhagic
components that damage endothelial and subendothelial structures of vessels, thereby
producing a prothrombotic terrain, causing hemorrhaging from places with capillary integrity
disorder. Other venom components act on hemocoagulation, largely in terms of
prothrombotic activation, changes in activity of platelets, increased fibrino(geno)lysis, and
other impacts. There is a regular and typical presence of enzymes and toxins, which cause the
release of histamine and plasmatic kinins with subsequent vasodilation, hypotension, reactive
tachycardia, sweating, smooth GIT muscle and bronchiole contraction. In addition, the
histamine released may bring about angioneurotic edema of the face. The minor neurotoxic
effect of the venom in some Vipera genus species will typically not cause envenoming in a
human.
 Envenoming and Snakebite Treatment in Specific Snake Groups 185

Figure 7. Range of certain vipers in Europe and Turkey (freely edited according to Bucherl, Buckley,
and Deulofue, 1968).

Although this type of toxin activity has been described for certain members of the genus,
such as V. palestinae, V. xanthina, V. aspis, V. latastei, V. ursine, and V. berus bosniensis, it
is only neurotoxicity of presynaptic type based on a phospholipase effect with the potential
cooperation of other enzymes. This kind of neurotoxicity may also participate in vasodilation
and hypotension by reducing vasoregulating structures.
186 Jiri Valenta

Aside from the venom components above, other enzymes that participate in local
damage, or even formation of necrosis, are found in the Vipera genus members. Nevertheless,
necrosis is not typical in an envenoming by these vipers, except for V. ammodytes, V. aspis,
V. latastei, V. palestinae, and V. xanthina.
Due to the similarity in venom composition and the process of envenoming, details are
provided only for the species below, including the nosed-horn viper (V. ammodytes) as it is
the most significant European viper in terms of toxinology. In addition, the common viper is
outlined (V. berus), being a representative of small snakes and the most abundant venomous
snake in Europe. There is the inclusion of a section covering the asp viper (V. aspis) due to it
possessing a wider range of toxins; the Palestinian viper (V. palestinae), as it is representative
of the large members of the genus responsible for the most severe courses of envenoming,
plus additional information on the Armenian mountain viper (V. raddei), and rock viper (V.
xanthina).
As the common viper (V. berus) is a very widespread species in the wild across Europe,
the related chapter provides an in-depth look at this species and includes data presented
elsewhere in this book.

Vipera Ammodytes, the Nose-Horned Viper

Subspecies. V. ammodytes ammodytes including the former subspecies - gregorwallneri,
illyrica and ruffoi; V. ammodytes meridionalis including the former montandoni subspecies
and V. ammodytes transcaucasiana.
Other names: EN: western sand viper, sand viper, long-nosed viper; FR: Vipre
ammodytes; DE: Sandotter, Hornotter.
Description: A medium-sized viper, it grows between 50-100 cm long and features a
scaly horn on the tip of its snout. The color of the dorsal part errs towards brown, brown/red,
gray to silver, often with a zigzag line along the back. When under threat, the snake easily
becomes animated and bites; striking over a short distance is possible. Having said that, it
may stay calm and hesitate before attacking and biting. It hunts at dusk; during colder
months, it is active during the day as well.
Home range and habitat: The nose-horned viper mostly inhabits arid, stony, and shrubby
terrains or open woodland, abandoned gardens, forest edges in lowlands and uplands to an
altitude of 2,000 m (Mount Olympus); human settlements and water prove not to be a
deterrent. The home range of V. ammodytes ammodytes includes S Austria, Hungary, SW
Italy, Slovenia, Croatia, Bosnia, Serbia, Albania, SW Romania, and NW Bulgaria. It has also
been introduced into Switzerland. V. ammodytes meridionalis extends the nose-horned vipers
home range to Greece, the Cyclades, NW Turkey, NW Syria, and Lebanon. V. ammodytes
transcaucasiana resides in NE Turkey, Georgia, Armenia, and Azerbaijan.
Toxins: Outside the territory of Turkey with V. xanthina, V. ammodytes is the most
dangerous European viper boasting quite a potent range of toxic components, 20 mg of dry
venom on average. In terms of toxin and enzyme content, this viper does not much differ
from other viperid snakes. Circulation toxins releasing histamine, plasmatic kinins, and other
circulation-afflicting substances, plus hemorrhagins and hemocoagulation-afflicting
compounds comprise the key parts of the venom structure. The effect of destructive and
digestion enzymes, i.e. proteases, esterases, phospholipases, etc., can most often be observed
via local damage, including necrosis; local damage is also a prevailing symptom of
envenomation following an attack by the nose-horned viper.
 Envenoming and Snakebite Treatment in Specific Snake Groups 187

Local symptoms of envenoming: Marks of a bite can be discreet; nevertheless,

envenoming cannot be precluded even if these are not apparent. The initial signs may not
involve pain, but a tendency towards feelings of stiffness, the release of blood, and edema,
plus difficult movements in lesser joints. The edema slowly expands, but in most cases it will
remain lesser or medium in size. Lymphangitis and lymphadenitis occur in the related area.
Even this phase may not exhibit any greater local pain. If the affliction is more severe, the
edema is more distinct and hemorrhagic, with developing ecchymoses, blisters and maybe
hemorrhagic bullae, and necrosis. Complications involving a perfusion disorder and
formation of compartment syndrome are uncommon; nevertheless, gangrene may occur in
cases of a highly severe local affliction.
Systemic symptoms of envenoming: As with the majority of the less venomous snake
species, envenoming starts with prodromal symptomatology, e.g. nausea, cold sweats,
vomiting, abdominal pain, and possibly diarrhea. Aside from these symptoms, a very intense
or even intolerable pain in the epigastrium, sensations of difficulty in breathing and weakness,
vertigo, shivering, syncope, angioneurotic syndrome with a swollen tongue and face, and
dysphagia have also been described. In grievous envenomings, hypotension, and arrhythmias
in terms of tachycardia occur, as does bradycardia. Hypotension can result in circulation
collapse and shock. Hemostasis disorders appear as laboratory abnormities, or manifest via
clinically evident gastrointestinal or urinary pathway hemorrhaging, mostly at a local and
exceptionally at a systemic level. A case of multiple hemorrhagic brain attacks is known
(Boviatsis et al., 2003).
Dyspnea may be caused by a certain level of pulmonary congestion, increased EVLW
due to vasodilation and endothelial damage, and probably also by the presence of
microthromboses in pulmonary vascular beds. Hematuria, hemoglobinuria, myoglobinuria,
hypoperfusion due to microthrombosis and hypotension or relative hypovolemia are factors
participating in renal failure; in addition, the direct impact of nephrotoxic venom components
is possible.
Laboratory findings: Laboratory results reveal neutrophilic leukocytosis, prolonged PT
and APTT, hypofibrinogenemia, thrombocytopenia, and increased FDP; urine exhibits
proteinuria, hemoglobinuria, erythrocyturia, and possibly myoglobinuria.
Mortality: Fatalities are rare.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. The patient, including the limb, should be kept rested and immobile; fix the
limb to a splint using bandaging. Analgesia is usually not necessary.
Specific therapy in form of administration of antivenom against European vipers is only
indicated in symptoms of systemic envenoming, such as prodromes, facial edema,
hypotension, hemorrhaging, significant laboratory findings, or other symptoms of systemic
envenoming.
Applicable antivenoms:

* EUROPEAN VIPER VENOM ANTISERUM, Institute of Immunology, Croatia;

*VIPERATAB, Protherics, USA, UK;
* VIPERFAV, Aventis Pasteur, France;
188 Jiri Valenta

Local treatment methods desired include mild cooling of the edema, limb elevation, and
gentle treatment of defects, and any necrectomy. The necessity for deeper debridement or
even fasciotomy is very rare.
Symptomatic therapy is subject to clinical manifestation. Mild and mostly vegetative
symptoms will require rest in bed with a temporary strict or very moderate sickness diet and
plenty of liquids. In instances of more severe courses of envenoming, therapy will require an
intense approach. Hypotension can be corrected by volumotherapy and administering
vasopressors. Catecholamine therapy can be applied in bradycardia. Due to possible renal
failure, sufficient hydration, intravasal volume, and diuresis must be maintained. The
discovery of DIC-like consumption coagulopathy necessitates standard treatment based on the
severity of the status, from boosting the AT-heparin inhibition complex and applying fresh-
frozen plasma, through to essential PLT and erythrocyte substitution. In extreme cases, even
the following steps are necessary based on vital indication: blocking fibrinolysis by antilysin
and administering factor concentrates if any lack of the same is diagnosed. Any developing
respiratory failure may require oxygen therapy, or even more rarely, application of continuous
positive airway pressure (CPAP).
Although the kinds of severe systemic affliction mentioned above tend to be exceptions
in cases of snakebite by V. ammodytes, and any therapeutic approach to the symptoms of
envenoming will be mostly limited to local treatment, laboratory tests and observation, a bite
from this viper species should not be underestimated.
Symptomatology of lighter and non-complicated envenomings will last 2-4 days. The
patient can be discharged after 24 hours following abatement of systemic symptoms; less
significant local damage can be resolved via outpatient treatment. Any persisting laboratory
results indicating mild prothrombotic activity should be managed by pre-emptive
miniheparinization; see chapter 5.4 Convalescence following envenoming.

Vipera Berus, the Common Viper

Subspecies. Vipera berus berus, V. berus bosniensis, V. berus sachalinensis.
Other names: EN: European or nordic viper (adder); FR: Vipre pliade; DE: Kreuzotter;
SK: zmija severna, vretenica obycajna.
Description: The common viper is the last wild venomous snake species remaining in
Central Europe. Its relatively heavy-set body can grow to 50-65 cm, with lengths documented
at 85-92 cm. The coloring is variable, with basic tones of brown, gray and black, but even
with tints of yellow, red, olive or blue, and silver. Their backs display a typical dark zigzag
stripe, which may be discontinuous or scattered; exceptionally, it may be even completely
missing. Specimens of the dark prester form and reddish chersea form lack this stripe. The
head is triangular and can be clearly distinguished from the body. Compared to colubrids, the
head possesses smaller scales. The pupil is vertically slotted. In the conditions of Central
Europe, common vipers are mostly active during the day and at dusk, but also at night in
warmer places and in hot summers.
Home range and habitat: The common viper dwells in a wide range of landscapes:
clearings in forests, both natural and man-made, stony and rocky forested and open terrains.
Furthermore, they can be found on vegetated and bare slopes and hillsides, plus those with
screes, as well as meadows near water, and the edges of swamps and bogs. The viper can be
also found in water in order to bypass an obstacle. Curiously, one case is described by
Mrtson et al. (2001) of a viper which caused a bite in salt water. In Central Europe, the
 Envenoming and Snakebite Treatment in Specific Snake Groups 189

common viper ranges in altitudes of up to 1,500 m, although in the Alps and Balkan
mountains it can be observed even at elevations of 2,000 to 2,500 m above sea level.
Vipera berus is found in Europe and Asia, in the zone bordered by England and Scotland
to the west - except Ireland. To the south, its home range is delimited by Central France, N
Italy and the Adriatic coasts as far as N Albania, Macedonia, and N Greece. The zone
continues along the southern side through Serbia, Bulgaria, Romania (V. berus bosniensis),
and Moldova, and then to the east through Ukraine, Russia, N Mongolia, N China, N Korea to
the eastern Russian coast, and Sakhalin Island (V. berus sachalinensis), with the northern
limit crossing Norway, Sweden, and Finland, except for the northernmost regions, from NW
Russia, the line of the home range declines to the south-east as far as the 60th parallel.
Epidemiology of the snakebite. The registered incidence of bites by the common viper
within individual European countries are in the order of dozens to hundreds of cases per year.
Sweden, for example, registered 136 hospitalized individuals bitten by the common viper in
1975, of which 27% exhibited only a minor local response, and of the remaining 73% of those
affected at a systemic level, 46% were described as light envenomings, 15% were moderate
and 12% severe. The mortality of this sample was zero. However, 44 deaths related to a viper
bite were recorded between 1911 and 1977 (Persson et Irestedt, 1981). In a Swiss sample of
113 bitten persons over a 16-year period, 13 lacked any signs of envenoming; of the
remaining 100 envenomed, 62% displayed a local and light reaction, 24% a moderate
response with vomiting, diarrhea, and hypotension, while 24% suffered a severe reaction with
either shock or angioneurotic edema. Mortality was zero (Stahel et al., 1985). In the Czech
Republic, 90 cases were consulted with the Toxinology Centre during 1999-2005, but over
half of them reported no venom injection at all, meaning nil or merely a slight local response
was registered. With this in mind, the case of a 3-year-old child bitten on the lower lip, while
bending forward and studying an intriguing creature it had found, could be considered unique
with a happy ending. 14 cases of systemic envenoming and 17 cases of isolated local reaction
were found within the above reported bites. Out of a group of 11 envenomed and hospitalized
children in Slovakia, venom was not injected at all in three of the patients, whereas a local
reaction was registered in 8 patients, and systemic symptoms were only shown in a single
child. Investigating the circumstances, localities, and, causes of bites proved very interesting,
demonstrating a lack of knowledge and unsound judgment on the part of the children, as they
attempted to catch or pet the snake (Dluhorucky et al., 2000).
Toxins: The venom of the common viper is that of enzymatic type; its composition is
relatively unfavorable from a toxinologic and clinical aspect. The lethal dose for a human, 15-
20 mg, can be compared to the venom of the Indian cobra (Naja naja) or the South American
rattlesnake (Crotalus durissus); it is four times lower than that of the eastern diamond-backed
rattlesnake (Crotalus adamanteus), even though the quantity of dry matter in the venom in an
adult common viper usually does not exceed 15 mg, which is about 60% of a lethal dose
estimated for a human. Nevertheless, research via collecting the venom from 20 adult vipers
showed that the quantity of dry matter exceeded this traditional limit in 3 vipers, exhibiting
values as great as 18, 28, and 39 mg (Vozenilek, 2000). Such a quantity of common viper
venom could have severe after-effects if injected. Fortunately, a much lower quantity of
venom - from 2 to 14 mg of dry matter - is found in most common vipers; moreover, a snake
will only discharge a minor amount or none at all if displaying defensive behavior.
Out of the diverse range of snake venom components, the common viper lacks paralyzing
postsynaptic neurotoxins, cardiotoxins, myotoxins, and necrotizing substances. However,
190 Jiri Valenta

neurotoxic compounds, like PLA2 with presynaptic effects, are still present in venoms of
certain common viper subspecies or individuals, at a level that can induce systemic
symptoms, for instance, in specific sections of the vegetative nerve system, but even in
innervations of facial muscles.
Components affecting hemocoagulation and cytotoxic substances are contained in the
venom to a negligible extent, so they generally apply merely at a local level. However, the
common viper still contains clinically dangerous groups of substances - circulation toxins
with vasodilation effects, and hemorrhagins increasing capillary permeability. These
compounds can cause losses in liquid, ions and proteins; subsequently, in the cases of the
highest severity, they can reduce blood elements in intravasal compartments.
Local symptoms of envenoming: At the very least, a minimal application of a toxin will
manifest itself by localized edema, which can sometimes exhibit a central livid tone; later on
it progresses and is accompanied by swollen regional lymph nodes. Typically, the edema will
reach maximum size within 48 hours following an attack; in more severe and rather rare
cases, it will even propagate from the afflicted limb to the torso. It is also accompanied by
feelings of pain and strain; in some cases the pain is simply nominal. The edema may be
hemorrhagic and accompanied by ecchymoses and changes in skin tone at the afflicted site
turning red or livid; later on, bruises change their color to tints of green and yellow. Blisters,
bullae, any significant localized bleeding or necrosis do not occur. Exceptionally, normally in
children, edema can be extreme in sized and transfer from the limb via lymph nodes to the
torso.
Sporadically, infection complications may occur i.e. phlegmon at and around the bitten
site.
Systemic symptoms of envenoming: A large number of common viper snakebite incidents
will only exhibit symptoms of local affliction or light systemic changes. On some occasions,
local signs are discreet and the envenomation manifests only with systemic symptoms.
To generalize the level of envenoming in V. berus, the Reid classification scheme is
sometimes used (Reid, 1976).

* A Minimum or zero reaction. Local edema, no reaction or only that caused by a shock
at a systemic level.
* B Light reaction. A larger edema with or without gastrointestinal complications,
however, no further affliction at a systemic level.
* C Medium reaction. Extensive edema, shock persists for less than two hours, further
signs of a light systemic affliction.
* D Severe reaction. Shock persists for over two hours or states of shock repeat. Further
signs of a severe systemic affliction.
* E Fatal reaction.

Just like for most other vipers, the first symptoms of systemic envenoming include
nausea, vomiting, excessive sweating, increased temperature, and thirst. Vomiting can occur
even several minutes after the snakebite, and is typically accompanied by abdominal pain like
colic, diarrhea - rarely with hemorrhaging - and sometimes incontinence. These symptoms
indicate a moderate to more significant level of envenoming and may persist for 48 hours
following the attack.
 Envenoming and Snakebite Treatment in Specific Snake Groups 191

In less than 10% of cases, a severe type of affliction can be represented by an

angioneurotic edema limited to the area of the lips, tongue, and face, perhaps assisted by
anaphylaxis. Any respiratory difficulties reported are likely to be caused by anaphylactoid
bronchospasm as well.
Other dangerous symptoms of envenoming include decreased systemic pressure,
circulation collapse, or even shock accompanied by tachycardia, cold sweats, paleness, and
altered consciousness. In the majority of cases, the circulation complication can be managed
within 2 hours; a longer persistence is exceptional. Provided incidence of circulatory changes
ranges from 20% to 40% of those envenomed; however, in other research such frequency is
not reached (Persson et Irestedt, 1981, Stahel et al., 1985, Audebert et al., 1992). The
vasoparalytic action of toxins and plasmatic kinins released is multiplied by extravasation of
water into the interstitium, caused by damage to the endothelium, endothelial junctions, and
subendothelium. The loss of water, ions, and proteins without blood elements will, if not
compensated, increase Hct and Hb levels. Significant affection of capillary beds can even
result in extravasation of erythrocytes, which will be conversely manifest via the discovery of
anemia without apparent hemorrhaging. Besides this, moderate anemia may also occur in
cases where the volume of dilated vascular system is replenished by using plasma volume
substitutes. Spontaneous bleeding after a bite from the common viper is a rarity, however, it
cannot be fully precluded. More often, even in 30% of severe envenomings, the course can be
complicated by hematuria.
In addition, clinical symptoms of neurotoxicity have been recorded. Weinert et al. (2002)
describe a case of persisting facial paresis that followed a bite to the face, probably caused by
damage to nerve endings. Occasionally, symptoms like ophtalmoplegia, eyelid ptosis,
dysphonia, and dysphagia have been registered in cases of V. berus snakebites, even though
such types of affection are normally typical for the venom of the asp viper (V. aspis). In some
cases of envenoming, CNS disorders like somnolence or fuzziness, and even unconsciousness
may occur. Cederholm et Lennmarken (1987) describe convulsion attacks without an EEG
correlate in a 15-month-old boy weighing 10 kg, with extensive local edema and suspected
edema of brain caused by mobilization of edema liquid.
Renal failure with temporary oliguria, proteinuria, and hemoglobinuria can occur in up to
6% of envenomings, potentiated by hypotension, extravasation, and hemolysis.
In extraordinary cases, temporary ECG changes like low or inversed T wave can be
registered; even atrioventricular block of stage 2 has occurred.
Cases described include an intrauterine fetal death following a snakebite suffered by a
woman in the 7th month of pregnancy, development of paralytic ileus in a 4-year-old child, and
successfully resuscitated respiratory and circulatory failure in a man, who reached a hospital
one kilometer away by running following an attack by a common viper (Persson et Irestedt,
1981).
In cases of common envenoming with systemic symptoms, full normalization of systemic
changes can be expected within 1-3 weeks. However, intermittent swelling and pain at the
affected site may persist for a number of months. Reid (1976) states that the recovery in
children is faster than in adults.
Laboratory findings: Leukocytosis presents the most frequent result found in envenoming
by V. berus. If significant, especially when it exceeds 20 x 109/l, it predicts a more severe
extent of envenoming. Increased Hb and Hct levels are caused by water that has escaped in
capillary integrity disorder. In rare cases, coagulation tests show thrombocytopenia - up to 14
192 Jiri Valenta

x 109/l, prolonged PT and APTT, increased levels of FDP with reduced FBG, and
prothrombin complex.
Possible renal failure relates to creatinine and urea found in both serum and urine;
nevertheless, the serum creatinine level might have been slightly increased even outside the
affliction of kidneys. The occurrence of metabolic acidosis is due to organ hypoperfusion. In
especially severe cases, an increased level of liver enzymes can be found.
Urine lab tests typically reveal proteinuria and hemoglobinuria, or erythrocyturia.
Mortality: Even though extremely rare after envenoming by European vipers, fatalities do
exist.
50 cases of death occurred across Europe in 1984; however, they involved victims of
snakebites from all European viper species, i.e. also V. ammodytes, V. aspis, and V. xanthina
in addition to those from V. berus. In the United Kingdom, 14 people died after suffering a
bite from the common viper over the last 100 years, with only a single fatality recorded in
England and Wales in 1950-72 (Reid, 1976). Audebert et al. (1992) provide a single death in
France for a set of 82 snakebites; another death in 1993 is presented by Bures et al. Sweden
registered 44 fatalities in 1911-1978, while in recent decades mortality has been described as
negligible. A single case of a fatality from obstructed airways and bronchospasm with
angioneurotic edema is known; the woman died despite extensive symptomatic treatment
(Karlson-Stiber et al., 1997).
Therapy: As a consequence of the high variability of venoms and their effects, each case
of a snakebite by a venomous snake, including all European vipers, must be handled on an
individual basis, and the possibility of unexpected complications arising may not be
precluded. Although the symptoms of envenoming do not largely pose any significant danger
for an adult, the approach taken to a snakebite from the common viper and other small
snakes of this genus must be serious, and the patient should be fully managed. As regards
children so affected, such an approach is mandatory as the quantity of venom in a possible
dose may be lethal considering the potential weight of a child.
First aid, including immobilization of the patient and fixing the limb using a splint and
loose bandage, is applicable even upon a bite from a small European viper, including the
common viper. Such a procedure is definitely indicated in children. Applying a pressure
immobilization bandage according to Sutherland is not indicated. For further aid and general
rules of treatment, see chapter 5 Snakebite: Therapy and prevention. The affected person
should be encouraged to calm down as well.
If there are no symptoms of reduced blood pressure, such as vertigo, weakness, or
syncope, the individual affected can be allowed to sit. No unnecessary or straining
movements are recommended. If medical aid is within a good reach, it should be called very
promptly, especially when local afflictions or systemic symptoms become apparent early; in
every case of a bitten child this is implicit.
Where pain is experienced that can be locally extensive, although this is not common,
analgesics are applied. Although the common vipers venom does not contain any significant
level of hemocoagulation-afflicting substances, administering salicylates is best avoided in
the initial phase due to reduced platelet function and increases in local hemorrhaging in the
edema, as well as encouraging a potential hemostasis disorder.
The development of any intense allergic reaction or anaphylactic shock is treated under
common guidelines, using adrenaline, corticoids, replenishing circulating volume, or
 Envenoming and Snakebite Treatment in Specific Snake Groups 193

management of the airways and mechanical ventilation; see chapter 5. 3. 2 Prevention and
treatment of anaphylactic reactions.
Handling ordinary symptoms of systemic envenoming, such as nausea, vomiting,
abdominal pain, diarrhea, weakness, sweating etc., is not necessary in this phase; just steady
management and observation of vital functions whilst the patient is being transported will be
satisfactory.
In hypotension due to vasodilation and extravasation, tension can be increased and
stabilized through supplied volume; in instances of circulation collapse or shock, measures
based on symptoms must be taken, i.e. volume compensation is supplemented by
vasopressure therapy using norepinephrine and oxygen therapy. The presence of signs of
systemic reaction indicates antivenom therapy should be applied.
Reids criteria (1976) for application of antivenom include a condition that at least one of
the following symptoms is detected:

* Persisting or repeated hypotension;

* Leukocytosis exceeding 20 x 109/l;
* Acidosis;
* ECG changes;
* Increased serum CC value;
* Extensive edema in adults.

According to stricter criteria, it is argued that indication presents grave symptoms of

envenoming with severe hypotension and shock being found (Efrati, 1979). In children, early
administration is recommended in the following symptoms of significant exposure:
circulation reaction, CNS symptomatology, acidosis, and leukocytosis (Cederholm et
Lennmarken, 1987). Another method involves the so-called Stockholm criteria, see chapter
5.3.1 Specific treatment - immunotherapy; Tab. 4. A clear benefit from applying antivenom
was only found in severe envenomings within a group of 100 envenomed patients by Stahel et
al. (1985), with hospitalization time reduced from 10 to 5 days, whilst in medium and mild
reactions, the period remained unaffected. However, application of antivenom in cases with
no symptoms of envenoming conversely prolonged the period of hospitalization from one to
two days. Some authors suggest that aside from the positive effect on the course of systemic
envenoming, treatment by antivenoms influence the size and severity of edema (Kleber et al.,
1998).
With regard to the facts above, indications for implementation of specific
immunotherapy, i.e. administration of a relevant antivenom, might be summed up as follows:

* Existing hypotension that is difficult or not possible to control by volumotherapy, the

necessity to use catecholamines, the recurrence of hypotension, the onset of circulation
collapse or shock;
* Clinical presence and recurrence of more severe systemic symptoms of envenoming,
namely within GIT or CNS;
* Presence of a high level of leukocytosis (above 20 109/l), acidosis, ECG changes,
increased levels of serum CC or other significant pathologic laboratory results, for instance,
prolonged PT and APTT, laboratory evidence of DIC, more severe fibrinolysis, hematuria,
proteinuria, or other symptoms of hemocoagulation dysregulation, etc.;
194 Jiri Valenta

* Existence of extensive edema, especially the hemorrhagic form;

* Occurrence of any more severe or persisting symptoms of systemic envenoming in
children without allergic anamnesis.

Applicable antivenoms:

* ANTITOXINUM VIPERICUM, Biomed, Poland;

* EUROPEAN VIPER VENOM ANTISERUM, Inst. of Immunology, Croatia;
* VIPERATAB, Protherics, USA, UK.

Currently, the use of VIPERATAB, Protherics, a sheep antivenom manufactured on the

basis of purified Fab-fragments of antigens, can be recommended as preferable. With
comparable clinical inhibiting effects, this preparation exhibits almost a zero incidence of
allergic reactions, including serum sickness, when compared to horse antivenoms. Applying
this antivenom will eliminate a number of objections against giving antivenom; nonetheless,
the issue of immunotherapy benefits in medium or even light symptoms of envenoming
remains unresolved. In such cases, a familiar pearl of wisdom should be applied: if
administration of a medicine is not indicated, it is contraindicated.
The antivenoms mentioned above can be used when necessary for envenomings by other
Vipera genus snakes as well.
The antivenom is applied preferably within a vein and diluted to 500 ml; see chapter 5. 3.
1 Specific treatment, immunotherapy. In children, the dose is not reduced.
Handling and therapy of a local affliction is not crucial, even though it can be extensive
in some cases. As the damage to tissue is typically not significant and V. berus toxins lack
necrotizing effects, gentle treatment of the afflicted tissue, limb elevation, and mild cooling is
sufficient. Giving corticosteroids will probably not influence the course of local changes;
nevertheless, early application of certain types of antivenoms can hinder development of
edema, although this does not mean extending the criteria for their application.
In cases where systemic symptoms of envenoming occur by the common viper, with a
subsequent decline in blood pressure leading up to circulatory failure, which is characterized
as capacity shock, symptomatic treatment is infinitely preferred plasma-expansion with
tonization of vascular beds using catecholamines, or -mimetic support of myocardium, when
necessary. As the circulatory failure therapy proceeds, retaining sufficient organ perfusion is
essential by providing adequate intravasal volume to avoid vasodilation and escape of liquids
into the interstitium. This can eliminate or reduce the affliction of organs, such as renal
failure, where severe cases involve symptoms of shock. In more severe local reactions with
hemorrhaging, or in cases involving the hemostasis disorder, dextran-like volume expanders
are not suitable to fill the circulation due to interference with platelet function. In addition,
applying corticosteroids is adequate in instances of more severe angioneurotic edema, tongue
edema, bronchospasm, etc. Tracheal intubation is indicated for occurrences of obstruction to
upper airways, although this is rare.
Preventing renal failure can be managed by maintaining perfusion pressure and supplying
liquids to retain adequate vascular volume and production of a satisfactory quantity of
primary urine if hemoglobinuria and proteinuria are exhibited. Support of diuresis and
mobilization of edemas, where indicated, can be achieved using manitol.
 Envenoming and Snakebite Treatment in Specific Snake Groups 195

Antibiotics are not indicated as a means of prevention; any potential administration is

dependant on a rise of inflammation determined by bacteria, such as phlegmons.
Symptomatology of lighter and uncomplicated envenomings will last approximately 2-4
days. The patient can be discharged for home treatment after 24 hours following abatement of
systemic or severe local symptoms, which in most cases involves severe edema. Any
potentially less significant local damage can be solved via treatment as an outpatient. Any
potentially persisting laboratory results indicating mild prothrombotic activity can be
managed by pre-emptive miniheparinization; see chapter 5.4 Convalescence following
envenoming.

Vipera Aspis, the Asp Viper

Currently, the asp viper (Vipera aspis) comprises 5-6 subspecies. Other names: FR:
Vipre aspic; DE: Aspisviper.
Resembling the common viper, this snake can grow to 45-65 cm, which is exceeded very
rarely. Unlike the common viper, the asp features an elongated snout and yellowish tip to its
tail. In most subspecies as well as individuals, the typical zigzag line splits into isolated spots.
The asp viper resides in mountainous and sub mountainous localities with sparse
vegetation in Central and S France, NW Spain, Elba, Italy, and Sicily, Switzerland and along
the south-western edge of Germany.
Some data related to a snakebite from the asp viper (V. aspis) indicate a more severe or
slightly different course of envenoming is possible to that of the common viper. Certain
subspecies or local forms seem to possess enhanced neurotoxic potency, in SE France this
may involve hybrids of V. ammodytes and V. aspis, or procoagulative potency; in addition,
higher rates of morbidity and mortality than those of toxins of V. berus cannot be fully
precluded. Pozio (1988) presents 3 fatalities and the occurrence of a hemocoagulation
disorder and ophtalmoplegia, in addition to conventional systemic reactions within a group of
286 persons envenomed in the Italian countryside, with V. aspis responsible for the most of
cases. Furthermore, other neurological symptoms are described: bilateral ptosis, dysphagia,
dysphonia, and paresthesia, with even paralysis at the bitten site not unheard of (Weinert et
al., 2002).
The procoagulative potency of the asp viper (V. aspis) can be proven based on isolating
the protein participating in direct prothrombin activation, as well as describing ileic and
mesenterial thrombosis with necrosis of the colon, and the necessity for hemicolectomia.
Even if small necrosis is possible aside from typical results already described under the
section related to V. berus in local afflictions upon envenoming by V. aspis, the course of
envenoming and local or systemic affliction found in most cases is identical to that mentioned
for V. berus. Envenomings by these two species are often very difficult to tell apart.
Applicable antivenoms:

* EUROPEAN VIPER VENOM ANTISERUM, Institute of Immunology, Croatia;

* VIPERATAB, Protherics, USA, UK.
* If applicable and if the antivenoms above are not available, ANTITOXINUM
VIPERICUM, a monovalent antivenom produced by Biomed, Poland, can be applied as well
owing to the high probability of identical venom components and their cross-immunity.
196 Jiri Valenta

Vipera Palestinae, the Palestinian Viper

Other names: FR: Vipre de Palestine; DE: Palstinaviper. Former names: V. xanthina
palestinae, Daboia palestinae.
Description: This rather robust, spectacular, and variegated viper of mostly nocturnal
activity is the largest Vipera genus member. It can grow up to 100 cm, with the maximum
length being 130 cm. The dorsal part of body exhibits a grayish or umber color with brownish
spots. It is the most common snake found in Israel. Of 826 treated snakebites in 1998-2001,
503 cases were accounted for by this species (Bentur et Cahana, 2003).
Home range and habitat: The species is an inhabitant of rocky, stony, as well as sandy
localities, fields, plantations, and forests; it even does not avoid human settlements. Its home
range includes the Middle East: Israel, Lebanon, W Jordan, and W Syria - largely the parts
along the Mediterranean Sea and the Jordan Valley.
Toxins: The venom content is similar to that of the most of Vipera genus species; it
contains hemorrhagins and hemocoagulation-active toxins, circulation toxins, and proteolytic
enzymes, for instance, proteinases, hyaluronidase, phosphodiesterase, phospholipases, and a
number of others. Toxin action causes among other things, the release of histamine and
plasmatic kinins, PLT dysfunction, thrombin activation dysfunction, and increased
fibrino(geno)lysis with subsequent hypofibrinogenemia. The quantity, nature, and
effectiveness of enzymatic and toxin range of the Palestinian viper causes affliction to the
circulatory system in particular, and explains the severity of endothelial damage,
hemocoagulation disorder, and significant local changes.
Local symptoms of envenoming: Bite marks executed by either one or two fangs or
possibly a deeper scratch may bleed slightly. The first symptom involves pain, localized
redness and progressive swelling. In most cases, painful and strained hemorrhagic edema
occur, maybe spreading over related lymph nodes to the torso, or even transferring to the
opposite side of the body. Ecchymoses and hemorrhagic blisters, potentially extending to
necrosis, appear on the skin near the site of the injury. Local changes are accompanied by
lymphangitis and lymphadenitis. The edema peaks at around day 3 or 4, regression can be
expected within a week, or even later.
Cases have been described of the edema progressing to the neck including dysphagia and
a risk of obstruction of airways, as well as those of edema descending to the epigastrium with
symptoms of urine retention and necessary catheterization.
Systemic symptoms of envenoming: Systemic envenoming can be noted through
prodromes involving nausea and vomiting followed by abdominal pain, diarrhea, increased
temperatures, sweating, restlessness, weakness, or even syncope. There is a risk of an
angioneurotic edema on the tongue, lips, and face.
Circulation affection is manifest by hypotension, changes in rhythm, possible
compensatory tachycardia, or conversely bradycardia; grievous cases may result in circulation
collapse and shock.
Hemocoagulation defects cause hemorrhaging; firstly from wounds, but later on
spontaneous bleeding from mucous membranes, into the organs and body cavities.
Gastrointestinal hemorrhaging is evident due to hematemesis with subsequent enterorrhagia,
but even via acute intestine hemorrhaging. Hematuria is relatively frequent; organ intradermal
bleeding is also possible, for example, myocardial hemorrhaging. Congestion occurs on the
lungs in the form of interstitial or even hemorrhagic edema, caused by endothelial damage
 Envenoming and Snakebite Treatment in Specific Snake Groups 197

with increased capillary permeability and a hemostasis disorder in terms of activation and
consumption.
Hemoglobinuria and myoglobinuria, accompanied by kidney perfusion disorder caused
by hypotension, as well as microthrombotization, result in potential renal failure, although
this is probably associated with a direct nephrotoxic effect of the venoms components.
Laboratory findings: Neutrophilic leukocytosis and anemia accompanying hemorrhaging
is typically found. Consequences of hemocoagulation defects involve thrombocytopenia and
hypoafibrinogenemia of variable levels with increased values of FDP and D-dim. PT and
APTT may be prolonged. High CC, LD, and AST values with an almost normal ALT level
have been recorded in biochemical laboratory tests, which ostensibly illustrates muscular
decomposition rather than liver affliction. This corresponds with myoglobinuria, which is
typically detected together with hemoglobinuria and proteinuria. The rest of the results are not
specific and correspond to the clinical status and the level of hypoperfusion formed.
Mortality: Snakebites from the Palestinian viper (V. palestinae) produce up to 5%
fatalities, which in most cases follow circulation shocks due to hypotension and extravasation,
or massive hemorrhaging into soft tissues with profound thrombocytopenia and fibrinolysis.
Lethality can probably be reduced by a suitable type of comprehensive treatment or timely
administration of antivenom.
Therapy: For first aid and general rules of treatment, see chapter 5 Snakebite: Therapy
and prevention. Limb immobilization and gentle local treatment can be recommended, with
mild cooling and elevation where pain, edema, and congestion are present. Analgesics
including opiates and antiphlogistics, except ASA, can be administered in case of intense
pain; sedation is also possible.
In case of snakebite from V. palestinae, specific therapy by applying a relevant
monovalent or polyvalent antivenom is indicated not only due to systemic affliction with
existence of prodromes, circulatory complications or hemocoagulation disorder, even though
manifest via laboratory results only, but also if progressive or severe local affliction exists.
Applicable antivenom:

* ANTI VIPERA PALESTINAE, Felsenstein Medical Research Center, Israel.

During hospitalization, mild cooling of the edema and elevation of the afflicted limb is
recommended. Common methods of skin defect treatment are applicable, including early
necrectomy. With regard to the serious local effects of toxins, potentially deeper debridement
or even fasciotomy cannot be precluded.
Hypotension is handled through increased supply of liquids in the form of volume
expanders and electrolytes; if this is ineffective, vasopressure therapy is applied. If
bradycardia persists, symptomatic treatment using relevant catecholamines should follow.
Hemocoagulation disorder requires that the intensity of the therapy be regulated based on
the severity of the process, from miniheparinization, including boosting AT activity as far as
substitution of erythrocytes, consumed or sequestered platelets or degraded and consumed
coagulation factors, see chapter 5. 3. 3. 6 Hemocoagulation disorders. In instances of
uncontrollable hemorrhaging, primarily due to activated fibrino(geno)lysis, medicine that
possesses antifibrinolytic effects can be also administered; however, avoiding potential
microthrombosis in the capillary system should be borne in mind.
198 Jiri Valenta

Respiratory failure in the form of incipient affection of the ALI/ARDS type will require
oxygen therapy, possibly using continuous positive airway pressure (CPAP), or even
mechanical ventilation.
The potential risk of renal failure can be tackled through increasing the supply of liquids
to retain sufficient perfusion of kidneys and to ensure production of a satisfactory quantity of
primary urine. However, any overdosing of liquids, especially with reduced diuresis, can
potentiate the generation of pulmonary edema in the terrain of the damaged pulmonary
capillary network.
The patient can be discharged for home treatment after 24 hours following abatement of
all systemic symptoms and normalization of significant laboratory results. A lighter local
affection can be solved by means of treatment as an outpatient. Any persisting laboratory
results indicating mild prothrombotic activity, can be managed by pre-emptive
miniheparinization; see chapter 5.4 Convalescence following envenoming.

Vipera Xanthina, the Rock Viper. Vipera Raddei, the Armenian Mountain Viper
The rock viper (Vipera xanthina) - whose scientific name should not be confused with the
former name V. xanthina palestinae (currently V. palestinae) - and the Armenian mountain
viper (Vipera raddei) rank alongside the Palestinian viper as the largest vipers in Turkey and
the Middle East.
They can reach lengths of 70-100 cm. Coloring is in hues of gray or brown, with yellow
tints in V. xanthina, mostly with a zigzag pattern on their backs.
They can be found in stony and often forested localities in the mountains and foothills of
Armenia, NE Turkey, and NW Iran (V. raddei), and W and Central Turkey (V. xanthina).
In general, the venoms composition corresponds to that of other Vipera snakes - see
above, with enzymatic components being the key parts; less significantly, the toxin range
involves components of specific toxins with smaller molecules. Primarily, kininogen-like
enzymes that attack vascular systems in terms of vasodilation and hemorrhagins can be
expected; in addition, there are components afflicting hemocoagulation in some ways, and
general cytotoxic enzymes: proteinases, hyaluronidase, esterases, phospholipases, etc.
Cases of envenoming by these two vipers have not been surveyed to a sufficient extent. It
is highly probable that envenoming takes place in a similar way to envenomation caused by
other Vipera subspecies, such as the Palestinian viper (V. palestinae). The Armenian
mountain viper (V. raddei) is typically held responsible for fatal snakebites to animals in its
home range.
The course of envenoming can be estimated based on the status of an adult man bitten by
the Armenian mountain viper (V. raddei) and hospitalized at authors workplace. A double
bite mark and localized edema without hemorrhagic signs were evident. Pain in the afflicted
limb as well as nausea and vomiting came immediately, followed by shivering and
dysesthesia of skin around the body. On entry, signs of a low-level reduction of hydration
were apparent, but circulation still remained stable. The patient exhibited no signs of
hemorrhagic diathesis. Laboratory findings did not show any apparent pathological values
except for leukocytosis: 11,100-15,100 x 109/l; CRP below 2 mg/l increased to 55 mg/l within
12 hours, D-dim of 461 /l was still decreasing. No further development was exhibited so the
patient was discharged for home treatment on day 3. However, such a light course documents
exposure to a smaller quantity of venom from a bite; in other cases, a more severe
envenoming can be expected, with hypotension, or even hemocoagulation disorder.
 Envenoming and Snakebite Treatment in Specific Snake Groups 199

A severe localized affliction following a snakebite from the rock viper (V. xanthina) has
been described, when fasciotomy of arm was required due to the formation of compartment
syndrome, even after application of antivenom and without manifestation of systemic
symptoms (Kuzbari et al., 1994).
No mortality has been described.
Applicable antivenoms:

EUROPEAN VIPER VENOM ANTISERUM, Institute of Immunology, Croatia (V.

xanthina, etc.).

No antivenom against the Armenian mountain viper (V. raddei) is available; if necessary,
some other antivenoms applicable for the Vipera genus members can be used owing to the
likeness of venom components and probability of cross-immunity.
Therapy corresponds to the procedures mentioned for other Vipera species; see above.
Potentially, the most severe symptoms of systemic envenoming include hypotension or even
circulation collapse with the necessity for volume compensation and catecholamine support -
see chapter 5. 3. 3. 5 Hypotension, shock, or hemocoagulation disorder - see chapter 5. 3. 3. 6
Hemocoagulation disorders.

REFERENCES
ALLOATTI, G., GATTULLO, D., DALLA VALLE, R., et al. The haemodynamic effect of
Bitis nasicornis (Rhinoceros Horned Viper) venom. Gen Pharmacol, 1991, 22, No. 1, pp.
203206.
AUDEBERT, F., SORKINE, M., BON, C. Envenoming by viper bites in France: clinical
gradation and biological quantification by ELISA. Toxicon, 1992, 30, No. 56, pp. 599
609.
BARKAGAN, ZS., MAMOT, AP., GLAZUNOVA, GA., et al. Effect of heparin on
fibrinogen formation during experimental toxic syndrome of disseminated intravascular
coagulation. Ukr Biokhim Zh, 1988, 60, No. 1, pp. 2329.
BEER, E., MUSIANI, R. A case of intestinal infarction following Vipera aspis bite. Toxicon,
1998, 36, No. 55, pp. 729733.
BENBASSAT, J., SHALEV, O. Envenomation by Echis coloratus (Mid-East Saw-scaled
Viper). Isr J Med Sci, 1993, 29, pp. 239250.
BENTUR, Y, CAHANA, A. Unusual local complications of Vipera palestinae bite. Toxicon,
2003, 41, No. 5, pp. 633635.
BOVIATSIS, EJ., KOUYIALIS, AT., PAPATHEODOROU, G., et al. Multiple hemorrhagic
brain infarcts after Viper envenomation. Am J Med Hyg, 2003, 68, No. 2, pp. 253257.
BURES, E., MALIN, F., FOURNIER, E., et al. A fatal case of Viper bite in adult in France.
Rev Med Interne, 1993, 14, No. 3, pp. 174176.
BCHERL, W., BUCKLEY, EE., DEULOFEU, V. (Eds). Venomous animals and their
venoms. Volume I. New York : Academia Press, 1968.
CEDERHOLM, I., LENNMARKEN, C. Vipera berus bites in children experience of early
antivenom treatment. Acta Paediatr Scand, 1987, 76, No. 4, pp. 682684.
200 Jiri Valenta

COPPOLA, M., HOGAN, DE. Venomous snakes of southwest Asia. Am J Emerg Med, 1992,
10, No. 3, pp. 230236.
EFRATI, P. Clinical manifestations and treatment of viper bite in Israel. Toxicon, 1969, 7,
No. 1, pp. 2931.
GALLISSEN, A., THEAKSTON, RD., BARTH, J., et al. Neurotoxicity, heamostatic
disturbances and haemolytic anaemia after a bite by a Tunisian Saw-scaled or Carpet
Viper (Echis pyramidum complex): failure of antivenom treatment. Toxicon, 1994, 32,
No. 8, pp. 937944.
GAN, ZR., GOULD, RJ., JACOBS, JW., et al. Echistatin. A potent platelet aggregation
inhibitor from the venom of the Viper, Echis carinatus. J Biol Chem, 1988, 263, No. 36,
pp. 1982719832.
GILTON, D., SHALEV, O., BENBASSAT, J. Treatment of envenomation by Echis coloratus
(Mid-East Saw Scaled Viper): a decision tree. Toxicon, 1989, 27, No. 10, pp. 11051112.
GRNLUND, J., VUORI, A., NIEMINEN, S. Adder bites. A report of 68 cases. Scand J of
Surg, 2003, 92, pp. 171174.
GUILLEMIN, I., BOUCHIER, C., GARRIGUES, T. et al. Sequences and structural
organization on phospholipase A2 genes from Vipera aspis aspis, V. aspis zinnikeri and
Vipera berus berus venom. Identification of the origin of a new Viper population based
on ammodytin I1 heterogenity. Eur J Biochem, 2003, 270, No. 13, pp. 26972706.
HUANG, TF., PENG, HC., PENG, JS., et al. An antiplatled peptide, gabonin, from Bitis
gabonica snake venom. Arch Biochem Biophys, 1992, 298, No. 1, pp. 1320.
ISMAIL, M., MEMISH, ZA. Venomous snakes of Saudi Arabia and the Middle East: a
keynote for travellers. Int J of Antimikrob Agents, 2003, 21, p. 164169.
JANSSEN, M., FREYVOGEL, TA., MEIER, J. Antigenic relationship between the veno, of
the night adder Causus maculatus and venoms of other Viperids. Toxicon, 1990, 28, No.
8, pp. 975983.
JANSSEN, M., MEIER, J., FREYVOGEL, TA. Purification and charakterization of
antithrombin III inactivating enzyme from the venom of the African Night Adder
(Causus rhombeatus). Toxicon, 1992, 30, No. 9, pp. 985999.
KARLSON-STIBER, C., PERSSON, H. Antivenom treatment in Vipera berus envenoming
report of 30 cases. J Intern Med, 1994, 235, pp. 5761.
KARLSON-STIBER, C., PERSSON, H., HEATH, A., et al. First clinical experience with
specific sheep Fab fragments in snake bite. Report of a multicentre study of Vipera berus
envenoming. J Intern Med, 1997, 241, p. 5358.
KEYLER, DE. Envenomation by the lowland viper (Proatheris superciliaris): Severe case
profile documentation. Toxicon 2008, 52, pp. 836-841.
KHADWAL, A., BHARTI, B., PODDAR, B., et al. Persistent coagulopathy in snake bite.
Indian J Pediatr, 2003, 70, No. 5, pp. 439441.
KLEBER, JJ., ZILKER, T. Adder bites in humans. Tierarztl Prax Ausg K Klientiere
Heimtiere, 1998, 26, No. 2, pp. 95100.
KNOEPFFLER, LF. Autoobservation denvenomation par morsure dAtheris sp. Toxicon,
1965, 2, pp. 257276.
KOMORI,Y., NIKAI, T., SUGIHARA, H. Isolation and characterisation of procoagulant
from the venom of Vipera aspis aspis. Int J Biochem, 1993, 25, No. 5, pp. 761767.
 Envenoming and Snakebite Treatment in Specific Snake Groups 201

KULARATNE, SA. Epidemiology and clinical picture of the Russells viper (Daboia russelli
russelli) bite in Anuradhpura, Sri Lanka: a prospective study of 336 patients. Southeast
Asian J Trop Med Public Health, 2003, 34, No. 4, pp. 855862.
KUZBARI, R., SEIDLER, D. DEUTINGER, M. Lokal complications after poisonous snake
bite. Handchir Mikrochir Plast Chir, 1994, 26, No. 1, pp. 4850.
De HARO, L., ROBBE-VINCENT, A., SALIOU, B., et al. Unusual neurotoxic
envenomations by Vipera aspis aspis snakes in France. Hum Exp Toxicol, 2002, 21, pp.
137145.
LATIFI, M. Variation in yield and letality of venoms from Iranian snakes. Toxicon, 1984, 22,
No. 3, pp. 373380.
LANOIE, LO., BRANCH, WR. Venoms and snakebite. J Herpetol Ass Afr, 1991, 39, p. 29.
LAVONAS, EJ., TOMASZEWSKI, CA., FORD, MD., et al. Severe Puff Adder (Bitis
arietans) envenomation with coagulopathy. J Toxicol Clin Toxicol, 2002, 40, No. 7, pp.
911918.
LIFSHITZ, M., KAPELUSHNIK, J., BEN-HAROSH, M., et al. Disseminated intravascular
coagulation after Cerastes vipera envenomation in 3-year-old child: a case report.
Toxicon, 2000, 38, No. 11, pp. 15931598.
LIFSHITZ, M., KASTEL, H., HARMAN-BOEHM, I. Cerastes cerastes envenomation in an
18 year old female: a case report. Toxicon, 2002, 40, pp. 12271229.
LIFSHITZ, M., PHILLIP, M., BERNSTEIN, T., et al. Snake bite by Cerastes vipera in
children: report of two cases. Wilderness Environ Med, 1995, 6, No. 3, pp. 269272.
MacKAY, N., FERGUSON, JC., McNICOL, GP. Effects of the venom of Rhinoceros Horned
Viper (Bitis nasicornis) on blood coagulation, platelet aggregation and fibrinolysis. J Clin
Pathol, 1970, 23, pp. 789796.
MARSH, N., GATTULLO, D., PAGLIARO, P., et al. The Gaboon Viper, Bitis gabonica:
hemorrhagic, metabolit, cardiovascular and clinical effect of the venom. Life Sci, 1997,
61, No. 8, pp. 763769.
MRTSON, M, TAITTONEN, M, ALANEN, M, et al. Vipera berus adder bite in the water,
complicated by rapid shock. A case history. Eur J Pediatr Surg, 2001, 11, No. 5, pp.
358360.
McNALLY, T., CONWAY, GS., JACKSON, L., et al. Accidental envenoming by a Gaboon
Viper (Bitis gabonica): the haemostatic disturbances observed and investigation of in
vitro haemostatic properties of whole venom. Trans R Soc Trop Med Hyg, 1993, 87, No.
1, pp. 6670.
MEBS, D., HOLADA, K., KORNALK, F., et al. Severe coagulopathy after a bite of a Green
Bush Viper (Atheris squamiger): case report and biochemical analysis of the venom.
Toxicon, 1998, 36, No. 10, pp. 13331340.
MEBS, D., KUCH, U., MEIER, J. Studies on venom and venom apparatus on Feas viper,
Azemiops Feae. Toxicon, 1994, 32, No. 10, pp. 12751278.
MEIER, J., WHITE, J. (Eds). Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995, 752 pp.
MYINT-LWIN, WARRELL, DA., PHILLIPS, RE., et al. Bites by Russells Viper (Vipera
russelli siamensis) in Burma: haemostatic, vascular and renal disturbances and response
to treatment. Lancet, 1985, 2, No. 8467, p. 12591264.
PAUL, V., PRAHLAD, KA., EARALI, J., et al. Trial of heparin in viper bites. J Assoc
Physicians India, 2003, 51, pp. 163166.
202 Jiri Valenta

PE, T., MYA, S., MYINT, AA., et al. Field trial of efficacy of local compression
immobilization first-aid technique in Russells Viper (Daboia russelli siamensis) bite
patients. Southeast Asian J Trop Med Public Health, 2000, 31, No. 2, pp. 364368.
PERSSON, H. Clinical toxicology of snakebite in Europe. In. MEIER, J., WHITE, J. (Eds),
Handbook of clinical toxicology of animal venoms and poisons. Boca Raton : CRC Press,
1995.
PERSSON, H., IRESTEDT, B. A study of 136 cases of Adder bite treated in Swedish
hospitals during one year. Acta Med Scand, 1981, 210, No. 6, p. 433439.
PHILLIPS, RE., THEAKSTON, RD., WARRELL, DA. Paralysis, rhabdomyolysis and
haemolysis caused by bites of Russells Viper (Vipera russelli pulchella) in Sri Lanka:
failure of Indian (Haffkine) antivenom. Q J Med, 1988, 68, No. 257, pp. 691715.
PORATH, A., GILON, D., SCHULCHYNSKA-CASTEL, H., et al. Risk indicators after
envenomation in human by Echis coloratus (Mid-East Saw Scaled Viper). Toxicon, 1992,
30, No. 1, pp. 2532.
POZIO, E. Venomous snake bites in Italy: epidemiological and clinical aspects. Trop Med
Parasitol, 1988, 39, No. 1, pp. 6266.
PUGH, RN., THEAKSTON, RD. A clinical study of viper bite poisoning. Ann Trop Med
Parasitol, 1987, 81, No. 2, pp. 135149.
RAMACHANDRAN, S., GANAIKABAHU, B., PUSHPARAJAN, K., et al. Myonecrosis
due to Russells Viper bites in Sri Lanka. Am J Trop Med Hyg, 1994, 50, No. 5, pp. 597
601.
RATHOD, K., SHETH, R., CHAVHAN, G., et al. Hemoperitoneum complicating snake bite:
rare CT features. Abdom Imaging, 2003, 28, No. 6, pp. 820821.
REID, HA. Adder bites in Britain. Br Med J, 1976, 2, No. 6028, pp. 153156.
ROBINSON, RF., BAKER, RS., MARTIN, S., et al. Use of Near Middle East antivenom
to treat African Bush Viper envenomation. Vet Hum Toxicol, 2004, 46, No. 5, pp. 264
265.
SHEBUSKI, RJ., RAMJIT, DR., BENCEN, HG., et al. Characterization and platelet
inhibitory activity of bitistatin, a potent arginine-glycine-aspartic acid-containing peptide
from the venom of the Viper Bitis arietans. J Biol Chem, 1989, 264, No. 36, pp. 21550
21556.
SCHAEFFER, RC. Jr. Heterogenity of Echis venoms from different sources. Toxicon, 1987,
25, No. 12, pp. 13431346.
STAHEL, E., WELLAUER, R., FREYVOGEL, TA. Poisoning by domestic Vipers (Vipera
berus and Vipera aspis). A retrospective study of 113 patients. Schweiz Med Wochenschr,
1985, 115, No. 26, pp. 890896.
STCKLIN, R., CRETTON, G. The ultimate database on venomous animals, snakes. CD-
rom, Geneva : Atheris Laboratories, 1998.
TAN, NH., PONNUDARAI, G. A comparativ study of the biological properties of venoms of
some world Vipers (subfamily Viperinae). Int J Biochem, 1992, 24, No. 2, pp. 331336.
TRAPE, JF., PEELMAN, P., CARME, B., et al. La gravite dune morsuare de serpent a
propos de trois observations au Congo. Ann Soc Belge Med Trop, 1992, 72, pp. 155157.
VALENTA, J., STACH, Z., FRICOVA, D. et al. Envenoming by the viperid snake
Proatheris superciliaris: A case report. Toxicon, 2008, 52, pp. 392-394.
VEST, DK. Preliminary studies on the venom of the Chinese snake Azemiops feae, Boulenger
(Feas viper). Toxicon, 1986, 24, No. 5, pp. 510513.
 Envenoming and Snakebite Treatment in Specific Snake Groups 203

VOZENILEK, P. Ty zmije. Praha : Ministerstvo zivotniho prosted CR, 2000, 79 pp.(in

Czech)
WARRELL, DA. Clinical toxicology of snakebite in Africa and the Middle East / Arabien
Peninsula. In MEIER, J., WHITE, J. (Eds), Handbook of clinical toxicology of animal
venoms and poisons. Boca Raton : CRC Press, 1995.
WARRELL, DA. Clinical toxicology of snakebite in Asia. In MEIER, J., WHITE, J. (Eds),
Handbook of clinical toxicology of animal venoms and poisons. Boca Raton : CRC Press,
1995.
WARRELL, DA., DAVIDSON, NM., GREENWOOD, BM., et al. Poisoning by bites of the
Saw-Scaled or Carpet Viper (Echis carinatus) in Nigeria. Q J Med, 1977, 46, No. 181,
pp. 3362.
WARRELL, DA., ORMEROD, LD., DAVIDSON, NM. Bites by Puff-adder (Bitis arietans)
in Nigeria, and value of antivenom. Br Med J, 1975, 4, No. 5998, p. 697700.
WARRELL, DA., ORMEROD, LD., DAVIDSON, NM. Bites by the Night Adder (Causus
maculatus) and Burrowing Vipers (genus Atractaspis) in Nigeria. Am J Trop Med Hyg,
1976, 25, No. 3, pp. 517524.
WARRELL, DA., POPE, HM., PRENTICE, CR. Disseminated intravascular coagulation
cause by the Carpet Viper (Echis carinatus): trial of heparin. Br J Haematol, 1976, 33,
No. 3, pp. 335342.
WEINERT, W., SATTLER, RW., MEBS, D. Persistent paresis of the facialis muscle after
European Adder (Vipera berus) bite on the forehead. Toxicon, 2002, 40, No. 11, pp.
16271629.
WEIS, JR., WHATLEY, RE., GLENN, JL., et al. Prolonged hypofibrinogenemia and protein
C activation after envenoming by Echis carinatus sochureki. Am J Trop Med Hyg, 1991,
44, No. 4, pp. 452460.
WILDI, SM., GMPERLI, A., BEER, G., et al. Severe envenoming by a Gaboon Viper (Bitis
gabonica). Swis Med Wkly, 2001, 131, No. 34, pp. 5455.

6.4.3. Subfamily: Crotalinae

Formerly grouped under a separate family, the Crotalinae subfamily currently

encompasses 18 genera including 154 species. More recently, the number of genera
recognized has even increased.
The anatomy of Crotaline snakes is similar to that of most viperids (Viperidae); in
addition, they resemble the rest of the family in many ways. According to the structure and
function of their venom apparatus, featuring large erectile fangs embedded in the maxilla,
they rank among solenoglyphous snakes, as well as other viperids. However, unlike the others
of the family, they differ fundamentally due to possessing heat sensing organs - a pair of deep
pits placed in the anterior part of their heads between the eyes and nostrils; see chapter 1. 3
Morphology of snakes.
Their venom composition roughly corresponds with that of other viperids, in that it
contains a significant proportion of enzymes, typically with extensive destructive potency
towards tissues, and frequently also components with hemocoagulation effects. Clinically, the
role of neurotoxins is only visible occasionally, except for certain species that is, e.g. C.
204 Jiri Valenta

durissus. Again, neurotoxins are those of enzymatic nature, being phospholipase-like

substances, with presynaptic effects.
Crotalinae snakes inhabit a major part of the American continent, as well as central and
south-eastern Asian regions. Within America and Japan, these animals are the most
significant as regards epidemiology of envenoming by snakes. Some of the species are
popular as pets, which again underlines their epidemiology significance.

6.4.3.1. Agkistrodon, Calloselasma, Deinagkistrodonon, Gloydius, and Hypnale

Genera.
Species: Currently, only three species are included in the Agkistrodon genus: the cantil
(Agkistrodon bilineatus), southern copperhead (Agkistrodon contortrix), and western
cottonmouth (Agkistrodon piscivorus). The Mexican moccasin (Agkistrodon taylori) is now
sometimes listed as a separate species. Other seven species formerly ranked among the genus
are now listed as Gloydius genus comprising 10 species, such as the mamushi (Gloydius
blomhoffii), Halys pit viper (Gloydius halys), Himalayan pit viper (Gloydius himalayanus),
etc. Calloselasma and Deinagkistrodon are monotypic genera that include the Malayan pit
viper (Calloselasma rhodostoma) and Chinese moccasin (Deinagkistrodon acutus),
respectively. The Hypnale genus, i.e. hump-nosed pit vipers, contains three species: the
hump-nosed moccasin (Hypnale hypnale), Sri Lanka hump-nosed viper (Hypnale nepa) and
Walls hump-nosed viper (Hypnale walli).
Other names: EN: cantil (A. bilineatus), copperhead (A. contortrix), water moccasin (A.
piscivorus). FR: trigonocphale bouche rose (C. rhodostoma). EN: hundred-pace viper; FR:
Agkistrodon rostre pointu (D. acutus). EN: Japanese or Chinese mamushi, doksa or Asiatic
(Siberian, Himalayan) pit viper; JAP: mamushi (Gloydius). EN: humpnose viper (Hypnale).
The Gloydius snakes are often still listed and named as Agkistrodon.
Description. Mamushis and pit vipers have a robust to heavyset and well-muscled
medium-sized body with average length of 50-120 cm; 189 cm for the conanti (Agkistrodon
piscivorus) is the maximum-evidenced length. The similar shape of body, but a lesser size:
these are the features of the hump-nosed viper, Hypnale; they can grow up to the length of
mere 30 to 45 cm, with the maximum of 56 cm. Their large head has a form of triangle. The
color is brownish, ferruginous, rubiginous, grayish, or even blackish; they mostly feature big
spots fused up to cross bands or also small pale or whitish spots on a dark background (A.
bilineatus, A. piscivorus).
The most species of this group are active particularly at night; the species ranging in
colder zones will be rather diurnal animals.
Mamushis and pit vipers are more or less nervous characters, with good motional skills
and the possibility of relatively quick attack; however, they lack any apparent aggressiveness.
In Northern Carolina, U.S., bites by the copperhead (A. contortrix) form the highest
percentage of cases of envenoming, while in the entire USA, 8.8% from the 4,400 snakebites
including non-venomous snakes reported in 1991 involved A. contortrix, and 1.5% can be
assigned to A. piscivorus. In Japan, roughly 3,000 mamushi (G. blomhoffi) bites have been
reported per year. In Sri Lanka, H. hypnale bites present 27% from the total number of cases
of envenoming. In terms of epidemiology, the Gloydius mamushis and pit vipers are an issue
in China and Korea as well.
Habitat and range. The Agkistrodon snakes inhabit Northern America; they range from
the southeast regions of the USA (A. piscivorus) over the central and southern part of the U.S.
 Envenoming and Snakebite Treatment in Specific Snake Groups 205

and NE Mexico (A. contortrix) as far as the western Mexican coast and NW Costa Rica (A.
bilineatus). Their habitats mostly involve forests and savannahs; they can often be found in
hilly grounds or near water surfaces as well as in flood zones of rivers (A. contortrix). The
conanti (A. piscivorus) is directly bound to the presence of water through the structure of its
diet.
The rest of the genera are found in Asia. Calloselasma rhodostoma inhabits woodlands,
primary forests and fields in the former territory of Indochina, while Deinagkistrodon acutus
ranges in hilly landscapes near water in SE China, N Vietnam and Taiwan. The home range
of the Gloydius snakes extends from N Iran (G. intermedius) and the coastland of the Caspian
Sea (G. halys) over Central Asia, Pakistan, N India and Nepal (G. himalayanus), Mongolia
and China (G. blomhoffi, G. halys, G. monticola, G. stauchi) as far as Korea and Japan (G.
blomhoffi, G. tsushimaensis) and to the south and eastern Russian portion of Siberia (G.
saxatilis, G. ussuriensis). They are in most cases inhabitants of woodland and stony habitats,
often in the neighborhood of water surfaces or managed farmland, but even in steppes and
semideserts (G. halys). Hypnale snakes live in S India and Sri Lanka, where they can be
found in woodlands, fields and grassy areas.
The group includes a snake species living in the highest altitude - this is the Himalayan
pit viper (Gloydius himalayanus), a dweller of forests in 3,000-4,000 m above sea level; this
animals was even found on the edge of the permanent ice zone, 5,300 m above sea level.
Toxins: In snakes of this family, venom largely consists of enzymes; in A. halys, LD50 for
mice IV is approximately about 0.8 mg/kg (Latifi 1984). Venom especially contains the
components with hemocoagulation effects as follows: prothrombin activators (e.g. aharin, a
kind of enzyme isolated from venom of G. halys that is similar to the venom components in
Echis and Bothrops snakes), the components activating additional factors of the plasmatic
coagulation system (such as F X from venom of C. rhodostoma), thrombin-like fibrinogen
converting enzymes isolated e.g. from venom of G. halys, direct fibrino(geno)lytic enzymes
isolated for example from venoms of A. contortrix and H. hypnale, platelets aggregation
inhibitors isolated for instance from venom of G. blomhoffi, platelets aggregation activating
elements (e.g. venom of H. hypnale) and others; generally, these components shows pro-
coagulation and anticoagulation effects at the same time, which depends namely on the dose
of venom.
Typical venom components include hemorrhagins and other substances increasing the
level of capillary permeability; clinically, presynaptic enzymatic neurotoxins are active as
well, such as agkistrodotoxin and PLA2 from G. blomhoffi venom.
Concerning local affliction, proteolytic and other cytotoxic enzymes are responsible for
affecting tissue, plus necrosis can arise as well.
Local symptoms of intoxication. All bites from mamushis and pit vipers are painful. In the
early stages, envenoming is accompanied by a development of edemas that will mostly affect
half of a leg, but may extend to an entire limb or even the trunk. A bite injury often bleeds to
a small extent; roughly, a quarter of those concerned (H. hypnale) exhibit painful
lymphadenopathy, including swelling of lymphatic nodes in the region. In worse cases, the
skin of the affected areas is erythematotic with developing petechiae and ecchymoses. More
severely, even a subcutaneous hematoma might very rarely form. Vesicles and bullae, largely
with blood content, precede the development of necrosis, with an incident rate of up to 10%
(A. contortrix, D. acutus). In most cases, necrosis will only affect the skin and can be
primarily found on fingers and after a use of a tourniquet. Exceptionally, they afflict deeper
206 Jiri Valenta

structures, i.e. hypodermis and muscles; more often, myotoxins or infection agents are
involved. Development of a compartment syndrome with the urgency of fasciotomy or a
long-term or permanent functional effect on the legs is rare but also possible; see 5.3.3.1
Local damage.
Any infectious complications are chiefly associated with necrosis; even gangrene
necessitating amputation or the development of sepsis may occur. Microorganisms isolated
from necrosis and infections have mainly included Enterococcus sp., Pseudomonas sp.,
Staphylococcus sp., and Clostridium sp.
Systemic symptoms of envenoming: Symptoms of systemic envenoming appear in about
one half of snakebites by the snakes of this group; the rest can be assessed as dry bites
with no venom released. A certain portion of snakebites by these snakes is associated with
only mild symptoms or takes place without any systemic symptoms at all, limited to local
affliction, such as in A. contortix and G. himalayanus.
Systemic envenoming mostly starts with the following prodromes: nausea, vomiting,
abdominal pain, diarrhea and increased temperature. Worse courses continue with shivering,
cold sweat, thirst, vertigo, weakness, palpitation, eye burning, stomach burning sensations (H.
hypnale), intestine distension that can rarely change even into an ileous status, and, in the
most severe cases of envenoming, lethargy to coma (G. blomhoffi, H. hypnale) or even
syncope and respiratory failure (D. acutus).
Hemostatic disorder is the main and fundamentally the most severe symptom.
Coagulopathy is manifest by defibrination, which is partly primary and partly secondary, as a
result of a DIC-like consumption disorder induced by prothrombin and other activators of the
plasmatic coagulation system or fibrinogen-converting enzymes. The hemostasis disorder is
primarily demonstrated through laboratory results; clinically, worse cases usually exhibit
hemorrhaging from the gums, nose, mucous membranes, small wounds, GIT, urinary tract, as
well as airways; retinal hemorrhaging has even been rarely described. Hemorrhaging
significant in terms of volume may even lead to symptoms of hypovolemic shock. Coronary
hypoperfusion caused by either hypotension or microthrombosis may result in changes in
ECG as regards T wave inversion and depressed ST section (C. rhodostoma). The incidence
of symptoms of hemocoagulation disorder ranges from very rare, e.g. A. contortrix and G.
himalayanus with over 10-24% of persons affected, just like H. hypnale and C. rhodostoma,
but D. acutus causes up to 40% of such incidences.
Hemocoagulation disorder, in terms of developing fibrin deposits and microthrombi in
glomerular capillaries, participates in oliguric renal failure, in association with possible
hemolysis, myoglobinemia, hypotension, and the nephrotoxic effects of the venom
components. An unusual yet possible occurrence of respiratory failure is respiratory failure of
ALI/ARDS type via, for example, G. blomhoffi, in addition to which H. hypnale presents a
similar complication with the participation of hemorrhagic venom components.
Other symptoms are associated with the presence of presynaptic neurotoxins. Within 1-48
hours following a snakebite, affliction of cranial nerves will occur and manifest as ptosis,
diplopia, hazy vision, dysphagia, difficulties in opening the mouth, plus indistinct and
generally myasthenic symptoms, as caused by G. blomhoffi and G. halys for instance. Cases
of ventilatory muscle paralysis with necessary mechanical ventilation described from China
seem not quite probable - the respiratory failure is more likely to derive from affection of
pulmonary tissue related to the ALI/ARDS syndrome; see above.
 Envenoming and Snakebite Treatment in Specific Snake Groups 207

The content of the myotoxic elements of the venom causes a certain extent of
rhabdomyolysis, which is manifest by pain and strain in certain muscular parts including
those of neck, back, chest, etc., e.g. in G. blomhoffi venom. In addition, neural or muscular
damage, if any, also relates to potential motional dysfunctions of limbs that may persist as
long as one year, e.g. A. contortrix.
Laboratory findings: Typical laboratory results include changes in hemocoagulation tests.
Hypofibrinogenemia or even afibrinogenemia occur, and an increase in FDP, mostly with a
significant percentage of D dim., as well as thrombocytopenia. A decrease in plasminogen,
alfa2-antiplasmin and AT levels is also possible. In more severe instances, extension of PT,
APTT, TT, and coagulation time according to Lee-White was discovered. However,
hypofibrinogenemia up to afibrinogenemia will only prevail in some cases as a result of
primary fibrinolysis, with no additional symptoms of consumption in progress.
Other laboratory tests may include indications of neutrophilic leukocytosis, hemolysis,
myoglobin, increases in CK and CRP, and proteinuria, myoglobinuria, and hemoglobinuria
through to hematuria can be found in urine.
Mortality: Cases of mortality following bites by some of the mamushi and pit viper
snakes are not rare. Between 1904 and 1971, 66 fatalities occurred in Taiwan, which means
24% cases of envenoming out of the recorded total were caused by the venom of D. acutus. In
D. acutus, present mortality following a bite ranges from 4.7 to 5.4%
In Thailand, envenoming by C. rhodostoma together with that by the Malayan krait
(Bungarus candidus) constitutes the highest mortality, with each of these species sharing 13
victims from the total of 46 described. In Japan, two fatal cases per year occur on average out
of approximately 3,000 bites by G. blomhoffi. Cases of death caused by G. blomhoffi and
rarely by H. hypnale bites have been recorded in China.
Reasons for fatal courses of envenoming usually include hemorrhage, predominantly
cerebral hemorrhage, DIC, respiratory and renal failure, shock and sepsis during gangrene
and necrosis.
Therapy: For first aid treatment and common principles of therapy, see chapter 5,
Snakebite: Therapy and precautions.
Application of a pressure immobilization bandage is not recommended due to the risk of
extending local damage through the persistence of the high concentration of venomous
hemorrhagic and cytotoxic components at the particular point. Nevertheless, immobilizing the
leg by using a looser bandage is a useful solution. Exhaustion of venom from the wound by,
for example, an extractor has not been proved as effective but not dangerous when compared
to other practices like cutting the wound, tourniquet, etc. A presence of pain acting locally or
in the leg may require opiate analgesics to be administered.
Applicable antivenoms:

* CROFAB, CROTALIDAE POLYVALENT IMMUNE FAB(OVINE), Protherics, the

USA (Agkistrodon contortrix, Agkistrodon piscivorus, etc.);
* POLYVALENT ANTIVENOM, Instituto Clodomiro Picado, Costa Rica (Agkistrodon
bilineatus, and other snakes);
* ANTIVENIN POLYVALENT, Bio Farma, Indonesia (Calloselasma rhodostoma, etc.);
* MALAYAN PIT VIPER ANTIVENIN, Thai Red Cross, Thailand (Calloselasma
rhodostoma, and others);
* AGKISTRODON ACUTUS, Nat. Inst. Prev. Med., Taiwan (Deinagkistrodon acutus).
208 Jiri Valenta

A certain level of cross immunity, thus the possibility of applying antivenoms in cases of
bites by other mamushi, e.g. a pit viper species, may be anticipated. Nevertheless, the effect
of certain severe venom components, such as prothrombin activators, is usually hard to
influence by any specific immunotherapy in most cases.
No H. hypnale antivenom is available; HAFFKIN POLYVALENT antivenom
administered in some cases has not been effective (Warrell 1995).
Applying antivenoms can be practicable in cases with the development of overall
symptoms, hemorrhage, hypotension, heavier neurotoxic symptoms, rhabdomyolysis
symptoms like muscle pain and tension, and in more serious laboratory findings, namely in
hemocoagulation lab tests, or when a high level of myoglobin is discovered. The effective
amount of antivenom will depend on the type and amount of venom or on the level of
severity. Generally speaking, it can range from 1-4 vials (D. acutus) up to 5-10 vials (C.
rhodostoma). Any positive effect should be demonstrated by an improved hemocoagulation
test. However, recurrent coagulopathy, including common defibrinations, may occur,
especially upon the application of antivenoms containing Fab (CroFab) accelerating
elimination from circulation.
Any contraindication of application of the antivenom as well as its unavailability,
insufficiency or low immunogenicity, and any persistence of severe symptoms of envenoming
can be treated by repeated plasmaferesis.
In some circumstances, there may be more grievous local envenoming symptoms. Any
developing dermal bullae or lesser necrosis as the predisposition of the occurrence of
infectious complications should be hastily removed and the area of the affection treated
adequately. In addition, the development of a compartment syndrome cannot be fully
precluded. In cases of any suspected disorder of district perfusion, a leg must be treated by
elevation and general administration of manitol, with doses of 0.5-2 g/kg IV, in the course of
about 30 minutes. If the risk of ischemia in the relevant area does not abate, fasciotomy could
be appropriate. However, this kind of treatment is never carried out preemptively; see also
chapter 5.3.3.1 Local damage, and chapter 6.4.3.3 Crotalus and Sistrurus genera: rattlesnakes
and ground rattlesnakes. There may be a necessity to amputate due to gangrene affecting
fingers.
Pre-emptive administration of antibiotics is not indicated, although sometimes
recommended; antibiotic therapy, if one is applied, is launched only upon occurrence of
infectious complications.
In case of hypotension or circulatory failure and shock, treatment is initiated with
volumotherapy, i.e. replenishing the circulating volume with infusions of crystalloids or
colloids. Including fresh-frozen plasma in the therapy will also positively influence a DIC-
like hemocoagulation disorder. If application of infusions fails to ensure satisfactory
stabilization of the circulation, or hypotension persists or any further increase in volume is
contraproductive, vasopressure therapy is indicated using norepinephrine in continual
infusion, which will provide sufficient perfusion pressures; see chapter 5.3.3.5 Hypotension,
shock.
Sufficient intravascular volume together with adequate perfusion pressure needs to be
maintained to retain diuresis in efforts to prevent renal failure.
By default, the hemocoagulation balance disorder should be treated by giving a sufficient
quantity of antivenom. Symptomatic therapy becomes necessary if antivenom cannot be
 Envenoming and Snakebite Treatment in Specific Snake Groups 209

applied or exists in insufficient quantity, and proves necessary to influence any later
secondary affliction that might occur, for instance, persisting prothrombotic activity.
Isolated hypofibrinogenemia without clinical signs of increased hemorrhaging will not
require any special symptomatic treatment. If this caused by a direct effect of venom
components on FBG, it cannot be controlled by means of symptomatic treatment, e.g. using
heparin. FBG substitution is not recommended unless bleeding had been caused by its low
level. A DIC-like consumption disorder, especially in the late phase, may not be sufficiently
manageable by immunotherapy, thus will require a symptomatic approach: therapy in form of
applying fresh-frozen plasma (10-20 ml/kg), and substituting AT with potential
miniheparinization (70-210 units/kg/24 h) by means of UFH or LMWH with a beneficial and
more intense anti-Xa effect based on the specific phase and course of the syndrome.
Naturally, the heparin therapy will not be indicated over the period of increased bleeding;
nevertheless, it may have a positive effect on managing hypercoagulation states associated
with the development of microembolisms. For potential substitution of platelets, erythrocytes
and FBG, ordinary guidelines will apply. Administering hemocoagulation factor concentrates
is not recommended; see chapter 5.3.3.6. Hemocoagulation disorders.
Light symptoms of neurotoxicity, i.e. ptosis, diplopia, dysphagia, light myasthenic
symptoms, etc. will abate without any specific therapy.
A patient can be discharged for home treatment after 24 hours following abatement of all
systemic symptoms of envenoming, normalization of significant laboratory findings, and
stabilization of the local affliction.
Any persisting laboratory symptomatology of less significant prothrombotic activity
should be resolved by preemptive miniheparinization, see chapter 5.4 Convalescence
following envenoming.

6.4.3.2. Atropoides, Bothriechis, Bothriopsis, Bothrocophias, Bothrops, Cerrophidion,

Lachesis, Ophryacus, and Porthidium Genera
Species: The Atropoides genus comprises three species of jumping pit vipers originally
classified into the Porthidium genus. Each of the Bothriechis and Bothriopsis genus, i.e. palm
pit vipers or forest pit vipers, respectively, contains seven snake species, a part of which was
once placed in Bothrops, the most extensive genus of this group, which now numbers 32
species, for example the common lancehead (Bothrops atrox), jararaca (Bothrops jararaca),
jararacussu (Bothrops jararacusu), Brazilian lancehead (Bothrops moojeni), Neuwieds
lancehead (Bothrops neuwiedi) and others. Note: former Bothrops asper seems to be only a
subspecies of B. atrox. A lesser number of species can be found in the Cerrophidion genus
with three members, formerly or even recently by some authors placed into the Porthidium
genus, the Lachesis genus with its four species, and Ophryacus, a monotypic genus with a
sole species - Ophryacus undulatus. On the other hand, the Porthidium genus currently
comprises nine species. More recently, a new genus named Bothrocophias containing five
species has been described, see chapter 7 List of venomous snakes.
Other names:
Barba amarilla, Caissaca, Mapanare, Terciopelo (B. atrox); Fer de Lance (B. lanceolatus,
B caribbaeus); Urutu (B. alternatus); Surucucu (Lachesis); Jararaca ilhao (B. insularis);
Jararaca pintada (B. neuwiedi); Jararacussu (B. jararacussu).
Description: Some snake species of the genera mentioned above typically reach lengths
of between 50 and 70 cm (Cerrophidion, Ophryacus, Porthidium), some others 100-200 cm
210 Jiri Valenta

(Bothriechis, Bothriopsis, Bothrops). The record is held by the viperids (Viperidae), in

particular the South American bushmaster (Lachesis muta), which boasts a documented
length of 365 cm and an unconfirmed 426 cm. The Fangs of this snake can measure up to 3.5
cm.
The majority of snakes of this group possess a rather slender, but well-muscled body. The
head is of a typical triangular form, and often features a striking striped or spotted pattern,
which is darker than overall coloring and also appears on their bodies. Background tones are
hues of green, sandy shades, brown, brown/gray, and brown/red.
These snakes are mostly arboreal or semi-arboreal, but can be terrestrial, e.g. Bothriechis
taeniatus, Bothrops ammodytoides, Bothrops pictus, Porthidium, and others. Most tend to be
nocturnal animals.
Generally, they possess very good and fast motion skills, and err towards short-tempered
behavior, whilst some are outright aggressive.
In terms of epidemiology, the lanceheads (Bothrops), especially B. atrox, B. jararaca, B.
moojenii, etc., comprise the most significant representatives due to their relative abundance,
extensive home ranges, high toxicity, and volume of venom. Some degree of preferring places
close to human settlements is shown by some lanceheads (Bothrops), hence is also an
essential factor. In the Brazilian state of Sao Paulo, 12,639 bites by a snake were recorded
from 1988 to 1993. Of this number, as many as 9,828 snakebites, i.e. 87% of incidents, and
68.3% of fatalities were caused by Bothrops (Ribeiro et al., 1998). The Vital Brazil Hospital,
Sao Paulo, experienced from 1989 to 1990 a total of 137 hospitalized cases of envenoming
following bites by B. jararaca (Franca, et al., 2003). Annually, it is estimated that 20,000
snakebite incidents occur throughout Brazil, 85% of which were caused by Bothrops snakes
(Benvenuti et al., 2003). In addition, members of this genus feature the greatest
epidemiological relevance throughout South America - they are responsible for nearly 90% of
all snakebites. Severe envenomation, though with a much lower incidence, is also accounted
for by a somewhat rarer snake, the South American bushmaster (Lachesis muta).
Habitat and range. The representatives of the genera above are found in diverse habitats;
most of them are forest dwellers, with a range of forest types from open and arid savannah-
like stands (e.g. Bothrops, Porthidium), through to dense woods - often oak/pine woodlands
(Bothriechis, Bothriopsis, Bothrops, Cerrophidion, Ophryacus, and Porthidium), with vast
swathes of forest, including cloud forests, being home to Atropoides, Bothrops, and Lachesis.
In addition, some species also seek out farmland and neighboring residential zones, as well as
plantations, fields or cleared areas (e.g. Bothrops and Lachesis). Their home range includes
Central and South America, from Central Mexico (Ophryacus, Porthidium) across Central
America, covering the entire span of South America as far as the middle portion of Argentina
in the south, i.e. Bothrops ammodytoides. They are absent only in Chile, their passage
blocked by the Cordillera mountain ranges.
Toxins: All members of the genera, namely the larger species, have available a relatively
good amount of venom. For example, at the Butantan Institute, Brazil, 1.76 mg of venom was
extracted from the South American bushmaster (Lachesis muta). In general terms, the venom
of adults in this snake group is not more highly effective than that of other snakes, at least
when it comes to doses tested on mice; see chapter 3.2 Effectiveness of snake venoms.
Nevertheless, this will not hinder its highly clinical effectiveness on humans, which is a given
due to the large amount of venom produced and its clinically unfavorable composition.
 Envenoming and Snakebite Treatment in Specific Snake Groups 211

The venoms usually contain components principally affecting hemocoagulation,

hemorrhagins, and cytotoxic enzymes.
Dysregulation of the coagulation system is the co-responsibility of enzymes that directly
activate prothrombin (Bothrops, Lachesis), thrombin-like fibrinogen-converting proteinases
cleaving FPA and FPB (e.g. batroxobin from B. atrox venom which can cleave FPA; it is
produced under the trade name of Reptilase and used in the laboratory to determine RT in
hemocoagulation tests), and components activating FX and FVIII, hence the coagulation
system. At the same time, PLT function is affected in terms of activation and increased
aggregability. Furthermore, fibrinolysis is increased within the action on hemocoagulation,
probably both primarily, i.e. by venom components, and secondarily - by hyperactivating
plasminogen as consumption coagulopathy proceeds. The overall effect of hemocoagulation
venom components of this snake group consists in initiating procoagulation. This is the way it
manifests in prey, and potentially in human victims in cases of extremely high exposure to the
venom. However, the majority of persons bitten arrive at medical facilities at the stage of
afibrinogenemia, featuring developed DIC and various levels of hemorrhaging.
The venoms composition is subject to change in the course of ontogenesis: the venom of
young common lanceheads (B. atrox) largely contains elements of prothrombin-converting
activity, while the venom in adults chiefly possesses a thrombin-like activity with a prevailing
effect of fibrinogen-converting enzymes.
Kininogenases comprise one type of clinically significant venom component - enzymes
involved in releasing endogenic hypotension substances like histamine, serotonine,
bradykinin, etc. In synergy with other components, they influence activation of inflammation
mediators, such as leukotrienes, prostaglandins, and others.
Hemorrhagins accompanied by a number of other destructive proteases destroy basal
membranes of peripheral vessels and capillaries, causing soluble components, and later also
particle components, to escape into the interstitium. This results in intravasal hypovolemia,
which causes or intensifies hypotension, potency of hemorrhagic complications, and affliction
of interstitium tissues, which could prove especially dangerous to the lungs.
Local destruction of tissues, or even the occurrence of necrosis, is determined by the high
activity of generally cytotoxic, largely enzymatic substances, such as proteinases, esterases,
hyaluronidases, and PLA2 including elements with myotoxic effects.
In some species of the Bothrops genus (B. insularis, B. neuwiedi), presynaptic and
clinically insignificant neurotoxicity has been discovered as well.
Other components are those that possess direct nephrotoxic effects (B. jararaca), and are
involved in resultant renal failure together with microthrombosis and hypovolemia.
The venom of freshly hatched common lanceheads (B. atrox) is more effective than that
of adults; similarly, the venom of the jararaca (B. jararaca), with its significant action on
hemocoagulation in subadult age, can largely cause local affliction if injected by an adult
(Horte et al., 1995). However, unlike in the species above, the venom of a newborn South
American bushmaster (L. muta) allegedly lacks almost any toxicity. Nevertheless, any such
information obtained from a laboratory should not be considered as either reliable in
husbandry practice or clinically. Indeed, the venoms of all species in the group must be
treated as highly dangerous.
Local symptoms of envenomation. The first signs of envenoming include pain and the
almost immediate development of edema at the site of affection. Both symptoms crop up in
98% of cases. The marks of a bite may be evident, but this may not be true in the early phase,
212 Jiri Valenta

especially if conducted by a young snake. Nevertheless, they frequently bleed. The painful
edema often propagates across the limb; lymphadenopathy follows with erythemas along the
lymph vessels, including painful enlargement of lymph nodes.
In further progress of the envenomation, ecchymoses occur on the skin in nearly a half of
incidents. At around 12 hours following exposure, vesicles with hemorrhagic or necrotic
content develop in 10% to 15% of persons affected, and necrosis forms in 5% to 10% (Horte
et al., 1995). This chiefly occurs after an attack by B. jararaca, predominantly to the fingers,
and if a constriction tourniquet is applied as a first aid measure. In most cases, necrosis is
localized on and under the skin, but may affect even deeper structures, such as muscles,
tendons, and bones. This leads to long-term disorders or even permanent damage, although
rarely posing a reason for amputation. This is a necessity in less than 1% of those affected, as
is treatment of compartment syndrome by means of fasciotomy. A severe local affliction is
worsened by disorders of tissue perfusion due to developed microthromboses, potential
myonecrosis, worsening local hemorrhages, and a severe edema of compartment syndrome
nature.
Abscesses occur in 5% - 10% of cases; in Brazil, following B. jararaca and B. moojeni
bites, even in 12% to 18% of cases. Infectious agents recorded include Staphylococcus
aureus, Morganella morganii, Escherichia coli, Providentia sp., and some anaerobic bacteria.
A tragic but curious incident involved a 5-year-old child who suffered a bite to the eye by
a Brazilian lancehead (B. moojeni), resulting in exophtalmus, necrosis, and necessary
enucleation (Bryndao et al., 1993).
Systemic symptoms of envenoming: System envenoming may not always be preceded by
prodromes, as is true of most snakebites; however, they do sometimes manifest, especially
upon a bite from the South American bushmaster (Lachesis muta), whose venom exhibits
neurotoxic activities on the autonomous system to some extent. This brings with it the usual
nausea, vomiting, abdominal pain, and diarrhea. Half of the persons so afflicted suffer
increased temperatures.
A severe case of envenoming appears as affection of the cardiovascular system.
Envenomation by the South American bushmaster (Lachesis muta) may result in bradycardia
or arrhythmia due to vagus nerve stimulation. Other cases produce hypotension or even shock
resulting from a massive release of vasoactive substances of the bradykinin kind. Such a
status is potentiated by sequestration of fluids to the site of edema and into the interstitium at
a systemic level, as well as by loss of blood in profound hemorrhaging. Circulation collapse
and shock may arise early on, and develop with extreme severity in some instances of major
envenomation, particularly when caused by Bothrops and Lachesis snakes.
Hemocoagulation effects present a typical display of envenoming in nearly all species of
this group, except for those triggered by Bothriechis lateralis, Porthidium nasutum, P.
ophryomegas, and P. picadoi, as no coagulation disorders have been found following
envenoming by these snakes. A less distinctive effect on the coagulation system is brought
about by the venom of the Neuwieds lancehead (Bothrops neuwiedi). Symptoms of the
affected hemocoagulation system will mostly occur after a certain time, 6-12 hours on
average. In terms of Bothrops snakes, a hemostasis disorder is often the only sign indicating a
systemic envenoming; it can only be registered through laboratory tests during the initial
phase and in mild cases of envenoming. Potential hypofibrinogenemia or afibrinogenemia
may not always result in hemorrhaging, although there are signs of increased bleeding in most
cases. The symptoms start with bleeding from the gums, wounds, and stabs, with continued
 Envenoming and Snakebite Treatment in Specific Snake Groups 213

hemoptysis, gastrointestinal hemorrhaging including hematemesis and later enterorrhage, as

well as hematuria with diuresis maintained. In severe forms, intradermal bleeding occurs to
organs, be it the lungs or brain. In a group of 309 patients bitten by Bothrops snakes in
Ecuador, cerebral hemorrhaging occurred in eight persons, i.e. in 2.6% (Mosquera et al.,
2003). Inducing a hemocoagulation disorder is not determined by a complete bite in which a
large amount of venom is released. The potent venom of a young common lancehead (B.
athrox) may produce a profound DIC-like disorder, even through a mere scratching by a
single fang (Kornalik et Vorlova, 1990).
As a major portion of hemocoagulation disorders resemble DIC, i.e. procoagulation in
certain stages and levels of severity, and microthromboses extending to thrombosis develop
as well. For example, a bite by Bothrops lanceolatus caused 11 cases of intensive cerebral,
pulmonary, and myocardial thrombotic complications requiring thrombolytic treatment within
12 to 96 hours in 50 patients in Martinique (Thomas et al., 1995). There has also been a
description of thrombotic ischemia in the arteria mesenterica superior catchment area, which
developed 3 days after a bite from the South American bushmaster (L. muta) (Rosenthal et al.,
2002).
In the course of DIC-like consumption coagulopathy, affliction of endothelial and
subendothelial structures is generated, including interstitial edema and microthromboses in
lungs, amongst other things. This causes respiratory failure of the ALI/ARDS type that
requires oxygen therapy or even mechanical ventilation. At the same time, hemorrhaging into
lungs may occur.
Acute oliguric renal failure with necessary hemodialysis is a common type of
complication and the most frequent cause of death reported. A prothrombotic status of the
hemocoagulation system, with intraglomerular production of fibrin deposits, hypovolemia,
and hypotension all giving rise to this kind of failure, plus there is probably a direct effect by
venom components on renal tubules (B. jararaca). Thus, acute renal failure is typically a
result of ischemia and direct toxin effects. Histologically, this involves acute tubular necrosis,
and less frequently cortical necrosis.
Laboratory test results in instances of envenoming by snakes of this group mostly reveal
symptomatology of a hemocoagulation disorder. In over half of those affected, coagulation of
blood will not occur; in laboratory tests according to Lee-White, the time will prolong to over
30 minutes. The disorder is usually DIC-like consumption coagulopathy, including activation
of fibrinolysis, i.e. PT, APTT, TT, and RT are prolonged. The FBG level is either lower or
even zero; reciprocal to this result is a decrease in FDP, including D-dim. A certain level of
thrombocytopenia is typical. AT activity could be just slightly decreased, especially in initial
stages of the disorder.
Urine, including the residual urine in oliguria, typically exhibits proteinuria and
hemoglobinuria. Renal failure will increase urea and creatinine serum levels.
ALI/ARDS pulmonary disorder is accompanied by a typical symptomatology of diffuse
flocculent densities and decreased oxemia.
Mortality: Snakebites caused by this snake group, especially concerning Bothrops and
Lachesis snakes, are associated with relatively high lethality. Fatality in most cases relates to
acute renal failure, respiratory failure, hemorrhaging, thrombosis, shock, and sepsis. In a
group of 309 envenomed persons in Ecuador, cerebral hemorrhaging was the cause in five out
of eight deaths.
214 Jiri Valenta

In Brazil, approximately 4,800 fatalities occurred in 1914. As therapeutic options

increased, the mortality rate subsequently decreased to 2.43% in 1949, 1.75% in 1972, and to
the recent figure of 0.59% of persons afflicted. In total, 60,647 cases of envenoming by
Bothrops snakes were registered in Brazil from 1986 to 1990, from which 234 affected
persons died, amounting to 0.39%. For the Lachesis genus, 1,529 cases of snakebite occurred
with 19 fatalities, which is a rate of 1.24% in mortality. Fatalities in Argentina for 1979
equaled six cases from a total of 109 snakebites, i.e. 5.5%, while Ecuador reported 5.4% for
the same period (Fan et Cardoso 1995).
Therapy: For first aid treatment and common principles of therapy, see chapter 5,
Snakebite: Therapy and precautions.
Application of a pressure immobilization bandage is not recommended due to the risk of
extension of local damage through the persistence of highly concentrated toxic hemorrhagic
and cytotoxic components at the point in question. Nevertheless, immobilizing the leg by
using a looser bandage is a useful option. Exhaustion of venom from the wound by, for
example, an extractor has not proven effective, but does not pose a danger unlike other
practices, e.g. cutting the wound, using a tourniquet, etc. Due to the potential risk of rapid
circulatory failure (L. muta), prompt transportation to a medical facility is recommended.
Available antivenoms:

* SORO BOTROPICO, Instituto Butantan, Brazil (Bothrops alternatus, B. jararaca, B.

jararacusu, B. moojeni, B. neuwiedi);
* POLYVALENT ANTIVENOM, Instituto Clodomiro Picado, Costa Rica (Atropoides
nummifer, Botriechis lateralis, Botriechis nigroviridis, Botriechis schlegeli, Bothrops asper,
Cerrophidion godmani, Lachesis muta stenophrys, Porthidium nasutum, Porthidium
ophryomegas).

In Central America, there is a producer of a sheep polyvalent antivenom, the Instituto

Clodomiro Picado in Costa Rica.
A certain level of cross immunity can be expected, i.e. the possibility of applying
antivenom relevant for bites by other members of this group; nevertheless, the effects of
certain significant venom components, such as prothrombin activators, are sometimes
difficult to control via specific immunotherapy.
Administering antivenom is indicated should worse systemic symptoms develop,
examples including hemorrhaging, hypotension, and a significant prolongation of blood
coagulation time discovered via laboratory tests, be it according to Lee-White, or PT, APTT,
and TT.
The low immunogenicity of certain venom components will be reason enough for the
necessary application of larger amounts of antivenom, where indicated. For example, the
Ministry of Health in Brazil recommends 10-20 vials of antivenom as an initial quantity in
cases of evident envenomation by the South American bushmaster (L. muta); but sometimes a
lower quantity may be sufficient. The initial two vials may settle the hemocoagulation
disorder within 6 hours (Salligan et al., 2004). Potential coagulopathy should be primarily
treated by means of sufficient quantity of antivenom.
In some circumstances, local envenoming symptoms may be more severe. Any
developing dermal bullae or possibly lesser necrosis, which is a predisposition to infectious
complications, should be hastily removed and the affected area treated adequately. In
 Envenoming and Snakebite Treatment in Specific Snake Groups 215

addition, the development of compartment syndrome cannot be fully precluded. In cases of

any suspected disorder of district perfusion, the limb must be treated by elevation and general
administration of manitol, with doses of 0.5-2 g/kg IV, in the course of about 30 minutes. If
the risk of ischemia in the relevant area does not abate, fasciotomy can be indicated.
However, this kind of treatment is never carried out preemptively; see also chapter 6.4.3.3
Crotalus and Sistrurus genera: rattlesnakes and ground rattlesnakes. There may be a necessity
to amputate due to gangrene afflicting fingers.
Pre-emptive administration of antibiotics is not indicated, although sometimes
recommended; antibiotic therapy, if one is applied, is commenced only upon occurrence of
infectious complications.
In hypotension of circulatory failure and shock, the treatment is initiated by
volumotherapy: the circulating volume is replenished using an infusion of crystalloids or
colloids. Including fresh-frozen plasma in the therapy can positively influence a DIC-like
hemocoagulation disorder, if any. If application of infusions fails to ensure satisfactory
stabilization of the circulation, or hypotension persists or any further increase in volume is
contraproductive, vasopressure therapy is indicated using norepinephrine in continual
infusion, which will provide sufficient perfusion pressures; see chapter 5.3.3.5 Hypotension,
shock.
Sufficient intravascular volume together with adequate perfusion pressure needs to be
continued in order to retain diuresis, thereby helping prevent renal failure.
The most typical symptom of envenoming - hemocoagulation disorder - should be
primarily treated and regulated by means of administering antivenom in sufficient quantity.
Symptomatic therapy becomes necessary if antivenom cannot be applied or insufficient
quantity is available, or for later regulation of secondary changes, for instance persisting
prothrombotic activity.
Isolated hypofibrinogenemia without clinical signs of increased hemorrhaging will not
require any special symptomatic treatment. If caused by a direct effect of venom components
on FBG, it cannot be controlled by means of symptomatic treatment, e.g. using heparin. FBG
substitution is not recommended in this case, unless a sublimit level of FBG causes
hemorrhaging (Fan et Cardoso, 1995).
A DIC-like consumption coagulopathy, especially in its later phase, may prove difficult
to control by means of immunotherapy to a satisfactory extent and require symptomatic
treatment: therapy using fresh-frozen plasma (10-20 ml/kg) and AT substitution with
potential miniheparinization (70-210 units/kg/24 h) by means of UHF or LMWH with a
beneficial and more intense anti-Xa effect based on the phase and progress of the syndrome.
Naturally, heparin therapy is not indicated during the period of increased bleeding;
nevertheless, it may have a positive effect on managing hypercoagulation states associated
with the development of microembolisms. For potential PLT, erythrocyte, and FBG
substitution, ordinary guidelines apply; application of hemocoagulation factor concentrates is
normally not recommended; see chapter 5. 3. 3. 6 Hemocoagulation disorders.
Contraindication of application, unavailability, insufficient quantity or poor effectiveness
of antivenom, as well as cases of persisting severe symptoms of envenoming, can be resolved
by repeated plasmaferesis.
A patient can be discharged for home treatment after 24 hours following abatement of all
systemic symptoms of envenoming, normalization of significant laboratory values, and
stabilization of the local affection. Any persisting laboratory symptomatology of less
216 Jiri Valenta

significant prothrombotic activity should be resolved by preemptive miniheparinization, see

chapter 5.4 Convalescence following envenoming.

6.4.3.3. Crotalus and Sistrurus Genera: Rattlesnakes and Ground Rattlesnakes

Overview of the species. The Crotalus genus comprises about 30 species and a number of
subspecies of true rattlesnakes, see chapter 7 List of venomous snakes. The number provided
in bibliography varies due to classifying some species as subspecies and vice versa. The best
known rattlesnakes and at the same time the most significant species in terms of
epidemiology include the eastern diamond-backed rattlesnake (Crotalus adamanteus),
western diamond-backed rattlesnake (Crotalus atrox), South American rattlesnake (Crotalus
durissus), timber rattlesnake (Crotalus horridus), red diamond rattlesnake (Crotalus ruber),
Mojave rattlesnake (Crotalus scutulatus), and Northern Pacific rattlesnake (Crotalus viridis).
The Sistrurus genus, i.e. ground rattlesnakes, includes 3 species of lesser rattlesnakes: the
massasauga (Sistrurus catenatus), pigmy rattlesnake (Sistrurus miliarius) and Mexican
massasauga (Sistrurus ravus) that is now however placed into the Crotalus genus (C. ravus
ssp.).
Other names: EN: Sidewinders (for rattlesnakes and ground rattlesnakes). Neotropical
rattlesnake, cascabel, cascauella, maracaboia (C. durissus). Prairie rattlesnake (C. viridis
viridis). Desert sidewinder (C. cerastes).
Description: Crotalus snakes come in sizes from 50 cm (C. aquilus, C. cerastes, C.
intermedius, C. pusillus) to 200 cm (C. adamanteus, C. atrox), with the longest documented
length of 244 cm attributed to the eastern diamond-backed rattlesnake (C. adamanteus), the
largest venomous snake of North America. These creatures possess a robust body with a
broad head and rather short tail featuring a rattle, which is a warning apparatus comprising
several loosely articulated beads of hardened skin. Vibrating the rattle will produce an
unmistakable and quite powerful sound that is used by the snake to alert and ward of potential
intruders. Rattlesnake coloring usually is in shades of gray or brown, sometimes with a
reddish tint; although they can also be olive, or sandy to yellow, with a varied linear, ring-like
or spotted pattern. When they defend or attack, these snakes can form a very large coil,
mostly to one side, from the anterior part of their body, thereby allowing them to deliver a
strike over quite a distance. Despite their seemingly thick bodies and rather slower frontal
movement, strikes can be carried out very swiftly.
Sistrurus snakes mostly grow to 45-90 cm in length; their body is covered in darker spots
on light background; anatomically, they differ little to Crotalus snakes.
In terms of epidemiology, members of the Crotalus genus are the most significant snakes
in North America. In the USA, bites by them account for 65% of the annual number of 7,000-
8,000 bites by venomous snakes, with C. adamanteus, C. atrox, C. viridis, and C. horridus
being held largely responsible. The epidemiological significance of Sistrurus snakes nowhere
near matches that of the Crotalus variety, due to the smaller quantity of venom available and
lower abundance.
In terms of private ownership, rattlesnakes are one of the snake genera favored by
collectors. This corresponds to the incidence of bites outside their home range. In SE France
and N Germany, 21 cases caused by rattlesnakes were registered in 20 years, while in the
Czech Republic, there were 5 such occurrences in 10 years.
Habitat and range. The majority of Crotalus snakes reside rather arid habitats, for
example sparse pine and broad-leaved forests (C. adamanteus, C. pusillus, C. ruber), bushes
 Envenoming and Snakebite Treatment in Specific Snake Groups 217

and grass plains (C. durissus, C. enyo, C. molossus, C. scutulatus, C. viridis) and rocky or
sandy semideserts (C. atrox, C. cerastes, C. mitchelli), but can be found even in humid places
- cloud forests, swamps and flood areas (C. horridus, C. intermedius).
Their home range stretches from S Canada and eastern (C. horridus) as well as south-
eastern part of the USA (C. adamanteus, with C. atrox ranging over a large part of this
territory), western, south-western and southern USA (C. mitchelli, C. molossus, C. ruber, C.
scutulatus) as well as Mexico (C. atrox, C. basilicus, C. enyo, C. intermedius, C. mitchelli, C.
molossus, C. ruber, C. viridis) to Central and South America as far as SE Peru (C. durissus).
Sistrurus snakes inhabit diverse habitats, from swamps to peat-bogs and also arid
woodland and mountain slopes across North America from Ontario, Canada, as far as Texas
(S. catenatus), Florida (S. miliarius) and Central Mexico (Sistrurus i.e. Crotalus ravus).
Toxins: In the venoms of Crotalus and Sistrurus snakes, similarly to those of other
viperids (Viperidae), enzymatic compounds dominate over specific toxins with smaller
molecules. Venom effects can be generally described as predisposed to causing hypotension
due to vasodilation and extravasation, hemorrhaging, hemocoagulation effects, nephrotoxic
effects, and cytotoxic actions, i.e. necrotizing and myotoxicity; in some species, even a
neurotoxic impact is possible.
In particular, the venoms contain kallikrein-like enzymes, kininogenases releasing
bradykinin, and other components causing vasodilation hypotension from kininogen.
Hypotension can be intensified by a hemorrhagin present in the venom that damages
endothelium and capillary integrity, and causes the fluid to escape into the interstitium. This
can result in, aside from formation of edema and flushing inflammation mediators, in severe
hypotension and circulation collapse up to shock.
Components with hemocoagulation effects, again largely those of enzymatic nature, are a
typical complex of elements. They include fibrinogen-converting thrombin-like enzymes, for
instance gyroxin, that have in experiments carried out on dogs caused intravascular
coagulation in the lungs, heart, and liver. Another example is crotalase isolated from eastern
diamond-backed rattlesnake (C. adamanteus) venom, which is capable of initiating or
inducing a disorder of the consumption coagulopathy kind. Other components significantly
involved in affecting hemostasis are fibrino(geno)lytic proteinases present in the venoms of
probably all members of the genus, e.g. an isolate from so-called crotalotoxin in the venom of
C. durissus vegrandis. The functioning of platelets is affected in terms of inhibited
aggregation by crotaviridin and crotavirin, polypeptides isolated from C. viridis venom.
Conversely, convulxin and crotalocytin actually activate platelets and increase their
aggregation.
The action of components with hemocoagulation effects results in hemostasis disorders,
largely including symptoms of increased hemorrhaging, as well as potential thrombotic
complications. The hemostasis disorder is potentiated by the presence of hemorrhagin-like
components.
Another important group of venom components comprises proteolytic enzymes and other
general cytotoxic components causing local destruction of tissues and necrosis. Enzyme
myotoxins, largely those of the PLA2 type, responsible for local myonecrosis with the risk of
rising compartment syndrome and myoglobinuria, can also be placed within this group of
toxins. Damage to erythrocytes, including hemolysis, develops in a similar manner. In
addition, venoms also contain locally acting hyaluronidases facilitating the venom to
penetrate from the bitten site by damaging the extracellular matrix of affected tissue.
218 Jiri Valenta

Precipitation of myoglobin and hemoglobin in renal tubules is typically indicated as the

main reason for renal failure. Naturally, other factors causing damage to kidneys worthy of
mention include microthrombi generated in renal glomerules as consumption coagulopathy
proceeds, hypoperfusion in hypotension, and the direct action of venom components, such as
that of nephrotoxic lysolecitin which is produced by PLA2 cleaving lecithin.
Venoms from some members of the genera above, such as the South American
rattlesnake (C. durissus) or Mojave rattlesnake (C. scutulatus), contain a clinically evident
proportion of presynaptic neurotoxins, largely made up of PLA2. Neurotoxic effects can be
assigned to, for example, crotoxin and crotamine from C. durissus terrificus venom or
Mojave toxin from C. scutulatus.
The previously mentioned crotoxin possesses a certain capacity for modulating the
immunity response, in addition to the activities listed above.
The aggressiveness of Crotalus venoms, especially that of their cytotoxic component,
may even become apparent via contact with mucous membranes. Despite existence of an
overall normal course of envenoming, obturating edema affecting the mucous membrane in
the airways, which necessitated fibrooptical intubation, occurred in a man who sucked a bite
by C. horridus.
Local symptoms of envenoming: Following a snakebite, the wound or at least scratching
is visible in almost every case due to the size of the fangs. In most persons afflicted, moderate
or intense burning pain or feelings of strain set in early. A worse level of pain is not typical
for a bite from the Mojave rattlesnake (C. scutulatus), while the South American rattlesnake
(C. durissus) only causes pain in about a half of incidents. The bite wound may bleed. Painful
edema develops that progressively expands to related lymph nodes, and even beyond, perhaps
to the torso. Regional lymph nodes become swollen. Skin on the body part afflicted is
erythemated, with developing ecchymoses, petechiae, and later also serous or hemorrhagic
vesicles, which is a sign of local hemorrhagic and hemocoagulation dysfunction. A sensation
of heat on the side of the envenomed area is usually reported. Within hours, ecchymoses as
well as edema may move to the skin on the opposite side of body. Damage to skin and
subcutaneous regions often results in necrosis at the bitten site and its surroundings. The
necessity for partial amputation may arise if a finger has been affected.
Occurrence of compartment syndrome, including elevation of compartment pressure to
levels constricting tissue perfusion (30-55 mmHg), means a severe local affliction, usually
accounted for by profound myonecrosis, including an increase in the percentage of water in
the damaged muscle possibly caused by penetrated myotoxic venom components, although
more often by a direct bite into the subfascial area. Damage to the vascular integrity of tissue
may be of secondary importance in syndrome development. In the early phase, this will be
manifest by pain in the given area, or conversely hypesthesia, sensations of strain, and
contraction of the muscle in question, with associated pain when passively extended. If
smaller areas are affected, e.g. thenar, a pulse wave may still be evident in the limb as well as
signs of venous return flow.
A worse course of local affliction is quite typical for envenomings by most rattlesnake
genera, exceptions being the South American rattlesnake (C. durissus) and Mojave
rattlesnake (C. scutulatus), whose venoms do not contain a high proportion of cytotoxic
components.
Furthermore, abscesses formed as a result of secondary infection of tissue in the damaged
area cannot be precluded.
 Envenoming and Snakebite Treatment in Specific Snake Groups 219

Local affection, following a bite by snakes of the Sistrurus genus, is typically a factor in
the majority of cases, this being of a less significant nature and only accompanied by pain,
edema, lymphadenopathy, and erythema - no necrosis occurs.
Systemic symptoms of envenoming: About a quarter of bites by Crotalus and Sistrurus
snakes will not be associated with the release of venom and will proceed without
envenoming. If envenomation has occurred, symptoms or at least laboratory findings should
become manifest within 8 hours following an incident. In order to facilitate judgment of the
severity of envenomation by Crotalus snakes, namely those from North America, criteria that
define the levels of affection have been developed and used in bibliography.
No envenoming:

* Bite marks are present;

* At a local level: no edema, skin changes, and paresthesia;
* At a system level: no symptoms;
* Laboratory: no findings.

Minimum envenoming:

* At a local level: edema, erythema or ecchymoses without progression;

* At a systemic level: none or minimal symptoms;
* Laboratory: no significant findings.

Mild envenoming:

* At a local level: the affliction spreads over a major part of the limb;
* At a systemic level: signs that pose no threat to life, e.g. nausea, vomiting, systolic
pressure exceeding 80 mmHg, light tachycardia, paresthesia, etc., no signs of hemorrhaging;
* Laboratory: positive laboratory findings, but lacking significant abnormalities.

Severe envenoming:

* At a local level: edema and ecchymoses that rapidly spread all over the limb;
* At a systemic level: signs threatening life, e.g. altered consciousness, systolic pressure
lower than 80 mmHg, severe tachycardia, signs of respiratory failure, etc., spontaneous
hemorrhaging;
* Laboratory: severe affliction including significantly prolonged coagulation times,
severe thrombocytopenia, hypofibrinogenemia, and other biochemical results in either serum
or urine.

A systemic envenoming mostly proceeds with nausea and vomiting; diarrhea may follow.
Paresthesia is quite common, either perioral that spreads to the tongue and crown of the head,
or a tingling sensation in the fingertips. Furthermore, the envenoming is accompanied by
spasms and fasciculations that may change from local sensations to those at a systemic level,
myalgia, sensations of warmth or conversely cold and chill, including cold sweats, thirst,
tastes in the mouth resembling chewing gum, menthol or metal, plus lethargy, overall
weakness, and vertigo. Typically, the majority of those envenomed suffer tachycardia,
220 Jiri Valenta

accelerated breathing, and slightly increased temperatures. Within milder cases of

envenoming, blood pressure remains normal.
Worse cases of envenoming will continue with hypotension, which is partly due to
dilation of the bloodstream in addition to extravasation, which is quite typical for severe cases
of envenoming by rattlesnakes. Endothelial damage increases vascular permeability, as well
as loss of water, electrolytes, albumin, other blood proteins, and even blood elements in cases
of extreme damage. In places with the highest concentration of venom, i.e. largely locally at
the bitten site, these symptoms are the worst. At a systemic level, the reduced circulating
volume is followed by hypovolemia with hypoalbuminemia, and potentially
hemoconcentration, which may result in distribution shock, including disorder of tissue
perfusion, lactate acidosis and renal failure; see below. The sharp rise of intensive life
threatening hypotension with shock typically poses a risk to as many as 7% of envenomed
persons (Juckett et al., 2002). Capillary affliction includes respiratory failure based on the
sequestration of water and ions into the pulmonary interstitium, or even the alveoli
(ALI/ARDS, pulmonary edema) or pleural cavity. Gross endothelial damage may be
exhibited by extravasation of erythrocytes, i.e. hemorrhaging, which affects the lungs,
myocardium, kidneys, peritoneal cavity, and rarely the CNS.
Impact on hemocoagulation occurs fairly frequently, with severity ranging from a
moderate level of hypofibrinogenemia or thrombocytopenia found via laboratory tests,
extending as far as a serious hemostasis disorder with symptoms of spontaneous bleeding -
from wounds, hematuria, hematemesis, enterorrhage, and internal hemorrhaging, thereby
signifying symptomatology of DIC-like consumption coagulopathy. However, less significant
cases of local hemorrhaging occur, with laboratory tests revealing thrombocytopenia,
hypofibrinogenemia up to afibrinogenemia, prolonged coagulation times, and the discovery of
FDP. Changes in hemocoagulation mostly persist for 7-14 days, with frequent recurrence,
sometimes regardless of antivenom being applied; see chapter 5.3.1 Specific treatment,
immunotherapy; particularly in relation to recurrent loss of PLT and FBG. Thrombocytopenia
arises based on PLT activation with subsequent aggregation, consumption and platelet
sequestration into the affected areas. It is the severity of local affliction, damaged vascular
wall, and PLT sequestration into these areas that may determine the level of
thrombocytopenia, especially a late or recurrent variety. The earlier occurrence of
thrombocytopenia is typically caused by aggregation proteins of the venom, or through
activation as consumption coagulopathy proceeds. Hypofibrinogenemia extending to
afibrinogenemia, if isolated, i.e. probably generated by direct fibrinolytic action of venom
components, will typically not result in symptoms of increased hemorrhaging.
Factors involved in the onset of renal failure include hypovolemia due to dilation and
extravasation, microthrombosis of the kidney vascular beds within DIC, hemolysis with
hemoglobinuria, rhabdomyolysis with myoglobinuria, and probably the direct nephrotoxic
effect of some venom components. Renal failure potentiated by myonecrosis with CC
elevation found in the laboratory is a relatively frequent complication of envenomings by
South American subspecies of the South American rattlesnake (C. durissus), while bites from
the Central American C. durissus durissus do not cause this type of affection.
A bite from rattlesnakes with venoms containing a clinically more significant proportion
of neurotoxins, e.g. the South American rattlesnake (C. durissus), Mojave rattlesnake (C.
scutulatus), and the timber rattlesnake (C. horridus), will generate disorders on
neuromuscular end-plates with neurotoxic symptoms like weak paralysis, as manifest
 Envenoming and Snakebite Treatment in Specific Snake Groups 221

clinically by ptosis, external ophtalmoplegia with blurred vision, anisocoria or mydriasis,

overall muscle weakness, and exhaustion. Any possible affection of respiratory muscles is
exhibited via accelerated shallow breathing; nevertheless, total paralysis of respiratory
muscles is not probable. What remains of utmost importance is that local affection following
an attack from the species above is mild, consequently giving no true indication as to the
extent of systemic envenoming. Underestimating the severity and providing insufficient
treatment can have significant after-effects.
Bites by Sistrurus snakes will proceed in most cases without a severe systemic response
and significant laboratory findings, the envenoming only manifest by local affliction.
However, even in such cases a snakebite should not be overly dismissed, as a systemic
envenoming similar to that caused by exposure to the venom of Crotalus snakes is still
possible, albeit rare.
Laboratory findings: As for non-specific findings, a mild level of neutrophilic
leukocytosis about 10 x 109/l is typically present in worse envenomings. Frequently, CC is
elevated, including MB-fraction, which in severe cases will average 5 kat/l, but might
exceed 33 kat/l, indicating a high predisposition for renal failure occurring. Elevated levels
of LD, myoglobin and AST are not unusual. The extent of elevated levels of tissue enzymes
simulates biochemical symptomatology of myocardial damage; however, troponin I was
found to be negative in children (Cupo et al., 2003). Intravascular hemolysis is accompanied
by either evidence of free hemoglobin or a positive result of Coombs test and decreased Hct.
Affected hemocoagulation is manifest by either ordinary hypofibrinogenemia, potentially
extending to afibrinogenemia, as well as isolated thrombocytopenia, or symptomatology of a
full DIC-like consumption disorder with prolonged PT, APTT, RT, and positive FDP results,
including very high D-dim levels, which may extend beyond 8 mg/l (the standard level being
below 0.5 mg/l). Thrombocytopenia as well as other symptoms found in the hemocoagulation
laboratory tests may arrive relatively late (thrombocytopenia even after 72 hours), persist for
several days, may react or not to the administration of antivenom, or possibly return to
pathological levels within hours or 7 days. PLT may display hypoaggregability due to the
impact of venom components. If that is the case, thrombocytopenia will not occur.
Glycosuria, proteinuria, hemoglobinuria, myoglobinuria, and even hematuria could be
found in urine.
Mortality: A high number of the 138 cases resulting in death over 10 years in the USA
involved cases of envenoming by Crotalus snakes. Out of 7,000-8,000 bites a year caused by
Crotalinae snakes, there are 5-12 fatalities, of which 95% are due to attacks from the eastern
diamond-backed rattlesnake (Crotalus adamanteus) and the western diamond-backed
rattlesnake (Crotalus atrox) (Juckett et Hancox, 2002, Shaw et Hosalkar, 2002).
In the Brazilian state of Sao Paulo, over 12,000 snakebites were analyzed for the period
from 1988 to 1993. From this number, 1,359 (12%) envenomings and 13 fatalities were
assigned to the South American rattlesnake (Crotalus durissus) (Ribeiro et al., 1998). A
different source calculates lethality via envenomation by this rattlesnake as 1.9% (Bucaretchi
et al., 2002). A fatal course may include acute renal failure.
Therapy: For first aid treatment and common principles of therapy, see chapter 5,
Snakebite: Therapy and precautions.
Application of a pressure immobilization bandage is debatable due to high local damage
to tissues, so is not recommended in most cases. If, however, several hours delay in receiving
eventual treatment is expected, and it is possible to put on the bandage within a few minutes
222 Jiri Valenta

of an attack, this can be a worthwhile option. In such cases, both arterial and venous
bloodstreams must be unrestrained, and also monitored to ensure the presence of a pulse and
to eliminate ischemic pain in the limb. Due to the general cytotoxic effect of the venom, this
is of particularly heightened importance. If measurement is possible, the recommended
pressure of the bandage is around 20 mmHg (Juckett et Hancox, 2002).
Even though using the widely recommended Sawyers extractor has not been proven as
effective in a satisfactory manner, it should not be ruled out. If one is applied, the process
must be carried out very soon after a bite, approximately 3-5 minutes. The extractor is kept in
place for about 30 minutes.
Available antivenoms:

* CROFAB CROTALIDAE POLYVALENT IMMUNE FAB (OVINE), Protherics, USA

(C. adamanteus, C. atrox, C. horridus, C. molossus, C. scutulatus, C. viridis, etc.);
* SORO ANTICROTALICO, Instituto Butantan, Brazil (C. durissus cascavella, C.
durissus collineatus, C. durissus terrificus);
* POLYVALENT ANTIVENOM, Instituto Clodomiro Picado, Costa Rica (C. durissus
durissus, and others).

In approximate terms, CROFAB is five times more effective than ANTIVENIN

(CROTALIDAE) POLYVALENT (ACP), Wyeth, USA, a horse antivenom produced in the
past which usually triggered allergic responses. Acute reactions to the antivenom upon ACP
administration reached 23-56%, while the figure for CROFAB is just 14%; as for serum
sickness, incidence of reactions for the former amounted to 18-86% compared to 16% for
CROFAB (Gold et al., 2002).
If envenomation is proven, even if only moderately severe local symptoms are exhibited,
application of 4-6 vials of CROFAB is advisable. If the state consequently improves, 2 vials
should be given at 6, 12, and 18 hours later. If symptoms still do not recede, the
administration schedule should be repeated. Even higher amounts of antivenom are
sometimes recommended, i.e. an initial 10-15 vials for mild envenomings and 15-20 vials in
severe cases, a dosage which is subsequently repeated based on patients status. Of course,
often a lesser amount proves sufficient - a total of 8 vials or even less. The initial vial of
antivenom should be diluted with 250-500 ml of electrolyte solution. A low rate of instillation
should be used for application over the first 10 minutes, with the remainder being instilled
within an hour. Application of the antivenom is recommended by the manufacturer of
CROFAB within 6 hours following the bite; nevertheless, a beneficial effect has been
demonstrated after 9 hours and even 52 hours. Treatment by means of giving a sufficient
quantity of effective antivenom will no only mitigate or even eliminate systemic symptoms of
envenoming, including early hemocoagulation disorders and laboratory results revealing
thrombocytopenia and hypofibrinogenemia, but should positively and preemptively influence
the severity of edema, development of compartment syndrome, and any necessary
fasciotomy. If edema continues to spread and compartment pressure increases, controlling
further development by administering additional vials of antivenom is advisable, see below.
Recurrence of symptoms or laboratory symptomatology is frequent, namely through the
use of CROFAB. This is explained by the progressive release of venom components from the
pool at the bitten site, but primarily due to rapid clearance of the antivenom.
 Envenoming and Snakebite Treatment in Specific Snake Groups 223

Mild dermal manifestation of an allergy, urticaria, as the venom is being applied may not
contraindicate the treatment and does not indicate the onset of anaphylaxis. Should there be a
threat of fasciotomy or severe symptoms of systemic envenoming, specific immunotherapy of
the patient can continue provided appropriate antiallergic measures are applied.
Special attention must be paid to local symptoms of envenoming as regards their severity.
To inspect an increase in edema, the affected limb is measured at multiple points above and
below the bitten site approximately every 15-20 minutes until the state becomes stabilized or
abates. The progression of edema towards the torso should also be monitored and its edges
recorded, for instance, by tracing lines on the skin. Skin afflicted by vesicles and necrosis
must be kept under tight control, requiring prompt removal of bullae and necrotic tissue as
well as proper care for the wound bed.
If severe edema has occurred and compartment syndrome is suspected, measuring
compartment pressure is appropriate. If pressure values rise above 30 mmHg and clinical
signs of the syndrome exist, applicable attempts to decrease pressure in the tissue include
elevation of the limb and administration of manitol (0.5-2 g/kg of weight) during 30 minutes
under parallel or even repeated application of a larger quantity of antivenom, i.e. 10-20 vials
within 60 minutes (Gold et al., 2003). Benefits have also been recorded via hyperbaric
oxygen therapy. Treating severe local symptoms of envenoming with a sufficient quantity of
antivenom is typically effective enough to avoid compartment syndrome and any necessary
fasciotomy. However, this must be applied if a risk of increased compartment pressure and
clinical symptoms of the syndrome, particularly pain when the muscle is passively extended,
still persist despite providing the adequate therapy discussed above. The time recommended
for this is an additional 60 minutes once antivenom has been instilled. As fasciotomy can be
associated with subsequent damage to nerves, contractures, skin deformities, and even partial
loss of function of the limb, it is applied only once all remaining conservative medical
procedures have been attempted. It must never be carried out preemptively.
As the incidence of primary infections is very low, antibiotics are not indicated; they are
applied only when infectious complications occur.
Hypotension or circulatory failure and shock can mostly be avoided by volumotherapy:
the circulating volume is replenished using an infusion of crystalloids or colloids. In addition,
including fresh-frozen plasma in the therapy can positively influence a hemocoagulation
disorder, if any. If application of infusions fails to ensure satisfactory stabilization of the
circulation, or hypotension persists or any further increase in volume is contraproductive,
such as in the case of respiratory failure (ALI/ARDS), vasopressure therapy is indicated using
norepinephrine in continual infusion, which will provide sufficient perfusion pressures; see
chapter 5.3.3.5 Hypotension, shock.
A satisfactory level of diuresis should be retained by maintaining sufficient intravascular
volume together with adequate perfusion pressure. Urine volume higher than 90 ml/h has a
preventative effect against renal failure.
Any persisting signs of hemocoagulation disorders must be treated symptomatically as
necessary. Isolated hypofibrinogenemia without clinical signs of increased hemorrhaging, as
well as persisting mild thrombocytopenia, will not require any special symptomatic treatment,
indicating repeated application of antivenom in most cases, especially in early phases of
envenoming. However, late and recurrent thrombocytopenia proves typically obstinate to
specific immunotherapy. In instances of critical reduction of platelets despite repeated
application of antivenom and symptomatic therapy of potential consumption element, the
224 Jiri Valenta

platelets must be substituted. A DIC-like consumption coagulopathy, again chiefly in its later
phase, may be difficult to control by means of immunotherapy to a satisfactory extent and
will require symptomatic treatment: therapy by means of fresh-frozen plasma (10-20 ml/kg)
and AT substitution with potential miniheparinization (70-210 units/kg/24 h). However,
heparinization is not indicated whenever intense hemorrhaging occurs. For potential PLT,
erythrocyte and FBG substitution, ordinary guidelines apply; application of hemocoagulation
factor concentrates is usually not recommended; see chapter 5.3.3.6 Hemocoagulation
disorders.
The level of severity of the clinically evident effect of neurotoxins in C. durissus and C.
scutulatus will not cause respiratory failure requiring mechanical ventilation. Nevertheless,
pulmonary affection of the ALI/ARDS type may still arise, and in very rare cases may reach a
level where mechanical ventilation must be applied. Such cases will require tracheal
intubation and supportive or managed mechanical ventilation.
Observation over 12-24 hours will be necessary in bites lacking evidence of envenoming,
even if caused by Sistrurus snakes. Following 24-48 hours once all symptoms of severe local
type and systemic envenoming have abated, a patient can be discharged from hospital.
Stabilized and minor local damage can be dealt with by means of outpatient treatment. Any
persisting laboratory symptomatology of less significant prothrombotic activity should be
resolved by preemptive miniheparinization, see chapter 5.4 Convalescence following
envenoming.

6.4.3.4. Ovophis - Mountain Pit Vipers, Protobothrops and Trimeresurus, Asian Pit
Vipers and Tropidolaemus - Temple Vipers
Species: The relatively extensive Trimeresurus genus contains about 36 species of
snakes. More recently, additional species have been described and others reclassified under
two snake genera: the Ovophis genus with its four species, i.e. the Chinese mountain pit viper
(Ovophis monticola), Ryukyu Island pit viper (Ovophis okinavensis), Tonkin pitviper
(Ovophis tonkinensis), and Chasens mountain pit viper (Ovophis chaseni); and the
Tropidolaemus genus containing the Waglers palm viper (Tropidolaemus wagleri). A new
Protobothrops genus has been recognized, comprising several forms that were once placed
into Trimeresurus, Trigonocephalus, and other genera - this involves Protobothrops cornutus,
Protobothrops elegans, Protobothrops flavoviridis, Protobothrops jerdonii, Protobothrops
kaulbacki, Protobothrops mucrosquamatus, Protobothrops tokarensis, and Protobothrops
xiangchengensis. In addition, monotypic Triceratolepidophis and Zhaoermia genera have
been described; the latter was formerly named Ermia, however, this name turned out to be
reserved for a genus of the Orthoptera insects. Furthermore, separation of some additional
genera from the Trimeresurus and Ovophis range has been suggested, such as Garthius,
Cryptelytrops, Parias, Viridovipera, Peltopelor, Popeia, and Himalayophis; however, general
acceptation of this proposal still remains an open issue.
Out of the number of snakes of the Trimeresurus and Protobothrops genera, the
following are examples of epidemiological importance: the white-lipped tree viper
(Trimeresurus albolabris), elegant pit viper [Protobothrops (Trimeresurus) elegans], redtail
(bamboo) pit viper (Trimeresurus erythrurus), Philippine pitviper (Trimeresurus
flavomaculatus), habu [Protobothrops (Trimeresurus) flavoviridis], common bamboo viper
(Trimeresurus gramineus), Kramers pit viper (Trimeresurus macrops), brown spotted pit
viper [Protobothrops (Trimeresurus) mucrosquamatus], mangrove viper (Trimeresurus
 Envenoming and Snakebite Treatment in Specific Snake Groups 225

purpureomaculatus), Stejnegers bamboo viper (Trimeresurus stejnegeri) and Sumatra pit

viper (Trimeresurus sumatranus); for other species, see chapter 7 List of venomous snakes.
Other names: EN: Asian arboreal pit viper; FR: Fer-de-Lance asiatique; JAP: Habu
(Trimeresurus). EN: (White-lipped) green pit viper; FR: Vipre des bambous (T. albolabris).
EN: Japanese habu (Protobothrops flavoviridis), Chinese habu (Protobothrops
mucrosquamatus), Chinese green pit viper (T. stejnegeri), Indo-Chinese mountain (pit) viper
(Ovophis).
Description: This group of genera comprises small to medium-sized snakes at lengths
from 40 cm (Trimeresurus borneensis, T. gracilis, T. gramineus) to 100-120 cm
(Protobothrops elegans, P. jerdoni, P. mucrosquamatus, P. tokarensis, Trimeresurus
flavomaculatus); the documented maximum of 160 cm attributed to T. sumatranus. Another
variety, Protobothrops flavoviridis, normally grows to between 130-230 cm, but a stated
length of 300 cm is unverified and would be an exceptional specimen of its genus. Snakes of
the genera above are slender but well-muscled animals, with a typical triangular head often
featuring a prominent snout. The color range may encompass green, green/yellow or
green/blue, but also tints of brown, brown/gray, and brown/red.
A majority of these snakes are arboreal or at least semi arboreal creatures, normally
active at night.
They can move relatively swiftly; some show quite short-tempered behavior with even
signs of aggressiveness. The Sumatra pit viper is typically referred to as the most aggressive
viperid. Nonetheless, this reputation does not put off snake keepers, in fact, the opposite is
true. One factor for this may be the quite attractive appearance of these snakes. In the Czech
Republic, 20 snakebites from Trimeresurus snakes were registered within the last 10 years.
In places within their home range, these snakes have a quite important role in terms of
epidemiology: Protobothrops mucrosquamatus is responsible for 50% of all envenomations
in the territories of Indonesia and Hong Kong, plus 30% of cases of envenoming in Taiwan
from 1904 to 1971 were caused by this snake. In Thailand, where snakes of this group cause
27% of snake bites, 278 cases of envenomation by Trimeresurus albolabris and T. macrops
were treated by just a single Bangkok hospital during 1987 to 1995 (Rojnuckarin et al., 1998).
Habitat and range. Pit vipers of the genera above inhabit scrubland, plantations, bamboo
and mangrove stands, woods and forests, primarily in hilly areas, but often near water or in
humid localities. Their home range covers a vast swathe of land in South and East Asia:
Pakistan, the Indian Peninsula region (including Nepal and Sri Lanka), S China, Taiwan, the
former Indochinese countries, Malaysia, Indonesia, the Philippines and the islands of Japan.
Toxins: As with other viperids (Viperidae) and Crotalinae snakes, venoms of the genera
above are largely composed of enzymatic components.
The venom contains kininogenases, kallikrein-like enzymes that can release bradykinin
from kininogen, as well as directly active enzymes potentiating bradykinin function, and
substances with direct effects on myocardium.
Furthermore, the venom contains components increasing vascular permeability, i.e.
hemorrhagins, for example mucrotoxin, a hemorrhagic factor in Protobothrops
(Trimeresurus) mucrosquamatus venom, and hemorrhagins isolated from Protobothrops
flavoviridis venom.
Resulting effects may include hypotension, circulation collapse, and shock; cases have
been reported of myocardial failure with increased pressure in the pulmonary trunk and
bradycardia (Protobothrops mucrosquamatus, P. flavoviridis).
226 Jiri Valenta

Hemocoagulation-affecting components, again largely those of an enzymatic nature,

present another typical complex of elements, comprising fibrinogen-converting thrombin-like
enzymes, such as elegaxobin from Protobothrops elegans venom, which cause consumption
coagulopathy. In addition, there are fibrino(geno)lytic proteinases, like those in
Protobothrops mucrosquamatus; specific inhibitors of plasmatic coagulation factors with
anticoagulation effects, for instance in T. stejnegeri and T. gramineus; PLT activators, e.g.
those in Protobothrops mucrosquamatus, and a number of others. The action of
hemocoagulation-affecting components results in hemostasis disorders, principally featuring
symptoms of increased hemorrhaging, as well as potential thrombotic complications.
Local damage of afflicted tissues is caused by a complex of cytotoxic enzymes. These
may even cause a certain degree of rhabdomyolysis on occasion; they are also responsible for
other things, such as necrosis and possible compartment syndrome.
Local symptoms of envenoming: Soon after envenomation, relatively intense pain is felt
and spreads progressively along with developing edema and lymphadenopathy. Edema
usually extends over a half of the limb, although it can rarely cross regional lymph nodes and
expand to the torso. In a nearly half of cases of bites from Trimeresurus albolabris,
lymphadenopathy occurs including swollen and painful regional lymph nodes. The skin of the
afflicted area may turn red, with ecchymoses forming, and, more rarely, petechiae. The bite
wound often bleeds, especially if cut open as part of incompetent first aid measures.
In the course of time, vesicles and later necrosis can develop. Necrosis primarily affects
localities of tight compartments - fingers and toes. The incidence of necrosis fluctuates at
around 2-3%, with the highest figure of 6.8% concerning bites by Protobothrops flavoviridis.
Blisters and necrotic portions of skin and sub-cutaneous areas are subject to the occurrence of
secondary infections, for which an incidence of about 5% is registered. Rarely, gangrene of
the fingers occurs, necessitating amputation; within a group of 80 persons probably
envenomed by Trimeresurus albolabris or Trimeresurus macrops in Bangkok, finger
amputation was necessary in 2 out of 9 affected patients.
Compartment syndrome in the front tibial region following a bite of a lower limb, with
tissue pressure that constricts perfusion, presents a significant local complication usually
arising after attacks by Prothobotrops flavoviridis.
Proof of the cytotoxic aggressiveness of venoms in this snake group is evidenced by a
case of lip and tongue edema which occurred following a wound being sucked after a bite.
Convalescence of a severe local affliction might last months; even permanent damage in
the manner of deformities (Protobothrops elegans) and ankylosis might be caused.
Systemic symptoms of envenoming: The severity of a local affliction does not correspond
to that of systemic affliction. Cases exist of severe local damage that presented minimum
systemic symptoms, as do instances of a severe progress lacking necrosis. Thus, severity of a
systemic envenomation should not be generally assessed according to the extent of local
symptoms. Indeed, the reverse is true: cases with a harsh local response tend to accompany a
lower degree of systemic response, while a less intensive local affliction is exhibited in cases
of envenoming complicated by hemorrhaging. This situation can be explained by the
establishment of a closed pool of venom in tight compartments, which will slow down
penetration of venom into the system whilst increased local devastation of tissue is occurring.
Systemic envenoming mostly starts with the following prodromes: nausea, vomiting,
abdominal pain, diarrhea, and increased temperatures. Harsher cases may include lethargy, or
possibly temporary syncope. Envenoming primarily continues with hypotension and
 Envenoming and Snakebite Treatment in Specific Snake Groups 227

hemocoagulation abnormities normally only found in laboratory tests. Decreased blood

pressure caused by vasodilation and extravasation of fluids may result in circulation collapse
or even shock, including tachypnea, cyanosis, and coma.
Hemostasis disorder is firstly evident only in laboratory results, but may not manifest
clinically at all in lighter cases. However, in more severe instances, it results in hemorrhaging,
usually of a local type, but also at a systemic level. Examples include hemorrhaging from the
gums, nose and into the GIT, hematuria, and more unusually fatal cerebral hemorrhaging, e.g.
via Protobothrops mucrosquamatus. Spontaneous bleeding occurs in nearly one fifth of those
envenomed by Trimeresurus albolabris. Susceptibility to hemorrhaging mainly occurs in
persons affected with whole blood clotting time (based on Lee-White) of longer than 15
minutes, the presence of thrombocytopenia with a platelet count less than 150 109/l, and a
bite wound not localized in the tight compartment of fingers.
In some cases, the hemostasis disorder is not in the nature of consumption coagulopathy,
but is probably due to increased fibrino(geno)lytic activity of venom components, resulting in
isolated defibrination. In other cases, like T. albolabris and T. stejnegeri, the action of
thrombin-like enzymes generates a DIC-like consumption disorder with relevant laboratory
results found - hemorrhaging or suspected microembolism entry into the lungs or kidneys,
including symptomatology of worsened oxemia or extraordinary cases of acute tubular
necrosis of the kidneys.
Cases of envenoming by Protobothrops flavoviridis and Trimeresurus macrops are not
associated with hemostasis disorders.
Other less frequent symptoms of envenoming described include a case of stool
incontinency, difficulties urinating (Ovophis chaseni), oliguric renal failure, ECG changes
(Protobothrops mucrosquamatus), and the death of a 10-week-old fetus in a pregnant woman
in Japan, who featured only a relatively light course of envenomation without signs of
increased bleeding (Nasu et al., 2004).
Generally, worse systemic envenomings can be expected following a snakebite from
Protobothrops elegans, P. flavoviridis, P. mucrosqamatus, and Trimeresurus albolabris,
while for the majority of other snakes of this group, the tendency is for a local affliction with
lighter systemic reactions to arise.
In instances when no symptoms are exhibited, a patient is observed for 24 hours. If
neither clinical nor laboratory symptoms of systemic response arise, a systemic envenomation
can be ruled out.
Laboratory findings: Specific findings in cases of envenoming by this group of snakes
are principally present in hemocoagulation laboratory tests; they normally resemble DIC.
Prevailing symptomatology includes hypofibrinogenemia, potentially extending to
afibrinogenemia, thrombocytopenia, and elevation of FDP, sometimes that of predominantly
non-stabilized forms, but often D-dim. Reduced levels of 2-antiplasmin and AT are
registered, probably a result of these substances being fully spent due to the inhibition of
hyperactivities of plasmin and thrombin. In addition, increased levels of soluble fibrin-
monomer complexes have been detected. In cases of worse hemostasis disorders,
prolongation of PT, APTT, and TT occurs. A laboratory form of hemocoagulation
dysbalance, such as a certain degree of hypofibrinogenemia and increased FDP (D-dim) level,
may persist for 2 weeks.
Neutrophilic leukocytosis is obligatory; based on the increased myoglobin level in serum
and urine, and signs of rhabdomyolysis cannot be precluded.
228 Jiri Valenta

Mortality: Before antivenom therapy was implemented, i.e. prior to 1905, the fatality of
envenomings by the habu (Protobothrops flavoviridis) in Japan amounted to 11-24%. Warrell
(1995) states that the mortality rate dropped owing to improved therapy, principally
antivenom treatment, to 0.9% in this country during 1962 to 1970, and even 0.54% between
1971 and 1984 from a total of 467 persons so affected.
In Taiwan, 8% of those envenomed by Protobothrops mucrosquamatus died in the period
1904 to 1971. In Indonesia, the lethality of snakebites from the white-lipped tree viper
(Trimeresurus albolabris) accounts for 2.4%. Individual cases of fatalities from bites by the
Chinese mountain pit viper (Ovophis monticola) and elegant pit viper (Protobothrops
elegans) have been described, as well as relatively frequent bites caused to people harvesting
tea in Java.
In the majority of victims, death was caused by hemorrhaging, namely of the cerebral
form.
Therapy: For first-aid treatment and ordinary principles of therapy, see chapter 5, Snake
bite: Therapy and precautions.
Application of a pressure immobilization bandage is not recommended due to the risk of
extending local damage through the persistence of highly concentrated cytotoxic venom
components at point in question. Nevertheless, immobilizing the leg by using a looser
bandage is useful.
Antivenom available:

GREEN PIT VIPER ANTIVENIN, Thai Red Cross, Thailand (T. albolabris and other
Thailand species).

For the remainder of the species, a certain level of cross-immunity is possible.

Application of antivenom is indicated in cases where worse systemic symptoms develop, such
as hemorrhaging and hypotension, or if laboratory findings show prolonged clotting time
(according to Lee-White - over 15 minutes), and thrombocytopenia below 150 109/l,
especially if a bite is located outside the tight compartment of a finger; this situation
facilitates an increased level of hemorrhaging. Of course, the prolonged clotting time test can
be replaced by another, e.g. PT, APTT, TT, or FBG level.
The antivenom is administered in an initial amount of 3-6 vials, which should establish
hemocoagulation balance. Recurrence of symptoms or severe laboratory symptomatology will
require repeated application of antivenom.
Special attention must be paid to local symptoms of envenoming for their relative
severity. Developing dermal bullae and necrosis, although typically not very large, are a
predisposition to occurrence of infectious complications. Prompt removal of bullae and
necrotic tissue as well as proper care for the wound bed is advisable. Compartment syndrome,
largely in the front tibial region following a bite in this area, presents a risk in exceptional
cases. It must be treated by elevating the limb and administering manitol, with doses of 0.5-2
g/kg IV in the course of about 30 minutes. If the risk of perfusion failure in the relevant area
does not abate, fasciotomy is indicated. However, this kind of treatment is never carried out
preemptively; see also chapter 6.4.3.3 Crotalus and Sistrurus genera: rattlesnakes and pygmy
rattlesnakes. There may be a necessity for amputation due to gangrene afflicting fingers.
 Envenoming and Snakebite Treatment in Specific Snake Groups 229

Pre-emptive administration of antibiotics is not indicated, although sometimes

recommended; antibiotic therapy, if one is applied, is introduced only upon the occurrence of
infectious complications.
For hypotension of circulatory failure and shock, treatment is initiated by volumotherapy:
the circulating volume is replenished using an infusion of crystalloids or colloid solutions, or
fresh-frozen plasma. In addition, including fresh-frozen plasma in the therapy can positively
influence a DIC-like hemocoagulation disorder, if any. If application of infusions fails to
ensure satisfactory stabilization of the circulation, or hypotension persists or any further
increase in volume is contraproductive, vasopressure therapy is indicated using
norepinephrine in continual infusion, which will provide sufficient perfusion pressures; see
chapter 5.3 3.5 Hypotension, shock.
Appropriate intravascular volume together with adequate perfusion pressure needs to be
maintained to retain sufficient diuresis, and prevent potential but rare renal failure.
Any signs of hemocoagulation disorders must be treated symptomatically as necessary, in
parallel with the application of antivenom. Isolated hypofibrinogenemia without clinical signs
of increased hemorrhaging, as well as persisting mild thrombocytopenia, will not require any
special symptomatic treatment and indicates repeated application of antivenom in most cases,
especially in the early phases of envenoming. A DIC-like consumption coagulopathy,
particularly in its later phase, may be difficult to control by means of immunotherapy to a
satisfactory extent and will require symptomatic treatment: therapy using fresh-frozen plasma
(10-20 ml/kg) and AT substitution with potential miniheparinization (70-210 units/kg/24 h)
based on the phase and progress of the syndrome. Heparin therapy is not indicated over the
period of increased bleeding; nevertheless, it may have a positive effect on managing
hypercoagulation states that may sometimes even be associated with the development of
microembolisms. For potential substitution of platelets, erythrocytes and FBG, ordinary
guidelines will apply. Administering hemocoagulation factor concentrates is not
recommended; see chapter 5.3.3.6. Hemocoagulation disorders.
A patient can be discharged for home treatment after 24 hours following abatement of all
systemic symptoms of envenoming, normalization of significant laboratory values, and
stabilization of the local affliction. Any persisting laboratory symptomatology of less
significant prothrombotic activity should be resolved by preemptive miniheparinization, see
chapter 5.4 Convalescence following envenoming.

REFERENCES
ANDREW, RK., GARDINER, EE., ASAZUMA, N., et al. A novel Viper venom
metalloproteinase, alborhagin, is an agonist at the platelet collagen receptor GPVI. J biol
Chem, 2001, 276, No. 30, pp. 2809228097.
ANGEL, MF., ZHANG, F., JONES, M., et al. Nectotizing fasciitis of the upper extremity
resulting from a Water Moccasin bite. South Med J, 2002, Sep, 95, No. 9, pp. 10901094.
ARI, AB. Patient with purely extraocular manifestation from a pit viper snakebite
(Agkistrodon halys brevicaudatus). Mil Med, 2001, 166, No. 7, pp. 667669.
230 Jiri Valenta

De CASTRO, I., BURDMANN, EA., SEGURO, AC., et al. Bothrops venom induces direct
renal tubular injury: role for lipid peroxidation and prevention by antivenom. Toxicon,
2004, 43, No. 7, pp. 833839.
BERBARTA, V., DART, RC. Effectiveness of delayed use of Crotalidae polyvalent immune
Fab (ovine) antivenom. J Toxicol Clin Toxicol, 2004, 42, No. 3, pp. 321324.
BENVENUTI, LA., FRANCA, FO., BARBARO, KC., et al. Pulmonary haemorrhage
causing rapid death after Bothrops jararacussa snakebite: a case report. Toxicon, 2003,
42, No. 3, pp. 331334.
BRYNDAO, EO., de BASTOS, HC., NISHIOKA, SA., et al. Lance-headed Viper (Bothrops
moojeni) bite wounding the eye. Rev Inst Med Trop Sao Paulo, 1993, 35, No. 4, pp. 381
383.
BUCARETCHI, F., HERRERA, SRF., HYSLOP, S., et al. Snakebites by Crotalus durissus
ssp. in children in Campinas, Sao Paulo, Brazil. Rev Inst Med Trop Sao Paulo, 2002, 44,
No. 3, pp. 133138.
COWLES, RA., COLLETTI, LM. Presentation and treatment of venomous snakebites at a
Nothern Academic Medical Center. Am Surg, 2003, 69, No. 5, pp. 445449.
CUPO, P., de AZEVEDO-MARQUES, MM., HERING, SE. Absence of myocardial
involvement in children victims of Crotalus durissus terrificus envenoming. Toxicon,
2003, 42, No. 7, pp. 741745.
DUMAVIBHAT, B., VISUDHISPHAN, S., MALASIT, P. Severe cases of Green Pit Viper
snake venom poisoning. J Med Assoc Thai, 1989, 72, No. 10, pp. 593596.
FAN, HW., CARDOSO, JL. Clinical toxicology of snake bites in South America. In MEIER,
J., WHITE, J. (Eds), Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995.
FRANCA, FO., BARBARO, KC., FAN, HW., et al. Envenoming by Bothrops jararaca in
Brasil: association between venom antigenemia and severiny at admission to hospital.
Trans R Soc Trop Med Hyg, 2003, 97, pp. 312317.
GAO, R, ZHANG, Y., MENG, QL., et al. Characterization of the three fibrinogenolytic
enzymes from Chinese Green Viper (Trimeresurus stejnegeri) venom. Toxicon, 1998, 36,
No. 3, pp. 457467.
GIBLY, RL., WALTER, FG., NOWLIN, SW., et al. Intravascular hemolysis associated with
North American Crotalid envenomation. J Toxicol Clin Toxicol, 1998, 36, No. 4, pp.
337343.
GOLD BS., BARISH, RA., DART, RC., et al. Resolution of compartemnt syndrome after
Rattlesnake envenomation utilizing non-invasive measures. J Emerg Med, 2003, 24, No.
3, p. 285288.
GOLD, BS., DART, RC., BARISH, RA. Bites of venomous snakes. N Engl J Med, 2002,
347, No. 5, pp. 347356.
GOLD, BS., WINGERT, WA. Snake venom poisoning in the United States: a review of
therapeutic practice. South Med J, 1994, 87, No. 6, pp. 579590.
GOMEZ, HF., DART, RC. Clinical toxicology of snakebite in North America. In MEIER, J.,
WHITE, J. (Eds), Handbook of clinical toxicology of animal venoms and poisons. Boca
Raton : CRC Press, 1995.
GUIMARARES, AQ., CRUZ-HOFLING, MA., FERREIRA De ARAUJO, PM., et al.
Pharmacological and histopathological charakterization of Bothrops lanceolatus (Fer de
lance) venom-induced edema. Inflamm Res, 2004, 53, No. 7, pp. 284291.
 Envenoming and Snakebite Treatment in Specific Snake Groups 231

GUTIRREZ, JM. Clinical toxicology of snakebite in Central America. In MEIER, J.,

WHITE, J. (Eds), Handbook of clinical toxicology of animal venoms and poisons. Boca
Raton : CRC Press, 1995, pp. 645666.
HOLSTEGE, CP., MILLER, MB., WERMUTH, M., et al. Crotalid snake envenomation. Crit
Care Clin, 1997, 13, No. 4, pp. 889921.
HORTE, MT., CARDOVO, JL., ASTRO, SC., et al. A randomised blinded comparison of
two doses of antivenom in the treatment of Bothrops envenoming in Sao Paulo, Brazil.
Trans R Soc Trop Med Hyg, 1995, 89, pp. 111114.
HORTE, MT., RIBEIRO, LA. Envenoming by the South American Pit Viper Bothrops
neuwiedi Wagner. Ann Trop Med Parasitol, 2000, 94, No. 7, pp. 731734.
HUTTON, RA., LOOAREESUWAN, S., HO, M., et al. Arboreal Green Pit Vipers (genus
Trimeresurus) of Southeast Asia: bites by T. albolabris and T. macrops in Thailand and
review of the literature. Trans R Soc Trop Med Hyg, 1990, 84, No. 6, p. 866874.
JUCKETT, G., HANCOX, JG. Venomous snakebites in the United States: management
review and update. Am Fam Physician, 2002, 65, No. 7, pp. 13671374.
KERNS, W. 2nd, TOMASZEWSKI, C. Airway obstruction following Canebrake Rattlesnake
envenomation. J Emerg Med, 2001, 20, No. 4, pp. 377380.
KONG, YL., CHAN, GTC. Coagulation problems in Pit Viper bite. J Hong Kong Med Assoc,
1988, 40, No. 3, pp. 210212.
KORNALIK, F., VORLOVA, Z. Non-specific therapy of a hemorrhagic diathesis after a bite
by a young Bothrops asper (Barba amarilla): a case report. Toxicon, 1990, 28, No. 12, pp.
14971501.
KULARATNE, SA., RATNATUNGA, N. Severe systemic effects of Merrems Hump-nosed
Viper bite. Ceylon Med J, 1999, 44, No. 4, pp. 169170.
LATIFI, M. Variation in yield and letality of venoms from Iranian snakes. Toxicon, 1984, 22,
No. 3, pp. 373380.
LAVONAS, EJ., GERARDO, CJ., OMALLEY, G., et al. Initial experience with Crotalidae
polyvalent immune Fab (ovine) antivenom in the treatment of Copperhead Snakebite.
Ann Emerg Med, 2004, 43, No. 2, pp. 200206.
LONATI, D., BUTERA, R., CIMA, M., et al. Exotic snakes in Europe. A case of Mexican
Moccasin (Agkistrodon bilineatus) snakebite. Presse Med, 2004, 33, No. 22, pp. 1582
1584.
LOVECCHIO, F., KLEMENT, J., WELCH, S., et al. Antibiotics after Rattlesnake
envenomation. J Emerg Med, 2002, 23, No. 4, pp. 327328.
MAGALHAES, A., FERREIRA, RN., RICHARDSON, M., et al. Coagulant trombin-like
enzymes from the venoms of Brasilian and Peruvian Bushmaster (Lachesis muta muta)
snakes. Comp Biochem Physiol B Biochem Mol Biol, 2003, 136, No. 2, pp. 255266.
MARTINS, AM., TOYAMA, MH., HAVT, A., et al. Determination of Crotalus durissus
cascavella venom components that induce renal toxicity in isolated rat kidneys. Toxicon,
2002, 40, No. 8, pp. 11651171.
MEIER, J., WHITE, J. (Eds). Handbook of clinical toxicology of animal venoms and poisons.
Boca Raton : CRC Press, 1995, 752 pp.
MOSQUERA, A., IDROVO, LA., TAFUR, A., et al. Stroke following Bothrops spp.
snakebite. Neurology, 2003, 60, No. 10, pp. 15771580.
NASU, K., UEDA, T., MIYAKAWA, I. Intrauterine fetal death cause by Pit Viper venom
poisoning in early pregnancy. Gynecol Obstet Incest, 2004, 57, No. 2, pp. 114116.
232 Jiri Valenta

NISHIOKA, SA., JORGE, MT., SILVEIRA, PV., et al. South American Rattlesnake bite and
soft-tissue infections: report of a case. Rev Soc Bras Med Trop, 2000, 33, No. 4, pp. 401
402.
OFFERMAN, SR., BARRY, JD., SCHNEIR, A., et al. Biphasic Rattlesnake venom-induced
tropbocytopenia. J Emerg Med, 2003, 24, 3, pp. 289293.
PINHO, FM., ZANETTA, DM., BURDMANN, EA. Acute renal failure after Crotalus
durissus snakebite: a prospective survey on 100 patients. Kidney Int, 2005, 67, No. 2, pp.
659667.
PREMAWARDENA, AP., SENEVIRATNE, SL., GUNATILAKE, SB., et al. Excessive
fybrinolysis: the coagulopathy following Merrems Hump-nosed Viper (Hypnale
hypnale) bites. Am J Trop Med Hyg, 1998, 58, No. 6, pp. 821823.
RIBEIRO, LA., ALBUQUERQUE, MJ., de CAMPOS, VA., et al. Death caused by
venomous snakes in the State of Sao Paulo, evaluation of 43 cases from 1988 to 1993.
Rev Assoc Med Bras, 1998, 44, No. 4, pp. 312318.
RODRIGUES-SIMONI, L., ZAMUNER, SR., COGO, JC., et al. Pharmacological evidence
for a presynaptic action of venoms from Bothrops insularis (Jararaca Ilhoa) and Bothrops
neuwiedi (Jararaca Pintada). Toxicon, 2004, 43, No. 6, pp. 633638.
ROJNUCKARIN, P., MAHASANDANA, S., INTRAGUMTHORNCHAI, T., et al.
Prognostic factors of Green Pit Vipers bites. Am J Trop Med Hyg, 1998, 58, No. 1, pp.
2225.
ROSENTHAL, R., MEIER, J., KOELZ, A., et al. Intestinal ischemia after Buschmaster
(Lachesis muta) snakebite a case report. Toxicon, 2002, 40, No. 2, pp. 217220.
SALLIGAN, R., COLE, J., BRITO, N., et al. Crotaline snake bite in the Ecuadorian Amazon:
Randomised double blind comparative trial of three South American polyspecific
antivenoms. BMJ, 2004, 329, No. 7475, pp. 1129.
SCHARMAN, EJ., NOFFSINGER, VD. Copperhead snakebites: clinical severiny of local
effects. Ann Emerg Med, 2001, 38, No. 1, pp. 5561.
SCHIER, JG., WIENER, SW., TOUGER, M., et al. Efficacy of Crotalidae polyvalent
antivenin for the treatment of Hognosed Viper (Porthidium nasutum) envenomation. Ann
Emerg Med, 2003, 41, No. 3, pp. 391395.
SELLAHEWA, KH., KUMARARATNE, MP. Envenomation by the Hump-nosed Viper
(Hypnale hypnale). Am J Trop Med Hyg, 1994, 51, No. 6, pp. 823825.
SHAW, BA., HOSALKAR, HS. Rattlesnake bites in children: antivenin treatment and
surgical indication. J Bone Joint Surg Am, 2002, 84A, No. 9, pp. 16241629.
SCHAPER, A., de HARO, L., DESEL, H., et al. Rattlesnake bites in Europe experiences
from southestern France and northern Germany. J Toxicol Clin Toxicol, 2004, 42, No. 5,
pp. 635641.
De SILVA, A. Trimeresurus trigonocephalus bites. The Snake, 1983, 15, pp. 9194.
De SILVA, A., WIJEKOON, AS., JAYASENA, L., et al. Haemostatic dysfunction and acute
renal failure following envenoming by Merrems Hump-nosed Viper (Hypnale hypnale)
in Sri Lanka: first autentic case. Trans R Soc Trop Med Hyg, 1994, 88, No. 2, pp. 209
212.
SILVEIRA, KS., BOECHEM, NT., de NASCIMENTO, SM., et al. Pulmonary mechanics
and lung histology in acute lung injury induced by Bothrops jararaca venom. Respir
Physiol Neurobiol, 2004, 139, No. 2, pp. 167177.
 Envenoming and Snakebite Treatment in Specific Snake Groups 233

SOTELO-CRUZ, N. Rattlesnake bite poisoning, health damage and treatment in children.

Gac Med Mex, 2003, 139, No. 4, pp. 317324.
STCKLIN, R., CRETTON, G. The ultimate database on venomous animals, snakes. CD-
rom, Geneva : Atheris Laboratories, 1998.
TAKESHITA, T., YAMADA, K., HANADA, M., et al. Case report: extraocular muscle
paresis caused by snakebite. Kobe J Med Sci, 2003, 49, No. 1, pp. 1115.
TANEN, DA., RUHA, AM., GRAME, KA., et al. Rattlesnake envenomations: unusual case
presentation. Arch Intern Med, 2001, 161, No. 3, pp. 474479.
THOMAS, L., TYBURN, B., BUCHER, B., et al. Prevention of thromboses in human patiens
with Bothrops lanceolatus envenoming in Martinique: failure of anticoagulants and
efficacy of a monospecific antivenom. Am J Trop Med Hyg, 1995, 52, No. 5, pp. 419
426.
THORSON, A., LAVONAS, EJ., ROUSE, AM., et al. Copperhead envenomation in the
Karolina. J Toxicol Clin Toxicol, 2003, 41, No. 1, pp. 2935.
VISUDHIPHAN, S., TONMUKAYAKUL, A., TUMLIANG, S., et al. Dark Green Pit Viper
(Trimeresurus popeorum) bite: clinical and serial coagulation profiles in 51 cases. Am J
Trop Med Hyg, 1989, 41, No. 5, pp. 570575.
WARRELL, DA. Clinical toxicology of snakebite in Asia. In MEIER, J., WHITE, J. (Eds),
Handbook of clinical toxicology of animal venoms and poisons. Boca Raton, New York,
London, Tokyo : CRC Press, 1995.
WINGERT, WA., CHAN, L. Rattlesnake bites in southern California and rationale for
recomended treatment. West J Med, 1988, 148, No.1, pp. 3744.
WHITAKER, R. Pit viper (Trimeresurus macrolepis Beddome) bites at a South Indian tea
estate. J Bombay Nat Hist Soc, 1973, 70, No. 1, pp. 207208.
ZAMUDIO, KR., HARDY, DL. Sr., MARTINS, M., et al. Fang tip spread, puncture distance,
and suction for snake bite. Toxicon, 2000, 38, No. 5, pp. 723728.
ZAMUNER, SR., da CRUZ-HOFLING, MA., CORADO, AP., et al. Comparison of the
neurotoxic and myotoxic effect of Brasilian Bothrops venom and their neutralisation by
commercial antivenom. Toxicon, 2004, 44, No. 3, pp. 259271.
ZHANG, Y., LEE, WH., GAO, R., et al. Effects of Pallas Viper (Agkistrodon halys pallas)
venom on blood coagulation and characterization of a protrombin activator. Toxicon,
1998, 36, No. 1, pp. 143152.
Chapter 7

LIST OF VENOMOUS SNAKES

The aim of the venomous snake overview below is not to provide full and complex
taxonomy in terms of zoology and systematics. Instead, the purpose is to catalog the names of
known venomous snakes, as well as those, namely from the colubrid family (Colubridae),
capable of causing envenomation through bites, even though they may merely cause a local or
a very light affection. The list of potentially venomous snakes may not be comprehensive due
to the general shortage of information available. In addition, it features snakes that are known
to possess venom apparatus, but for which no envenoming has been described as a result of
rarity or a benign course.

7.1. FAMILY: COLUBRIDAE, COLUBRIDS

Genus: Ahaetulla, formerly Dryophis, vine snakes
Ahaetulla dispar1* Gnthers vine snake or Indian bronzeback (India)
Ahaetulla fasciolata* Speckle-headed whipsnake (Indonesia, Malaysia, Singapore,
Thailand)
Ahaetulla fronticincta* Burmese vine snake (India and Burma)
Ahaetulla nasuta* Long-nosed whipsnake (Sri Lanka, India, Malaysia)
Ahaetulla mycterizans* Malayan green whipsnake (Indonesia, Thailand, Laos, W
Malaysia)
Ahaetulla perroteti* Western Ghats bronzeback (India)
Ahaetulla prasina ssp.* Oriental whipsnake or Asian vine snake (Sri Lanka, India,
Malaysia)
Ahaetulla pulverulenta* Brown-speckled whipsnake (E Himalayas, former Indochinese
region and sea along the archipelagos between E India and N Australia)
Genus: Amblyodipsas, purple-glossed snakes, see Atractaspididae, Aparallactinae
Genus: Amplorhinus

1 * This snake taxon features animals with venom of limited effectiveness or quantity. Snakebites by this species
are not dangerous, and do not pose a threat to the life of a human, except in remote cases or due to extreme
allergic reaction. In some instances, this asterisk may mark a species of unknown toxicity or unproven clinical
course of envenoming, and for which a low level of peril is expected; examples include some members of the
colubrid family (Colubridae). Nonetheless, even these snakes should not be underestimated and any
unnecessary exposure to risk should be avoided.
236 Jiri Valenta

Amplorhinus multimaculatus* Cape reed snake (S and E South Africa and E Zimbabwe)
Genus: Arrhyton (coasts of the Caribbean Gulf and Cuba)
Arrhyton ainictum* Cuban island racer
Arrhyton callilaemum*
Arrhyton dolichura* Habana island racer
Arrhyton exiguum* Ground snake
Arrhyton funereum*
Arrhyton landoi* Schwartzs island racer
Arrhyton polylepis*
Arrhyton procerum*
Arrhyton redimitum*
Arrhyton supernum*
Arrhyton taeniatum* Gnthers island racer
Arrhyton tanyplectum* St Vincent island racer
Arrhyton vittatum* Common island racer
Genus: Balanophis
Balanophis ceylonensis* Sri Lankan keelback blossom krait (Sri Lanka)
Genus: Boiga, boigas or cat snakes
Boiga andamanensis2** Andaman cat snake (India and the Andaman Islands)
Boiga angulata** Leyte cat snake (the Philippines)
Boiga barnesi** Barnes cat snake (Sri Lanka)
Boiga beddomei** Beddomes cat snake (Sri Lanka and India)
Boiga bengkuluensis** (Sumatra)
Boiga blandingii** (Uganda and W Kenya)
Boiga bourreti** Blandings tree snake (Vietnam)
Boiga ceylonensis** Sri Lankan cat snake (Sri Lanka, India, the Andaman Islands)
Boiga cyanea** Green cat snake (India, former Indochina, S China)
Boiga cynodon** Dog-toothed cat snake (SE Asia and the Philippines)
Boiga dendrophila** Gold-ringed cat snake or mangrove snake
-- B. dendrophila annectens (Borneo)
-- B. dendrophila dendrophil (Java)
-- B. dendrophila divergens (the Philippines)
-- B. dendrophila gemmicincta (Indonesia - Sulawesi)
-- B. dendrophila latifasciata (the Philippines)
-- B. dendrophila levitoni (the Philippines - Panay)
-- B. dendrophila melanota (mainland SE Asia, Malayan Peninsula, Indonesia)
-- B. dendrophila multicincta (the Philippines)
-- B. dendrophila occidentalis (Indonesia)
Boiga dightoni** Pirmad cat snake (India)
Boiga drapiezii** White-spotted cat snake (Indonesia, Malaysia, the Philippines,
Singapore, Thailand)

2 ** This snake is one of a low to moderately dangerous taxon. In most cases, health complications arise following
envenomation by these snakes. Cases of grievous affliction and threat to life of a healthy adult are rare;
nevertheless, fatalities have been described involving some of these species, especially when adequate
treatment is absent. Therefore, the twin asterisks also refer to snake taxons where a clinical course of
envenoming has not been described, but an indicated level of risk can be analogically presumed.
 List of Venomous Snakes 237

Boiga flavescens see B. irregularis

Boiga forsteni** Forstens cat snake (India and Sri Lanka)
Boiga gokool** Arrowback tree snake (India)
Boiga guangxiensis** (China and Vietnam)
Boiga hexagonata see B. cyanea
Boiga irregularis** Brown catsnake or brown tree snake (Indonesia, New Guinea,
Australia)
Boiga jaspidea** Jasper cat snake (SE Asia)
Boiga kraepelini** Kelung cat snake (N Taiwan and S China)
Boiga multifasciata** Many-banded tree snake (India, Nepal, Bhutan)
Boia multimaculata (multomaculata)** Many-spotted cat snake (SE Asia and Indonesia)
Boiga nigriceps** Black-headed cat snake (Thailand, China, Indonesia, Malaysia)
Boiga nuchalis** (India and Nepal)
Boiga ocellata** Gray cat snake or eyed cat snake (India, Bangladesh, former Indochina,
NW Malaysia)
Boiga ochracea** Orange cat snake (India and Bhutan)
Boiga philippina** Philippine cat snake (the Philippines)
Boiga pulverulenta** Fischers cat snake (W and C Africa)
Boiga quincunciata** (India and Burma)
Boiga saengsomi** Banded cat snake (Thailand)
Boiga schultzei** (the Philippines)
Boiga tanahjampeana** Tanahjampea cat snake (Tanahjampea Island near Indonesia)
Boiga trigonata** Indian gamma snake (Iran, Afghanistan, Pakistan, Nepal, India, Sri
Lanka)
Boiga wallachi** Nicobar cat snake (India and the Nicobar Islands)
Genus: Calamodontophis
Calamodontophis paucidens* Tropical forest snake (S Brazil)
Genus: Cerberus
Cerberus microlepis* Dog-faced water snake (coastal S India, SE Asia, N Australia)
Cerberus rynchops* New Guinea bockadam (coastal S India, SE Asia, N Australia)
Genus: Clelia, mussuranas
Clelia bicolor* Two-colored mussurana (Brazil and Argentina)
Clelia clelia ssp.* (N Central America, N South America)
Clelia equatoriana* Equatorial mussurana (E Panama, NW Ecuador, Colombia)
Clelia errabunda* Underwoods mussurana (the Antilles - Saint Lucia)
Clelia husami* (Brazil)
Clelia montana* (Brazil - Sao Paulo)
Clelia occipitolutea* Black mussurana (N Brazil, Uruguay, Argentina)
Clelia quimi* (Brazil)
Clelia plumbea* (N Central America and N South America)
Clelia rustica* (Brazil, Uruguay, Argentina)
Clelia scytalina* Mexican snake eater (Central America)
Genus: Coluber, racers
Coluber sp. A genus of a collective nature with a rather diverse taxonomy, it comprises
some 30 species of slightly venomous or non-venomous colubrids. More recently, species
238 Jiri Valenta

once ranked amongst the genus have been reclassified under other genera, for instance
Hierophis, Hemorrhois, Platyceps, etc.
Coluber ravergieri see Hemorrhois ravergieri
Coluber rhodorachis see Platyceps rhodorachis
Genus: Coniophanes, black-striped snakes (North, Central and South America, Texas to
Peru)
Coniophanes alvarezi* Chiapan stripeless snake
Coniophanes andresensis* Andresens snake
Coniophanes bipunctatus* Two-spotted snake
Coniophanes dromiciformis* Peters running snake
Coniophanes fissidens* Yellowbelly snake
Coniophanes imperialis* Black-striped snake
Coniophanes joanae*
Coniophanes lateritius* Stripeless snake
Coniophanes longinquus*
Coniophanes meridanus* Peninsula stripeless snake
Coniophanes piceivittis ssp.* Copes black-striped snake
-- Coniophanes piceivittis frangivirgatus*
Coniophanes quinquevittatus* Five-striped snake
Coniophanes schmidti* Faded black-striped snake
Genus: Conophis (Central America)
Conophis biserialis see Conopsis biserialis
Conophis lineatus* Road guarder
Conophis morai*
Conophis nasus see Conopsis nasus
Conophis pulcher* Beautiful road guarder
Conophis vittatus* Striped road guarder
Genus: Conopsis (Central America)
Conopsis biserialis* Two-lined Mexican earth snake
Conopsis nasus* Largenose earth snake
Genus: Crotaphopeltis
Crotaphopeltis acarina see C. braestrupi and C. hippocrepis
Crotaphopeltis barotseensis* Barotse water snake (Zambia and N Botswana)
Crotaphopeltis braestrupi* (Somalia and Burkina Faso)
Crotaphopeltis degeni* (N Sudan, Uganda, Kenya)
Crotaphopeltis hippocrepis* (W and C Africa)
Crotaphopeltis hotamboeia* Red-lipped snake (E Africa from Somalia as far as RSA)
Crotaphopeltis tornieri* Werners water snake (Tanzania and N Malawi)
Genus: Dipsadoboa (Africa)
Dipsadoboa aulica* Marbled tree snake
Dipsadoboa duchesnei*
Dipsadoboa elongata*
Dipsadoboa flavida ssp.* Cross-bared tree snake
Dipsadoboa shrevei* Shreves tree snake
Dipsadoboa underwoodi*
Dipsadoboa unicolor* Gnthers green tree snake
 List of Venomous Snakes 239

Dipsadoboa viridis ssp.*

Dipsadoboa werneri* Werners tree snake
Genus: Dispholidus
Dispholidus typus3*** African boomslang
-- D. typus kivuensis (N Zambia to SW Kenya)
-- D. typus punctatus (N Angola, W Democratic Republic of Congo - DRC, NW Zambia)
-- D. typus typus (Sub-Saharan Africa)
Genus: Dromophis
Dromophis lineatus* Lined Olympic snake (C Africa)
Dromophis praeornatus* Striped swamp snake (W Africa)
Genus: Dryophis see Ahaetulla
Genus: Elapomorphus
Elapomorphus lemniscatus ssp.* Dumerils diadem snake (Brazil, Uruguay, Paraguay,
Bolivia, Argentina)
Elapomorphus lepidus* Minas Gerais snake (Brazil)
Elapomorphus mertensi see Phalotris mertensi
Elapomorphus nasutus see Phalotris nasutus
Elapomorphus punctatus see Phalotris punctatus
Elapomorphus quinquelineatus* Raddis lizard-eating snake (Brazil)
Elapomophus spegazzinii ssp.* Spegazzinis diadem snake (Argentina)
Elapomorphus tricolor see Phalotris tricolor
Elapomorphus wuchereri* Wucherers lizard-eating snake (Brazil)
Genus: Enhydris, water snakes
Enhydris albomaculata* (Indonesia)
Enhydris alternans* Reuss water snake (Indonesia)
Enhydris bennetti* Bennetts water snake (SE China)
Enhydris bocourti* Bocourts water snake (Vietnam, Thailand, Cambodia, W Malaysia)
Enhydris chinensis* Chinese water snake (N China, Taiwan, Hainan, N Vietnam)
Enhydris doriae* (Sarawak)
Enhydris dussumieri* Dussumiers water snake (India and Bangladesh)
Enhydris enhydris* Rainbow water snake (Pakistan, India, Malaysia, S China, SE Asia)
Enhydris indica* (W Malaysia)
Enhydris innominata* Tay Minh water snake (Vietnam and Thailand)
Enhydris jagori* Jagors water snake (Former Indochina)
Enhydris longicauda* Longhead water snake (Cambodia)
Enhydris maculosa* Blanfords spotted water snake (Burma, Indonesia, probably SE
China)
Enhydris matannensis* Boulengers water snake (Indonesia)
Enhydris pahangensis* Pahang water snake (W Malaysia)
Enhydris pakistanica* Sind River snake (Pakistan)

3 *** This snake taxon is classified as highly dangerous. Envenoming following a snakebite to a human is typically
a serious process often resulting in death unless adequate and full-ranging treatment is provided.
In certain descriptions of home range, the following abbreviations have been used: N (north, northern), NW and NE
(north-west, north-western or north-east, north-eastern, respectively), S (south, southern), SW and SE (south-
west, south-western or south-east, south-eastern, respectively), W (west, western), E (east, eastern), C
(central).
240 Jiri Valenta

Enhydris plumbea* Yellowbelly water snake (SE China, former Indochina, Malaysia)
Enhydris polylepis* Macleays water snake (Papua-New Guinea and N Australia)
Enhydris punctata* Spotted water snake (NE India)
Enhydris sieboldi* Siebolds water snake (India and W Malaysia)
Enhydris smithi* Smiths water snake (Thailand)
Genus: Eteirodipsas
Eteirodipsas colubrina see Madagascarophis colubrinus
Genus: Ficimia, hooknosed snakes (North and Central America, S Texas to N Honduras)
Ficimia hardyi* Hardys hook-nosed snake
Ficimia olivacea* Mexican hook-nosed snake
Ficimia publia* Blotched hook-nosed snake
Ficimia ramirezi* Ramirezs hook-nosed snake
Ficimia ruspator* Guerreran hook-nosed snake
Ficimia streckeri* Streckers hook-nosed snake
Ficimia variegata* Tehuantepec hook-nosed snake
Genus: Fordonia
Fordonia leucobalia* Crab-eating water snake or white-bellied mangrove snake (India,
former Indochina, Malaysia, the Philippines, Papua-New Guinea, N Australia)
Genus: Heterodon
Heterodon nasicus ssp.* Western hog-nosed snake (from the south to the north
throughout the central zone of the USA)
Heterodon platirhinos* Eastern hog-nosed snake (E USA)
Heterodon simus* Southern hog-nosed snake (N USA)
Genus: Hemorrhois
Hemorrhois ravergieri* Spotted whip snake (Kos Island near Greece, Turkey, the Middle
East and a part of Central Asia to China)
Genus: Homalopsis, water snake
Homalopsis buccata* Puff-faced water snake or masked water snake (India to SE Asia)
Genus: Chrysopelea, flying snakes (Sri Lanka, S India, Burma, Malaysia, Indonesia, the
Philippines)
Chrysopelea ornata* Golden tree snake or ornate flying snake
Chrysopelea paradisi* Paradise tree snake
Chrysopelea pelias* Twin-barred tree snake or banded flying snake
Chrysopelea rhodepleuron* Moluccan flying snake
Chrysopelea taprobanica* Indian flying snake
Genus: Ialtris (Dominican Republic and Haiti)
Ialtris agyrtes* Barreras fanged snake
Ialtris dorsalis* Brown fanged snake
Ialtris parishi* Parishs fanged snake
Genus: Imantodes
Imantodes cenchoa ssp.* Blunt-headed treesnake (tropical South America and Central
America)
Imantodes gemmistratus* Central American tree snake (Mexico to Colombia)
Imantodes inornatus* Western tree snake (Honduras to Ecuador)
Imantodes lentiferus* Amazon Basin tree snake (Ecuador, Colombia, Brazil, Venezuela,
French Guyana, Peru, Bolivia)
 List of Venomous Snakes 241

Imantodes phantasma* Phantasma tree snake (Panama)

Imantodes tenuissimus* Yucatn blunthead snake (Mexico)
Genus: Ithycyphus (Madagascar)
Ithycyphus blanci*
Ithycyphus goudoti* Forest night snake
Ithycyphus miniatus* Tiny night snake
Ithycyphus oursi*
Ithycyphus perineti*
Genus: Langaha (Madagascar)
Langaha alluaudi* Southern leafnose snake
Langaha madagascariensis*
Langaha nasuta see L. madagascariensis
Langaha pseudoalluaudi*
Genus: Leimadophis (Central and South America)
Leimadophis attahuallpae see Saphenophis atahuallpae
Leimadophis pygmeus see Umbrivaga pygmaea
Leimadophis simonsii see Philodryas simonsii
Genus: Leptodeira
Leptodeira annulata* Banded cat-eyed snake (tropical South America)
Leptodeira bakeri* Bakers cat-eyed snake (Venezuela and Aruba)
Leptodeira frenata ssp.* Rainforest cat-eyed snake (Mexico, Guatemala, Belize)
Leptodeira maculata* Southwestern cat-eyed snake (Mexico and Panama)
Leptodeira nigrofasciata* Black-banded cat-eyed snake (Mexico to Panama)
Leptodeira punctata* Western cat-eyed snake (Mexico)
Leptodeira rubricata* Costa Rican cat-eyed snake (Costa Rica)
Leptodeira septentrionalis* Northern cat-eyed snake (N Texas and NE Mexico)
Leptodeira splendida ssp.* Splendid cat-eyed snake (Mexico)
Genus: Leptophis (Central and South America)
Leptophis ahaetulla ssp.* Parrot snake
Leptophis cupreus* Copper parrot snake
Leptophis depressirostris* Copes parrot snake
Leptophis diplotropis ssp.* Pacific Coast parrot snake
Leptophis mexicanus ssp.* Mexican parrot snake
Leptophis modestus* Cloud forest parrot snake
Leptophis nebulosus* Olivers parrot snake
Leptophis riveti* Despaxs parrot snake
Leptophis santamartensis*
Leptophis stimsoni* Gray lora
Genus: Liophis (Central and South America, the Caribbean)
Liophis albiceps*
Liophis albiventris see L. epinephelus ssp.
Liophis almadensis* Almaden ground snake
Liophis amarali* Amarals ground snake
Liophis amazonicus see L. miliaris ssp.
Liophis andinus*
Liophis angustilineatus*
242 Jiri Valenta

Liophis anomalus*
Liophis atraventer*
Liophis bimaculatus see L. epinephelus ssp.
Liophis boursieri*
Liophis brazili see L. frenatus
Liophis breviceps ssp.* Short ground snake
Liophis canaima see L. breviceps ssp.
Liophis carajascinsis see L. carajasensis
Liophis carajasensis*
Liophis ceii*
Liophis chrysostomus see L. miliaris ssp.
Liophis cobellus ssp.*
Liophis coralliventris see L. jaegeri ssp.
Liophis cursor* Lacpdes ground snake
Liophis dilepis* Lemas ground snake
Liophis elegantissimus*
Liophis epinephelus ssp.*
Liophis festae* Drab ground snake
Liophis flavifrenatus* Fronted ground snake
Liophis fraseri see L. epinephelus ssp.
Liophis frenatus*
Liophis guentheri*
Liophis ingeri see L. cobellus
Liophis jaegeri ssp.* Jaegers ground snake
Liophis joberti*
Liophis juliae* Julias ground snake
Liophis leucogaster*
Liophis lineatus* Lined ground snake
Liophis longiventris* Long ground snake
Liophis maryellanae* Maryellens ground snake
Liophis melanauchen*
Liophis melanostigma*
Liophis melanotus* Shaws black-backed snake
Liophis meridionalis*
Liophis miliaris ssp.* Military ground snake
Liophis mossoroensis see L. miliaris ssp.
Liophis obtusus*
Liophis oligolepis*
Liophis ornatus* Ornate ground snake
Liophis paucidens* Hoges ground snake
Liophis perfuscus* Tan ground snake
Liophis poecilogyrus ssp.*
Liophis problematicus* Problem ground snake
Liophis pseudocobella see L. epinephelus ssp.
Liophis purpurans see L. miliaris
Liophis reginae ssp.* Royal ground snake
 List of Venomous Snakes 243

Liophis sagittifer ssp.* Arrow ground snake

Liophis steinbachi*
Liophis subocularis*
Liophis tachymenoides* syn. Philodryas tachymenoides
Liophis taeniurus* Thin ground snake
Liophis torrenicolus*
Liophis triscalis* Three-scaled ground snake
Liophis tristriatus*
Liophis typhlus ssp.* Blind ground snake
Liophis vanzolinii*
Liophis viridis* Crown ground snake
Liophis vitti*
Liophis williamsi* Williams ground snake
Liophis zweifeli see L. reginae ssp.
Genus: Lygophis
Lygophis coralliventris see Liophis coralliventris
Lygophis flavifrenatus see Liophis flavifrenatus
Lygophis lineatus see Liophis lineatus
Lygophis paucidens see Liophis paucidens
Genus: Macropisthodon
Macropisthodon flaviceps* Orangeneck keelback or yellow-headed keelback (Indonesia,
Malaysia, Thailand)
Macropisthodon plumbicolor ssp.* Lead keelback (India and Sri Lanka)
Macropisthodon rhodomelas* Blueneck keelback (Indonesia, Malaysia, Singapore,
Thailand)
Macropisthodon rudis ssp.* Red keelback (Taiwan and the neighboring part of China)
Genus: Macroprotodon
Macroprotodon cucullatus ssp.* False smooth snake (N Pyrenean Peninsula, across N
Africa as far as Israel)
Genus: Madagascarophis, Malagasy cat-eyed snakes
Madagascarophis citrinus* (Madagascar)
Madagascarophis colubrinus* (Madagascar)
Madagascarophis meridionalis* (Madagascar)
Madagascarophis ocellatus* (Madagascar)
Genus: Malpolon
Malpolon moilensis* False cobra or Moila snake (N Africa and Near East)
Malpolon monspessulanus* Montpellier snake (SE Europe, NE Africa, Pyrenean
Peninsula, N Sahara)
-- M. monsspesulanus insignitus (Balkans, NE Africa, Middle East)
-- M. monsspesulanus monsspesulanus (SW Europe, Greece, NW Africa)
Genus: Masticophis (North and Central America and N South America)
Masticophis anthonyi* Clarion Island whip snake
Masticophis aurigulus* Baja California striped whip snake
Masticophis bilineatus ssp.* Sonoran whip snake
Masticophis flagellum ssp.* Coach whip
Masticophis lateralis ssp.* California whipsnake
244 Jiri Valenta

Masticophis lineolatus see M. bilineatus ssp.

Masticophis mentovarius ssp.* Neotropical whip snake
Masticophis pulchericeps*
Masticophis schotti* Schotts whip snake
Masticophis taeniatus ssp.* Striped whipsnake
Genus: Myron
Myron richardsonii* Richardsons grey mangrove snake (coastal N Australia, New
Guinea, and the Aru Archipelago)
Genus: Oxybelis, vine snakes
Oxybelis aeneus* Mexican vine snake (Arizona to N South America)
Oxybelis acuminatus* (Central and South America)
Oxybelis argentus (argenteus)* syn. Xenoxybelis argenteus (South America - Colombia
to Bolivia)
Oxybelis brevirostris* Copes vine snake (Honduras to NW South America)
Oxybelis fulgidus* Amazonian vine snake (N Central America and N South America)
Oxybelis microphthalmu see O. aeneus
Oxybelis wilsoni* (Honduras)
Genus: Oxyrhopus (Central and South America, Mexico to Peru)
Oxyrhopus clathratus* Dumrils false coral snake
Oxyrhopus doliatus* Bibrons false coral snake
Oxyrhopus fitzingeri ssp.* Fitzingers false coral snake
Oxyrhopus formosus* Formosa false coral snake
Oxyrhopus guibei*
Oxyrhopus leucomelas* Werners false coral snake
Oxyrhopus marcapatae* Boulengers false coral snake
Oxyrhopus melanogenys ssp.* Tschudis false coral snake
Oxyrhopus occipitalis*
Oxyrhopus petola ssp.* Calico false coral snake
Oxyrhopus rhombifer ssp.* Amazon false coral snake
Oxyrhopus trigeminus* Brazilian false coral snake
Oxyrhopus venezuelanus*
Genus: Phalotris
Phalotris mertensi* formerly Elapomorphus mertensi (Brazil)
Phalotris nasutus* formerly Elapomorphus nasutus (Brazil)
Phalotris punctatus* formerly Elapomorphus punctatus (NE Argentina)
Phalotris tricolor* (Brazil, Bolivia, Argentina, Uruguay)
Genus: Philodryas, green snakes
Philodryas aestiva ssp.* Brazilian green racer (SW Brazil to N Argentina and Uruguay)
Philodryas arnaldoi* Arnaldos green racer (Brazil)
Philodryas baroni* Barons green racer (Argentina)
Philodryas bolivianus* (Bolivia)
Philodryas borelli see P. varius
Philodryas burmeisteri see P. trilineata
Philodryas carbonelli see P. olfersii
Philodryas chamissonis* Chilean green racer (Chile)
Philodryas cordata* (Venezuela)
 List of Venomous Snakes 245

Philodryas elegans* syn. Alsophis elegans (Ecuador, Peru, Chile)

Philodryas hoodensis* Hood racer (the Galapagos and Ecuador)
Philodryas inca* Tropical green racer (South America)
Philodryas laticeps* (Bolivia)
Philodryas latirostris* (Bolivia)
Philodryas livida* (Brazil)
Philodryas mattogrossensis* Miranda green racer (SW Brazil, Paraguay, Bolivia)
Philodryas nattereri* Paraguay green racer (Paraguay, C and W Brazil)
Philodryas olfersii ssp.* Lichtensteins green racer (Brazil to Argentina and Uruguay)
Philodryas oligolepis* Gomes green racer (Brazil)
Philodryas patagoniensis* Patagonia green racer (Brazil to Argentina and Uruguay)
Philodryas psammophidea* Gnthers green racer (Brazil to Argentina)
Philodryas pseudoserra* syn. Tropidodryas striaticeps (Brazil)
Philodryas serra* syn. Tropidodryas serra (Brazil)
Philodryas simonsii* (South America)
Philodryas tachymenoides* Schmidts green racer (South America)
Philodryas trilineata* (Argentina, maybe up to Bolivia)
Philodryas varius* Jans green racer (Bolivia)
Philodryas viridissima* Common green racer (N Venezuela to Argentina)
Genus: Philothamnus
Philothamnus angolensis* Western green snake (Cameroon and Congo-Brazzaville to
Namibia and S Mozambique)
Philothamnus battersbyi* Battersbys green snake (NE Africa: Ethiopia to Tanzania)
Philothamnus bequaerti* Bequaerts green snake (the Central African Republic,
Cameroon, Uganda, S Sudan, W Ethiopia, W and N DRC)
Philothamnus carinatus* Thirteen-scaled green snake (W, C and E Africa: Guinea to
Kenya)
Philothamnus dorsalis* Striped green snake (coastal W Africa, Gabon to Angola)
Philothamnus girardi* Girards green snake (the Gulf of Guinea countries)
Philothamnus heterodermus ssp.* Variable green snake (W and C Africa)
Philothamnus heterolepidotus* Slender green snake (W, C and E Africa)
Philothamnus hoplogaster* green water snake (E Africa)
Philothamnus hughesi* Hughes green snake (W, C and N DRC, Congo-Brazzaville,
Cameroon)
Philothamnus irregularis* Northern green bush snake (E Africa)
Philothamnus macrops* Usambara green snake (coastal Tanzania)
Philothamnus natalensis ssp.* Natal green snake (SE Africa: Mozambique to the
Republic of South Africa - SA)
Philothamnus nitidus ssp.* Green bush snake (W and C Africa: Ghana to Congo-
Brazzaville)
Philothamnus ornatus* Ornate green snake (Angola, Zambia to N Botswana)
Philothamnus punctatus* Spotted green snake (Mozambique, E Tanzania, Kenya,
Somalia, E Ethiopia, N Malawi)
Philothamnus semivariegatus* Variegated green snake (Sub-Saharan Africa)
Philothamnus thomensis* (So Tom)
Genus: Platyceps
246 Jiri Valenta

Platyceps rhodorhachis* Braid snake or Jans cliff racer (NE Africa, Near and Middle
East to NW India)
Genus: Psammophis
Psammophis aegiptius* (N Africa: SE Algeria to Israel)
Psammophis angolensis* Dwarf sand snake (Tanzania and Zanzibar)
Psammophis ansorgii* Link-marked sand racer (Angola)
Psammophis biseriatus* Two-striped sand racer (NE Africa)
Psammophys brevirostris* (N, W and S Africa)
Psammophis condanarus ssp.* Sand snake (N India and Burma)
Psammophis crucifer* Cross-marked or montane grass snake (SE RSA and S Zimbabwe)
Psammophis elegans ssp.* Elegant sand racer (W Africa)
Psammophis jallae* Jallas sand snake (N Africa)
Psammophis leightoni ssp.* Cape sand snake (N Africa)
Psammophis leithii* Pakistan sand racer (Afghanistan, Pakistan and W India)
Psammophis leopardinus* Leopard grass snake (Angola and Zambia)
Psammophis lineolatus* syn. Taphrometopon lineolatum, Steppe ribbon racer (C Asia to
Mongolia and China)
Psammophis longifrons* Long sand racer (India)
Psammophis namibensis* Namib sand snake (N Africa))
Psammophis notosticus* Karoo sand snake Or whip snake (N Africa)
Psammophys orientalis* Eastern stripe-bellied sand snake (N Africa to Ethiopia and
Sudan)
Psammophis phillipsi ssp.* Phillips sand snake (V, C and W Africa)
Psammophis pulcher* Boulengers sand racer (Ethiopia)
Psammophis punctulatus ssp.* Speckled sand racer (NE Africa)
Psammophis rukwae ssp.* Rukwa sand racer (NW Africa)
Psammophis schokari* Schokari sand racer (N Africa, SW Asia, Pakistan, NW India)
Psammophis sibilans ssp.* Short-snouted grass snake (N, W and S Africa)
Psammophis subteniatus ssp.* Stripe-bellied sand snake (N Africa)
Psammophis tanganicus* Western link-marked sand racer (NE Africa: from S Libya as
far as Tanzania)
Psammophis trigrammus* Western sand snake (Namibia, Angolan and RSA border
regions)
Psammophys trinasalis* Fork-marked sand snake (N Africa)
Psammophis zambiensis* (Zambia)
Genus: Psammophylax
Psammophylax rhombeatus* Spotted or Rhombic skaapsteker (N Africa and SW Angola)
Psammophylax tritaeniatus* Striped skaapsteker (Angola and SE Africa)
Psammophylax variabilis ssp.* Grey-bellied grass snake (E Africa)
Genus: Pseudoboa (Central and South America)
Pseudoboa coronata* Crowned false boa
Pseudoboa haasi* Paran false boa
Pseudoboa neuwiedii* Neuwieds false boa
Pseudoboa nigra* Black false boa
Pseudoboa serrana*
Genus: Ptychophis
 List of Venomous Snakes 247

Ptychophis flavovirgatus* (Brazil)

Genus: Pythonodispas
Pythonodispas carinata* Western keeled snake (Namibia and Angola)
Genus: Rhabdophis, keelback snakes
Rhabdophis adleri** (Hainan and China)
Rhabdophis angeli** (Vietnam)
Rhabdophis auriculata ssp.** (the Philippines)
Rhabdophis barbouri** Barbours water snake (the Philippines)
Rhabdophis callichroma** (Vietnam, S China - Hainan)
Rhabdophis chrysargoides** (Indonesia)
Rhabdophis chrysargo** Speckle-bellied keelback (SE Asia: Burma to the Philippines)
Rhabdophis conspicillatus** (Malaysia and Indonesia)
Rhabdophis himalayanus** Orange-collared keelback (N India, Nepal, Burma, SW
China)
Rhabdophis leonardi** Burmese keelback (China and Burma)
Rhabdophis lineata** Zigzag-lined water snake (the Philippines)
Rhabdophis murudensis** (Malaysia)
Rhabdophis nigrocincta** Black-striped keelback (Thailand, Vietnam, China)
Rhabdophis nuchalis**
-- R. nuchalis nuchalis (N Vietnam and China)
-- R. nuchalis pentasupralabialis (China and W Sichuan)
Rhabdophis spilogaster** Northern water snake (the Philippines)
Rhabdophis subminiatus** Red-necked keelback (N China, Hainan, Vietnam, Thailand,
Burma, NE India, Sumatra, Java, Borneo)
-- R. subminiatus helleri (N China, Hong Kong, Laos, N Thailand)
-- R. subminiatus subminiatus (mainland SE Asia, Hainan)
Rhabdophis swinhonis** Swinhoes grass snake (Taiwan)
Rhabdophis tigrinus,** Tiger grooved-neck keelback or tiger keelback or Japanese grass
snake
-- R. tigrinus tigrinus (Japan)
-- R. tigrinus formosanus (Taiwan)
-- R. tigrinus lateralis (China, Korea, E Russia)
Genus: Saphenophis (Central and South America)
Saphenophis atahuallpae* Atahuallpa saphenophis snake
Genus: Siphlophis (Central and South America)
Siphlophis cervinus* Panama spotted night snake
Siphlophis compressus* Tropical flat snake
Siphlophis leucocephalus* Common spotted night snake
Siphlophis longicaudatus* Brazilian spotted night snake
Siphlophis pulcher* Guanabara spotted night snake
Siphlophis worontzowi* Worontzows spotted night snake
Genus: Spalerosophis (N Africa to the Middle East)
Spalerosophis arenarius*
Spalerosophis atriceps*
Spalerosophis diademy ssp.*
Spalerosophis dolichospilus* Mograbin diadem snake
248 Jiri Valenta

Spalerosophis josephscotreccii*
Spalerosophis microlepis*
Genus: Stenorrhina (Central and South America, from Mexico as far as Ecuador)
Stenorrhina degenhardtii ssp.* Degenhardts Scorpion-eating snake
Stenorrhina freminvillei* Slaty grey snake
Genus: Tachymenis
Tachymenis affinis* Boulengers slender snake (Peru)
Tachymenis attenuata ssp.* Walkers slender snake (Bolivia and Peru)
Tachymenis elongata* Depaxs slender snake (Peru)
Tachymenis chilensis ssp.* Chilean slender snake (Chile and Argentina)
Tachymenis peruviana ssp.* Peru slender snake (SW Bolivia, Peru, Argentina)
Tachymenis surinamensis* (Surinam)
Tachymenis tarmensis* Slender snake (Peru)
Genus: Tantilla (North, Central and South America, from the central zones of the USA
as far as Argentina)
Tantilla albiceps* Barbours centipede snake
Tantilla alticola* Boulengers centipede snake
Tantilla andinista* Andes centipede snake
Tantilla armillata*
Tantilla atriceps* Mexican blackhead snake
Tantilla bairdi* Bairds blackhead snake
Tantilla bocourti* Bocourts blackhead snake
Tantilla boipiranga*
Tantilla brevicaudata (brevicauda)* Mertens centipede snake
Tantilla brevis* syn. Tantillita canula
Tantilla briggsi* Briggs centipede snake
Tantilla calamarina* Pacific Coast centipede snake
Tantilla canula* syn. Tantillita canula
Tantilla capistrata* Capistrata centipede snake
Tantilla cascadae* Michoacn centipede snake
Tantilla coronadoi* Guerreran centipede snake
Tantilla coronata* Southeastern crowned snake
Tantilla cucullata* Big bend blackhead snake
Tantilla cuesta* Wilsons centipede snake
Tantilla cuniculator* Peten centipede snake
Tantilla deppei* Deppes centipede snake
Tantilla deviatrix*
Tantilla eiseni see T. rubra
Tantilla equatoriana* Equator centipede snake
Tantilla excubitor* syn. Tantillita brevissima
Tantilla flavilineata* Yellow-lined centipede snake
Tantilla fraseri*
Tantilla gracilis* Flathead snake
Tantilla hendersoni* Peten centipede snake
Tantilla hobartsmithi* Southwestern blackhead snake
Tantilla impensa*
 List of Venomous Snakes 249

Tantilla insulamontana* Mountain centipede snake

Tantilla jani* Jans centipede snake
Tantilla johnsoni*
Tantilla lempira* Menas centipede snake
Tantilla longifrontalis*
Tantilla melanocephala* Blackhead snake
Tantilla mexicana*
Tantilla miniata see T. rubra
Tantilla miyatai*
Tantilla moesta* Blackbelly centipede snake
Tantilla morgana see T. rubra
Tantilla nigra* Black centipede snake
Tantilla nigriceps* Plains blackhead snake
Tantilla oaxacae* Oaxacan centipede snake
Tantilla oolitica* Rim rock crowned snake
Tantilla petersi* Peters blackhead snake
Tantilla planiceps* Western blackhead snake
Tantilla relicta ssp.* Florida crowned snake
Tantilla reticulata* Reticulate centipede snake
Tantilla robusta*
Tantilla rubra* Big bend blackhead snake
Tantilla schistosa* Red earth centipede snake
Tantilla semicincta* Ringed centipede snake
Tantilla sertula*
Tantilla shawi* Potos centipede snake
Tantilla slavensi* Slavens centipede snake
Tantilla striata* Striped centipede snake
Tantilla supracincta* Banded centipede snake
Tantilla taeniata* Central American centipede snake
Tantilla tayrae* Volcan Tacana centipede snake
Tantilla tecta*
Tantilla trilineata* Brazilian three-lined centipede snake
Tantilla triseriata* Mexican three-lined centipede snake
Tantilla tritaeniata* Three-banded centipede snake
Tantilla vermiformis* Hallowells centipede snake
Tantilla virgata see T. reticulata
Tantilla vulcani*
Tantilla wilcoxi* Chihuahuan blackhead snake
Tantilla yaquia* Yaqui blackhead snake
Genus: Taphrometopon
Taphrometopon lineolatum see Psammophis lineolatus
Genus: Tarbophis
Tarbophis see Telescopus
Genus: Telescopus
Telescopus dhara* Arabian tiger snake (Z, C and NE Africa)
Telescopus fallax ssp.* Mediterranean cat snake (Balkans, Syria, Iran, Georgia, Armenia)
250 Jiri Valenta

Telescopus gabesiensis see T. obtusus

Telescopus gezirae* (E Sudan)
Telescopus guentheri see T. dhara
Telescopus guidimakaensis see T. obtusus
Telescopus hoogstraali* (Israel)
Telescopus iberus* (E Turkey, S Iran, S Russia)
Telescopus nigriceps* (Jordan and Iraq)
Telescopus obtusus* (N and NE Africa)
Telescopus pulcher* (Somalia)
Telescopus rhinopoma* Indian desert tiger snake (the Middle East)
Telescopus semiannulatus* Western tiger snake (SE Africa)
Telescopus tessellatus * Soosan tiger snake (Iraq)
Telescopus variegatus* (W Africa)
Genus: Thamnodynastes (South America)
Thamnodynastes almae*
Thamnodynastes chaquensis*
Thamnodynastes chimanta* Rozes coastal house snake
Thamnodynastes corocoroensis*
Thamnodynastes duida*
Thamnodynastes gambotensis*
Thamnodynastes hypoconia*
Thamnodynastes longicaudus*
Thamnodynastes marahuaquensis*
Thamnodynastes pallidus* Northern coastal house snake
Thamnodynastes rutilus*
Thamnodynastes strigatus* Coastal house snake
Thamnodynastes strigilis*
Genus: Thamnophis (North and Central America)
Thamnophis angustirostris* Longnose garter snake
Thamnophis atratus ssp.* Aquatic garter snake
Thamnophis brachystoma* Shorthead garter snake
Thamnophis butleri* Butlers garter snake
Thamnophis chrysocephalus* Goldenhead garter snake
Thamnophis couchii* Western Aquatic garter snake (Oregon and California, the USA)
Thamnophis cyrtopsis ssp.* Blackneck garter snake
Thamnophis elegans ssp.* Western terrestrial garter snake
Thamnophis eques ssp.*
Thamnophis exsul* Montane garter snake
Thamnophis fulvus* Highland garter snake
Thamnophis gigas* Giant garter snake
Thamnophis godmani* Godmans garter snake
Thamnophis hammondii* Two-striped garter snake
Thamnophis marcianus ssp.* Checkered garter snake
Thamnophis melanogaster* Blackbelly garter snake
Thamnophis mendax* Tamaulipan montane garter snake
Thamnophis ordinoides* Northwestern garter snake
 List of Venomous Snakes 251

Thamnophis proximus ssp.* Western ribbon snake

Thamnophis radix ssp.* Eastern Plains garter snake
Thamnophis rossmani* Rossmans garter snake
Thamnophis rufipunctatus ssp.* Narrowhead garter snake
Thamnophis sauritus ssp.* Eastern ribbon snake
Thamnophis scalaris* Longtail Alpine garter snake
Thamnophis scaliger* Short-tail Alpine garter snake
Thamnophis sirtalis ssp.* Common garter snake
Thamnophis sumichrasti* Sumichrasts garter snake
Thamnophis valida ssp.* West Coast garter snake
Thamnophis vicinus viz. T. cyrtopsis
Genus: Thelotornis, twig snakes
Thelotornis capensis** Bird snake, twig snake or vine snake
-- T. capensis capensis (E Botswana and NE RSA)
-- T. capensis mossambicanus (Mozambique, as far as S Somalia to the north)
-- T. capensis oatesi (Lake Tanganyika, as far as C Angola to the west)
-- T. capensis schilsi (Burundi)
Thelotornis kirtlandii** Forest twig snake (W and C Equatorial Africa)
Thelotornis usambaricus** Usambara vine snake (Tanzania and Kenya)
Genus: Thrasops (Tropical Africa)
Thrasops aethiopissa* syn. Rhamnophis aethiopissa Large-eyed green treesnake or
splendid dagger-tooth tree snake
Thrasops flavigularis* Yellow-throated bold-eyed tree snake
Thrasops jacksonii* Black tree snake
Thrasops occidentalis* (Western) Black tree snake
Genus: Trimorphodon, lyre snakes (North and Central America)
Trimorphodon biscutatus ssp.* Chihuahuan desert lyre snake
Trimorphodon lyrophanes see T. biscutatus ssp.
Trimorphodon tau* Mexican lyre snake
Trimorphodon vandeburghi see T. biscutatus ssp.
Trimorphodon vilkinsonii* Texas lyre snake
Genus: Umbrivaga (Central and South America)
Umbrivaga pygmaea* Amazon tropical forest snake
Genus: Waglerophis
Waglerophis merremi* Waglers snake (South America)
Genus: Xenochrophis, painted keelbacks (Asia, from Afghanistan as far as Indonesia)
Xenochrophis asperrimus* Boulengers keelback
Xenochrophis bellula*
Xenochrophis cerasogaster* Painted keelback
Xenochrophis flavipunctatus ssp.* Yellow-spotted keelback
Xenochrophis maculatus*
Xenochrophis piscator* Asiatic water snakes
Xenochrophis punctulatus*
Xenochrophis sanctijohannis* St. Johns keelback
Xenochrophis trianguligerus* Triangle keelback
Xenochrophis vittatus* Striped keelback
252 Jiri Valenta

Genus: Xenodon (Central and South America, Mexico to Argentina)

Xenodon bertholdi see X. rabdocephalus
Xenodon guentheri*
Xenodon neuwiedii* Neuwieds false fer-de-lance
Xenodon rabdocephalus* False fer-de-lance
Xenodon severus* Amazon false fer-de-lance
Xenodon suspectus see X. rabdocephalus
Xenodon werneri*
Genus: Xylodentophis
Xyelodontophis ulugurensis** (Tanzania - the Uluguru mountain range)

7.2. FAMILY: ATRACTASPIDIDAE

7.2.1. Subfamily: Atractaspidinae

Genus: Atractaspis
Atractaspis aterriima* Western forest mole viper (W and C Africa)
Atractaspis battersbyi* Battersbys mole viper (DRC)
Atractaspis bibronii** Southern or Bibrons burrowing asp (N Africa)
Atractaspis boulengeri* Boulengers mole viper
-- A. boulengeri boulengeri Boulengers mole viper (Gabon)
-- A. boulengeri matschiensis (Cameroon)
-- A. boulengeri mixta (DRC)
-- A. boulengeri schmidti (DRC)
-- A. boulengeri schultzei (DRC)
-- A. boulengeri vanderborghti (DRC)
Atractaspis coalescens* Mole viper (Cameroon)
Atractaspis congica* Eastern Congo burrowing asp
-- A. congica congica Eastern Congo burrowing asp (Cameroon, N Angola, DRC)
-- A. congica leleupi (DRC)
-- A. congica orientalis (DRC and N Zambia)
Atractaspis corpulenta* Fat mole viper
-- A. corpulenta corpulenta Fat mole viper (Cameroon, Gabon, Congo-Brazzaville, DRC)
-- A. corpulenta kivuenzis (DRC)
-- A. corpulenta leucura (Liberia, Cte dIvoire, Ghana)
Atractaspis dahomeyensis* Bocages mole viper (SW Africa, Guinea to Cameroon)
Atractaspis duerdeni* Duerdens or beaked burrowing asp (N Africa)
Atractaspis engaddensis** Israeli mole viper (Israel and Sinai)
Atractaspis engdahli* Engdahls mole viper (Somalia)
Atractaspis fallax* False mole viper (Ethiopia, Somalia, Kenya)
Atractaspis irregularis** Variable mole viper
-- A. irregularis angeli (Eritrea)
-- A. irregularis bipostocularis (Kenya, NW Tanzania, Uganda, Rwanda, DRC)
 List of Venomous Snakes 253

-- A. irregularis irregularis Variable mole viper (Guinea and Liberia to Cameroon,

Gabon)
-- A. irregularis parkeri (W DRC, Cameroon, Congo, N Angola)
-- A. irregularis uelensis (DRC, NW Uganda and the neighboring territory of Sudan)
Atractaspis leucomelas* White mole viper (Ethiopia and Somalia)
Atractaspis microlepidota** Small-scaled burrowing asp
-- A. microlepidota andersonii (NE Egypt, Israel, SW Arabian Peninsula)
-- A. microlepidota magrettii (E Sudan, Ethiopia, Eritrea, N Somalia)
-- A. microlepidota microlepidota Small-scaled burrowing asp (Sub-Saharan Africa: the
zone from Senegal as far as Somalia)
Atractaspis micropholis* Sahelian burrowing asp (C to W Africa, Mauritania to Mali)
Atractaspis phillipsi see A. microlepidota andersonii
Atractaspis reticulata* Reticulate mole viper
-- A. reticulata brieni (DRC)
-- A. reticulata heterochilus (C Africa, Cameroon to DRC)
-- A. reticulata reticulata (Cameroon)
Atractaspis scorteccii* Scorteccis mole viper (Somalia)

7.2.2 Subfamily: Aparallactinae

Genus: Amblyodipsas, glossy snakes (Sub-Saharan Africa)

Amblyodipsas concolor* Natal purple-glossed snake (RSA and Swaziland)
Amblyodipsas dimidiata* Mpwapwa purple-glossed snake (N Tanzania)
Amblyodipsas katangensis* Katanga purple-glossed snake (DRC and N Zambia)
Amblyodipsas micropthalma* Eastern purple-glossed snake (RSA and S Mozambique)
Amblyodipsas polylepis* Common purple-glossed snake (Angola, Namibia, Botswana,
DRC, Zambia, Mozambique, Zimbabwe, Malawi, RSA, Tanzania, Kenya)
-- Amblyodipsas polylepis hildebrandtii* Common purple-glossed snake (sometimes
classified as a separate subspecies described from Zanzibar)
Amblyodipsas rodhaini* (DRC) Rodhains purple-glossed snake
Amblyodipsas teitana* (Kenya) Teitana purple-glossed snake
Amblyodipsas unicolor* Western purple-glossed snake (Senegal to Tanzania)
Amblyodipsas ventrimaculata* Kalahari purple-glossed snake (Namibia, Botswana,
Zimbabwe, Zambia)
Genus: Aparallactus, centipede eaters (Sub-Saharan Africa)
Aparallactus capensis* Cape centipede eater
Aparallactus guentheri* Black centipede eater
Aparallactus jacksonii*
Aparallactus lineatus* Lined centipede-eater
Aparallactus lunulatus* Reticulated centipede eater
Aparallactus modestus* Western Forest centipede-eater
Aparallactus moeruensis* Zaire centipede-eater
Aparallactus niger*
Aparallactus nigriceps* Mozambique centipede eater
Aparallactus turneri* Malindi centipede-eater
254 Jiri Valenta

Aparallactus werneri* Usambara centipede-eater

Genus: Brachyophis
Brachyophis revoili* Revoils Short snake (Kenya and Somalia)
Genus: Cyanodontophis see Polemon
Genus: Chilorhinophis
Chilorhinophis butleri* Butlers two-headed snake (N Sudan)
Chilorhinophis carpenteri* Liwale two-headed snake (Mozambique and Tanzania)
Chilorhinophis gerardi* Gerards black and yellow burrowing snake (DRC, Zambia,
Zimbabwe, Tanzania)
Genus: Hypoptophis
Hypoptophis wilsoni* African bighead snake (C Africa)
Genus: Homoroselaps see Elapidae
Genus: Macrelaps
Macrelaps microlepidotus** Natal black snake (N Africa)
Genus: Micrelaps
Micrelaps bicoloratus* Kenya two-headed snake (Kenya and Tanzania)
Micrelaps boettgeri* Boettgers two-headed snake (NE Africa, Somalia to Kenya)
Micrelaps muelleri* (Israel)
Micrelaps vaillanti* Somali two-headed snake (Somalia)
Genus: Elapocalmus see Polemon
Genus: Elapotinus (in parallel listed under Colubridae)
Elapotinus picteti* Jans snake (tropical Africa)
Genus: Miodon see Polemon
Genus: Polemon, formerly also Cyanodontophis, Elapocalmus, Miodon (W and C
Africa)
Polemon acanthias* Reinhardts snake-eater
Polemon barthii* Guinea snake-eater
Polemon bocourti* Bocourts snake-eater
Polemon christyi* Eastern snake-eater
Polemon collaris* Collared snake-eater
Polemon fulvicollis* African snake eater
Polemon gabonensis* Gabon snake-eater
Polemon gracilis* Graceful snake-eater
Polemon griseiceps* Cameroon snake-eater
Polemon leopoldi*
Polemon neuwiedi* Ivory Coast snake-eater
Polemon notatus* syn. P. notatum
Polemon robustus* Zaire snake-eater
Genus: Xenocalamus (C and S Africa)
Xenocalamus bicolor* Slender quill-snouted snake
Xenocalamus mechowii* Elongate quill-Snouted snake
-- X. mechowii inornatus
-- X. mechowii mechowii
Xenocalamus michelli* Michells quill-snouted snake
Xenocalamus sabiensis* Sabi quill-snouted snake
Xenocalamus transvaalensis* Transvaal quill-snouted snake
 List of Venomous Snakes 255

7.3. FAMILY: ELAPIDAE, ELAPIDS

7.3.1. Subfamily: Elapinae

Genus: Aspidelaps, shield-nosed cobras

Aspidelaps lubricus* South African coral snake (N Africa)
-- A. lubricus cowlesi (SW Angola and NW Namibia)
-- A. lubricus infuscatus (C Namibia)
-- A. lubricus lubricus South African coral snake (RSA and S Namibia)
Aspidelaps scutatus* Intermediate shield-nose snake (N Africa)
-- A. scutatus intermedius (RSA)
-- A. scutatus fulafula (SE Zimbabwe and S Mozambique)
-- A. scutatus scutatus, syn. A. scutatus bachrani Intermediate shield-nose snake (RSA,
Botswana, SW Zimbabwe, Namibia)
Genus: Boulengerina, water cobras
Boulengerina annulata*** Ringed water cobra
-- B. annulata annulata (E Cameroon, Gabon, DRC, Congo-Brazzaville)
-- B. annulata stormsi (sides of the Lake Tanganyika)
Boulengerina christyi*** Christys water cobra (N Congo-Brazzaville, W DRC, probably
inc. NW Angola)
Genus: Bungarus, kraits
Bungarus andamanensis*** South Andaman krait (the Andaman Islands)
Bungarus bungaroides*** Northeastern Hill krait (India and N Burma)
Bungarus caeruleus*** Indian krait (Indian subcontinent and Sri Lanka)
Bungarus candidus*** Blue krait (Vietnam, Malaysia, Sumatra, Java, Bali, Celebes)
Bungarus ceylonicus*** Ceylon krait (Sri Lanka)
Bungarus fasciatus*** Banded krait (N India, Indonesia, SE Asia)
Bungarus flaviceps*** Red-headed krait (mainland SE Asia, Malaysia, Indonesia)
-- B. flaviceps baluensis (Borneo)
-- B. flaviceps flaviceps (N Thailand, S Burma, S Cambodia, Vietnam, Malaysia,
Indonesia)
Bungarus javanicus see B. candidus
Bungarus lividus*** Lesser black krait (India)
Bungarus magnimaculatus*** Burmese krait (N Burma)
Bungarus multicinctus*** Many-banded krait (Burma, S China, Taiwan)
-- B. multicinctus multicinctus (N China, Taiwan, Hainan, Hong Kong)
-- B. multicinctus wanghaotingi (Burma, NW Laos, SW China, N Vietnam)
Bungarus niger*** Greater black krait (E Himalayas and Assam)
Bungarus sindanus*** Sind krait
-- B. sindanus razai (E Afghanistan and NW Pakistan)
-- B. sindanus sindanus (N Pakistan and the neighboring part of W India)
-- B. sindanus walli (India)
Bungarus walli see Bungarus sindanus walli
Genus: Calliophis, Oriental coral snakes or Asian coral snakes
Caliophis beddomei* (SW India)
256 Jiri Valenta

Calliophis bibroni* Bibrons coral snake (India)

Calliophis bivirgata*** Blue Malaysian coral snake
-- C. bivirgatus bivirgatus (Java)
-- C. bivirgatus flaviceps (Burma, Thailand, Cambodia, Malayan Peninsula, Singapore,
Indonesia)
-- C. bivirgatus tetrataenia (Borneo)
Calliophis calligaster* syn. Hemibungarus calligaster
-- C. calligaster calligaster (the Philippines, Luzon and Mindoro islands)
-- C. calligaster gemiannulis (the Philippines, Cebu, Negros, Panay and Masbate islands)
-- C. calligaster mcclungi (Polillo Island near the Philippines)
Calliophis gracilis* Spotted coral snake (Malaysia, Sumatra, Singapore)
Calliophis intestinalis* Banded Malaysian coral snake
-- C. intestinalis bilineata (the Philippines)
-- C. intestinalis everetti (Borneo - Sabah)
-- C. intestinalis intestinalis (Indonesia)
-- C. intestinalis lineata, syn. C. nigrotaeniata, C. sumatrana (N Thailand, Malayan
Peninsula, Indonesia)
-- C. intestinalis philippina (the Philippines)
-- C. intestinalis suluensis (the Philippines)
-- C. intestinalis thepassi (Borneo and E Malaysia)
Calliophis japonicus* see Hemibungarus japonicus Japanese coral snake
Calliophis kellogi* syn. Sinomicrurus kelloggi, see Hemibungarus kellogi
Calliophis macclellandi** Macclellands coral snake, syn. Sinomicrurus macclellandi
-- C. macclellandi macclellandi (India, N Burma, S China, Vietnam, Thailand, Hainan)
-- C. macclellandi iwasakii (Japan)
-- C. macclellandi swinhoei (Taiwan)
-- C. macclellandi univirgatus (Nepal and India)
Calliophis maculiceps* Small-spotted coral snake
-- C. maculiceps atrofrontalis (N Vietnam and Cambodia)
-- C. maculiceps hughi (Thailand)
-- C. maculiceps maculiceps Small-spotted coral snake (N Burma, S Thailand, N
Malayan Peninsula)
-- C. maculiceps michaelis (C and S Laos)
-- C. maculiceps smithi (C Thailand)
Calliophis melanurus* Indian coral snake
-- C. melanurus melanurus (N and E India)
-- C. melanurus sinhaleyus (Sri Lanka)
Calliophis nigrescens* Black coral snake (N and W India)
Calliophis sauteri see Hemibungarus japonicus sauteri
Genus: Dendroaspis, mambas
Dendroaspis angusticeps*** Eastern green mamba (Tanzania, Mozambique, RSA)
Dendroaspis jamesoni*** Jamesons mamba (W and C Equatorial Africa)
-- D. jamesoni jamesoni (Ghana to Central African Republic, Congo-Brazzaville, E DRC,
Angola)
-- D. jamesoni kaimosae (E DRC, Rwanda, Uganda, W Kenya)
Dendroaspis polylepis*** Black mamba (C Africa)
 List of Venomous Snakes 257

Dendroaspis viridis*** Western green mamba (W Africa, So Tom, probably S Senegal

and Togo)
Genus: Elapsoidea, venomous or African garter snakes
Elapsoidea boulengeri see E. semiannulata boulengeri
Elapsoidea broadleyi* (N Somalia)
Elapsoidea chelazzii* Somali garter snake syn. E. chelazziorum (a type locality near
Afgoi, S Somalia)
Elapsoidea guentherii* (N Congo-Brazzaville, S DRC, N and C Angola, C Zambia, N
and C Zimbabwe)
Elapsoidea laticincta* Werners garter snake (N Sudan, Central African Republic, N
Uganda, N DRC to SW Ethiopia)
Elapsoidea loveridgei* Loveridges garter snake
-- E. loveridgei colleti (E DRC, SW Uganda, Rwanda, Burundi)
-- E. loveridgei loveridgei (C and S Kenya, N Tanzania)
-- E. loveridgei multicincta (NE DRC, Uganda, W Kenya, NW Tanzania, S Ethiopia)
-- E. loveridgei scalaris see E. guentherii
Elapsoidea nigra* Black garter snake (NE Tanzania)
Elapsoidea semiannulata* Angolan garter snake
-- E. semiannulata boulengeri Boulengers garter snake (N Tanzania to RSA)
-- E. semiannulata moebiusi (N Mauritania, Senegal to Central African Republic,
Cameroon, Congo-Brazzaville, DRC)
-- E. semiannulata semiannulata (Angola, SW DRC, NW RSA, W Zambia to N
Namibia)
Elapsoidea sundevalli** Sundevalls garter snake or African garter snake
-- E. sundevalli decosteri (N Mozambique and NE RSA)
-- E. sundevalli fitzsimonsi (W Botswana, Namibia and the neighboring territory of RSA)
-- E. sundevalli longicauda (SE Zimbabwe, S Mozambique, RSA)
-- E. sundevalli media (RSA)
-- E. sundevalli sundevalli (RSA and Swaziland)
Elapsoidea trapei* (Senegal)
Genus: Hemachatus, cobra
Hemachatus haemachatus*** Rinkhals, ring-necked spitting cobra, or ringhals (N
Africa)
Genus: Hemibungarus, Asian or oriental coral snakes
Hemibungarus calligaster see Calliophis calligaster
Hemibungarus hatori* syn. Sinomicrurus hatori (NE Taiwan)
Hemibungarus japonicus*, syn. Sinomicrurus japonicus, Japanese coral snake, see
Calliophis japonicus
-- H. japonicus boettgeri (Japan)
-- H. japonicus japonicus (Japan)
-- H. japonicus sauteri see H. sauteri
-- H. japonicus takarai (Okinawa)
Hemibungarus kelloggi* Kelloggs coral snake (N China)
Hemibungarus macclellandi see Calliophis macclellandi
Hemibungarus sauteri* syn. Sinomicrurus sauteri (Taiwan)
Genus: Homoroselaps
258 Jiri Valenta

Homoroselaps dorsalis* Striped harlequin snake or striped dwarf garter snake (NE RSA
and W Swaziland)
Homoroselaps lacteus* Spotted harlequin snake (N RSA)
Genus: Leptomicrurus (sometimes included in Micrurus genus synonyms)
Leptomicrurus collaris** Guyana blackback coral snake
-- L. collaris breviventris (Venezuela and Guyana)
-- L. collaris collaris (SE Venezuela to French Guyana and the neighboring territory of
Brazil)
Leptomicrurus narduccii** Andean blackback coral snake
-- L. narduccii melanotus (Colombia, Ecuador, Peru, Brazil)
-- L. narduccii narduccii (Bolivia)
Leptomicrurus renjifoi** (E Colombia)
Leptomicrurus scutiventris** (the border region of SE Colombia, S Venezuela, NW
Brazil and NE Peru)
Genus: Maticora
Maticora beddomei* see Calliophis beddomei
Maticora bivirgatus*** see Calliophis bivirgatus
Maticora intestinalis* see Calliophis intestinalis
Maticora maculiceps* see Calliophis maculiceps
Maticora nigrescens* see Calliophis nigriscens
Genus: Micruroides
Micruroides euryxanthus** Western coral snake
-- M. euryxanthus australis (Mexico)
-- M. euryxanthus euryxanthus (the USA, N Mexico, Tiburn)
-- M. euryxanthus neglectus (Mexico)
Genus: Micrurus, coral snake
Micrurus albicinctus** (NW Brazil)
Micrurus alleni** Allens coral snake (E Nicaragua, Costa Rica to W Panama)
Micrurus altirostris** (Uruguay, NE Argentina, S Brazil)
Micrurus ancoralis** Regal coral snake
-- M. ancoralis ancoralis (SW Colombia and NW Ecuador)
-- M. ancoralis jani (E Panama and Colombia - the Pacific part)
Micrurus annellatus** Annellated coral snake
-- M. annellatus annellatus (SE Ecuador, C and SE Peru)
-- M. annellatus balzani (Peru and W Bolivia)
-- M. annellatus bolivianus (C Bolivia)
Micrurus averyi** Black-headed coral snake (N Guyana, Brazil - the Manaus territory)
Micrurus baliocoryphus** (NE Argentina, between the Paran and Uruguay rivers)
Micrurus bernardi** (Mexico)
Micrurus bocourti** Ecuadorian coral snake (coastal Ecuador, probably inc. the
neighboring territory of NW Peru)
Micrurus bogerti** Bogerts coral snake (Mexico)
Micrurus brasiliensis** (Brazil)
Micrurus browni** Browns coral snake (N Mexico)
-- M. browni browni (N Mexico to W Guatemala mountains)
-- M. browni importunus (Guatemala)
 List of Venomous Snakes 259

-- M. browni taylori (Mexico)

Micrurus catamayensis** Catamayo coral snake (Ecuador)
Micrurus circinalis** (Trinidad and Gaspare islands, NE Venezuela)
Micrurus clarki** Clarks coral snake (N Costa Rica, Panama to W coast of Colombia)
Micrurus corallinus** Painted coral snake (N Brazil, N Argentina, S Paraguay)
Micrurus decoratus** Brazilian coral snake (SE Brazil)
Micrurus diana** (E Bolivia)
Micrurus diastema** Variable coral snake
-- M. diastema affinis (N Mexico)
-- M. diastema aglaeope (NW Honduras)
-- M. diastema alienus (N Mexico - N Yucatn)
-- M. diastema apiatus (N Mexico and Guatemala)
-- M. diastema bernadi see M. bernardi
-- M. diastema diastema (N Mexico, Belize, N and C Guatemala, NW Honduras)
-- M. diastema macdougalli (N Mexico)
-- M. diastema sapperi (N Mexico, W Guatemala, Belize)
Micrurus dissoleucus** Pygmy coral snake
-- M. dissoleucus dissoleucus (NE Colombia and Venezuela)
-- M. dissoleucus dunni (Panama Canal as far as NW Colombia)
-- M. dissoleucus melanogenys (NE Colombia)
-- M. dissoleucus meridensis see M. meridensis
-- M. dissoleucus nigrirostris (N Colombia)
Micrurus distans** West Mexican coral snake
-- M. distans distans (Mexico)
-- M. distans michoacanensis (Mexico)
-- M. distans oliveri (Mexico)
-- M. distans zweifeli (Mexico)
Micrurus dumerilii**
-- M. dumerilii antoquiensis (Colombia)
-- M. dumerilii carinicauda (Colombia to NW Venezuela)
-- M. dumerilii colombianus (NE Colombia)
-- M. dumerilii dumerili (Colombia)
-- M. dumerilii transandinus (N Panama and W Colombia)
-- M. dumerilii venezuelensis (N Venezuela)
Micrurus elegans** Elegant coral snake
-- M. elegans elegans (Mexico)
-- M. elegans veraepacis (Mexico and Guatemala)
Micrurus ephippifer** Oaxacan coral snake
-- M. ephippifer ephippifer (Mexico - Oaxaca, the Pacific part)
-- M. ephippifer zapotecus (Mexico - Oaxaca)
Micrurus filiformis** Slender coral snake
-- M. filiformis filiformis (Brazil)
-- M. filiformis subtilis (N and SE Colombia, E Ecuador, N Peru, W Brazil as far as
Manaus)
Micrurus frontalis*** Southern coral snake
-- M. frontalis altirostris see M. altirostris
260 Jiri Valenta

-- M. frontalis baliocoryphus see M. baliocoryphus

-- M. frontalis brasiliensis see M. brasiliensis
-- M. frontalis diana see M. diana
-- M. frontalis frontalis (N Brazil, S Paraguay and the neighboring areas of NE
Argentina)
-- M. frontalis multicinctus see M. altirostris
-- M. frontalis pyrhocryptus see M. pyrhocryptus pyrhocryptus
-- M. frontalis tricolor see M. pyrhocryptus tricolor
Micrurus frontifasciatus, Bolivian coral snake see M. lemniscatus
Micrurus fulvius** Eastern coral snake
-- M. fulvius fitzingeri see M. tener fitzingeri
-- M. fulvius fulvius (SE USA)
-- M. fulvius maculatus see M. tener maculatus
-- M. fulvius microgalbineus see M. tener microgalbineus
-- M. fulvius tener see M. tener tener
Micrurus hemprichii** Hemprichs coral snake
-- M. hemprichii hemprichii (E Colombia, S Venezuela to French Guyana and the
neighboring territories of NE Brazil)
-- M. hemprichii ortoni (Colombia, Ecuador, N Peru and the neighboring territory of
Brazil as far as NE Bolivia)
-- M. hemprichii rondonianus (a type locality - Usina hidroelectrica Samuel, a water
power plant, the State of Rondonia, W Brazil)
Micrurus hippocrepis** Mayan coral snake (N Belize and E Guatemala)
Micrurus ibiboboca** Caatinga coral snake (E Brazil, N Surinam, N French Guyana)
Micrurus isozonus** Venezuela coral snake (NE Colombia, N and C Venezuela)
Micrurus langsdorffi** Langsdorffs coral snake
-- M. langsdorffi langsdorffi (N Colombia, E Ecuador, N Peru, Colombia)
-- M. langsdorffi ornatissimus see M. ornatissimus
Micrurus laticollaris** Balsan coral snake
-- M. laticollaris laticollaris (N Mexico - the Balsas River valley)
-- M. laticollaris maculirostris (N Mexico - the states of Colima and Jalisco)
Micrurus latifasciatus** Broad-ringed coral snake (N Mexico and SE Guatemala)
Micrurus lemniscatus*** South American coral snake
-- M. lemniscatus carvalhoi (NE and C Brazil)
-- M. lemniscatus diutius (E and SE Venezuela, Trinidad, C and S Guyana, Surinam,
French Guyana)
-- M. lemniscatus helleri (N Colombia, S Venezuela, NW Brazil, Bolivia)
-- M. lemniscatus lemniscatus (NE Brazil, N Guyana, Surinam)
Micrurus limbatus** Tuxtlan coral snake
-- M. limbatus limbatus (the northern coast of the Mexican state of Veracruz)
-- limbatus spilosomus (Mexico - S Veracruz)
Micrurus margaritiferus** Speckled coral snake (Peru)
Micrurus medemi** (C Colombia)
Micrurus meridensis** (Venezuela)
Micrurus mertensi** Mertens coral snake (SW Ecuador and W Peru)
Micrurus mipartitus** Redtail coral snake
 List of Venomous Snakes 261

-- M. mipartitus anomalus (E Colombia, the neighboring part of NW Venezuela)

-- M. mipartitus decussatus (W and C Colombian Andes, W Ecuador)
-- M. mipartitus mipartitus (E Panama and W Colombia)
-- M. mipartitus popayanensis (Colombia - the Popayan and Cauca regions)
-- M. mipartitus semipartitus see M. mipartitus rozei
-- M. mipartitus rozei (N Venezuela)
Micrurus multifasciatus** Many-banded coral snake
-- M. multifasciatus hertwigi (N Nicaragua to W Panama)
-- M. multifasciatus multifasciatus (C Panama)
Micrurus multiscutatus** Cauca coral snake (Colombia)
Micrurus nebularis** Cloud forest coral snake (Mexico)
Micrurus nigrocinctus** Central American coral snake
-- M. nigrocinctus babaspul (Nicaragua)
-- M. nigrocinctus coibensis (Panama)
-- M. nigrocinctus divaricatus (N and C Honduras to C Belize)
-- M. nigrocinctus mosquitensis (Costa Rica and NW Panama)
-- M. nigrocinctus nigrocinctus (W Nicaragua, W Costa Rica, Panama)
-- M. nigrocinctus ruatanus see M. ruatanus
-- M. nigrocinctus zunilensis (N Mexico, Guatemala, Salvador, S Honduras)
Micrurus oligoannelatus** (Colombia - Cauca region)
Micrurus ornatissimus** (N Colombia, E Ecuador, N Peru, NW Brazil)
Micrurus pachecogili** (C Mexico)
Micrurus paraensis** (NE and C Brazil)
Micrurus ornatissimus** (N Colombia, E Ecuador, N Peru, NW Brazil)
Micrurus peruvianus** Peruvian coral snake (Peru)
Micrurus petersi** Peters coral snake (Ecuador)
Micrurus proximans** Nayarit coral snake (Mexico)
Micrurus psyches** Carib coral snake
-- M. psyches circinalis see M. circinalis
-- M. psyches donosoi see M. paraensis
-- M. psyches medemi see M. medemi
-- M. psyches paraensis see M. paraensis
-- M. psyches psyches (SE Colombia to French Guyana)
-- M. psyches remotus see M. remotus
Micrurus putumayensis** Putumayo coral snake (SE Colombia, NE Peru, NW Brazil)
Micrurus pyrhocryptus**
-- M. pyrhocryptus pyrhocryptus (Brazil, W and SW Bolivia, the neighboring part of
Paraguay, N Argentina)
-- M. pyrhocryptus tricolor (Brazil and E Paraguay)
Mircurus remotus** (the border regions of Venezuela, Brazil, and Colombia)
Micrurus rondonianus see M. hemprichii rondonianus
Micrurus ruatanus** Roatan coral snake (Honduras)
Micrurus sangilensis** Santander coral snake (N Colombia)
Micrurus serranus** (Bolivia)
Micrurus spixii** Amazon coral snake
-- M. spixii martiusi (E Brazil)
262 Jiri Valenta

-- M. spixii obscurus (E Colombia, E Ecuador, E Peru, S Venezuela, NW Brazil to

Bolivia)
-- M. spixii princeps (NW and C Bolivia)
-- M. spixii spixii (Brazil)
Micrurus spurrelli** (W and C Colombia)
Micrurus steindachneri** Steindachners coral snake
-- M. steindachneri orcesi (C Ecuador)
-- M. steindachneri steindachneri (SE Ecuador)
Micrurus stewarti** Panamanian coral snake (Panama)
Micrurus stuarti** Stuarts coral snake (SW Guatemala)
Micrurus surinamensis*** Aquatic coral snake
-- M. surinamensis nattereri (E Colombia, S Venezuela, Brazil)
-- M. surinamensis surinamensis (Colombia to French Guyana, Brazil - Amazon Basin,
Bolivia)
Micrurus tener** Texas coral snake
-- M. tener tener (the USA - SW Arkansas to S Texas, Mexico - N Coahuila, Nuevo
Len, Tamaulipas)
-- M. tener fitzingeri (the Mexican State of Guanajuato to the State of Morelos, probably
inc. Zacatecas)
-- M. tener maculatus (Mexico - the State of Tamaulipas)
-- M. tener microgalbineus (Mexico - S Tamaulipas to C Guanujato)
Micrurus tschudii** Desert coral snake
-- M. tschudii olssoni (SW Ecuador and NW Peru)
-- M. tschudii tschudii (the Pacific part of the Andes in Peru)
Genus: Naja, cobras
Naja anchietae*** Anchietas cobra (N Angola, S DRC, N and C Namibia, N Botswana,
W Zambia, NW Zimbabwe)
Naja annulifera*** Snouted cobra
-- N. annulifera anchietae see N. anchietae
-- N. annulifera annulifera (N Zambia, Malawi, Mozambique, Zimbabwe, E Botswana)
Naja atra*** Chinese cobra (N China, Taiwan, Mainland Southeast Asia)
Naja haje*** Egyptian cobra
-- N. haje arabica (SW Saudi Arabia, Yemen, SW Oman)
-- N. haje legionis (SE Morocco, NW Western Sahara to N Algeria)
-- N. haje haje Egyptian cobra (C Tunisia, N Libya to Egypt, the southern edge of Sahara
to Ethiopia to the north, NE DRC, Uganda, Kenya)
Naja kaouthia*** Monocellate cobra (Bengal, Nepal, E Himalayas, SW China)
Naja katiensis*** Katian spitting cobra (W Africa)
Naja mandalayensis*** (Burma)
Naja melanoleuca*** Black and white cobra (African forests and savannahs)
Naja mossambica*** Mozambique spitting cobra (SE Tanzania, S Zambia, Malawi,
Mozambique to RSA, SE Angola)
Naja naja*** Indian cobra (E Pakistan, S Nepal, India, Sri Lanka, W Bangladesh)
Naja nigricollis*** Black-necked spitting cobra
-- N. nigricollis nigricincta (N Namibia and SW Angola)
-- N. nigricollis nigricollis (Senegal, S Mauritania to S Sudan, Ethiopia, Angola, Malawi)
 List of Venomous Snakes 263

-- N. nigricollis woodi (RSA, Namibia)

Naja nivea*** Cape cobra (RSA and SW Africa)
Naja nubiae*** Nubian spitting cobra (Egypt, Sudan, Chad, Niger, Eritrea)
Naja oxiana*** Central Asian cobra (the Southern Caucasus to Afghanistan and
Kashmir)
Naja pallida*** African cobra or red spitting cobra (N Egypt, NE Sudan, Ethiopia,
Eritrea, Somalia, Kenya, NE Tanzania)
Naja philippinensis*** Philippine cobra (the Philippines)
Naja sagittifera*** (Andaman)
Naja samarensis*** Peters cobra (the Philippines)
Naja siamensis*** Indochinese spitting cobra (E Burma, Thailand, W Laos, Cambodia, S
Vietnam)
Naja sputatrix*** Indonesian cobra (Malaysia; Java, Bali, Sumbawa, Flores, Komodo
and Sulawesi islands)
Naja sumatrana*** Equatorial spitting cobra or golden spitting cobra (N Thailand,
Malaysia, Singapore, Indonesia to the Philippines)
Genus: Ophiophagus
Ophiophagus hannah*** King cobra (SE and S Asia)
Genus: Paranaja
Paranaja multifasciata** Many-banded snake
-- P. multifasciata anomala (E Cameroon)
-- P. multifasciata duttoni (DRC)
-- P. multifasciata multifasciata (N DRC and Congo-Brazzaville)
Genus: Pseudohaje
Pseudohaje goldii** African tree cobra, Golds forest cobra, Goldies false cobra, or tree
cobra (Africa from Nigeria as far as Uganda)
Pseudohaje nigra** Hoodless cobra (Sierra Leone, Liberia, Ghana, Togo)
Genus: Walterinnesia
Walterinnesia aegyptia** Desert cobra (Egypt, Israel, Syria, Iraq, Iran, Lebanon, Jordan)

7.3.2. Subfamily: Hydrophiinae

7.3.2.1. Terrestrial Species (Formerly: Oxyuraninae Subfamily)

Genus: Acanthophis, death adders
Acanthophis antarcticus*** Common death adder (Australia and New Guinea)
-- A. antarcticus antarcticus Common death adder
-- A. antarcticus cliffrosswelingtoni
-- A. antarcticus schistos
Acanthophis barnetti see A. laevis
Acanthophis crotalusei see A. laevis
Acanthophis cummingi see A. hawkei
Acanthophis groenveldi see A. laevis
Acanthophis hawkei*** (N Australia)
Acanthophis laevis*** (New Guinea, Indonesia - Seram and Tanimbar islands)
Acanthophis macgregori see A. laevis
264 Jiri Valenta

Acanthophis praelongus*** Northern death adder (N Australia, New Guinea, Torres

Strait Islands, Seram Island and Tanimbar Islands to the west)
Acanthophis pyrrhus*** Desert death adder (C and W Australia)
Acanthophis rugosus*** (N Australia and Irian Jaya, Indonesia)
Acanthophis wellsi*** (Pilbara, Australia)
Genus: Aspidomorphus
Aspidomorphus diadema see Furina diadema
Aspidomorphus lineaticollis * Striped crown snake (NE Papua-New Guinea)
Aspidomorphus muelleri * Mllers crown snake (New Guinea as far as Misool, Salawati
and Seram islands to the west, and New Britain as well as New Ireland islands to the
east)
-- A. muelleri muelleri Mllers crown snake (New Guinea)
-- A. muelleri interruptus (New Britain, Duke of York and New Ireland islands)
Aspidomorphus schlegeli * Schlegels crown snake (E Indonesia and NW Papua-New
Guinea)
Genus: Austrelaps, copperheads or Australian copperheads
Austrelaps labialis** Pygmy copperhead (N Australia)
Austrelaps ramsayi** Highlands copperhead (Australian mountain ranges from E
Victoria as far as New South Wales)
Austrelaps superbus** Australian copperhead (SE Australia, Tasmania and Bass Straits
Islands)
Genus: Cacophis, dwarf-crowned snakes
Cacophis churchilli* (Australia)
Cacophis harriettae* White-crowned snake (Australia)
Cacophis krefftii* Kreffts dwarf snake (Australia)
Cacophis squamulosus* (Australia)
Genus: Demansia
Demansia atra see D. vestigiata
Demansia calodera* Black-necked whipsnake (W Australia, S Papua-New Guinea)
Demansia olivacea** Marble-headed whip snake (N and NW Australia)
Demansia papuensis** Papuan whip snake
-- D. papuensis melanea (N Australia)
-- D. papuensis papuensis (SE Irian Jaya and NE Australia)
Demansia psammophis** Yellow-faced whip snake
-- D. psammophis cupreiceps (W Australia)
-- D. psammophis psammophis (SE to E Australia)
-- D. psammophis reticulata (coastal W Australia)
Demansia rufescens* (W Australia)
Demansia simplex* Grey whipsnake (W Australia)
Demansia torquata* Collared whip snake (Australia)
Demansia vestigiata** Black whip snake (N Indonesian New Guinea)
Demansia textilis see Pseudonaja textilis
Genus: Denisonia
Denisonia devisi** De Viss banded snake (Australia)
Denisonia maculata** Ornamental snake (Australia)
Denisonia superba see Austrelaps superbus
 List of Venomous Snakes 265

Denisonia gouldii see Suta gouldii

Genus: Drysdalia, crowned snakes
Drysdalia coronata see Elapognathus coronata
Drysdalia coronoides* White-lipped snake (SE Australia, Tasmania and Bass Straits
Islands)
Drysdalia mastersii* Masters snake (SE coast of W Australia, coastal S Australia)
Drysdalia rhodogaster* Mustard-bellied snake (Australia)
Genus: Echiopsis
Echopsis atriceps see Paroplocephalus atriceps
Echiopsis curta** Bardick snake (southern W Australia, coastal S Australia, SW New
South Wales, NW Victoria and the neighboring part of S Australia)
Genus: Elapognathus
Elapognathus coronata* Crowned snake (SW part of West Australia and the neighboring
islets)
Elapognathus minor* Short-nosed snake or little brown snake (SW Australia)
Genus: Furina
Furina barnardi* Yellow-naped snake (NW Australia)
Furina diadema* Red-naped snake (W Australia)
Furina dunmalli* Dunmalls snake (W Australia)
Furina ornata* Orange-naped snake (Australia)
Furina tristis* Brown-headed or grey-naped snake (N and NE Australia, Papua-New
Guinea)
Genus: Glyphodon
Glyphodon tristis see Furina tristis
Glyphodon barnardi see Furina barnardi
Glyphodon harriettae see Cacophis harriettae
Genus: Hemiaspis
Hemiaspis damelii** Grey snake (inland SE Australia as far as the eastern coast)
Hemiaspis signata** Marsh snake, swamp snake, or black-bellied swamp snake (coastal
E Australia)
Genus: Hoplocephalus
Hoplocephalus bitorquatus** Pale-headed snake (Australia)
Hoplocephalus bungaroides** Broad-headed snake (Australia)
Hoplocephalus stephensii** Stephenss banded snake (Australia)
Genus: Loveridgelaps
Loveridgelaps elapoides** Solomons small-eyed snake (the Solomon Islands)
Genus: Micropechis
Micropechis ikaheka*** New Guinea small-eyed or Ikaheka snake
-- M. ikaheka ikaheka (New Guinea and the neighboring islands)
-- M. ikaheka fasciatus (Aru Archipelago)
Genus: Notechis, tiger snakes
Notechis ater*** Black tiger snake
-- N. ater ater (SE part of S Australia)
-- N. ater humpreysi (Tasmania and the neighboring islands)
-- N. ater niger (Spencer Gulf islands)
-- N. ater occidentalis see N. scutatus occidentalis
266 Jiri Valenta

-- N. ater serventyi (Chappel and Badger islands, Bass Strait islets)

Notechis scutatus*** Mainland tiger snake (SE Australia)
-- N. scutatus occidentalis (SW part of W Australia and the neighboring islets)
Genus: Ogmodon
Ogmodon vitianus* Fiji cobra (Fiji)
Genus: Oxyuranus, taipans
Oxyuranus microlepidotus*** Fierce snake or inland taipan (inland Australia, border of
Victoria and New South Wales)
Oxyuranus scutellatus*** Coastal taipan
-- O. scutellatus canni Papuan taipan (N coast of Papua-New Guinea)
-- O. scutellatus scutellatus Coastal taipan (N and NE Australia)
Genus: Parapistocalamus
Parapistocalamus hedigeri* Bougainville or Hedigers coral snake (Bouganville Island,
the Solomon Islands)
Genus: Paroplocephalus
Paroplocephalus atriceps* Lake Cronin snake (SW coast of W Australia)
Genus: Pseudechis, black snakes
Pseudechis australis*** Mulga snake or king brown snake (Australia and New Guinea)
Pseudechis butleri** Spotted mulga snake (the middle-west part of W Australia)
Pseudechis colletti** Colletts snake (NE Australia)
Pseudechis guttatus** Blue-bellied black snake (E Australia)
Pseudechis papuans** Papuan black snake (E New Guinea and neighboring islands)
Pseudechis pailsei (Validity of the species has been disputed.)
Pseudechis porphyriacus** Red-bellied black snake (E and SE Australia)
-- P. porphyriacus eipperi (Validity of the subspecies has been disputed.)
-- P. porphyriacus rentoni (Validity of the subspecies has been disputed.)
Genus: Pseudonaja, brown snakes
Pseudonaja affinis** Dugite or spotted brown snake
-- P. affinis affinis (coastal SW Australia)
-- P. affinis exilis (Rottnest Island)
-- P. affinis tanneri (Boxers Island)
Pseudonaja elliotti** (Australia - W part of New South Wales)
Pseudonaja guttata** Speckled brown snake or spotted brown snake (Australia)
Pseudonaja inframacula** Peninsula brown snake (N Australia)
Pseudonaja ingrami** Ingrams brown snake (Australia, the Barkly Tableland region)
Pseudonaja modesta** Ringed brown snake (W Australia to the north of the Northern
Territory, inland S Australia, SW Queensland)
Pseudonaja nuchalis** Gwardar or western brown snake (W and S Australia, the
Northern Territory, W New South Wales, NW Victoria)
Pseudonaja textilis*** Eastern brown snake (NE Australia)
-- P. textilis pughi (ssp. described in 2003.)
Genus: Rhinoplocephalus
Rhinoplocephalus bicolor* Square-nosed snake (SW part of West Australia)
Rhinoplocephalus boschmai* syn. Unechis boschmai, U. carpentariae Carpentaria whip
snake (Australia and Indonesian part of New Guinea)
Rhinoplocephalus incredibilis* (Prince of Wales Island, Torres Straits)
 List of Venomous Snakes 267

Rhinoplocephalus nigrescens * Eastern small-eyed snake (E Australia)

Rhinoplocephalus nigrostriatus * Australian black-striped snake (Australia, S Papua-
New Guinea)
Rhinoplocephalus pallidiceps * Western Carpentaria snake (N Australia)
Genus: Salomonelaps
Salomonelaps par** Solomons coral snake (the Solomon Islands)
Genus: Simoselaps
Simoselaps anomalus * Northern desert banded snake (NW coast of W Australia to SW
Northern Territory and NW part of S Australia)
Simoselaps approximans * North-western shovel-nosed snake (NW Australia)
Simoselaps australis* Eastern shovel-nosed snake, coral snake, Australian coral snake (E
Australia)
Simoselaps bertholdi* Southern desert banded snake, desert banded snake (Australia)
Simoselaps bimaculatus* Black-naped burrowing snake (SW Australia to C S Australia)
Simoselaps calonotus* Black-striped burrowing snake (SW coast of Australia)
Simoselaps fasciolatus* Narrow-banded shovel-nosed snake
-- S. fasciolatus fasciatus (Central S Australia)
-- S. fasciolatus fasciolatus (SW Australia)
Simoselaps incinctus * Unbanded shovel-nosed snake (Australia)
Simoselaps littoralis * West-coast banded snake (C part of W coast of West Australia)
Simoselaps minimus * Dampierland burrowing snake (NW West Australia)
Simoselaps morrisi* (Australia - the Northern Territory)
Simoselaps roperi Northern shovel-nosed snake (W Australia to the Northern Territory)
Simoselaps semifasciatus*Southern shovel-nosed snake, half-girdled snake
-- S. semifasciatus campbelli (NE Queensland)
-- S. semifasciatus roperi
-- S. semifasciatus semifasciatus Southern shovel-nosed snake (SW and S Australia)
-- S. semifasciatus woodjonesii Cape York shovel-nosed snake (N Queensland)
Simoselaps warro* North-eastern plain-nosed (Australia)
Genus: Suta
Suta atriceps see Paroplocephalus atriceps
Suta dwyeri * Variable black-naped snake (Australia)
Suta fasciata* Rosens snake (W Australia)
Suta flagellum* Whip hooded snake (SE Australia)
Suta gouldii* Australian black-headed snake (SW West Australia)
Suta monachus* Hooded snake (Australia)
Suta nigriceps* Gnthers black-headed snake (N West Australia to NW Victoria and
SW New South Wales)
Suta ordensis* Ord curl snake (NW Australia)
Suta punctata * Little spotted snake (NW West Australia to C Australia and W C
Queensland)
Suta spectabilis* Spectacled hooded snake
-- S. spectabilis bushi (a type locality - Scaddan in W Australia)
-- S. spectabilis nullarbor (Australia - Nullarbor Plain)
-- S. spectabilis spectabilis Spectacled hooded snake (SE Australia)
Suta suta* Curl snake (C and E Australia)
268 Jiri Valenta

Genus: Toxicocalamus
Toxicocalamus buergersi* Buergers forest snake (N Papua-New Guinea)
Toxicocalamus grandis* Setekwa River forest snake (a type locality - River Setekwa,
Indonesian New Guinea)
Toxicocalamus holopelturus* Mt Rossel forest snake (Mt Rossel, Rossel Island)
Toxicocalamus longissimus* Woodlark or Fergusson Island forest snake (Woodlark and
Ferguson islands)
Toxicocalamus loriae* (New Guinea and Papua-New Guinea)
Toxicocalamus misimae* Misima Island forest snake (Misima Island near Papua-New
Guinea)
Toxicocalamus preussi* Preusss Sepik forest snake (N New Guinea)
-- T. preussi angusticinctus
-- T. preussi preussi Preusss forest snake
Toxicocalamus spilolepidotus* (a type locality - Papua-New Guinea, only two
individuals)
Toxicocalamus stanleyanus* (Indonesia)
Genus: Tropidechis
Tropidechis carinatus** Rough-scaled snake or Clarence River snake (coastal zones, NE
and E Australia)
Tropidechis sadlieri** (Australia - N Queensland)
Genus: Unechis see Rhinoplocephalus
Genus: Vermicella
Vermicella annulata* Eastern bandy bandy
-- V. annnulata annulata (Australia except NE and SE territories)
-- V. annulata snelli see V. snelli
Vermicella intermedia*
Vermicella snelli* (W Australia, Pilbara to S Northern Territory)
Vermicella multifasciata* Northern bandy bandy (N W Australia to Northern Territory)
Vermicella vermiformis*

7.3.2.2. Aquatic Species: True Sea Snakes and Sea Kraits

(formerly: Hydrophiidae family, Hydrophiinae and Laticaudinae subfamilies)
Genus: Acalyptophis
Acalyptophis peronii** Spiny-headed seasnake (the sea territories between China,
Taiwan and Australia)
Genus: Aipysurus
Aipysurus apraefrontalis** Short-nosed seasnake (Australian and Indonesian seas)
Aipysurus duboisii** Reef shallows seasnake (Melanesian, Australian and New Guinea
sea)
Aipysurus eydouxii** Spine-tailed seasnake (Thailand, Indonesian and N Australia sea)
Aipysurus foliosquama** Leaf-scaled seasnake (Indonesian and Australian sea)
Aipysurus fuscus** Timor reef snake (Sulawesi and Timor sea)
Aipysurus laevis** Olive-brown seasnake
-- A. laevis laevis (New Guinea, Australia, Melanesia)
-- A. laevis pooleorum see A. pooleorum
Aipysurus pooleorum** (coastal W Australia)
 List of Venomous Snakes 269

Aipysurus tenuis** (coastal NW Australia)

Genus: Astrotia
Astrotia stokesi*** Stokes seasnake (E Pacific Ocean and N Australia)
Genus: Disteira
Disteira kingii** Spectacled or kings seasnake (V, N and W coast of Australia)
Disteira major** see Hydrophis Olive-headed or greater seasnake (V, S and W coast of
Australia)
Disteira nigrocincta** (the sea along E India and around Sri Lanka)
Disteira walli** Walls sea snake (Malayan Archipelago sea)
Genus: Emydocephalus
Emydocephalus annulatus** Turtle-headed seasnake, egg-eating sea snake (W Pacific
Ocean to N coast of Australia)
Emydocephalus ijimae** Turtlehead sea snake (S Chinese, Taiwan and Japanese sea)
Genus: Enhydrina, seasnakes
Enhydrina schistosa*** Common or beaked seasnake (the Indian Ocean, the sea territory
between E India and N Australia)
Enhydrina zweifeli*** Sepik or Zweifels beaked seasnake (New Guinea)
Genus: Ephalophis
Ephalophis greyi (greyae)** North-western mangrove seasnake (coastal W Australia)
Genus: Hydrelaps
Hydrelaps darwiniensis** Port Darwin seasnake (the sea territory between N Australia
and S New Guinea)
Genus: Hydrophis, seasnakes
Hydrophis atriceps** Black-headed seasnake (the Burmese sea to Thailand, Java, New
Guinea, Australia and the Philippines)
Hydrophis belcheri** Faint-banded seasnake (Thailand, Indonesian and New Guinea sea)
Hydrophis bituberculatus** Peters sea snake (Sri Lanka and Thailand sea)
Hydrophis brookei (brookii)** (Malaysian, Thailand, Vietnamese and Indonesian sea)
Hydrophis caerulescens** syn. Polyodontognathus caerulescens Dark blue-banded sea
snake (S and SE Asia and Indonesian sea)
Hydrophis cantoris** syn. Microcephalophis cantoris (the seas of Pakistan, India, Sri
Lanka, Burma, Thailand, and Malaysia)
Hydrophis coggeri** Slender-necked seasnake (Oceania)
Hydrophis cyanocinctus** Asian annulated sea snake (the southern coast of Asia as far as
Japan)
Hydrophis czeblukovi** Fine-spined seasnake (Arafura Sea)
Hydrophis elegans** Elegant or bar-bellied seasnake (E, S, W coast of Australia)
Hydrophis fasciatus** Striped sea snake (the Indian Ocean to the northern coast of
Australia)
Hydrophis geometricus** (N coast of W Australia)
Hydrophis gracilis** syn. Microcephalophis gracilis (the coast of the Indian Ocean from
the Gulf of Persia as far as Australia and Melanesia)
Hydrophis inornatus** Plain seasnake (Indonesian, Philippines and Australian sea)
Hydrophis klossi** Kloss sea snake (Thailand, Malaysian and Indonesian sea)
Hydrophis laboutei** (New Caledonian sea)
Hydrophis lamberti** Lamberts sea snake (Thailand, Singapore and Philippine sea)
270 Jiri Valenta

Hydrophis lapemoides** Persian Gulf sea snake (the coast of the Indian Ocean from the
Gulf of Persia as far as Malaysia)
Hydrophis major see Disteira major
Hydrophis mamillaris** Bombay sea snake (coastal Pakistan, India and Sri Lanka)
Hydrophis macdowelli** Small-headed Or McDowells seasnake (N coast of Australia)
Hydrophis melanocaphalus** Slender-necked seasnake (waters of SE Asia, from
Australia as far as S Japan)
Hydrophis melanosoma** Black-banded or robust seasnake (Malaysian, Indonesian and
Australian sea)
Hydrophis obscurus** Russels sea snake (coastal E India, Sri Lanka and Burma)
Hydrophis ornatus ssp.** Ornate reef seasnake (the Indian Ocean, W Pacific Ocean)
Hydrophis pacificus** Pacific seasnake (Australia and New Guinea)
Hydrophis parviceps** (the South China Sea and coastal Vietnam)
Hydrophis semperi** Lake Taal snake (the Lake Taal, Luzon, the Philippines)
Hydrophis sibauensis** (Sibau River, W Borneo, Indonesia)
Hydrophis spiralis** Yellow sea snake (the Indian Ocean, the waters of archipelagos
between E India and N Australia)
Hydrophis stricticollis** Collared sea snake (coastal E India, Sri Lanka, Burma)
Hydrophis torquatus ssp.** West Coast black-headed sea snake (the South China Sea to
the waters near Borneo and Sumatra)
Hydrophis vorisi** Estuarine seasnake (New Guinea)
Genus: Kerilia
Kerilia jerdonii ssp.** Jerdons sea snake (Indian, Sri Lankan and Borneo seas)
Genus: Kolpophis
Kolpophis annandalei** Bighead sea snake (the South China Sea from Thailand as far as
Indonesia)
Genus: Lapemis
Lapemis curtus** Shaws sea snake (the Indian Ocean)
Lapemis hardwickii** Hardwickes spine-bellied seasnake (the sea territory from E India
to Australia)
Genus: Laticauda, Sea kraits
Laticauda colubrina** Colubrine or yellow-lipped sea krait (the sea territory between E
India, Japan and Australia)
Laticauda crockeri** Crockers sea snake (the Lake Te Nggano, Rennell Island - the
Solomon Islands)
Laticauda laticaudata** Common or blue-lipped sea krait (the sea territory between E
India, Japan, Australia and Polynesia)
-- L. laticaudata affinis
-- L. laticaudata wolffi
Laticauda schistorhynchus** (New Guinea, Melanesian and Polynesian seas)
Laticauda semifasciata** (Philippine, Chinese, Taiwan and Japanese seas)
Genus: Microcephalophis
Microcephalophis gracilis see Hydrophis gracilis
Microcephalophis cantoris see Hydrophis cantoris
Genus: Parahydrophis
 List of Venomous Snakes 271

Parahydrophis mertoni** Arafura smooth or northern mangrove seasnake (Indonesian,

New Guinea and Australian seas)
Genus: Pelamis
Pelamis platurus** Yellowbelly sea snake or pelagic sea snake (tropical zones of the
Indian and Pacific Ocean)
Genus: Polyodontognathus
Polyodontognathus caerulescens see Hydrophis caerulescens
Genus: Praescutata
Praescutata viperina see Thalassophina viperina
Genus: Thalassophis
Thalassophis anomalus** Anomalous sea snake (the Gulf of Siam and Indonesian seas)
Genus: Thalassophina
Thalassophina viperina** Schmidts sea snake (the Indian Ocean: the Persian Gulf to the
South China Sea)

7.4. FAMILY: VIPERIDAE, VIPERIDS

7.4.1. Subfamily: Azemiopinae

Genus: Azemiops
Azemiops feae* Feas viper (Burma, S China, N Vietnam)

7.4.2. Subfamily: Viperinae

Genus: Adenorhinos
Adenorhinos barbouri* Uzungwe Mountain bush viper (SW Tanzania)
Genus: Atheris, bush vipers
Atheris acuminata* Acuminate bush viper (W Uganda)
Atheris anisolepis see Atheris squamiger anisolepis
Atheris barbouri see Adenorhinos barbouri
Atheris broadley* (Cameroon)
Atheris ceratophorus* syn. A. ceratophora (E Tanzania)
Atheris chloroechis* syn. A. chlorechis (Africa from Guinea as far as Gabon)
Atheris desaixi* Ashes bush viper (Kenya)
Atheris hindii see Montatheris hindii
Atheris hirsuta* (Cte dIvoire)
Atheris hispidus* African hairy bush viper, syn. A. hispida (DRC, isolated patches of
populations in SW Uganda and W Kenya)
Atheris katangensis* Katanga Mountain bush viper (DRC)
Atheris laeviceps see A. squamiger anisolepis
Atheris nitschei* Great Lakes bush viper (E DRC, Rwanda, SW Uganda, Burundi to NW
Tanzania)
-- A. nitschei nitschei see A. nitschei
272 Jiri Valenta

-- A. nitschei rungweensis see A. rungweensis

Atheris rungweensis* Mt Rungwe bush viper (SW Tanzania, NE Zambia, N Malawi)
Atheris squamiger** Rough-scaled bush viper, syn. A. squamigera
-- A. squamiger anisolepis (N Congo-Brazzaville and N Angola)
-- A. squamiger robustus (the province of Orientale, DRC)
-- A. squamiger squamiger (SE Nigeria to NW Angola, DRC to S Uganda, W Kenya,
Ghana)
Atheris superciliaris see Proatheris superciliaris
Atheris subocularis* (Cameroon)
Genus: Bitis, puff or African adders, or African vipers
Bitis albanica** (RSA - E Cape Region)
Bitis arietans*** African puff adder
-- B. arietans arietans African puff adder (Africa, the savannahs from Morocco to
S Africa and Arabia)
-- B. arietans somalica (Somalia, N Kenya, SE Ethiopia)
Bitis armata* (RSA)
Bitis atropoides see B. armata
Bitis atropos** Mountain adder
-- B. atropos atropos Mountain adder (RSA, Swaziland, Lesotho and Zimbabwe)
-- B. atropos unicolor (N Africa)
Bitis caudalis* Horned puff adder (SW Angola, Namibia, Botswana, SW Zimbabwe,
RSA)
Bitis cornuta** Many-horned adder (W RSA and SW Namibia)
-- B. cornuta albanica see Bitis albanica
-- B. cornuta cornuta see Bitis cornuta
Bitis gabonica*** Gabon viper
-- B. gabonica gabonica Gabon adder (Nigeria, S Sudan, Uganda, W Kenya, S Tanzania,
Mozambique, RSA)
-- B. gabonica rhinoceros see B. rhinoceros
Bitis heraldica* Angolan adder or Bocages horned adder (NW and C Angola)
Bitis inornata* Plain mountain adder (N RSA)
Bitis lachesis see B. arietans
Bitis nasicornis*** Rhinoceros viper (N Sudan, Uganda, Congo-Brazzaville, Gabon)
Bitis parviocula** Ethiopian mountain adder (C and SW Ethiopia)
Bitis peringueyi* Peringueys adder (Angola and SW Africa)
Bitis rhinoceros*** (Guinea and Sierra Leone to Togo)
Bitis rubida* Red adder (RSA)
Bitis shneideri* Namaqua dwarf adder (Namibia)
Bitis worthingtoni* Kenya horned viper (Kenya)
Bitis xeropaga* Desert mountain adder (NW RSA and SW Namibia)
Genus: Causus, night adders
Causus bilineatus* Two-lined night adder (C Angola, NW Zambia, S DRC, Rwanda)
Causus defilippii* Snouted night adder (the SE coasts of Kenya, E and S Tanzania,
Malawi, Mozambique, E Zambia, Zimbabwe to RSA)
Causus lichtensteinii* Forest night adder (N Guinea, Sierra Leone to W Kenya and S
Sudan)
 List of Venomous Snakes 273

Causus maculatus* West-African night adder (Senegal and Gambia to Cameroon, S

Chad, Central African Republic and S Sudan)
Causus resimus* Green night adder (C and E Africa)
Causus rhombeatus* Common or rhombic night adder (C Africa)
Genus: Cerastes
Cerastes cerastes** Desert horned viper (Sahara to Arabia)
-- C. cerastes hoofieni (recently reclassified as a separate subspecies - SW Arabian
Peninsula)
-- C. cerastes karlhartli, C. cerastes mutila (formerly separate subspecies, recently
included in synonyms of a nominotypic subspecies)
Cerastes gasperettii** Arabian horned viper (Jordan, Iraq, Kuwait, Arabian Peninsula to
SW Iran)
-- C. gasperetti mendelssohni (Jordan and Israel)
Cerastes vipera* Sahara sand viper (Sahara inc. edges)
Genus: Daboia
Daboia russelli*** Russells or chain viper, syn. Vipera russelli
-- D. russelli russelli, includes the formerly separate D. r. pulchella and nordicus
subspecies (E Pakistan, India, W Bangladesh, Sri Lanka),
-- D. russelli siamensis, includes the formerly separate D. r. formosensis, limitis, and
sublimitis subspecies (N China, C and S Burma, C Thailand, Taiwan, Indonesia),
Genus: Echis, saw-scaled or carpet vipers
Echis carinatus*** Saw-scaled viper
-- E. carinatus astolae (Astola Island near Pakistan)
-- E. carinarus carinatus Saw-scaled viper (C and S India)
-- E. carinatus multisquamatus (SE Azerbaijan, Iran, Turkmenistan, Uzbekistan, SW
Tajikistan, N Afghanistan)
-- E. carinatus sinhaleyus (N and E part of Sri Lanka)
-- E. carinatus sochureki (Oman, S Afghanistan, Pakistan, N India)
Echis coloratus*** Palestine saw-scaled viper (the Arabian Peninsula, SE Egypt, Israel,
Jordan, Oman)
-- E. coloratus terraesanctae (recently reclassified as a separate subspecies - Israel and
Jordan)
Echis hughesi*** Hughes saw-scaled viper (Somalia)
Echis jogeri*** Jogers saw-scaled viper (Mali)
Echis leucogaster*** Romans saw-scaled viper (Senegal, Mauritania, the southern edge
of Sahara as far as Sudan, SE Morocco, S Algeria)
Echis megalocephalus*** Cherlins saw-scaled viper (Eritrea)
Echis multisquamatus see E. carinatus multisquamatus
Echis ocellatus*** West African carpet viper (Senegal, SW Mauritania, S Mali, Sahel as
far as SW Chad)
Echis omanensis*** (E Oman, the United Arabian Emirates)
Echis pyramidum*** Egyptian saw-scaled viper (NE Algeria, Tunisia, coastal Libya as
far as Egypt)
-- E. pyramidum aliaborri (sometimes also listed as a subspecies of E. carinatus) (NE
Kenya)
-- E. pyramidum leakeyi (W Kenya)
274 Jiri Valenta

-- E. pyramidum lucidus (Tunisia, N Libya, NW Egypt)

-- E. pyramidum pyramidum (NE Egypt, as far as S Sudan, Eritrea, N Somalia and NE
Kenya)
Echis sochureki see E. carinatus sochureki
Genus: Eristicophis
Eristicophis macmahoni*** McMahons desert viper (the Afghanistan and Pakistan
border, E Iran)
Genus: Macrovipera, large Palearctic vipers, formerly Vipera and Daboia genera
Macrovipera deserti*** Desert viper, syn. Daboia (C and S Tunisia, NW Libya, NE
Algeria)
Macrovipera lebetina*** Levantine viper
-- M. lebetina lebetina Levantine viper (Cyprus and Turkey)
-- M. lebetina chernovi (Turkmenistan)
-- M. lebetina obtusa, syn. M. lebetina euphratica (from N Syria across Turkey, Iraq, Iran
and W Pakistan as far as Afghanistan)
-- M. lebetina transmediterranea (Algeria)
-- M. lebetina turanica (NE Iran, Turkmenistan, Uzbekistan, Afghanistan, N Pakistan, N
India)
Macrovipera mauritanica*** Moorish viper, sometimes also listed as a species of
Daboia genus (NW Morocco and N Algeria)
Macrovipera schweizeri*** Cyclades blunt-nosed viper (Milos, Kimolos, Polinos, and
Siphnos islands, Greece)
Genus: Montatheris, Kenya mountain or Hinds viper
Montatheris hindii* (Kenya)
Genus: Montivipera
A proposal exists that a group containing species from the range of Vipera xanthina (i.e.
V. xanthina, V. albizona, V. bornmuelleri, V. bulgardaghica and V. wagneri) and
Vipera raddei (i.e. V. raddei, V. albicornuta and V. latifii) should be isolated and
listed under a separate genus Montivipera.
Genus: Proatheris
Proatheris superciliaris** Lowland swamp viper (SW Tanzania, S Malawi to C
Mozambique)
Genus: Pseudocerastes
Pseudocerastes fieldi see P. persicus fieldi
Pseudocerastes persicus** Persian horned viper
-- P. persicus fieldi Fields horned viper (Iraq, Jordan, Israel, Sinai)
-- P. persicus persicus (Iran, Pakistan, E part of the Arabian Peninsula)
Genus: Vipera, Palearctic or Eurasian vipers
Vipera albizona*** Central Turkish mountain viper (the province of Sivas, Turkey)
Vipera albicornuta see V. raddei albicornuta
Vipera ammodytes** Nose-horned viper
-- V. ammodytes ammodytes (N Tyrol, Austria, former Yugoslavia, Romania, NW
Bulgaria)
-- V. ammodytes meridionalis (Greece, Albania, Asia Minor, Syria, the Cyclades)
-- V. ammodytes montandoni (W Black Sea region)
-- V. ammodytes transcaucasiana (South Caucasus)
 List of Venomous Snakes 275

Vipera anatolica* (Taurus Mountains, S Turkey)

Vipera aspis** Asp viper
-- V. aspis aspis European asp (Pyrenean Mountains, S France, S Black Forest, the Alps,
Elba, the northern part of former Yugoslavia)
-- V. aspis atra Black asp (C Switzerland to N Italy, the neighboring part of SE France)
-- V. aspis francisciredi Central Italian asp (N and C Italy, Elba)
-- V. aspis hugyi, syn. montecristi Southern Italian asp (Calabria and Sicily)
-- V. aspis zinnikeri Gascony asp (SW France)
Vipera atra see V. aspis atra
Vipera barani** Turkish viper (NW, NE Turkey, possibly the neighboring part of
Georgia)
Vipera berus** Common or European viper
-- V. berus berus Common or European viper (N and C Europe, southwards to N Italy,
Russia)
-- V. berus bosniensis Balkan cross adder (former Yugoslavia, Bulgaria)
-- V. berus sachalinensis Sakhalin Island adder (Sakhalin and Far East)
Vipera bornmuelleri** Lebanon viper (Lebanon and the neighboring parts of Jordan,
Syria and Israel)
Vipera darevskii** Darevskys viper (SE Armenia and the neighboring part of Georgia)
Vipera dinnicki** Dinniks viper (the Greater Caucasus)
Vipera ebneri* (SW Turkmenistan and the neighboring territory of N Iran)
Vipera eriwanensis* (NE Turkey to S Caucasus and E Uzbekistan)
Vipera hugyi see V. aspis hugyi
Vipera kaznakovi** Kaznakovs viper (W Caucasus and Turkey)
Vipera latastei** Latastes viper
-- V. latastei gaditana (coastal S Portugal and SW Spain, Morocco, N coast of Algeria to
NW Tunisia)
-- V. latastei latastei (N Portugal and Spain)
Vipera latifii*** Latifis viper (Iran)
Vipera lotievi* Caucasian meadow viper (the northern slopes of the Greater Caucasus)
Vipera magnifica* (W Caucasus)
Vipera monticola* Atlas mountain viper (Morocco the Greater Atlas)
Vipera nikolskii** Nikolskis viper (SW Russia and Ukraine to W Kazakhstan)
Vipera orlovi* (W Caucasus)
Vipera palestinae*** Palestine viper, syn. Daboia palestinae (Israel, W Jordan, W Syria)
Vipera pontica Pontic adder see V. barani
Vipera raddei*** Armenian mountain viper
-- V. raddei albicornuta (N Iran)
-- V. raddei kurdistanica (SE Turkey)
-- V. raddei latifi see Vipera latifii
-- V. raddei raddei (Armenia, NE Turkey, NW Iran)
Vipera renardi* Steppe viper
-- V. renardi renardi (Ukraine, Russia, Kazakhstan, Azerbaijan, China)
-- V. renardi parursinii (NW China)
-- V. renardi tienshanica (Tian Shan in Kazakhstan, Kyrgyzstan and NW China)
Vipera russellii see Daboia russelli
276 Jiri Valenta

Vipera sachalinensis see V. berus sachalinensis

Vipera seoanei** Baskian viper
-- V. seoanei cantabrica (C Spain)
-- V. seoanei seoanei Baskian viper (N Spain, N Portugal, SW France)
Vipera transcaucasiana see V. ammodytes transcaucasiana
Vipera ursinii* Meadow viper
-- V. ursinii rakosiensis (originally isolated patches of populations in SE Austria,
Hungary and W Romania; the subspecies is now getting extinct)
-- V. ursinii ursinii (Italy and SE France)
-- V. ursinii anatolica see V. anatolica
-- V. ursinii graeca (the Pindos Mountains, Greece)
-- V. ursinii macrops (Krk Island near Greece, Bosnia and Herzegovina, Montenegro, N
Macedonia, NE Albania)
-- V. ursinii moldavica (lowlands from Romania across Moldavia as far as W Ukraine
steppes)
-- V. ursinii wettsteini see V. ursinii ursinii
Vipera wagneri** Ocellated mountain viper (NE Turkey and NW Iran)
Vipera xanthina*** Rock viper (the European part of Turkey, W Asia)
-- V. xanthina bornmuelleri see V. bornmuelleri
-- V. xanthina xanthina see V. xanthina
-- V. xanthina albizona see V. albizona
-- V. xanthina bulgardaghica - considered by some as a separate species, but disputed by
others who list the subspecies as a variation of V. xanthina (Bulgar-Dagh Mountains,
S Turkey)
Vipera zinnikeri see V. aspis zinnikeri

7.4.3. Subfamily: Crotalinae

Genus: Agkistrodon
Agkistrodon acutus see Deinagkistrodon acutus
Agkistrodon bilineatus*** Cantil (Mexico to Nicaragua)
-- A. bilineatus bilineatus (the Pacific coastal plains of Mexico, Guatemala, Salvador)
-- A. bilineatus howardgloydi (Honduras, Nicaragua, NW Costa Rica)
-- A. bilineatus russeolus (N Yucatn and the N part of Belize)
-- A. bilineatus taylori see A. taylori
Agkistrodon blomhoffii see Gloydius blomhoffii
Agkistrodon contortrix** Southern copperhead (C and S USA and NE Mexico)
-- A. contortrix contortrix (Maryland to Texas and Oklahoma)
-- A. contortrix laticinctus (C and N Texas to Kansas)
-- A. contortrix mokasen (Connecticut to Virginia and Carolina, Indiana)
-- A. contortrix phaeogaster (NE Oklahoma, E Kansas, C and W Missouri, SE Iowa,
Nebraska)
-- A. contortrix pictigaster (Mexico - Coahuila, Chihuahua; Texas - the Trans-Pecos
region)
Agkistrodon halys see Gloydius halys
 List of Venomous Snakes 277

Agkistrodon intermedius see Gloydius intermedius

Agkistrodon monticola see Gloydius monticola
Agkistrodon piscivorus*** Western cottonmouth (SE USA)
-- A. piscivorus conanti (Florida and the neighboring areas of S Georgia and SE
Alabama)
-- A. piscivorus leucostoma (the USA and Mexican border - E Oklahoma, S Illinois and
SW Alabama)
-- A. piscivorus piscivorus (SE Virginia, C Georgia, E Alabama)
Agkistrodon rhodostoma see Calloselasma rhodostoma
Agkistrodon saxalis see Gloydius intermedius saxatilis
Agkistrodon shedaoensis see Gloydius shedaoensis
Agkistrodon strauchi see Gloydius strauchi
Agkistrodon taylori*** Mexican Moccasin (NE Mexico)
Agkistrodon ussuriensis see Gloydius ussuriensis
Genus: Atropoides, jumping pit vipers
Atropoides mexicanus** Central American jumping pitviper (Central America - Belize to
C Panama)
Atropoides nummifer** Jumping pit viper
-- A. nummifer mexicanus see A. mexicanus
-- A. nummifer nummifer Jumping pit viper (Mexico)
-- A. nummifer occiduus see A. occiduus
Atropoides occiduus** (Central America - Mexico to Salvador)
Atropoides olmec** Olmecan pit viper (N Mexico)
Atropoides picadoi** Picados Jumping pitviper (Costa Rica and NW Panama)
Genus: Bothriechis, palm pit vipers
Bothriechis aurifer** Yellow-blotched palm pit viper (Mexico and C Guatemala)
Bothriechis bicolor** Guatemala palm pit viper (Mexico, Guatemala, isolated patches of
populations in W Honduras)
Bothriechis bilineatus see Bothriopsis bilineata
Bothriechis lateralis** Side-striped palm pit viper (Costa Rica to inland Panama)
Bothriechis marchi** Marchs palm pit viper (isolated patches of populations in NW
Honduras)
Bothriechis nigroviridis** Black-speckled palm pit viper (C Costa Rica to W Panama)
Bothriechis oligolepis see Bothriopsis oligolepis
Bothriechis punctatus see Bothrops punctatus
Bothriechis rowleyi** Rowleys palm pit viper (Mexico)
Bothriechis schlegelii** Eyelash palm pit viper (from S Mexico across Central America
as far as W Colombia)
Bothriechis supraciliaris** (SW Costa Rica)
Bothriechis thalassinus** (E Guatemala and W Honduras)
Bothriechis taeniatus see Bothriopsis taeniata
Genus: Bothriopsis, forest pit vipers
Bothriopsis albocarinata see B. pulchra
Bothriopsis bilineata** Two-striped forest pit viper (N Colombia, SW Venezuela,
Ecuador, Bolivia, Brazil)
Bothriopsis chloromelas** (the Peruvian Andes)
278 Jiri Valenta

Bothriopsis medusa** Venezuela forest pit viper (Venezuela)

Bothriopsis oligolepis** Inca forest pit viper
-- B. oligolepis oligolepis (N Peru and NW Bolivia)
-- B. oligolepis albocarinata see Bothriopsis pulchra
Bothriopsis peruviana, Peru forest pit viper, syn. B. chloromelas and B. oligolepis
Bothriopsis pulchra** (the Andes to the east, from S and C Colombia across Ecuador to
N Peru)
Bothriopsis punctata see Bothrops punctatus
Bothriopsis taeniata** Speckled forest pit viper (Colombia, Venezuela, Guyana, Brazil,
Bolivia, Peru, Ecuador)
Genus: Bothrocophias
Bothrocophias campbelli*** (the NW coasts of S America)
Bothrocophias colombianus** (Colombia)
Bothrocophias hyoprora** (N Colombia, E Ecuador, NE Peru, W Brazil, N Bolivia)
Bothrocophias microphthalmus*** (C Colombia, C Ecuador, Peru to NW Bolivia)
Bothrocophias myersi*** (the NW coasts of S America)
Genus: Bothrops, lanceheads, American lanceheads, or American lance-headed vipers
Bothrops alcatraz*** Alcatrazes lancehead (Alcatrazes Island near Brazil)
Bothrops alternatus*** Urutu (NE and C Argentina, Uruguay, S Paraguay, S Brazil,
isolated patches in E Argentina)
Bothrops ammodytoides* Patagonia lancehead (W and C Argentina)
Bothrops andianus** Andean lancehead (Peru)
Bothrops asper see Bothrops atrox
Bothrops atrox*** Common lancehead (Central and South America)
-- B. atrox atrox, B. atrox xanthogrammus; more recently not listed as subspecies
Bothrops barnetti** Barnetts lancehead (the N coast of Peru and the neighboring
territory of SW Ecuador)
Bothrops bilineatus see Bothriopsis bilineata
Bothrops brazili*** Brazils lancehead (N Colombia to French Guyana, E Ecuador, NE
and E Peru)
Bothrops campbelli see Bothrocophias campbelli and Bothrocophias myersi in part.
Bothrops caribbaeus*** Saint Lucia lancehead (Saint Lucia Island)
Bothrops castelnaudi see Bothriopsis taeniata
Bothrops colombianus see Bothrocophias colombianus
Bothrops cotiara*** Cotiara (N Brazil and NE Argentina)
Bothrops diporus** Chaco lancehead (N and E Paraguay and the neighboring areas of S
Brazil, Argentina)
Bothrops erythromelas*** Caatinga lancehead (NE Brazil)
Bothrops fonsecai*** Fonsecas lancehead (SE coast of Brazil)
Bothrops iglesiasi see Bothrops lutzi
Bothrops insularis*** Queimada jararaca (Queimada Grande Island)
Bothrops isabelae see Bothrops atrox
Bothrops itapetiningae*** Sao Paulo lancehead (N C Brazil)
Bothrops jararaca*** Jararaca (Brazil and N Argentina)
Bothrops jararacussu*** Jararacussu (Brazil, Bolivia, Paraguay, N Argentina)
Bothrops jonathani*** Jonathans lancehead (Bolivia)
 List of Venomous Snakes 279

Bothrops lanceolatus*** Martinique lancehead (Martinique)

Bothrops leucurus*** Whitetail lancehead (Brazil)
Bothrops lojanus*** Lojan lancehead (Ecuador)
Bothrops lutzi*** Sertao lancehead (Brazil)
Bothrops marajoensis*** Maraj lancehead (N Brazil)
Bothrops mattogrossensis** Mato Grosso lancehead (Bolivia and the neighboring part of
Brazil)
Bothrops medusa see Bothriopsis medusa
Bothrops microphthalmus see Bothrocophias microphthalmus
Bothrops moojeni*** Brazilian lancehead (E Paraguay to C Brazil and NE Argentina)
Bothrops muriciensis*** Murici lancehead (the Murici Forest region, E Brazil)
Bothrops neuwiedi** Neuwieds lancehead (Brazil, Bolivia, Paraguay, N Argentina)
-- B. neuwiedi bolivianus see B. mattogrossensis
-- B. neuwiedi diporus see B. diporus
-- B. neuwiedi goyazensis
-- B. neuwiedi lutzi, syn. bahiensis see B. lutzi
-- B. neuwiedi mattogrossensis see B. mattogrossensis
-- B. neuwiedi meridionalis, syn. fluminensis see B. neuwiedi
-- B. neuwiedi neuwiedi Neuwieds lancehead
-- B. neuwiedi paranaensis (Brazil)
-- B. neuwidei pauloensis see B. pauloensis
-- B. neuwiedi piauhyensis see B. lutzi
-- B. neuwiedi pubescens, syn. B. riograndensis see B. pubescens
-- B. neuwiedi urutu
Bothrops nummifer see Atropoides nummifer
Bothrops oligolepis see Bothriopsis oligolepis
Bothrops osbornei see Bothrops punctatus
Bothrops pauloensis** Black-faced lancehead (Brazil)
Bothrops peruvianus see Bothriopsis oligolepis
Bothrops pictus*** Desert lancehead (coastal Peru)
Bothrops pirajai*** Pirajas lancehead (Brazil)
Bothrops pradoi see B. leucurus
Bothrops pubescens** Pampas lancehead (Brazil)
Bothrops pulcher see Bothrocophias myersi
Bothrops punctatus*** (Pacific Panama across Colombia to Ecuador)
Bothrops sanctaecrucis*** Bolivian lancehead (Bolivia)
Bothrops schlegelii see Bothriechis schlegeli
Bothrops taeniatus see Bothriopsis taeniata
Bothrops venezuelensis*** Venezuela lancehead (N and C Venezuela)
Bothrops xanthogrammus see B. atrox
Genus: Calloselasma
Calloselasma rhodostoma** Malayan pit viper (N Burma, Thailand, Cambodia, Laos,
Vietnam)
Genus: Cerrophidion, montane pit vipers
Cerrophidion barbouri*** Barbours montane pit viper (Mexico)
280 Jiri Valenta

Cerrophidion godmani*** Godmans montane pit viper (Central America - from Mexico
as far as Costa Rica)
Cerrophidion petlalcalensis*** (E Mexico)
Cerrophidion tzotzilorum*** Tzotzil montane pit viper (Mexico)
Genus: Crotalus, rattlesnakes
Crotalus abysus see C. oreganus abyssus
Crotalus adamanteus*** Eastern diamond-backed rattlesnake (SE USA - from SE
Carolina as far as Florida, and S Mississippi and SE Louisiana to the west)
Crotalus angelensis see C. mitcheli angelensis
Crotalus aquilus** Queretaran dusky rattlesnake (C Mexico)
Crotalus atrox*** Western diamond-backed rattlesnake (Oklahoma to C Mexico and
California)
Crotalus basiliscus*** Mexican West Coast rattlesnake (the W coast of Mexico)
Crotalus catalinensis** Santa Catalina Island rattlesnake (the Santa Catalina Islands near
California)
Crotalus cerastes** Sidewinder
-- C. cerastes cerastes Mojave Desert sidewinder (the Mojave Desert)
-- C. cerastes cercobombus Sonoran sidewinder (the Sonora Desert, N Mexico)
-- C. cerastes laterorepens Colorado Desert sidewinder (the Colorado Desert, NW
Mexico)
Crotalus cerberus*** (the USA)
Crotalus concolor*** (the USA)
Crotalus durissus*** South American rattlesnake
-- C. durissus cascavella (Brazil)
-- C. durissus collilineatus (Brazil)
-- C. durissus culminatus see Crotalus simus culminatus
-- C. durissus cumanensis, syn. C. durissus pifanorum (NE Colombia, Venezuela, W
Guyana)
-- C. durissus dryinas - more recently one of C. durissus durissus synonyms (Guyana,
French Guyana, Surinam)
-- C. durissus durissus (SE Mexico, SW Nicaragua, Honduras to NW and C Costa Rica)
-- C. durissus marajoensis (Maraj Island)
-- C. durissus ruruima (Venezuela, N Brazil, and the neighboring part of Guyana)
-- C. durissus terrificus (SE Peru, Bolivia, Paraguay, N Uruguay, C Argentina, S Brazil)
-- C. durissus totonacus see C. totonacus
-- C. durissus trigonicus (SW Guyana)
-- C. durissus tzabcan see C. simus tzabcan
-- C. durissus unicolor Aruba Island rattlesnake (Aruba Island)
-- C. durissus vegrandis (Venezuela and the neighboring areas of Colombia)
Crotalus enyo** Lower California rattlesnake
-- C. enyo cerralvensis (the island of Cerralvo near Mexico)
-- C. enyo enyo (Mexico - N and C part of the Californian Peninsula and the neighboring
islands)
-- C. enyo furvus (Mexico - W Californian Peninsula)
Crotalus exsul see C. ruber exsul
Crotalus helleri*** (Coronado del Sur Island, the USA as far as Mexico)
 List of Venomous Snakes 281

Crotalus horridus*** Timber rattlesnake (SE, NE and E of the central USA, Canada -
Ontario)
-- C. horridus atricaudatus, C. horridus horridus - more recently not listed as a
subspecies
Crotalus intermedius** Mexican smallhead rattlesnake
-- C. intermedius gloydi (SW USA, N Mexico)
-- C. intermedius intermedius (N Mexico)
-- C. intermedius omiltemanus (N Mexico)
Crotalus lannomi** Autlan long-tailed rattlesnake (Mexico - Jalisco, Puerto los Mazos)
Crotalus lepidus** Rock rattlesnake
-- C. lepidus klauberi Banded rock rattlesnake (N USA, NW Mexico)
-- C. lepidus lepidus Mottled rock rattlesnake (N USA and the neighboring areas of NE
Mexico)
-- C. lepidus maculosus (Mexican Sierra Madre Occidental)
-- C. lepidus morulus (Mexico)
Crotalus lutosus*** (the USA)
Crotalus mitcheli*** Southwestern speckled rattlesnake
-- C. mitcheli angelensis (Angel de la Guarda Island)
-- C. mitcheli mitcheli (W Mexico)
-- C. mitcheli muertensis (El Muerto Island)
-- C. mitcheli pyrrhus (SW USA)
-- C. mitcheli stephensis (east of C California and SW Nevada)
Crotalus molossus*** Black-tailed rattlesnake
-- C. molossus estebanensis (San Estban Island)
-- C. molossus molossus (SW USA, the neighboring areas of Mexico, Tiburn Island)
-- C. molossus nigrescens (Mexico)
-- C. molossus oaxacus (Mexico)
Crotalus oreganus***
-- C. oreganus abyssus (Arizona)
-- C. oreganus caliginis see C. helleri
-- C. oreganus cerberus see C. cerberus
-- C. oreganus concolor see C. concolor
-- C. oreganus helleri see C. helleri
-- C. oreganus lutosus see C. lutosus
-- C. oreganus oreganus (SW Canada to W coast of the USA and NE Karolina)
Crotalus polystictus** Mexican lancehead rattlesnake (the N part of the Mexican
Plateau)
Crotalus pricei** Twin-spotted rattlesnake
-- C. pricei miquihuanus (Mexican Sierra Madre Oriental)
-- C. pricei pricei (SE Arizona)
Crotalus pusillus** Tancitaran dusky rattlesnake (Mexico)
Crotalus ravus** Mexican massasauga
-- C. ravus brunneus (Mexico - the mountain range of the State of Oaxaca)
-- C. ravus exiguus (Mexico - the State of Guerrerro)
-- C. ravus ravus (Mexico - the central plains of Altiplanicia)
Crotalus ruber*** Red diamond rattlesnake (SW USA and NW Mexico)
282 Jiri Valenta

-- C. ruber exsul (Cedros Island, Mexico)

-- C. ruber lorenzoensis (San Lorenzo Sur Island, Mexico)
-- C. ruber lucasensis (the southern part of the Californian Peninsula, San Margarita and
San Jos islands)
-- C. ruber ruber, syn. C. ruber monserratensis, C. ruber elegans (SW USA, NW
Mexico)
Crotalus scutulatus*** Mojave rattlesnake (SW USA to C Mexico)
-- C. scutulatus scutulatus (the USA to C Mexico)
-- C. scutulatus salvini (Mexico)
Crotalus simus***
-- C. simus simus (Mexico to Costa Rica)
-- C. simus culminatus (SW Mexico)
-- C. simus tzabcan (from Yucatn as far as North Belize and Guatemala)
Crotalus stejnegeri** Longtail rattlesnake (Mexico)
Crotalus tancitarensis** (Mexico - the State of Michoacan)
Crotalus tigris**Tiger rattlesnake (the USA, NW Mexico)
Crotalus tortugensis** Tortuga Island rattlesnake (Tortuga Island)
Crotalus totonacus*** (NE Mexico)
Crotalus transversus** Cross-banded mountain rattlesnake (Mexico)
Crotalus triseriatus** Central Plateau dusky rattlesnake
-- C. triseriatus aquilus see Crotalus aquilus
-- C. triseriatus armstrongi (Mexico, the Mesa Central and Sierra Madre Occidental
mountains)
-- C. triseriatus triseriatus (Mexico, the Transverse Volcanic Cordillera mountains)
Crotalus unicolor see Crotalus durissus unicolor
Crotalus vegrandis see Crotalus durissus vegrandis
Crotalus viridis*** Northern Pacific rattlesnake (SW USA and N Mexico)
-- C. viridis abyssus see C. oreganus abyssus
-- C. viridis caliginis see C. helleri
-- C. viridis cerberus see C. cerberus
-- C. viridis concolor, syn. C. viridis decolor see Crotalus concolor
-- C. viridis helleri see C. helleri
-- C. viridis lutosus see C. lutosus
-- C. viridis nuntius (the USA)
-- C. viridis oreganus see C. oreganus oreganus
-- C. viridis viridis (the USA, S Canada, Mexico)
Crotalus willardi** Ridge-nosed rattlesnake
-- C. willardi amabilis (Sierra del Nido, Mexico)
-- C. willardi meridionalis (Mexico)
-- C. willardi obscurus (Mexico and New Mexico, the USA)
-- C. willardi silus (Mexico)
-- C. willardi willardi (the USA and Mexico)
Genus: Cryptelytrops see Trimeresurus
Genus: Deinagkistrodon
Deinagkistrodon acutus*** Chinese moccasin (SE China, N Vietnam, Taiwan, Laos)
Genus: Garthius see Ovophis
 List of Venomous Snakes 283

Genus: Gloydius, Asian moccasins

Gloydius blomhoffii** Mamushi
-- G. blomhoffii blomhoffii (Japan)
-- G. blomhoffii brevicaudus, syn. G. blomhoffii dubitatus see G. brevicaudus
-- G. blomhoffii ussuriensis see G. ussuriensis
-- G. blomhoffii siniticus (China)
Gloydius caliginosus see G. ussuriensis
Gloydius brevicaudus** (Korea and NE China)
Gloydius halys** Halys pit viper
-- G. halys boehmei (E Afghanistan)
-- G. halys caraganus (from the Volga River delta to E Kazakhstan as far as Tajikistan to
the south, and Kyrgyzstan and NW China to the east)
-- G. halys cognatus (N China)
-- G. halys halys (Russia, Mongolia, China)
-- G. halys mogoi (Mongolia and S Siberia), more recently included in G. halys halys
synonyms
-- G. halys caucasicus (SE Azerbaijan, North Iran, S Turkmenistan, NW Afghanistan)
-- G. halys stejnegeri (N and SE Mongolia and the neighboring part of China)
Gloydius himalayanus** Himalayan pit viper (NE Pakistan, N India to C Nepal)
Gloydius intermedius** Central Asian pit viper (E Turkmenistan, E Kazakhstan, S
Siberia, SE Russia, Mongolia, China, Korea)
-- G. intermedius caucasicus see G. halys caucasicus
-- G. intermedius intermedius
-- G. intermedius saxatilis
-- G. intermedius stejnegeri see G. halys stejnegeri
Gloydius monticola** Likiang pit viper (China)
Gloydius saxatilis see G. intermedius saxatilis
Gloydius shedaoensis** Shedao Island pit viper (Shedao Island)
Gloydius strauchi** Strauchs pit viper (SW China)
Gloydius tsushimaensis** Tsushima Island pit viper (Japan)
Gloydius ussuriensis** Ussuri mamushi (Korea, E China, SE Russia)
Genus: Himalayophis see Trimeresurus
Genus: Hypnale, hump-nosed pit vipers
Hypnale hypnale** Hump-nosed moccasin (N India)
Hypnale nepa* Sri Lanka hump-nosed viper (SW Sri Lanka)
Hypnale walli* Walls hump-nosed viper (SW Sri Lanka)
Genus: Lachesis, bushmasters
Lachesis acrochorda*** (Panama across Colombia to Ecuador)
Lachesis melanocephala*** Black-headed bushmaster (SE Costa Rica)
Lachesis muta*** South American bushmaster
-- L. muta melanocephala see L. melanocephala
-- L. muta muta (Colombian equatorial forests to Trinidad, southwards as far as Bolivia,
the Andes - Ecuador and Colombia)
-- L. muta rhombeata, syn. L. muta noctivaga (the SE coast of Brazil), more recently
included in Lachesis muta synonyms
-- L. muta stenophrys see L. stenophrys
284 Jiri Valenta

Lachesis stenophrys*** Central American bushmaster (Costa Rica to Panama)

Genus: Ophryacus, Mexican horned pit vipers
Ophryacus melanurus** (N Mexico)
Ophryacus undulatus** Mexican horned pit viper (Mexico)
Genus: Ovophis, mountain pit vipers
Ovophis chaseni** Chasens mountain pitviper (a type locality - Kiau, Mt. Kinabalu, the
province of Sabah, Borneo) - also listed under a newly recognized Garthius genus
Ovophis monticola** Chinese mountain pit viper
-- O. monticola convictus (Vietnam, Cambodia, Thailand, W Malaysia, Indonesia)
-- O. monticola makazayazaya (N China and Taiwan)
-- O. monticola monticola (India, Nepal, Bangladesh, Burma, S China)
-- O. monticola orientalis (N and SE China)
-- O. monticola zayuensis see O. zayuensis
-- O. monticola zhaokentangi (China)
Ovophis okinavensis** Ryukyu Island pit viper (Japan)
Ovophis tonkinensis** Tonkin pitviper (Vietnam)
Ovophis zayuensis** (Tibet)
Genus: Parias see Trimeresurus
Genus: Peltopelor see Trimeresurus
Genus: Popeia see Trimeresurus
Genus: Porthidium, hognosed pit vipers
Porthidium arcosae** (type localities - Aqua Blanca, Manab, Mexico)
Porthidium almawebi see Bothrocophias campbelli and Bothrocophias myersi
Porthidium barbouri see Cerrophidion barbouri
Porthidium colombianum see Bothrocophias colombianus
Porthidium dunni** Dunns hognose viper (Mexico)
Porthidium godmani see Cerrophidion godmani
Porthidium hespere** Western hognose viper (a type locality - Municipio de Ixlahuacn,
Colima, Mexico)
Porthidium hyoprora see Bothrocophias hyoprora
Porthidium lansbergii**
-- P. lansbergii arcosae see Porthidium acrosae
-- P. lansbergii lansbergi (C Panama, N Colombia, W Venezuela)
-- P. lansbergii rozei, syn. P. lansbergii venezuelensis (coastal Venezuela), more recently
Porthidium lansbergii synonyms
Porthidium melanurum see Ophryacus melanurus
Porthidium microphtalmum see Bothrocophias microphthalmus
Porthidium nasutum** Rainforest hognosed pitviper (isolated patches of populations in S
Mexico to W Colombia and NW Ecuador)
Porthidium nummifer see Atropoides nummifer
Porthidium olmec see Atropoides olmec
Porthidium ophryomegas** Slender hog-nosed pitviper (Pacific Central America from
Guatemala as far as Panama)
Porthidium porrasi** (Costa Rica)
Porthidium picadoi see Atropoides picadoi
Porthidium tzotzilorum see Cerrophidion tzotzilorum
 List of Venomous Snakes 285

Porthidium volcanicum** (Costa Rica)

Porthidium yucatanicum** Yucatn hognose viper (Mexico)
Genus: Protobothrops, Asian pit vipers
Protobothrops cornutus** Fan-Si-Pan horned pit viper (N Vietnam)
Protobothrops elegans** Elegant pit viper (Japan)
Protobothrops flavoviridis*** Habu (Japan)
Protobothrops jerdonii** Bourrets pit viper
-- P. jerdoni bourreti (N Vietnam)
-- P. jerdoni jerdoni (India, Nepal, Burma, China)
-- P. jerdoni xanthomelas (N China)
Protobothrops kaulbacki** Kaulbacks lance-headed pit viper (a type locality - Pang-
nam-dim, N Burma)
Protobothrops mucrosquamatus*** Brown spotted pit viper (India, Bangladesh, S China,
Burma, N Vietnam, Taiwan, Hainan)
Protobothrops tokarensis** Tokara habu (Japan)
Protobothrops xiangchengensis** Kham Plateau pit viper (China - W Sichuan and
Yunnan)
Genus: Sistrurus, ground rattlesnakes
Sistrurus catenatus** Massasauga
-- S. catenatus catenatus (SE Canada and the USA)
-- S. catenatus edwardsii (the USA and N Mexico)
-- S. catenatus tergeminus (SW plains, the USA)
Sistrurus miliarius** Pigmy rattlesnake
-- S. miliarius barbouri (the USA - SW South Carolina to Florida)
-- S. miliarius miliarius (the USA - the lowlands along the coast of the Atlantic Ocean
from North Carolina as far as Georgia and C Alabama)
-- S. miliarius streckeri (the USA - SW Kentucky, western C Alabama, W Mississippi to
SW Tennessee, E Texas)
Sistrurus ravus Mexican Massasauga see Crotalus ravus ssp
Genus: Triceratolepidophis
Triceratolepidophis sieversorum** Three horned-scaled pit viper (Vietnam - the province
of Quang Binh and the neighboring areas of Laos)
Genus: Trimeresurus, Asian pit vipers, Asian lanceheads or lance-headed vipers
Trimeresurus albolabris** White-lipped tree viper (NE India, S China, Hainan, Thailand,
Vietnam, Hong Kong, Malayan Peninsula) - also listed under a newly recognized
Cryptelytrops genus
-- T. albolabris albolabris
-- T. albolabris insularis see T. insularis
-- T. albolabris septentrionalis see T. septentrionalis
Trimeresurus andersoni** Andersons pitviper - also listed under a newly recognized
Cryptelytrops genus (the Andaman and Nicobar Islands)
Trimeresurus barati** Barat bamboo pitviper (Indonesia)
Trimeresurus borneensis** Borneo pit viper (N Thailand, Malaysia, Indonesia, Brunei)
Trimeresurus brongersmai** Brongersmas pit viper (Indonesia)
Trimeresurus cantori** Cantors pit viper - also listed under a newly recognized
Cryptelytrops genus (the Nicobar Islands)
286 Jiri Valenta

Trimeresurus convictus see Ovophis monticola convictus

Trimeresurus cornutus see Protobothrops cornutus
Trimeresurus elegans see Protobothrops elegans
Trimeresurus erythrurus** Redtail (bamboo) pit viper - also listed under a newly
recognized Cryptelytrops genus (India, E Bengal, Burma, Bangladesh)
Trimeresurus fasciatus** Banded pit viper - also listed under a newly recognized
Cryptelytrops genus (Indonesia)
Trimeresurus flavomaculatus** Philippine pitviper - also listed under a newly recognized
Parias genus (the Philippines - Balete, Camiguin, Jolo, Luzon, Mindanao, Mindoro,
and Polillo islands)
-- T. flavomaculatus flavomaculatus
-- T. flavomaculatus halieus
-- T. flavomaculatus mcgregori see T. mcgregori
Trimeresurus flavoviridis see Protobothrops flavoviridis
Trimeresurus fucatus** Siamese Peninsula pitviper - also listed under a newly
recognized Popeia genus (N Thailand)
Trimeresurus gracilis** Kikuchi habu (inland Taiwan, mountain ranges)
Trimeresurus gramineus** Common bamboo viper (N and C India)
Trimeresurus gumprechti** Gumprechts green pitviper - also listed under a newly
recognized Viridovipera genus (NE Thailand, China - Yunnan, Hainan, NW
Vietnam, Laos, Burma)
Trimeresurus hageni** Indonesian pit viper or Hagens pitviper - also listed under a
newly recognized Parias genus (N Thailand, Malayan Peninsula, Indonesia).
Trimeresurus huttoni see Tropidolaemus huttoni
Trimeresurus insularis** White-lipped island pitviper - also listed under a newly
recognized Cryptelytrops genus (E Indonesia)
Trimeresurus jerdoni see Protobothrops jerdoni ssp.
Trimeresurus kanburiensis** Kanburi pit viper - also listed under a newly recognized
Cryptelytrops genus (Kanburi, SW Thailand)
Trimeresurus kaulbacki see Protobothrops kaulbacki
Trimeresurus labialis** Island pit viper, Nicobar bamboo pitviper - also listed under a
newly recognized Cryptelytrops genus (the Andaman and Nicobar Islands)
Trimeresurus macrolepis** Large-scaled pit viper - also listed under a newly recognized
Peltopelor genus (N India).
Trimeresurus macrops** Kramers pit viper, large-eyed pitviper - also listed under a
newly recognized Cryptelytrops genus (Thailand, Cambodia to S Vietnam).
Trimeresurus malabaricus** Malabarian pit viper (SW coast of India)
Trimeresurus malcolmi** Malcolms pitviper - also listed under a newly recognized
Parias genus (Borneo)
Trimeresurus mangshanensis** Mangshan pitviper - also listed under a newly recognized
Zhaoermia genus (a type locality - Mangshan, the province of Hunan, China)
Trimeresurus mcgregori** McGregors pitviper - also listed under a newly recognized
Parias genus (the Philippines - Batan)
Trimeresurus medoensis** Green bamboo leaf pit viper, Motuo bamboo pitviper - also
listed under a newly recognized Viridovipera genus (India, N Burma, SE China)
Trimeresurus monticola see Ovophis monticola ssp.
 List of Venomous Snakes 287

Trimeresurus mucrosquamatus see Protobothrops mucrosquamatus

Trimeresurus nebularis** Cameron highlands pit viper - also listed under a newly
recognized Popeia genus (Malaysia)
Trimeresurus popeiorum** Popes tree viper or Popes bamboo pit viper - also listed
under a newly recognized Popeia genus
-- T. popeiorum barati see T. barati
-- T. popeiorum popeiorum (E India to Malayan Peninsula)
-- T. popeiorum sabahi see T. sabahi
Trimeresurus puniceus** Ashy pit viper, flat-nosed pitviper (Indonesia)
Trimeresurus purpureomaculatus** Shore pit viper or mangrove viper - also listed under
a newly recognized Cryptelytrops genus (W Thailand, Burma, Malaysia, Indonesia)
-- T. purpureomaculatus andersoni see T. andersoni
-- T. purpureomaculatus purpureomaculatus
Trimeresurus sabahi** Sabah bamboo viper (Borneo)
Trimeresurus septentrionalis** - also listed under a newly recognized Cryptelytrops
genus (Nepal, India, Bangladesh)
Trimeresurus schultzei** Schultzes pit viper - also listed under a newly recognized
Parias genus (the Philippines)
Trimeresurus stejnegeri** Chinese green tree viper, Stejnegers bamboo pitviper - also
listed under a newly recognized Viridovipera genus
-- T. stejnegeri stejnegeri (N China, N Vietnam, Cambodia, E Thailand, Hainan, Taiwan)
-- T. stejnegeri chenbihuii (Hainan, China)
-- T. stejnegeri yunnanensis see T. yunnanensis
Trimeresurus strigatus** Horseshoe pitviper (N India)
Trimeresurus sumatranus** Sumatra pit viper - also listed under a newly recognized
Parias genus (Indonesia, Malaysia)
-- T. sumatranus malcolmi see T. malcolmi
-- T. sumatranus sumatranus
Trimeresurus tibetanus** Tibetan bamboo pitviper (a type locality - Chokosumo,
Nyalam Co., Tibet, China), also listed under a newly recognized Himalayophis genus
Trimeresurus tokarensis see Protobothrops tokarensis
Trimeresurus tonkinensis see Ovophis tonkinensis
Trimeresurus trigonocephalus** Ceylon pit viper, Sri Lankan green pitviper (Sri Lanka)
Trimeresurus truongsonensis** (C Vietnam)
Trimeresurus venustus** Beautiful pitviper - also listed under a newly recognized
Cryptelytrops genus (a type locality - Thung Song, Nakhon Si Thammart, Thailand)
Trimeresurus vogeli** Vogels pit viper - also listed under a newly recognized
Viridovipera genus (Thailand, Cambodia, Laos, Vietnam)
Trimeresurus xiangchengensis see Protobothrops xiangchengensis
Trimeresurus yunnanensis** Yunnan bamboo pitviper - also listed under a newly
recognized Viridovipera genus (Nepal, E India, China, N Burma)
Trimeresurus zayuensis see Ovophis zayuensis
Genus: Tropidolaemus, temple vipers
Tropidolaemus huttoni** Huttons pitviper (N India)
Tropidolaemus wagleri** Waglers palm viper, Waglers pit viper, temple pitviper
(Borneo, Malaysia, Sumatra, Sulawesi, the Philippines)
288 Jiri Valenta

-- T. wagleri alboviridis
-- T. wagleri celebensis
-- T. wagleri philippensis
-- T. wagleri schlegelii
-- T. wagleri wagleri
Genus: Viridovipera see Trimeresurus
Genus: Zhaoermia see Trimeresurus

REFERENCES
CAMPBELL, JA., LAMAR, WW. The venomous Reptiles of the western hemisphere.
Comstock, Ithaca, London : Cornell University Press, 2004, 1032 pp.
CAMPBELL, JA., LAMAR, WW. The venomous Reptiles of Latin America. Ithaca, London :
Cornell University Press, 1989, 425 pp.
McDIARMID, RW., CAMPBELL, JA., TOURE, TA. Snake species of the world. A
taxonomic and geographic reference. Vol. 1. Washington DC : Herpetologists' League,
1999, 512 pp.
GOLAY, P. Checklist and keys to the Terrestrial Proteroglyphs of the world. Geneva :
Elapsoidea, 1985, 91 pp.
GOLAY, P., SMITH, HM., et al. Endoglyphs and other major venomous snakes of the world.
Geneva : Azemiops S.A. Herpetological Data Center, 1993, 478 pp.
GUMPRECHT, A., TILLACK, F., et al. Asian Pitvipers. Berlin : GeitjeBooks, 2004, 368 pp.
HARDING, KA., WELCH, KRG. Venomous snakes of the world a checklist. Oxford :
Pergamon Press, 1980.
HUTCHINSON, MN. The generic classification of the Australian terrestrial Elapid snakes.
Memoirs of the Queensland Museum, 1990, 28, pp. 397405.
OSHEA, M. Venomous snakes of the world. London : New Holland Publishers, 2005.
STCKLIN, R., CRETTON, G. The ultimate database on venomous animals, snakes. CD-
rom, Geneva : Atheris Laboratories, 1998.
WSTER, W., BUSH, B., et al. Taxonomic contributions in the amateur literature:
comments on recent descriptions of new genera and species by Raymond Hoser.
Litteratura Serpentium, 2001, 21, pp. 6779, 8691.
 GLOSSARY
(hemo)coagulation A complex process by which blood forms clots.
abscess Limited suppurative inflammation.
acidosis An increased acidity of tissues, when tissue ph falls below
7.38.
adaptive radiation Evolution of an animal or plant group into a wide variety of
types adapted to specialized modes of life.
adherence Adhesion
affection Affection in terms of a disease or a morbid symptom.
affinity An inherent likeness or relationship.
agent A substance causing a disease.
agglutination The act of clumping together or adhesion of particles.
aggravation An increasing in seriousness or severity of subjective
symptoms of disease.
aggregability A tendency to aggregate.
aggregation The act of aggregating, or the state of being aggregated.
albuminuria A pathological condition where albumin is present in the
urine. It is a type of proteinuria.
alteration A pathological change or disorder.
alveolus A small cell containing air in the lungs, a sac-like dilation of
the alveolar ducts in the lung.
amnesia A short-term memory condition in which memory is
disturbed; the loss of memory.
analgesia The inability to feel pain while still conscious.
analgesic A medicine used to relieve pain.
anaphylactic shock Anaphylactic shock, the most severe type of anaphylaxis
leading to systemic vasodilation associated with a sudden
drop in blood pressure.
anaphylactoid Anaphylactic-like reaction.
ancestral Of, relating to, or evolved from an ancestor or ancestors.
angioneurotic edema The rapid edema of the lips, eyes, tongue, and neck of
mostly allergic origin.
anguimorph A member of the Anguimorpha taxon.
anisocoria A condition characterized by an unequal size of the pupils.
ankylosis A stiffness of a joint.
290 Jiri Valenta

anticoagulant A substance that prevents coagulation and can be used in

vivo as a medication for thrombotic disorders.
antiemetic Preventing or alleviating vomiting.
antigenemia The level of an antigen in circulating blood.
antihistaminics Anti-allergic medicaments.
antiphlogistics Medicaments that reduce inflammation.
anuria Nonpassage of urine.
anxiety Anxiety is a psychological and physiological state
characterized by cognitive, somatic, emotional, and
behavioral components.
anxious Causing or fraught with or showing anxiety.
apoptosis The process of cell death.
aquatic Relating to water; living in or near water, taking place in
water.
arteria mesenterica superior Superior mesenteric artery; arises from the anterior surface
of the abdominal aorta.
ascites A pathologic accumulation of fluid in the peritoneal cavity.
aspiration The entry of secretions or foreign material (herein the
stomach content) into the trachea and lungs.

ataxia Unsteady and clumsy motion of the limbs or trunk due to a

failure of the gross coordination of muscle movements.
axon or nerve fiber A long, slender projection of a nerve cell, or neuron, that
conducts electrical impulses away from the neuron's cell
body or soma.
basic Denoting or of the nature of or containing a base.
benign Not dangerous to health; not recurrent or progressive.
blepharospasm Twitching of an eyelid.
blood circulation The course of the blood from the heart through the arteries,
capillaries, and veins back again to the heart.
blood clot or thrombus A coagulated mass of blood.
bolus Referring to an injection or treatment given over a
short period of time.
bradycardia Excessively slow heart beat.
bronchial Relating to or associated with the bronchi.
bronchopneumonia An inflammation of the lungs.
bronchospasm A sudden constriction of the muscles in the walls of the
bronchioles accompanied by dyspnea; mostly of an allergic
nature.
cardiotoxic Causing damage to the tissues of the heart; toxic for the
heart.
circulus vitiosus Vicious circle.
clearance The rate at which a substance is removed or cleared from the
body.
clotting ability The ability of clotting.
coagulation The process by which blood forms solid clots.
 Glossary 291

coagulopathy A disease, which limits the coagulation ability of the blood.

compartment One of the parts in which an area is either partially or fully
subdivided.
compartment syndrome Compartment syndrome is an acute medical problem
following injury, surgery or in most cases repetitive and
extensive muscle use, in which increased pressure (usually
caused by edema of tissues) within a confined space (fascial
compartment) in the body impairs blood supply. Without
prompt recognizing and treatment, it may lead to necrosis of
the tissues, with possible necessity of limb amputation.
complement system A cascade of proteins in the blood that form part of innate
immunity.
congestion Overfullness of the tissue.
conjunctival Of or relating to the conjunctiva.
conjunctivitis An inflammation of the conjunctiva.
constipation Irregular and infrequent or difficult evacuation of the
bowels.
contractility The capability or quality of shrinking or contracting.
contracture A pathological contraction of a muscle, a spasm, either
temporary or as a result of fibrous conversion.
convulsion A medical condition where body muscles contract and relax
rapidly and repeatedly, resulting in an uncontrolled shaking
of the body.
corneal Of or related to the cornea.
coronarospasm A contraction in one location in the muscles in the
wall of an artery in the
heart.
coronary: coronary vessels Blood vessels surrounding the heart.
cranial polyneuritis Multiple mononeuropathy involving several cranial nerves.
craniocaudally From head end to opposite end of body or lower limbs.
curare-like A neurotoxin with effects similar to that of curare, i.e.
muscular paralysis.
cytotoxic The quality of being toxic to cells.
debridement The removal, typically surgical, of necrotic, infected or
foreign material from a severe wound.
defibrination Removal of fibrin from the blood.
demarcation The boundary of a specific area.
deposit Matter that has been deposited by some natural process
(herein used for fibrin deposits).
desquamation The shedding of epithelial elements, chiefly of the skin, in
scales or small sheets, exfoliation.
diaphragmatic Pertaining to diaphragm.
diathesis Constitutional predisposition to a particular disease or
abnormality.
diplopia Visual impairment in which an object is seen as two objects.
discrepancy A difference between conflicting facts.
292 Jiri Valenta

distal motor neuropathy Damage of peripheral sections of motor nerves.

distension Enlargement.
diuresis Excretion of urine.
diversification The back of the body of a vertebrate or any analogous
surface (as the upper or outer surface of an organ or
appendage or part).
dorsum The back of the body of a vertebrate or any analogous
surface (as the upper or outer surface of an organ or
appendage or part).
dysarthria A speech disorder.
dysesthesia A sensation disorder.
dysfunction Any disturbance in the function of an organ or body part.
dysphagia A difficulty in swallowing.
dysphonia A phonation disorder.
dyspnea Shortness of breath.
ecchymosis The escape of blood from ruptured blood vessels into the
surrounding tissue to form a purple or black-and-blue spot
on the skin.
efflorescence Any red eruption of the skin.
Emetic A medicine that induces nausea and vomiting.

encephalopathy Any disorder or disease of the brain.

endothelium The thin layer of cells that line the interior surface of blood
vessels.
Enucleation Surgical removal of a ball-like formation, e.g. an eye,
without cutting into or dissecting it.
Epigastrium The upper central region of the abdomen.
epistaxis Occurrence of hemorrhage from the nose.
erythema Redness of the skin.
erythrocyturia Occurrence of red blood cells in urine.
etiology The cause of a disease.
excretion The process of eliminating waste products of metabolism
and other non-useful materials.
exhaustion Serious weakening and loss of energy.
expiration, see shelf life
extracellular Located or occurring outside a cell or cells.
Extrasystole Premature heart contraction.
extravasation A discharge or escape of fluid or even blood elements
outside a vascular system.
extravascular Situated or occurring outside a vessel or the vessels.
eye accommodation A process by which the vertebrate eye changes optical power
to maintain a clear image (focus) on an object as its distance
changes.
facial Of or concerning the face.
fascia The soft tissue component of the connective tissue system
that permeates the human body.
 Glossary 293

fasciculation Rapid muscular twitching of contiguous groups of muscle

fibers.
fasciotomy Incision through a fascia.
fatality An individual instance of death.
fever A frequent medical sign that describes an increase in internal
body temperature to levels above normal.
fibrin A fibrous protein (also called Factor Ia) involved in the
clotting of blood.
fibrinogen A protein present in blood plasma; converts to fibrin through
the action of enzymes when blood clots.
fibrinogenolysis The proteolytic destruction of fibrinogen in circulating
blood.
fibrinolysis The process wherein a fibrin clot, the product of coagulation,
is broken down.
fluid therapy Therapy whose basic objective is to restore the volume and
composition of the body fluids to normal with respect to
water-electrolyte balance.
fluidothorax see pleural effusion
gastrointestinal Of or relating to the stomach and intestines.
glomerulus A capillary tuft surrounded by Bowman's capsule in
nephrons of the vertebrate kidney.
glycemia The concentration of glucose in the blood.
glycosylation The enzymatic process that links saccharides to produce
glycans.

half-life The interval required for the quantity to be excreted or

decayed to half of its initial value.
hematemesis Vomiting of blood.
hematolysis Lysis of erythrocytes with the release of hemoglobin.
hematuria The presence of erythrocytes in the urine that is manifest by
red color.
hemicolectomy The surgical resection of a half of the large intestine.
hemocoagulation A process of blood clotting.
hemoconcentration A condition of decrease in the volume of plasma in relation
to the number of red blood cells; increase in the
concentration of red blood cells in the circulating blood.
hemodialysis A method for removing waste products from the blood by
means of a dialysis machine.
hemodynamic Relating to or involved in hemodynamics.
hemoglobin The red blood pigment contained in the red blood cells.
hemoglobinuria A condition in which hemoglobin is found in abnormally
high concentrations in the urine, which is manifest by red
color of the urine.
hemolytic Relating to or involving or causing hemolysis.
hemoptysis The expectoration (coughing up) of blood or of bloodstained
sputum from the lungs.
294 Jiri Valenta

hemorrhage Bleeding, i.e. the loss of blood from the circulatory system.
hemostasis A complex process, which causes the bleeding process to
stop.
heparin Heparin, a polysaccharide, widely used as an anticoagulant
in medicine.
heparinization A process of treating with heparin.
hibernation A state of inactivity and metabolic depression in animals,
e.g. in winter.
hyalinous Herein amorphous or fibrous.
hyperbaric medicine Also known as hyperbaric oxygen therapy (HBOT), the
medical use of oxygen at a level higher than atmospheric
pressure.
hypercoagulation An increased tendency for clotting of the blood.
hyperfibrinolysis Markedly increased fibrinolysis.
hyperkalemia An elevated blood level of the electrolyte potassium.
hypertension High blood pressure.
hypoalbuminemia A medical condition where levels of albumin in blood serum
are abnormally low.
hypoesthesia A reduced sense of touch or sensation, or a partial loss of
sensitivity to sensory stimuli.
hypogastrium An area of the human abdomen residing below the
umbilicus.
hypotension A condition of abnormally low blood pressure.
hypovolemia A state of decreased blood volume; more specifically,
decrease in volume of blood plasma.
chemosis The swelling (or edema) of the conjunctiva.
iatrogenic Caused by or resulting from medical treatment or advice.
idiopathic Arising spontaneously or from an obscure or unknown
cause.
ileus An obstruction of the intestines.
immunogenicity The ability of an antigen to provoke an immune response.
incidence A number of new cases of disease within a specified period
of time.
incipient Only partly in existence; imperfectly formed.
induce Cause to occur.
inhibit Limit the range or extent of.
inhibitor A molecule, which represses or prevents another molecule
from engaging in a reaction.
inotropy The force of muscle contraction.
instillation The introduction of a fluid (by pouring or injection) drop by
drop.
insufficiency The condition of being insufficient or inadequate to the
performance of the allotted duty.
intact Not impaired or diminished in any way.
interference The act of hindering or obstructing or impeding.
intermittent Occurring at separated intervals, having periods of cessation
 Glossary 295

of activity.
interstitium Thin connective tissue, which surrounds the nerves and
vessels.
intima The innermost layer of a vessel.
intracerebral Occurring or situated within the cerebrum.
intradermal Within a dermal tissue layer.
intramuscular Inside a muscle or the muscles.
intrauterine Inside the uterus.
intravenous Inside the vein.
intubation The introduction of a tube into the trachea to allow for
breathing.
ischemia A restriction in blood supply.
junction A type of structure connecting e.g. cells.
lactatemia or blood lactate The concentration of lactates dissolved in the blood.
leukocytosis An elevated white blood cell count above the normal range.
leucopenia A decrease in the number of leukocytes found in the blood.
lucidity A lucid state of mind; not confused.
lymphadenitis A disease or swelling of the lymph nodes.
lymphadenopathy A disease of the lymphatic tissue.
lymphangitis A disease or inflammation of the lymphatic channels.
lymphatic Of or relating to or produced by lymph.
lyophilization A method of drying without destroying physical structure;
material is frozen and then warmed in a vacuum so that the
ice sublimes.
mandible The lower jawbone.
maxilla The upper jawbone.
median The middle value of an ordered set of values.
melena Abnormally dark tarry feces containing predigested
blood.
mesentery The peritoneum responsible for connecting the jejunum and
ileum to the back wall of the abdomen.
micturition Urination.
monophyletic taxon A taxon genetically deriving from a common ancestor.
monotypic taxon Any taxon that has a single immediately subordinate taxon.
morbidity The proportion of people getting ill during a given time
interval.
mortality The ratio of the total number of deaths to the total
population.
mortality The proportion of people dying during a given time interval.
muscarinic effect A vegetative reaction characterized by symptoms including
increased salivation, decreased heartbeat, increased tension
of splanchnic muscles, etc.
muscular Of or relating to or consisting of muscle.
myasthenia A disease characterized by muscular weakness.
mydriasis Reflex pupillary dilation.
myocardium The heart muscle.
296 Jiri Valenta

myoglobin A protein of muscular cells that is released in the process of

decomposition of the cells.
myoglobinemia Concentration of free myoglobin in the blood.
myoglobinuria The presence of myoglobin in the urine, which is manifest
by dark color of the urine.
myolysis Breakdown of muscular tissue.
myonecrosis Myonecrosis is a condition of necrotic damage to muscle
tissue.
myotoxin A substance that induce rapid necrosis of muscle.
nausea A state of sickness.
necrectomy Surgical removal of necrosed tissue.
necrosis Death of tissue.
nephron A basic structural and functional unit of the kidney
consisting of glomerules and tubules.
nephropathy Damage to or disease of the kidney.
nervus facialis The facial nerve.
nervus medianus Median nerve; a major nerve of the upper limb.
neuropathy Any pathology of the peripheral nerves.
neurotoxic Damaging a nerve tissue.
nomenclature A system of words used to name organisms.
occlusion Closure or blockage.
oculomotor paralysis A condition of paralysis of muscles controlling eye
movements.
oliguria Abnormally small production of urine.
ontogenesis The process of an individual development of an organism.
ophtalmoplegia Paralysis of the one or more extraocular muscles.
oxygen therapy The administration of oxygen as a medical intervention.
oxygenation The process of providing with oxygen.
palatal and Paralysis of palate and glossopharyngeal nerve (IX).
glossopharyngeal paralysis
panophtalmitis Inflammation of the whole eye.
paralysis Loss of the ability to move a body part.
paraphyletic taxon A group composed of a collection of organisms, including
the most recent common ancestor of all those organisms.
Unlike a monophyletic group, a paraphyletic taxon does not
include all the descendants of the most recent common
ancestor.
parenteral Administered by means other than through the alimentary
tract (as by intramuscular or intravenous injection).
paresis A slight or partial paralysis.
paresthesia Abnormal skin sensations.
pelagic Relating to or occurring or living in or frequenting the open
ocean.
perception The process of perceiving.
perfusion Flow; herein a flow of blood through organs or tissues.
perioral Situated or occurring around the mouth.
 Glossary 297

peritoneum A transparent membrane that lines the abdominal cavity and

covers most of the viscera.
petechiae Minute red or purple spots on the surface of the skin as the
result of tiny hemorrhages of blood vessels in the skin.
phlegmon A spreading diffuse inflammatory process of a subcutaneous
or submucous tissue.
photophobia A symptom of excessive sensitivity to light.
phyletic order A sequence followed in listing of taxa which aids ease of use
and roughly reflects the evolutionary relationships among
the taxa.
pleural Of or pertaining to the pleura or pleurae, or to the
sides of the thorax.
pleural effusion An abnormal accumulation of fluid in the pleural space.
poikilocyte A degenerated form of an erythrocyte.
polyneuritis A state of inflammation of many nerves simultaneously.
polyneuropathy A neurological disorder that occurs when many peripheral
nerves throughout the body malfunction simultaneously.
polyphyletic taxon A taxon composed of unrelated organisms descended from
more than one ancestor.
pool Herein a deposit of venom.
precipitation The condensation of a solid from a solution during a
chemical reaction.
precursor A compound that participates in the chemical reaction that
produces another compound.
prevalence In epidemiology, the total number of cases of the disease in
the population at a given time.
prodromes An early unspecific symptom that a disease, herein
envenomation, is developing.
proteinuria The presence of excessive protein in the urine.
pseudobulbar palsy A disorder of the swallowing reflex and speech caused by
damage to the nerves of the related area.
ptosis Dropping of the upper eyelid caused by muscle paralysis and
weakness.
putrid In an advanced state of decomposition.
pyrogen A substance that induces fever.
Quinckes edema Involves swelling of tissues under the skin of the neck and
face, often caused by an allergic reaction. It can result in
suffocation.
rabies An acute viral disease of the nervous system of warm-
blooded animals.
recanalization Restoration of the continuity of a lumen.
rectal Of or involving the rectum.
regurgitation A back movement, e.g. the reflex act of ejecting the contents
of the stomach through the mouth.
relapse The return of symptoms and signs of a disease after a period
of improvement.
298 Jiri Valenta

renal Pertaining to the kidney.

retroperitoneum/extraperito An area occupying the most posterior aspect of the
neum abdominal cavity.
reversible Capable of going through a series of changes in either
direction, forward or backward, as a reversible chemical
reaction.
rhabdomyolysis The destruction of skeletal muscle cells.
salivation The secretion of saliva.
sedation The act of calming, especially by the administration of a
sedative.
sedative A medication with tranquilizing properties.
sequence homology The situation where nucleic acid or protein sequences are
similar because they have a common evolutionary origin.
shelf life Shelf life is that length of time that medicine is given before
it is considered unsuitable for sale or consumption.
schistocytes Fragments of red blood cells found in the circulation.
spasm A convulsive contraction of a muscle.
spasticity A state of hypertonicity or increase over the normal tone of a
muscle, with heightened deep tendon reflexes.
stasis An abnormal state in which the normal flow of a fluid (such
as blood) is slowed or stopped.
stereotaxy A surgical technique that uses medical imaging to precisely
locate in three dimensions an anatomical site to which a
surgical instrument or a beam of radiation is directed.
ST-segment A part of the electrocardiographic tracing.
subarachnoid Beneath the arachnoid membrane.
subcapsular Situated or occurring below a capsule.
subconjunctival Situated or occurring beneath the conjunctiva.
subfascial Situated or occurring beneath a fascia.
subspecies A taxonomic group that is a division of a species.
subterrestrial Subterranean; dwelling underground.
superficial Being or affecting or concerned with a surface.
tachycardia The excessive rapidity in the action of the heart.
taxon An animal or plant group or category, at any level, in a
system for classifying plants or animals.
taxonomy Classification or division of living organisms into ordered
groups or categories.
terrestrial Of or relating to or inhabiting the land.
thenar The prominence of the palm above the base of the thumb.
thrombin An enzyme (hemocoagulation factor) that acts on fibrinogen
to produce fibrin.
thrombocytopenia A decrease in the number of platelets in the blood.
thrombophilia A pathologic tendency to the occurrence of thrombi.
thrombosis, thrombotization The formation, development or presence of a thrombus.
thrombus A coagulated mass of blood.
tibial Relating to or located near a tibia.
 Glossary 299

transgression The spreading of the sea over land.

trauma Any physical damage to the body caused by violence or
accident or fracture.
tremor An involuntary trembling or quivering.
tubulus or tubule A minute tube lined with glandular epithelium; as, the
uriniferous tubules of the kidney.
ulceration The formation or development of an ulcer.
urethra The tube that conveys urine from the bladder to the outside.
urticarial Relating to or marked by urticaria.
uveitis An inflammation of part or all of the uvea.
varanoid A member of the Varanoidea taxon.
vascular Of or relating to or having vessels.
vasoconstriction The functional diminution of the caliber of vessels.
vasodilation, vasodilatation The increase in the internal diameter of a blood vessel that
results from relaxation of smooth muscle within the wall of
the vessel.
vasodilating Causing vasodilation.
vasopressor An agent causing elevation of blood pressure by stimulating
contraction of the muscular tissue of the capillaries and
arteries.
vasospasm The contraction of smooth muscle within the wall of the
vessel, mostly of pathologic origin, that causes a decrease in
blood flow.
vegetative Relating to bodily functions mediated by involuntary
vegetative nerves.
vertigo A reeling sensation.
volume expansion An increase in the amount of fluid in the vessels (intravasal
volume).
vomiting or emesis The act of repeated regurgitation of stomach contents.
 AUTHORS AFFILIATION
Dr Jiri Valenta, an anesthesia resuscitation and intensive care specialist, has worked for
20 years as the head of the intensive care unit in the Department of Anesthesia, Resuscitation
and Intensive Care at the General Teaching Hospital, Charles University, Prague.
In cooperation with the world renowned expert on toxinology, Professor Dr Frantisek
Kornalik, DrSc, he founded the Clinical Toxinology Center for the consultation and treatment
of patients envenomed by snakes and other venomous creatures.
This center has assisted hundreds of victims bitten by either European vipers or other
snakes exotic to Europe. None of these cases has resulted in mortality, irrespective of their
seriousness. Dr Valenta also functions as a keeper of antivenoms for the Czech Republic.
Furthermore, the author has published articles on intensive care and clinical toxinology in
the Czech Republic as well as abroad.
 INDEX
abscess 73 - West 89, 92, 93, 109, 112, 122-124,
abdominal pain 67 159, 173, 237-239, 245, 246, 254,
Acalyptophis 268 256, 257, 262
Acanthophis 23, 29, 30, 35, 134, 135, African puff adder 20, 29, 41, 109, 161-
148, 263, 264 164, 272
- antarcticus 323 (Fig) African tree snake 88
acanthoxin 35 aggregoserpentin 41
Acrochordoidea 2 Agkistrodon 12, 14, 29, 35, 41, 43, 44, 45,
acutin 43 70, 72, 204, 205, 207, 276, 277
adder 134, 161, 165, 188 Agkistrodon bilineatus 324 (Fig)
Adenorhinos 159, 271 - contortrix 324 (Fig)
afaacytin 42, 44, 167 - taylori 324 (Fig)
Afai 173 agkistrodotoxin 35, 205
Afghanistan 94, 104, 113, 179, 181, 237, Aglypha 7
246, 251, 255, 263, 273, 274, 283 Ahaetulla 91, 235, 239
Afgoi 257 - prasina 324 (Fig)
afibrinogenemia 43, 44, 78, 86, 89, 139, Aipysurus 152, 153, 268, 269
142, 174, 197, 207, 211, 220, 227 Alabama 277, 285
Africa 20, 37, 88-94, 98, 102, 108, 109, Albania 89, 186, 189, 274, 276
112, 115, 116, 123, 159, 161, 166, Alcatrazes Island 278
167, 238, 239, 245, 253, 254, 263, Algeria 173, 181, 246, 273-275
271, 272 ALI/ARDS 38, 77, 175, 198, 206, 213,
- Central 109, 112, 122, 124, 159, 173, 220, 223, 224
237-239, 245, 254, 256, 273 Alps 12, 189, 275
- East 90, 93, 109, 112, 236, 238, 245, Altiplanicia 281
273 Amazon 240, 244, 251, 252, 261, 262
- North 89, 93, 94, 112, 173, 184, 243, America 5, 12, 91, 93, 94, 204
246, 254, 255, 257, 272 - Central 12, 94, 126, 153, 237-240, 243,
- North-eastern 112, 173, 245, 246, 254 277, 280, 284
- South 88, 89, 91-93, 98, 100, 103, 109, - Central and South 22, 91-94, 210, 217,
112, 123, 161, 162, 236, 245, 246, 240-252, 278
254, 263, 272 - North 2, 5, 11, 21, 22, 92-94, 126, 127,
204, 216-219, 240, 243, 250, 251
304 Index

- South 22, 23, 73, 92-94, 126, 129, 153, Arrhyton 91, 92, 236
241, 244, 245, 250, 251, 278 Aru Archipelago 149, 244, 265
Amblyodipsas 100, 235, 253 Aruba 241, 280
ammodytin 35 Asia 2, 11, 12, 21, 94, 102, 112, 116, 159,
Amplorhinus 91, 235, 236 189, 205, 251, 269, 274
anaphylaxis 71, 191, 223, 289 - Central 93, 112, 173, 184, 205, 240, 246
ancrod 44 - East 225
Andaman Island 112, 236, 255 - South 94, 107, 225, 263, 269
Andes 11, 248, 261, 262, 277, 278, 283 - South-eastern 91-93, 104, 107, 112
Angel de la Guarda 281 - South-western 246
angiotensin 37 - West 184, 276
angiotensin converting enzyme 37 Asia Minor 94, 274
Angola 90, 94, 112, 159, 162, 239, 245, Asian arboreal pit viper 225
246, 251-253, 255-257, 262, 272 asp viper 18, 34, 37, 41, 51, 55, 183, 186,
Aniliidae 1 191, 195, 275
Antarctica 2, 11 Aspidelaps 102, 255
antibiotic 73, 100, 118, 125, 127, 145, - lubricus 324 (Fig)
156, 165, 183, 195, 208, 215, 223, Aspidomorphus 148, 264
229 Aspisviper 195
antigens 47, 51-55, 69, 100, 162, 194 Assam 255
antihistaminic 56, 64, 65, 69, 71 asthma attack 47
Antilles 237 Astola 273
Antillophis 92 Astrotia 152-154, 269
antithrombin 40, 44 Atheris 12, 40, 159, 160, 271, 272
antivenom 34, 51-56, 62, 66-72, 74-79, - nitschei 324 (Fig)
81 - squamiger 324 (Fig)
Aparallactinae 4, 98, 100, 235, 253 Atlantic Ocean 11, 12, 285
Aparallactus 100, 253, 254 Atractaspid 98
applaggin 41 Atractaspididae 2, 4, 9, 12, 13, 38, 39, 76,
Aqua Blanca 284 97, 235, 252
Arabian horned viper 166, 167, 273 Atractaspidinae 4, 98, 100, 252
Arabian Peninsula 161, 167, 173, 253, Atractaspis 13, 37, 39, 98-101, 252, 253
273, 274 - irregularis 324 (Fig)
Arafura Sea 269 atrioventricular block see AV-block
Argentina 94, 210, 214, 237, 239, 244, Atropoides 209, 210, 214, 277, 279, 284
245, 248, 252, 258-261, 278-280 - nummifer 325 (Fig)
arietin 41 atroxase 44
Arizona 129, 244, 281 Australia 1, 23, 51, 65, 134, 135, 140-
- (Sonoran) coral snake 129 145, 149, 153, 158, 237, 263-270
Arkansas 262 - East 137, 147-149, 153, 264-269
Armenia 181, 186, 198, 249, 275 - North 91-93, 134, 153, 235, 240, 244,
Armenian mountain viper 183, 184, 186, 264, 269
198, 199, 275 - North-eastern 148, 265, 266
arrhythmia 79, 115, 119, 120, 122, 125, - North-western 87, 265
127, 138, 141, 148, 155, 162, 163, - South 148, 265, 267
165, 174, 179, 182, 187, 212
 Index 305

- South-eastern 136, 138, 148-150, 264- - arietans 325 (Fig)

268 - gabonica 325 (Fig)
- South-western 137, 148, 149, 265, 267 - nasicornis 325 (Fig)
- West 134, 148, 150, 264-269 bitiscetin 41
Austrelaps 136, 137, 264 bitistatin 41, 162
Austria 186, 274, 276 black desert cobra 124
AV-block 99, 120, 135, 142 Black Forest 124, 275
Avicena viper 166 Black Sea region 274
Azemiopinae 4, 158, 271 black snake 29,35, 143, 144, 254, 266
Azemiops 158, 271 - tiger snake 38, 39, 138, 265
Azerbaijan 173, 186, 273, 275, 282 bleeding 143, 145,161, 163, 165, 167,
Badger 266 168, 172, 175, 177, 178, 190,196,
Balanophis 91, 236 209, 212, 213, 215, 220, 227, 229
Balearic Islands 12 blepharospasm 66, 114
Balete 286 blue-bellied black snake 143, 266
Bali 113, 255, 263 bluntnose viper 180
Balkan, Balkans 94, 189, 275 Boidae 2
Balkans 243, 249 Boiga 85, 87, 236, 237
Balsas River 260 - cyanea 325, 326 (Fig)
bandage, pressure immobilization 61-65, - dendrophila 326 (Fig)
103, 105, 108, 110, 116, 117, 121, boigas see Boiga
125, 128, 135, 138, 140, 142, 144, Bolivia 93, 239, 240, 244, 245, 248, 258-
146-150, 156, 193, 207, 214, 221, 262, 277-280, 283
222, 228 Bongare 104
banded coral snake 261 Booidea 2
bandy bandy 268 boomslang 31, 42, 43, 85, 88, 90, 91
Bangladesh 112, 113, 169, 237, 239, 262, Borneo 108, 113, 236, 247, 255, 256,
273, 284-287 270, 284-287
Bankoraj 173 Bosnia 186, 276
Barba amarilla 209 - and Herzegovina 76
Barkly Tableland 266 Bothriechis 209, 210, 212, 277, 279
Baskian viper 183, 184, 276 - schlegelii 326 (Fig)
Bass Straits Islands 264-266 Bothriopsis 209, 210, 277-279
Batan 286 Bothrocophias 209, 278, 279, 284
batroxobin 43, 211 bothropasin 39
Belize 241, 259-261, 276, 277, 282 Bothrops 11, 12, 15, 22, 29, 31, 37, 39-
Bengal 262, 286 43, 46, 54, 64, 70, 77, 79, 93, 181,
Benin 20 184, 205, 209, 210-214, 277-279
Bhutan 237 - alternatus 326 (Fig)
bilineobin 43 - atrox 326 (Fig)
bird snake 90, 251 - neuwiedi 327 (Fig)
bite wound 72, 99, 114, 127, 129, 143, Botswana 98, 103, 238, 245, 251, 253,
218, 226, 227 255, 257, 262
Bitis 5, 9-11, 14, 20, 29, 33-35, 37, 40, Bouganville Island 266
41, 44, 54, 55, 75, 76, 109, 161-164, Boulengerina 122, 125, 255
181, 272 - christyi 327 (Fig)
306 Index

Brachyophis 100, 254 Canary Islands 12

bradycardia 75, 120, 138, 142, 163, 187, cantil 43, 204
188, 196, 197, 212, 225 Cape Region 272
bradykinin 37, 76, 162, 211, 212, 217, Cape Verde Islands 12
225 cardiac failure 99
Brazil 22, 51, 91, 126-129, 210, 214, 237, cardiotoxin, cardiotoxins 37, 38, 41, 66,
239, 244, 245, 247, 248-262, 277-280, 75, 76, 104, 114, 118-120, 124, 145,
283 162, 163, 189
bronchospasm 56, 71, 191, 192 cardiovascular system 163, 212
brown snake 35, 43, 143, 145, 146, 265, Caribbean 12, 91, 93, 153, 236, 241
266 Caribbean Gulf 236
- tree snake 87, 237 Caribbean Islands 91
Brunei 285 carinactivase 42
Bulgar-Dagh 276 carinatin 41
Bulgaria 89, 186, 189, 274, 275 Carolina 47, 130, 204, 276, 280, 285
Bungarinae 66, 102, 122 carpet viper 173, 273
bungarotoxin 35, 36, 87, 104 Cascabel 216
Bungarus 21, 35, 36, 61, 69, 70, 75, 103, Cascauella 216
104, 106, 117, 119, 207, 236, 255 Caspian Sea 89, 112, 205
Burkina Faso 238 cat snake 87, 236, 237, 249
Burma 21, 91-93, 113, 158, 169, 171, Cauca 261
235, 237, 239, 246, 247, 255, 256, Caucasus 263, 274, 275
262, 263, 270, 271, 273, 279, 285-287 caudoxin 35
Burrowing asp 37, 98, 252, 253 Causinae 157, 165
- cobra 123 Causus 20, 44, 55, 165, 166, 272, 273
Burundi 162, 251, 257, 271 - rhombeatus 327 (Fig)
bushmaster 22, 40, 43, 210-214, 283, 284 Cebu 256
C protein 45, 86, 142 Cedros 282
Cacophis 148, 149, 264, 265 centipede eaters 253
Caenophidia 2 Central African Republic 245, 256, 257,
Caissaca 209 273
Calabria 275 Cerastes 14, 19, 42-44, 55, 70, 160, 166-
Calamodontophis 91, 237 168, 179, 180, 216, 217, 273
calciseptin 35 - cerastes 327 (Fig)
California 243, 250, 280, 281 - vipera 327 (Fig)
Californian Peninsula 280, 282 cerastobin 43
Calliophinae 102, 106 Cerberus sp. 91, 237
Calliophis 106, 107, 256-258 Cerralvo 280
Calloselasma 21, 40, 41, 42, 44, 69, 204, Cerrophidion 209, 210, 214, 279, 280,
205, 207, 277, 279 284
Cambodia 86, 113, 139, 255, 256, 263, - godmani 327 (Fig)
279, 284, 286, 287 Chad 167, 263, 273
Cameroon 112, 245, 252, 253, 255, 257, Chappel 266
263, 271-273 Charina 2
Camiguin 113, 286 chemosis, conjunctival 114, 170
Canada 11, 21, 22, 217, 281, 282, 285 Chihuahua 276
 Index 307

Chile 11, 210, 244, 248 114-117, 119-125, 255, 257, 262, 263,
Chilorhinophis 100, 254 266
China 86, 91, 92, 105, 116, 184, 204-207, Cobra
237, 240, 243, 246, 247, 268, 270, - African tree 124, 263
275, 283-287 - black and white 20, 111, 112, 116, 262
- East 283 - black-necked spitting 20, 41, 44, 111,
- North 184, 189, 239, 247, 255, 257, 262, 112, 114, 116, 262
273, 283-285, 287 - Central Asian 111, 112, 116, 263
- North-eastern 283 - desert 124, 263
- North-western 275, 283 - Egyptian 29, 111, 112, 116, 181, 262
- South 86, 91, 93, 102-105, 107, 112, - hoodless 124, 263
153, 158, 169, 225, 236, 237, 239, - Chinese 37, 111, 114, 116, 262
247, 255, 256, 270, 271, 284, 285 - Indian 21, 28-31, 54, 61, 69, 111, 116,
- South-eastern 112, 205, 239, 240, 284, 189, 262
286 - Indochinese spitting 36, 111, 112, 263
- South-western 112, 247, 255, 262, 283 - king 5, 14, 36, 61, 102, 119, 120, 143,
- West 93 263
Chinese green pit viper 225 - monocellate 55, 111, 112, 262
habu 39, 225, 228, 285, 286 - Mozambique spitting 111, 112, 262
Chinese moccasin 39, 41, 43, 54, 204, - ringed water 122, 255
282 cobrotoxin, cobrotoxins 36, 38
Chinese mountain pit viper 224, 228, 284 Colima 260, 284
Chokosumo 287 Colletts snake 266
Cholophidia 1 Colombia 237, 240, 244, 258-262, 277-
Chrysopelea 91, 240 280, 283, 284
- ornata 328 (Fig) Colorado 280
Clarence River snake 147, 268 Coluber 91, 237, 238
Clelia 91, 237 colubrid, colubrids 2-6, 9, 12, 13, 18, 30,
Cleopatra viper 166 31, 42, 43, 85, 86, 88, 91-95, 100,
clotase 43 102, 123, 158, 188,235, 237
coagulation 32, 35, 39, 40, 42, 67, 77, 78, Colubridae 2-5, 8, 13, 30, 42, 85, 123,
87, 89, 109, 131, 136, 138, 139, 141, 235, 254
143, 146, 148, 167, 172, 174, 178, Colubrinae 3, 4, 85
191, 197, 205-207, 211, 212, 214, Colubroidea 2-4
217, 219, 220, 226 common viper 11, 12, 18, 19, 29, 30, 34,
coagulopathy 54, 69, 95, 105, 116, 139, 55, 61, 181, 183, 184, 186, 188-192,
141, 143, 146, 147, 149, 155, 163, 194, 195, 275
169, 170, 174, 182, 188, 206, 208, compartment syndrome, pressure 68, 72,
211, 213, 214, 218, 220, 224, 227, 118, 163, 171, 181, 183, 187, 199,
229 206, 208, 212, 215, 217, 218, 222,
- consumption see coagulation 223, 226-228
- disseminated intravascular see DIC complement 45, 55, 75, 88, 114, 120,
Coahuila 262, 276 174
Cobra 5, 9, 12-15, 20, 21, 28-31, 36-38, Congo 98, 159, 162, 239, 245, 252, 253,
41, 44-47, 51, 54, 55, 61, 66, 69, 71, 255-257, 263, 272
75, 77, 89, 102, 103, 108, 111, 112, Coniophanes 91, 238
308 Index

conjunctivitis 114 - ruber 330 (Fig)

Connecticut 276 - scutulatus 330 (Fig)
Conophis 92, 238 - tigris 330 (Fig)
convalescence 78, 81 - viridis 330 (Fig)
convulxin 41 Crotaphopeltis 92, 238
copperhead 29, 41, 44, 45, 136, 204, 264, crotoxin 35, 46, 54, 218
276 Cryptelytrops 224, 282, 285-287
coral snake 29, 30, 38, 64, 65, 102, 103, Cuba 236
106, 107, 125-127, 129, 244, 255-262, Cyanodontophis 254
267 Cyclades 180, 181, 186, 274
Coralilla, Coralillo 126 Cyprus 181, 274
Coronado del Sur 280 Czech Republic 18, 19, 85, 167, 189, 216,
Coronella austriaca 85 225
Corsica 12 Daboia 21, 30, 31, 33-35, 39-45, 54, 55,
corticosteroids 56, 64, 65, 70, 71, 118, 64, 69, 72, 74, 77-79, 168-171, 179,
125, 194 196, 273-275
Costa Rica 22, 156, 205, 214, 241, 248, - russelli 330 (Fig)
259, 261, 276, 277, 280, 282-285 daboiatoxin 35
cottonmouth 14, 29, 41, 204, 277 death adder 23, 29,30, 35, 134,263, 264
Couleuvre de Moila 89 Deinagkistrodon 39, 41, 43, 54, 204, 205,
- de Montpellier 89 207, 276, 282
Crete 12 Demansia 43, 148, 264
Croatia 55, 186 dendroaspin 36, 109
cross-immunity 106, 108, 121, 128, 144, Dendroaspis 5, 13, 14, 29, 31, 34-36, 61,
195, 199, 228 70, 75, 102, 108, 109, 122, 256, 257
crotalase 44, 217 - angusticeps 330 (Fig)
Crotalidae 3, 222 - jamesoni 331 (Fig)
Crotalinae 5, 6, 12, 33, 34, 37, 40, 43, 45, - polylepis 331 (Fig)
47, 67, 69, 74, 80, 82, 157, 158, 203, - viridis 331 (Fig)
204, 221, 225, 276 dendrotoxins 34, 35, 109
crotalotoxin 39, 217 Denisonia 148, 264, 265
Crotalus 5, 6, 12, 14, 15, 22, 29-31, 33- desert horned viper 42-44, 166, 167, 273
35, 37, 39-41, 44-46, 54, 55, 63, 64, desert Leventin viper 180
66, 69, 70, 72, 75-77, 79, 158, 172, - sidewinder 216, 280
189, 208, 215, 216-221, 280-282 - viper 179, 180, 181, 274
- adamanteus 328 (Fig) diadem snake 239, 247
- atrox 328 (Fig) diarrhea 46, 47,67, 74, 99, 107, 141, 149,
- cerastes 328 (Fig) 150, 160, 169, 181, 187, 189, 190,
- cerberus 328 (Fig) 193, 196, 206, 212, 219, 226
- durissus 328 (Fig) DIC 40, 42, 43, 76-80, 86-91, 94, 116,
- durissus unicolor 329 (Fig) 120, 121, 136-140, 143, 145, 147,
- helleri 329 (Fig) 162, 163, 165, 167-169, 172, 174,
- horridus 329 (Fig) 175, 178, 182, 183, 188, 193, 206-
- lutosus 329 (Fig) 209, 211, 213, 215, 220, 221, 224,
- mitcheli 329 (Fig) 227, 229
- ravus 329 (Fig) Dinilysia 1
 Index 309

Dipsadoboa 92, 238, 239 edema 38, 45, 47, 56, 61, 63, 64, 67, 68,
Dispholidus 13, 31, 39, 40, 42, 43, 85, 88, 71-73, 77, 81, 114, 118, 120, 123,
239 148, 158, 160, 163, 166, 167, 169,
- typus 331 (Fig) 175, 180, 181, 187, 190, 193-196,
disseminated intravascular coagulation see 211, 212, 218, 219, 223, 226
DIC - angioneurotic 56, 64, 71, 169, 184, 189
Disteira 152, 269, 270 - pulmonary 38, 87, 116, 175, 198, 220
Doksa 204 - Quinkes 56
Dominican Republic 92, 240 edrophonium 75, 106, 111, 118, 122, 128
Dromicus 92 Egypt 89, 98, 112, 124, 127, 173, 179,
Dromophis 6, 92, 239 253, 262, 263, 273, 274
Dryophis 91, 235, 239 El Muerto 281
Drysdalia 148, 265 elapid snakes, elapids, Elapidae 2-4, 8, 9,
dugit 145 12-14, 28, 30, 33, 37, 39, 40, 44, 45,
Duke of York 264 47, 61, 66, 71, 73-75, 77, 79, 100,
Duvernoys gland 8, 85 -87, 89 102, 108, 109, 111, 122, 134, 143,
dwarf-crowned snakes 148, 264 146
dysarthria 33, 66, 67, 75, 104, 107, 115, - terrestrial, Austropapuan 39, 40, 45, 61,
120, 123, 124, 127, 135, 139, 141, 76, 77, 79, 134, 143, 146, 148, 153,
146, 155, 170 263
dysphagia 33, 66, 67, 75, 90, 99, 104, Elapinae 3, 4, 102, 255
110, 115, 120, 127, 135, 140, 141, Elapocalmus 100, 254
155, 170, 172, 180, 187, 191, 195, Elapognathus 149, 265
196, 206, 209 Elapomorphus 92, 239, 244
dysrhythmia 32, 114 Elapotinus 100, 254
eastern brown snake 35, 43, 145, 146, 266 Elapsoidea 122-124, 257
eastern coral snake 125-127, 260 Elba 195, 275
eastern diamond-backed rattlesnake 5, 22, Emydocephalus 152, 269
30, 40, 41, 54, 64, 189, 216, 217, 221 endothelium 32, 33, 37, 38, 40, 43, 45,
- coral snake 125-127, 260 82, 170, 174, 191, 217
ecarin 42, 86, 87, 174 England 19, 189, 192
ECG 37, 67, 76, 99, 115, 120, 135, 142, Enhydrina 28-30, 46, 152-154, 156, 269
155, 157, 170, 182, 191, 193, 206, Enhydris 92, 239, 240
227 enzymes 27, 28, 32-46, 68, 72, 75-79, 81
Echide carne 173 Ephalophis 152, 269
Echiopsis 134, 148, 265 Eristicophis 179, 180, 274
Echis 6, 14, 20, 21, 30, 31, 33, 39-43, 52, - macmahoni 332 (Fig)
64, 66, 69, 77, 78, 80, 86, 88, 109, Eritrea 252, 253, 263, 273, 274
160, 172-174, 176, 177, 179, 180, Ermia 224
205, 273, 274 Eteirodipsas 92, 240
- carinatus 331 (Fig) Ethiopia 98, 162, 245, 246, 252, 253, 257,
- ocellatus 332 (Fig) 262, 263, 272
- pyramidum 332 (Fig) Europische Eidechsenatter 89
echistatin 41, 174 Europe 2, 11, 18, 102, 159, 183-186, 189,
Ecuador 22, 94, 213, 214, 237, 240, 245, 192
248, 258-262, 277-279, 283, 284 - Central 183, 188, 275
310 Index

- North 275 Fordonia 92, 240

- South-eastern 243 forest pit viper 209, 277, 278
- South-western 93, 243 forest twig snake 251
European adder see European viper France 19, 110, 164, 189, 192, 195, 216,
- viper 5, 74, 158, 186, 192, 275 275, 276
extravasation 32, 33, 37, 38, 46, 65, 74, French Guyana 240, 258, 260-262, 278,
76, 80, 122, 163, 170, 175, 178, 182, 280
183, 191, 193, 197, 217, 220, 227 Furina 149, 264, 265
exuvia 6 Gabon 122, 162, 245, 252, 253, 255, 271
eyelash palm pit viper 277 Gabon adder see Gabon viper
eyes, affection 114, 118, 123, 125 Gabon viper 11, 14, 15, 29, 44, 54, 161,
False Fer de Lance 252 163, 164, 272
false-horned viper 179 gabonase 44, 162
fangs, aglyphous 8, 10 gabonin 41
- erectile 10, 157, 159, 203 Galapagos 245
- opistoglyphous 8, 10 Gambia 273
- proteroglyphous 8, 10 gangrene 63, 73, 164, 165, 187, 206-208,
- solenoglyphous 8, 10 215, 226, 228
Far East 184, 275 Gargantilla 126
fasciculation 109 garter snakes 122, 257
fasciculins 34, 109, 111 Garthius 224, 282, 284
fasciotomy 72, 73, 118, 163, 172, 183, Gaspare 259
188, 197, 199, 206, 208, 212, 215, gastrointestinal (affection) 67, 99, 137,
222, 223, 228 163, 171, 175, 176, 187, 190, 196,
Feas viper 158, 271 213
Fer de Lance 209 Georgia 186, 249, 275
Fer de Lance asiatique 225 Georgia (U.S.) 277, 285
Ferguson 268 Germany 160, 195, 216
fever 114, 160 Ghana 20, 109, 159, 245, 252, 256, 263,
fibrin 40, 43, 44, 68, 78, 80, 170-172, 272
174-176, 206, 213 Gigantophis 1
fibrinogen 38, 43, 44, 46, 68, 78, 86, 205, gjurza 180
206, 211, 217, 226 glandula maxillaris 7
fibrinolysis 38, 80, 86, 87, 90, 142, 165, Gloydius 12, 34, 41, 42, 70, 158, 204,
170, 172, 188, 193, 197, 207, 211, 205, 276, 277, 283
213 - halys 332 (Fig)
fibrolase 44 - intermedius 332 (Fig)
Ficimia 92, 240 Glyphodon 149, 265
Fields horned viper 179, 274 Glyphodonta 8
fierce snake 140 Golds cobra 124
Fiji 149, 266 Golden tree snake 240
Finland 11, 18, 189 gold-ringed cat snake 236
flavoxobin 44 Great Lakes bush viper 159, 271
Flores 113, 169, 263 Greater Atlas 275
Florida 217, 249, 277, 280, 285 - Caucasus 275
flying snake 240 Greece 186, 189, 240, 243, 274, 276
 Index 311

- Pindos Mountains 276 Hemorrhois 91, 238, 240

Green cat snake 236 hemostasis 40, 45, 46, 76, 88, 90, 136,
green pit viper 225 137, 141, 172, 175, 177, 178, 182,
Greenland 11 187, 192, 194, 197, 206, 212, 217,
Guam 87 220, 226. 227
Guanajuato 262 heparin 42, 78-80, 89, 129, 136, 140, 143,
Guarda camino 92 146, 147, 168, 172, 174, 178, 183,
Guatemala 241, 258-262, 276, 277, 282, 188, 209, 215, 229
284 - low molecular weight heparin 79, 143,
Guerrerro 281 161, 165, 168, 178, 209, 215
Guinea 271, 272 heparinization 81, 146, 148, 161, 178,
Gulf of Persia 12, 269, 270 224
Gulf of Siam 271 Herzegovina 89, 276
Guyana 240, 258, 260-262, 278, 280 Heterodon 85, 92, 95, 240
Gwardar 145, 266 Hierophis 238
gwardar or western brown snake 266 Himalaya 113
habu 39, 224, 225, 228, 285, 286 Himalayan pit viper 12, 158, 204, 205,
Hainan 86, 104, 107, 112, 119, 239, 247, 283
255, 256, 285-287 Himalayophis 224, 283, 287
Haiti 92, 240 Homalopsinae 4
Halys pit viper 35, 41, 204, 283 Homalopsis 92, 95, 240
Hamadryad 119 Homoroselaps 100, 123, 124, 254, 257,
hannalgesin 36 258
harlequin snake 123, 258 Honduras 92, 240, 244, 259, 261, 276,
Hawaiian Islands 11 277, 280
Hemachatus 15, 63, 66, 107, 123-125, Hong Kong 225, 247, 255, 285
184, 257 Hoodless cobra 124, 263
hematoma 167, 205 Hoplocephalus 137, 265
Hemiaspis 149, 265 horned pit viper 284, 285
Hemibungarus 106, 107, 256, 267 horned puff adder 35, 272
hemocoagulation 20, 31, 38, 40, 42, 45, Hornotter 186
46, 63-65, 67-69, 72, 74, 76, 77, 78, humpnose viper 204
80, 81, 86, 88-91, 94, 95, 99, 104, hump-nosed pit vipers 204, 283
105, 115, 120, 124, 127, 134, 135, hundred-pace viper 204
137-150, 158-162, 164-172, 174-178, Hungary 186, 276
180-184, 190-193, 195-199, 203, 205- hyaluronidases 33, 109, 126, 162, 166,
209, 211-215, 217, 218, 220-224, 174, 211, 217
226-229 Hydrelaps 152, 269
hemoglobinuria 80, 116, 139, 140, 147, Hydrophiidae 3, 102, 133, 134, 152, 268
164, 171, 175, 176, 187, 191, 192, Hydrophiinae 4, 45, 102, 133, 152, 154,
194, 197, 207, 213, 220, 221 263, 268
hemorrhage 31, 77, 80, 87, 88, 139, 175, Hydrophis 152-154,269-271
176, 207, 208 hypercoagulation 40, 43, 68, 138, 140,
hemorrhagins 33, 37-40, 45, 46, 72, 76, 148, 209, 215, 229
77, 162, 186, 190, 196, 198, 205, 211, hyperkalemia 45, 79, 80, 155, 157
225 hypertension
312 Index

Hypnale 204-208, 283, 333 (Fig) Iran 113, 116, 124, 167, 173, 179-181,
hypofibrinogenemia 40, 78, 89, 144, 146, 189, 205, 237, 249, 250, 253, 273-
170, 182, 183, 187, 196, 207, 209, 276, 283
212, 215, 219-223, 227, 229 Iraq 89, 124, 179, 181, 182, 250, 263,
Hypoptophis 100, 254 273, 274
hypotension 31, 32, 36-38, 45-47, 56, 65, Ireland 11, 189, 264
67, 71, 74, 76, 78, 80, 114, 115, 120, Irian Jaya 264
122, 139, 146, 150, 158, 160, 162- Israel 1, 19, 89, 98, 124, 167, 173, 179,
164, 166, 168-172, 179, 182-184, 181, 196, 197, 243, 246, 250, 252-
187-189, 191, 193, 196-199, 206, 208, 254, 263, 273-275
211-215, 217, 218, 220, 223, 225, Italy 18, 89, 186, 189, 195, 275, 276
226, 228, 229 Ithycyphus 92, 241
Ialtris 92, 240 Jacobsons organ 6
Iceland 11 Jalisco 260, 281
Illinois 277 Japan 21, 51, 86, 87, 107, 204, 205, 207,
Imantodes 92, 240, 241 225, 227, 228, 247, 256, 257, 269,
immunity 51-55, 106, 108, 121, 128, 144, 270, 283-285
195, 199, 208, 214, 218, 228 Japanese habu 225
immunogenicity 28, 36, 51, 52, 54, 99, jararaca 22, 29, 31, 39, 181, 209-214, 278
208, 214 Jararaca ilhao 209
immunotherapy 66, 67, 75, 77, 138, 140, - pintada 209
142, 165, 193, 194, 208, 209, 214, jararacussu 22, 29, 209, 278
215, 220, 223, 224, 229 jararhagin 39
India 21, 52, 86, 87, 91-93, 102-108, 112, Java 105, 113, 169, 228, 236, 247, 255,
113, 116, 119, 155, 156, 169, 173, 256, 263, 269
181, 205, 225, 235-237, 239, 240, Jolo 286
243, 246, 247, 255, 256, 262, 269, Jordan 89, 173, 179, 181, 196, 250, 263,
270, 273, 274, 283-287 273-275
Indian Ocean 23, 269-271 jumping pit viper 277
Indian Peninsula see India Kanburi 286
Indian subcontinent see India Kangaroo Island 136
Indiana 276 Kansas 276
Indochina 107, 112, 205, 236, 237, 239, Kashmir 181, 263
240 Kazakhstan 275, 283
Indo-Chinese mountain (pit) viper 225 Kentucky 285
Indonesia 86, 87, 91, 84, 102, 104, 107, Kenya 20, 98, 109, 159, 162, 173, 236,
113, 119, 150, 169, 225, 228, 235- 238, 239, 245, 251-254, 256, 257,
237, 239, 240, 243, 247, 251, 255, 262, 263, 271-274
256, 253, 264, 268, 270, 273, 284-287 keratitis 114
infection 73, 114, 118, 122, 143, 145, Kerilia 152, 270
165, 175, 183, 190, 206, 218 Kiau 284
inhibitor 41, 44, 73, 75, 128 kidney failure see renal failure
Inland (western) taipan 28, 35, 140, 141 kidneys 46, 68, 80, 170, 183, 192, 198,
Iowa 276 218, 220, 227
Kimolos 181, 274
King brown snake 143, 266
 Index 313

- cobra 5, 14, 36, 47, 61, 102, 119, 120, Leptophis 93, 241
143, 263 Lesotho 272
kinin 24, 36, 37, 55, 162 lesser cerastes viper 166
kininogenases 37, 211, 217, 225 leukocytosis 67, 68, 74, 87, 95, 103, 105,
Kolpophis 152, 270 107, 116, 121, 124, 125, 127, 135,
Komodo 113, 169, 263 138, 155, 158, 160, 164, 166, 170,
Korea 86, 153, 184, 189, 204, 205, 247, 176, 180, 182, 187, 191, 193, 197,
283 198, 207, 221, 227
Kos 240 Leventin viper 180
krait (sea) 3, 36, 45, 54, 61, 77, 102, 133, Liberia 162, 252, 253, 263
134, 152-154, 268 Libya 181, 246, 262, 273, 274
krait see Bungarus Liophis 92, 93, 241- 243
Kreuzotter 188 lizard-eating snake 239
Krk 276 LMWH see heparin, low molecular weight
Kuwait 181, 273 heparin
Kyrgyzstan 275, 283 Lomblen 113, 169
Lachesis 22, 40, 43, 64, 70, 76, 77, 161, long-glanded coral snake 107
209-214, 283, 284 Long-nosed viper 186
Lake Taal, Luzon 270 Louisiana 280
- Te-Nggano, Solomon Island 154 Loveridgelaps 149, 265
Lamprophiinae 3, 4 Lowland swamp viper 159, 274
lancehead see Bothrops Luzon 113, 256, 270, 286
Langaha 92, 241 Lygophis 93, 243
- madagascariensis 333 (Fig) lymph nodes 56, 71, 73, 104, 114, 120,
languor 74, 95, 103, 104, 110, 135, 154, 124, 135, 143, 154, 160, 163, 166,
166 167, 169, 175, 180, 181, 190, 196,
Laos 86, 112, 113, 135, 247, 255, 256, 212, 218, 226
263, 279, 282, 285-287 lymphadenitis 90, 93, 95, 139, 141, 143,
Lapemis 152, 153, 270 187, 196
Lapparentophis defrennei 1 lymphadenopathy 73, 99, 103, 114, 123,
Latastes viper 183, 275 124, 137, 139, 142, 145, 147, 149,
Laticauda 36, 152-154, 270 150, 154, 160, 163, 166, 167, 180,
Laticaudinae 3, 152, 268 181, 205, 212, 219, 226
LD0 28 mFezi 112
LD100 28, 29, 161 Macedonia 189, 276
LD50 28, 86, 88, 90, 99, 113, 119, 136, MacMahons viper 179
141, 145, 154, 158, 159, 174, 179, Macrelaps 100, 101, 154
181, 184, 205 Macropisthodon 93, 243
leaf-nosed viper 179 Macroprotodon 93, 243
Lebanon 173, 181, 186, 196, 263, 275 Macrovipera 19, 20, 33, 39-43, 55, 64,
lebetase 44 76, 78, 79, 180-182, 274
lebetin 181 - lebetina 333 (Fig)
Leimadophis 92, 241 - mauritanica 333 (Fig)
Lepidosauria 4 - schweizeri 333 (Fig)
Leptodeira 92, 241 Madagascar 11, 92, 93, 241, 243
Leptomicrurus 102, 129, 258 Madagascarophis 93, 240, 243
314 Index

Madtsoia 1 - Coahuila 262, 276

mainland Southeast Asia 262 - Chihuahua 276
mainland tiger snake 28, 29, 35, 38, 39, Michoacn 248
42, 46, 52, 79, 128, 138, 140, 146, Micrelaps 100, 254
266 Microcephalophis 269, 270
Malawi 159, 238, 245, 253, 262, 272, 274 microembolization see microthrombi
Malayan pit viper 21, 40, 204, 279, 313 Micronesia 11
Malaysia 87, 91, 102, 104, 107, 112, 113, Micropechis 149, 265
119, 153, 156, 225, 235-237, 239, microthrombi 46, 77, 80, 87, 88, 169,
240, 243, 247, 255, 256, 263, 269, 170, 172, 174, 175, 206, 218
270, 284, 285, 287 Micruroides 102, 129, 258
Mali 112, 167, 253, 273 Micrurus 12, 22, 29, 30, 61, 70, 102, 125-
Malpolon 6, 18, 85, 89, 243 129, 258-262
- monspessulanus 333 (Fig) - fulvius 334 (Fig)
Malta 12 Middle East 19, 20, 24, 89, 91, 93, 94, 98,
mamba see Dendroaspis 160, 173, 183, 184, 196, 198, 240,
mamushi 42, 204, 207, 208, 283 243, 246, 247, 250
mamushigin 42 Milos 181, 274
Manab 284 Mindanao 113, 286
Manaus 258, 259 Mindoro 113, 256, 286
mangrove snake 236 Miodon 254
Mangshan 286 Misima 268
Mangashan pit viper 286 Misool 264
many-banded snake 123, 263 Mississippi 280, 285
many-spotted snake 291, 237 Missouri 276
Mapanare 209 MLD 181
Maracaboia 216 MODS 77, 86
Maraj 279, 280 Moila snake 89, 243
Martinique 12, 213, 279 Mojave
Maryland 276 - desert sidewinder 280
Masbate 113, 256 - rattlesnake 216, 218, 220, 282
massasauga 216, 281, 285 - toxin 35, 218
Masticophis 93, 243, 444 Moldova 189
Maticora 106-108, 285 Mole viper 39, 98, 252, 253
Maticorinae 102, 106 Mongolia 91, 189, 205, 246, 283
Mauritania 98, 112, 253, 277, 262, 273 montane pit viper 279, 280
meadow viper 183, 184, 275, 276 Montatheris 159, 271, 274
Mediterranean Sea 12, 196 Montenegro 89, 276
meisothrombin 42, 78, 87, 88, 174, 178 Montivipera 183, 274
Melanesia 268, 269 Montpellier snake 89, 243
Mesa Central 282 moojeni protease A 39
metalloproteinases 32, 39, 40 Moorish viper 180, 181, 274
Mexican Plateau 281 Morelos 262
Mexico 22, 52, 93, 94, 126, 129, 205, Morocco 89, 112, 167, 180, 181, 262,
210, 217, 240, 241, 244, 248, 252, 272-275
258-262, 276, 277, 279-282, 284, 285
 Index 315

Mozambique 103, 111, 112, 162, 245, Natricinae 3, 4, 12, 85

251, 253-257, 262, 172, 174 nausea 27, 47, 56, 67, 71, 74
Mt Kinabalu 284 Nebraska 276
mucrotoxin 40, 225 necrosis (tissue) 32, 33, 54, 71, 72, 81,
multiple organ dysfunction syndrome see 93, 99, 103, 113-116, 118, 121, 122,
MODS 126, 154, 165, 167-170, 181, 183,
mulga 143, 144, 266 186, 187, 195, 196, 205-208, 212,
multactivase 43 214, 217-219, 223, 226, 228
Municipio de Ixlahuacn 284 necrosis (tubular, cortical) 46, 47, 87, 89,
Murici 279 169-171, 213
mussurana 237 Negros 256
mutalysin II 40 neostigmine 75, 105, 106, 111, 119, 122,
Myanmar 21 128, 135, 136, 156
mydriasis 105, 110, 155, 221 neotropical rattlesnake 216
myocardial ischemia 76, 99, 100, 140, Nepal 87, 107, 108, 112, 113, 119, 205,
146 225, 237, 247, 256, 262, 283-285, 287
myoglobin 45, 46, 74, 79, 105, 127, 129, nephrotoxicity 46, 80
136, 138, 139, 142, 144, 145, 155, neurotoxicity 31, 35, 47, 54, 65, 70, 74,
156, 164, 169, 171, 182, 206-208, 75, 99, 103, 104, 107, 115, 116, 121,
218, 221, 227 124, 127, 135, 137-142, 144-146, 150,
myoglobinemia see myoglobin 155, 156, 169-171, 179, 185, 191, 211
myoglobinuria 33, 46, 68, 80, 105, 135, neurotoxins 13, 30-34, 36, 53, 54, 63-68,
139, 140, 144, 147, 155, 157, 164, 74, 75, 79, 87, 94, 103, 104, 107, 109,
170, 171, 187, 197, 207, 217, 220 113, 116, 120, 124, 126, 129, 134,
myonecrosis 32, 38, 45, 47, 54, 68, 79, 136, 137, 141, 143, 150, 154, 179,
169-171, 212, 217, 218, 220 205, 220
myotoxicity 134, 143, 150, 154, 155, 217 Neuwieds lancehead 209, 212, 279
myotoxin, myotoxins 33, 45, 46, 52, 54, Nevada 281
68, 72, 79, 126, 136, 137, 139, 144, New Britain 264
148, 150, 154, 155, 189, 206, 217 - Ireland 264
Myron 93, 244 New Guinea 23, 87, 91-93, 134, 140, 141,
Naja 12, 20, 21, 28-31, 33, 36-38, 40, 41, 143, 145, 148-150, 237, 240, 244,
44, 45, 54, 55, 61, 63, 66, 69-71, 75, 263-271
77, 103, 104, 107, 111-113, 115-118, New Hebrides 11
120, 121, 123, 124, 181, 184, 189, New South Wales 264-267
262, 263 New Zealand 11
- annulifera 334 (Fig) Nicaragua 258, 261, 276, 280
- atra 334 (Fig) Nicobar Islands 237, 285, 286
- haje 335 (Fig) Niger 167, 263
- kaouthia 335 (Fig) Nigeria 20, 99, 109, 112, 159, 162, 173,
- mossambica 335 (Fig) 263, 272
- naja 335 (Fig) night adder 20, 44, 165, 166, 272, 273
- oxiana 335 (Fig) nordic viper 188
Nakhon Si Thammart 287 North America see America North
Namibia 94, 98, 103, 245-247, 253, 255, Norway 11, 189
257, 262, 263, 272 nose-horned viper 18, 35, 55, 186, 274
316 Index

notecarin 42 Pacific Ocean 11, 12, 23, 155, 169-171

Notechis 23, 28, 29, 35, 38, 38, 42, 46, painted keelbacks 94, 251
52, 70, 75, 79, 121, 128, 138, 140, Pakistan 21, 104, 113, 119, 169, 173, 179,
144, 265, 266 181, 205, 225, 237, 239, 346, 355,
notexin 35, 46 262, 269, 270, 273, 274, 283
Nuevo Len 262 Palaeonaja 2
Nullarbor Plain 267 Palstinaviper 196
Nyalam Co. 287 Palawan 113
Oaxaca 259, 281 pale (broad) headed snake 137
Oceania 11, 23, 269 Palestine
ocellated mountain viper 276 Palestine saw-scaled viper 173, 178, 273
Ogmodon 149, 266 Palestine viper 19, 41, 275
Okinawa 257 palm pit viper 277
Oklahoma 276, 277, 280 Pama 104
Oman 179, 262, 273 Panama 153, 156, 237, 241, 258, 259,
Ontario 217, 281 261, 262, 277, 279, 283, 284
Ophidia 4, 5 Panay 236, 256
Ophiophagus 5, 12, 14, 36, 61, 70, 102, Papua-New Guinea 23, 141, 145, 149,
119-121, 143, 263 150, 240, 264-268
- hannah 336 (Fig) Parademansia microlepidota 28
Ophryacus 209, 210, 284 paradoxin 35, 141
ophtalmoplegia 67, 99, 104, 107, 115, Paraguay 92, 239, 245, 259-261, 278-280
170, 191, 195, 221 Parahydrophis 152, 270, 271
Opistoglypha 8 paralysis (muscular) 33, 34, 36, 63, 66,
ornate flying snake 240 67, 74, 75, 103-111, 115-125, 127-
orange-banded snake 149 129, 135, 136, 139, 141, 143, 145,
Oregon 250 147, 148, 155, 156, 170, 172, 206,
organ, Jacobsons 6 220, 221
- auditory 6 Paran 246, 258
- vomeronasal 6 Paranaja 123-125, 263
- thermo-sensitive 6 Parapistocalamus 149, 266
Oriental (Asian) coral snake 107, 255, Parias 224, 284, 286, 287
257 Paroplocephalus 149, 265-267
Oriental whipsnake or Asian vine snake parrot snakes 93
235 Pee-un 104
oscutatin 42 Pelamis 152-154, 156, 271
Otter 183 Peltopelor 224, 284, 286
Ovophis 224, 225, 227, 228, 282, 284, peninsula brown snake 145, 266
286, 287 Persian horned viper 179, 274
Oxybelis 93, 244 Peru 93, 217, 238, 240, 244, 245, 248,
Oxyrhopus 93, 244 258-262, 278-280
Oxyuraninae 134, 148, 150, 153, 263 Peruvian Andes 277
Oxyuranus 5, 23, 28-30, 35, 38, 42, 46, Phalotris 239, 244
54, 70, 75, 79, 134, 139, 140, 142, Philippines 87, 91, 102, 107, 112, 113,
266 119, 153, 225, 236, 237, 240, 247,
Pachyrhachis problematicus 1, 2 256, 263, 269, 270, 286, 287
 Index 317

Philodryas 92, 93, 241, 243-245 prothrombin 40, 42, 43, 46, 54, 77, 86-88,
Philothamnus 93, 95, 245 90, 94, 120, 137, 139, 141, 143, 145,
phlegmon 172, 190 147, 160, 174, 177, 181, 192, 195,
Phoorsa 173 205, 206, 208, 211, 214
phospholipase A see PLA2 Protobothrops 35, 39-41, 44, 46, 224-
pigmy rattlesnake 216, 285 228, 285-287
Pilbara 264, 268 - flavoviridis 336 (Fig)
Pindos 276 Psammophis 6, 93, 246, 249, 164
pit viper 12, 21, 35, 39-41, 44, 46, 56, - lineolatus 336 (Fig)
158, 204, 205, 207, 208, 224, 225, Psammophylax 93, 246
228, 229, 277-280, 283-287 Pseudechis 29, 35, 143, 144, 266
PLA2 32-35, 38, 41, 45-47, 74, 79, 103, pseudexins 35
107, 113, 120, 134, 136, 139, 141, Pseudoboa 93, 246
154, 169, 179, 190, 205, 211, 217 Pseudocraste de Perse 179
plasmaferesis 81, 160, 177, 208, 215 Pseudocerastes 19, 179, 180, 274
plasmin 39, 43, 135, 162, 227 - persicus 336 (Fig)
platelets see PLT Pseudohaje 124, 125, 263
Platyceps 91, 238, 245, 246 Pseudonaja 23, 30, 35, 43, 140, 144, 145,
PLT 32, 38, 40-42, 74, 78, 79, 89, 91, 99, 146, 264, 266
116, 120, 121, 135, 136, 141, 160, ptosis 33, 66, 67, 75
162, 167, 174, 177, 182, 184, 188, Ptychophis 94, 246, 247
196, 197, 205, 209, 211, 215, 217, Puerto los Mazos 281
220, 221, 223, 224, 229 Puff adder 20, 29, 35, 41, 109, 161, 164,
Poecilopholis 100 272
Poland 19, 194 Pyrenean Mountains 275
Polemon 100, 254 Pyrenean Peninsula 243
Polillo 256, 286 Python reticulatus 5
Polinos 281, 274 Pythonodipsas 94
Polynesia 11, 270 Quang Binh 285
Polyodontognathus 269, 271 Queensland 266-268
Pontic adder 275 Queimada Grande 278
Popayan 261 Quinkes edema 56
Popeia 224, 284, 286, 287 racers 91, 237
Porthidium 209, 210, 212, 214, 284, 285 rainbow water snake 239
Porthidium ophryomegas 336 (Fig) rattlesnake 5, 6, 12, 15, 22, 29, 30, 34, 35,
Portugal 89, 275, 276 39-41, 44-46, 51, 54, 55, 63, 64, 66,
Praescutata 152, 271 75, 79, 189, 216-221, 280-282, 285
prairie rattlesnake 216 recurrence of symptoms 53, 69, 81, 193,
Prince of Wales Island 266 220, 222, 228
Proatheris 159, 160, 272, 274 red diamond rattlesnake 30, 39, 216, 281
prodromes of envenoming 73, 74 red-bellied black snake 29, 35, 143, 144,
proteases 32, 33, 39, 42, 44, 78, 126, 182, 266
186, 211 red-lipped snake 238
proteinases see proteases rednecked keelback 86
Proteroglypha 9, 10, 102 Reids criteria 193
318 Index

renal failure 33, 45, 46, 54, 68, 76-80, 81, Salvador 261, 276, 277
86-89, 105, 106, 129, 135-142, 145- San Estban 281
148, 150, 155, 156, 160, 164, 165, - Jos 282
167, 170-172, 175-179, 182, 183, 187, - Lorenzo Sur 282
188, 191-194, 197, 198, 206-208, 211, - Margarita 282
213, 215, 218, 220, 221, 223, 227, Sand horned viper 166
229 Sandotter 186
Reptilase 40, 211 Sangchur 104
Reptilia 4 Santa Catalina 280
Republic of South Africa 88, 89, 98, 100, So Paulo 126, 128
103, 109, 110, 112, 117, 124, 162, So Tom 112, 245, 257
164, 245 Saphenophis 92, 241, 247
resistance, vascular 32, 36-38, 76, 100, SarafEn Gedi 98
162 sarafotoxins 37, 38, 76
respiratory failure see ALI/ARDS Sarawak 239
rhabdomyolysis 45, 68, 79, 105, 106, 134, Sardinia 12
136-139, 142, 144, 145, 147, 148, Saudi Arabia 89, 124, 181, 262
155, 156, 171, 207, 208, 220, 226, saw-scaled viper see Echis
227 Sawyer extractor 63
Rhabdophis 9, 42, 85, 86, 88, 247 Scaddan 267
Rhamphiophis 6 Scotland 189
rhinoceros viper 161, 272 sea kraits 3, 9, 10, 14, 36, 45, 54, 61, 77,
Rhinoplocephalus 149, 266-268 133, 134, 152, 154, 128, 270
rhodostoxin sea snakes 3, 9, 10, 11, 12, 14, 28, 34, 36,
ringed brown snake 145, 266 40, 45, 54, 61, 69, 77, 102, 121, 133,
ringhals 15, 123, 257 134, 152-154, 268
rock viper 18, 19, 55, 183, 184, 186, 198, Senegal 13, 20, 88, 109, 112, 173, 253,
199, 276 257, 262, 273
Romans saw-scaled viper 42, 173, 273 Seram 263, 264
Romania 184, 186, 189, 274, 276 Serbia 186, 189
Rondonia 260 Serpent lunetes 112
Rossel 268 - arlequin 123
Rottnest 266 - corail 103, 126, 129
rough-scaled bush viper 272 - - dAfrique du Sud 103
rough-scaled snake 174, 268 - - dl Arizona 129
Russells viper see Daboia Serpent corail du Cap 103
Russia 11, 86, 184, 189, 247, 250, 275, - - fin 129
283 - darbre 87
Rwanda 162, 252, 256, 257, 271, 272 - - du Cap 88
Sabah 256, 284, 287 - de mer 152
Sahara 112, 166, 243, 262, 273 - des paltuviers 87
- horned (sand) viper 166 - jarretire 122
Sahel 273 - liane de Kirtland 90
Sakhalin 11, 184, 189, 275 - - du Cap 90
Salawati 264 - ratier brun 87
Salomonelaps 149, 267 - - des mangroves 87
 Index 319

- tigrer dAsie 86 - solenoglyphous 3, 8, 10, 30, 73, 159, 203

Serpentes 4 Solenoglypha see snakes solenoglyphous
serpins 44 Solomon Islands 149, 154, 265-267, 270
serum sickness 56, 70, 71, 81, 194, 222 Somalia 88, 112, 162, 167, 173, 238, 245,
Setekwa 268 250-254, 257, 263, 272-274
Shedao 283 Sonora Desert 280
shield-nose snake 102, 255 South African (western) coral snake 102,
shivering 74, 95, 160, 175, 187, 198, 206 255
shock South American bushmaster see Lachesis
- anaphylactic 47, 56, 65, 70, 71 South Carolina 47, 285
- circulatory 32, 36-38, 45, 47, 67, 71, 76, South China Sea 153, 270, 271
77, 80 Southern Caucasus 263
shore pit viper or mangrove viper 287 southern copperhead 29, 41, 44, 45, 204,
Sibau 270 276
Siberia 205, 283 Spain 89, 195, 275, 276
Siberian (Himalayan) pit viper 204 Spalerosophis 94, 247, 248
Sichuan 247, 284 speed of attack 5
Sicily 195, 275 spitting cobra 20, 36, 41, 44, 66, 111,
side-stabbing snakes 98 112, 114, 116, 123, 125, 257, 262,
sidewinder 216, 280 263
Sierra del Nido 282 Squamata 4
- Leone 263, 272 Sri Lanka 21, 47, 87, 91, 93, 104, 105,
- Madre Occidental 281 107, 112, 113, 119, 169, 171, 173,
- - Oriental 281 204, 205, 225, 235-237, 240, 243,
Simoliophis 1 255, 256, 262, 269, 270, 273, 283,
Simoselaps 150, 267 287
Sinai 98, 179, 252, 274 Stenorrhina 94, 248
Singapore 107, 113, 235, 236, 243, 256, Stephens banded snake 137
263, 269 steppe ribbon racer 246
Siphlophis 94, 247 Stiletto snakes 98
Siphnos 181, 274 Stockholm criteria 67, 193
Sistrurus 6, 51, 158, 172, 208, 215, 216, stone breaker 104
217, 119, 221, 224, 228, 285 Straits 264-266
- catenatus 336 (Fig) Sudan 89, 99, 109, 162, 173, 238, 245,
Sivas 274 246, 250, 253, 254, 257, 262, 263,
skaapsteker 93, 246 272-274
slender hog-nosed pitviper 284 Sulawesi 236, 263, 268, 287
slough 6 Sumatra 113, 225, 236, 247, 255, 256,
Slovakia 189 270, 287
Slovenia 89, 186 Sumbawa 113, 263
small-scaled snake 140 Surinam 248, 260, 280
smooth snake 85, 243 Surucucu 209
snakes, opistoglyphous 3, 8, 10, 30, 42, Suta 149, 150, 265, 267
85 Swaziland 253, 257, 258, 272
- proteroglyphous 3, 8, 10, 30, 102, 134,
153
320 Index

sweating 67, 74, 99, 105, 110, 115, 120, textarin 43

154, 155, 160, 163, 184, 190, 193, textilotoxin 35
196 Thailand 93, 113, 116, 121, 169, 207,
Sweden 11, 18, 189, 192 225, 228, 235-237, 239, 240, 243,
swelling 73, 191, 196, 205, see also 247, 255, 256, 263, 268-270, 273,
edema 279, 284-287
Switzerland 19, 186, 195, 275 Thalassophina 152, 271
Syria 181, 186, 196, 249, 263, 274, 275 Thalassophis 152, 271
system, hemocoagulation see Thamnodynastes 94, 250
hemocoagulation Thamnophis 94, 122, 250, 251
- cardiovascular see cardiovascular thanatosis 15
Taal 270 Thelotornis 13, 39, 40, 42, 85, 90, 251
tachycardia 74, 75, 99, 105, 124, 163, Thrasops 88, 94, 251
166, 167, 169, 170, 182, 184, 187, thread coral snake 129
191, 196, 219 thrombin 35, 39, 40, 42-45, 54, 68, 78,
Tachymenis 94, 248 86-88, 141, 143, 146, 162, 166-168,
Tagerza 180 174, 178, 181, 196, 205, 211, 217,
taicatoxin 38, 141 226, 227
taipan 28, 135, 141-143, 154, see also thrombocytopenia 41, 78, 86, 89, 138,
Oxyuranus 139, 142, 144, 146, 164, 167, 169,
taipoxin 35, 46, 141 170, 176, 187, 191, 197, 207, 213,
Taiwan 86, 104, 107, 112, 116, 119, 168, 219-223, 227-229
169, 205, 207, 225, 228, 237, 239, thrombotization 40
243, 247, 255-257, 262, 268-270, 273, Thung Song 287
282, 284-287 Tian Shan 275
Taiwan Russells viper 168 Tibet 158, 284, 287
Tajikistan 113, 273, 283 Tiburn 258, 281
Tamaulipas 262 Tic-Polonga 168
Tanahjampea 237 tiger grooved-neck keelback 42, 86, 87,
Tanganyika 122, 251, 255 247
Tanimbar 263, 264 tiger snake 38, 39, 52, 137, 140, 144, 149,
Tantilla 5, 94, 248, 249 250 see also Notechis, Telescopus
Tanzania 112, 159, 162, 238, 245, 246, timber rattlesnake 39, 41, 216, 220, 281
251-254, 256, 257, 262, 263, 271, Timor 268
272, 274 TNF 37
Taphrometopon 146, 249 Tobago 12
Tarbophis 94, 249 Togo 257, 263, 272
Tasmania 23, 134, 136, 138, 264, 265 tongue 6, 104, 115, 123, 124, 155, 187,
Taurus 275 191, 194, 196, 219, 226
Telescopus 94, 95, 249, 250 Torres Straits 266
Te-Nggano 154 Tortuga 282
Terciopelo 209 tourniquet 61, 63, 65, 205, 207, 212, 214
test, conjunctival 70 Toxicocalamus 150, 268
- dermal 70 toxins 13, 27-46
Texas 92, 93, 126, 217, 238, 240, 241, Trans-Pecos 276
251, 262, 276, 285 Transverse Volcanic Cordillera 282
 Index 321

tree black forest cobra 124 217, 221, 222, 240, 248, 250, 258,
Triceratolepidophis 224, 285 260, 262, 276, 277, 280-282, 285
Trigonocphale bouche rose 204 Uzbekistan 113, 181, 273-275
Trimeresurus 12, 15, 21, 35, 39-42, 44, Uzungwe mountain bush viper 159, 271
46, 69, 70, 76, 79, 158, 224-228, 282- variable mole viper 98, 252, 253
288 vascular resistance 38, 76, 162
- albolabris 337 (Fig) vasoconstriction 37, 99, 110
- gumprechti 337 (Fig) vasodilation 31, 36, 37, 46, 65, 76, 159,
- popeiorum 337 (Fig) 163, 170, 184, 185, 187, 190, 193,
- purpureomaculatus 337 (Fig) 194, 198, 217, 227
Trimorphodon 94, 251 vasospasm, coronary 99
trimucrotoxin 35, 46 Venezuela 23, 240, 241, 244, 245, 258-
Trinidad 12, 259, 260, 283 262, 277-280, 284
triwaglerin 42 venom components 29-47
Tropidechis 147, 148, 168 venomous garter snakes 122
Tropidolaemus 42, 224, 286, 287 ventilation (pulmonary, mechanical) 64,
- wagleri 337 (Fig) 66, 71, 75, 77, 88, 90, 103, 105, 106,
Tropidophiidae 2 108, 111, 118, 121, 122, 127-129,
tumor necrosis factor see TNF 135-145, 147, 148, 156, 160, 172,
Tunisia 181, 262, 273-275 175, 179, 183, 193, 198, 206, 213,
Turkey 18, 89, 181, 183-186, 198, 204, 224
250, 274-276 Veracruz 260
- Bulgar-Dagh Mountains 276 Vermicella 150, 268
- province of Sivas 274 vertigo 74, 99, 107, 110, 115, 123, 124,
- Taurus Mountains 275 137, 160, 167, 187, 192, 206, 219
Turkmenistan 113, 181, 273-275, 283 Victoria 264-267
turtle-headed seasnake 269 Vietnam 52, 86, 112, 113, 158, 205, 236,
twig snake 85, 90, 251 237, 239, 247, 255, 256, 263, 270,
Tyrol 274 271, 279, 282, 284-287
Uganda 112, 159, 162, 236, 238, 245, vine snake 90, 236, 244, 251
252, 253, 256, 257, 262, 263, 271, viper see Bitis, Daboia, Echis,
272 Macrovipera, Vipera
Ukraine 189, 275, 276 viper minute 180
Ular Lampeh 86 Vipera 2, 11, 18, 19, 29, 30, 34, 35, 37,
- Picung 86 41, 42, 44, 47, 74, 76, 158, 168, 181,
Ularburong 87 183, 184, 186, 188, 189, 195, 196,
Uluguru 252 198, 273-276
Umbrivaga 92, 241, 251 - albizona 340 (Fig)
Umi-Hebi 152 - ammodytes 338 (Fig)
Unechis 149, 266, 268 - aspis 338 (Fig)
United Arabian Emirates 273 - berus 338 (Fig)
United Kingdom 19, 192 - dinnicki 338 (Fig)
Uruguay 237, 239, 244, 245, 258, 280 - ebneri 339 (Fig)
Urutu 209, 278, 279 - kaznakovi 339 (Fig)
USA 17, 18, 21, 22, 51, 94, 126, 128, - latifii 340 (Fig)
129, 187, 194, 195, 204, 207, 216, - nikolskii 339 (Fig)
322 Index

- palestinae 339 (Fig) vomiting see nausea

- raddei 339 (Fig) von Willebrands factor 41, 142
- renardi 339 (Fig) Waglers pit viper 287
- seoanei 340 (Fig) Waglerophis 94, 251
- wagneri 340 (Fig) Walterinnesia 124, 125, 263
Vipre 158, 159, 161, 166, 168, 179, 180, water cobras 122, 255
183, 186, 188, 195, 196 water moccasin 204
- ammodytes 186 water snakes 92, 239, 251
- arboricole 159 West African carpet viper 173, 273
- aspic 195 western cottonmouth 14, 29, 41, 204, 277
- cornue 166 whip snake 91, 240, 243, 244, 246, 264,
- dAvicena 166 266
- de lAtlas 180 white-lipped green pit viper 225
- de Levant 180 white-lipped tree viper 224, 228, 285
- de McMahon 179 Wonambi 1
- de Palestine 196 Woodlark 268
- de Russell 168 Xenocalamus 100, 254
- des bambous 225 Xenochrophis 94, 251
- des Cyclades 180 Xenodon 94, 252
- des sables Perse 179 Xenodontinae 4
- du Gabon 161 Yamakagashi 86
- du Sahara 180 Yemen 173, 262
- hbraique 161 Yugoslavia 274, 275
- heurtande 161 Yunnan 285-287
- pliade 188 Zacatecas 262
viperid snakes 7, 9, 33, 39, 45, 74-76, Zambia 112, 162, 238, 239, 245, 246,
158, 166, 180, 186 252-254, 257, 262, 272
Viperidae 2, 4, 14, 28, 30, 31, 33, 34, 37, Zanzibar 109, 112, 246, 253
39, 41-45, 63, 64, 71, 74-77, 79, 80, Zhaoermia 224, 286, 288
113, 134, 157-159, 203, 210, 225, 271 Zimbabwe 103, 123, 162, 236, 246, 253-
Viperinae 5, 12, 14, 34, 37, 40, 45, 47, 255, 257, 262, 272
67, 69, 74, 80, 82, 158, 159, 181, 184, zmeja 183
271 zmija severna 188
Viridovipera 224, 286-288
Volga 283
 PICTURES

Agkistrodon contortrix, photo P. Velensky

Acanthophis antarcticus, photo V.T. Jirousek

Agkistrodon taylori, photo V.T. Jirousek

Agkistrodon bilineatus, photo V.T. Jirousek

324 Pictures

Ahaetula prasina, photo P. Velensky

Atheris nitschei, photo V.T. Jirousek

Atheris squamiger, photo V.T. Jirousek

Aspidelaps lubricus, photo P. Velensky

Atractaspis irregularis, photo V.T. Jirousek

 Pictures 325

Atropoides nummifer, photo V.T. Jirousek

Bitis nasicornis 1, photo V.T. Jirousek

Bitis arietans, photo P. Velensky

Bitis nasocornis, photo V.T. Jirousek

Bitis gabonica gabonica, photo V.T. Jirousek

Boiga cyanea, photo P. Velensky

326 Pictures

Boiga cyanea, photo V.T. Jirousek Bothrops alternatus, photo P. Velensky

Bothrops atrox, photo J. Valenta

Boiga dendrophila, photo V.T. Jirousek

Bothrops atrox, photo V.T. Jirousek

Bothriechis schlegelii, photo V.T. Jirousek
 Pictures 327

Bothrops neuwiedi, photo V.T. Jirousek

Cerastes cerastes, photo P. Velensky

Boulengerina christyi, photo V.T. Jirousek

Cerastes vipera, photo P. Velensky

Causus rhombeatus, photo V.T. Jirousek

Cerrophidion godmani, photo V.T. Jirousek

328 Pictures

Crotalus cerastes, photo P. Velensky

Chrysopelea ornata, photo V.T. Jirousek

Crotalus cerberus, photo V.T. Jirousek

Crotalus adamanteus, photo V.T. Jirousek

Crotalus durissus terrificus, photo P. Velensky

Crotalus atrox, photo V.T. Jirousek

 Pictures 329

Crotalus durissus unicolor, photo P. Velensky

Crotalus lutosus, photo V.T. Jirousek

Crotalus mitscheli stephensis, photo V.T. Jirousek

Crotalus helleri, photo V.T. Jirousek

Crotalus ravus, photo V.T. Jirousek

Crotalus horridus, photo P. Velensky

330 Pictures

Crotalus ruber, photo V.T. Jirousek Crotalus viridis, photo P. Velensky

Daboia russelli, photo V.T. Jirousek

Crotalus scutulatus, photo V.T. Jirousek

Dendroaspis angusticeps, photo P. Velensky

Crotalus tigris, photo V.T. Jirousek

 Pictures 331

Dendroaspis jamesoni, photo V.T. Jirousek Dispholidus typus, photo V.T. Jirousek

Dendroapis polylepis, photo P. Velensky Echis carinatus, photo J. Valenta

Echis carnatus, photo V.T. Jirousek

Dendroaspis viridis, photo P. Velensky
332 Pictures

Gloydius halys caraganus, photo V.T. Jirousek

Eristicophis macmahoni, photo V.T. Jirousek

Gloydius intermedius saxatilis, photo V.T.

Echis ocellatus, photo V.T. Jirousek Jirousek

Echis pyramidium pyramidium, photo V.T. Hemachtus haemachatus, photo V.T. Jirousek
Jirousek
 Pictures 333

Macrovipera mauritanica, photo P. Velensky

Hypnale sp., photo V.T. Jirousek

Macrovipera schweizeri, photo V.T. Jirousek

Langaha madagascariensis, photo P. Velensky

Malpolon monspessulanus, photo P. Velensky

Macrovipera lebetina obtusa, photo V.T. Jirousek

334 Pictures

Micrurus fulvius, photo V.T. Jirousek

Naja atra albinic form, photo V.T. Jirousek

Naja annulifera, photo V.T. Jirousek

Naja atra, photo V.T. Jirousek

 Pictures 335

Naja mossambica, photo V.T. Jirousek

Naja haje haje, photo V.T. Jirousek

Naja naja, photo V.T. Jirousek

Naja kaouthia, photo V.T. Jirousek

Naja oxiana, photo V.T. Jirousek

336 Pictures

Psammophis linoleatus, photo P. Velensky

Ophiophagus hannah, photo P. Velensky

Porthidium ophryomegas, photo V.T. Jirousek

Pseudocerastes persicus, photo V.T. Jirousek

Sistrurus catenatus tergeminus, photo V.T.

Jirousek

Protobothrops flavoviridis, photo V.T. Jirousek

 Pictures 337

Sistrurus miliarius, photo P. Velensky

Trimeresurus popeiorum, photo P. Velensky

Trimeresurus albolabris, photo V.T. Jirousek

Trimeresurus purpureomaculus, photo V.T.

Jirousek

Tropidolaemus wagleri, photo V.T. Jirousek

Trimeresurus gumprechti, photo V.T. Jirousek

338 Pictures

Vipera ammodytes montandoni, female, photo P.

Velensky
Vipera berus, male, photo P. Velensky

Vipera aspis atra, photo V.T. Jirousek

Vipera berus melanotic form, photo V.T. Jirousek

Vipera berus, female, photo P. Velensky

Vipera dinnicki, photo V.T. Jirousek

 Pictures 339

Vipera ebneri, photo V.T. Jirousek

Vipera palaestinae, photo V.T. Jirousek

Vipera raddei, photo V.T. Jirousek

Vipera kaznakovi, photo V.T. Jirousek

Vipera nikolskii, photo V.T. Jirousek

Vipera renardi, photo P. Velensky
340 Pictures

Vipera seoanei seoanei, photo V.T. Jirousek

Vipera latifii, photo V.T. Jirousek

Vipera wagneri, photo V.T. Jirousek

Vipera albizona, photo V.T. Jirousek