Schistosomiasis

Presentation contents
 Introduction.
 History & epidemiology.
 Types & Morphology.
 Life cycle.
 Pathogenesis.
 Immunology.
 Clinical features.
 Investigations.
 Treatment.
 Complications.
 Management of complications.
 Prevention & Control.

Schistosomiasis or
( Snail Fever ) is an
important cause of
disease in many parts
of the world, most
commonly in places
with poor sanitation.
School-age children who live in these areas are often
most at risk because they tend to swim or bath in water
containing infectious cercariae.
If you live in, or travel to, areas where Schistosomiasis
is found & are exposed to contaminated freshwater,
you are at risk.

Areas where human Schistosomiasis is found include:
S.Mansoni & S.Haematobium distributed throughout Africa.
There is risk of infection in freshwater in southern & sub-
Saharan Africa–including the great lakes & rivers as well
as smaller bodies of water.

In Sudan specially, due to
agriculture & irrigation of
cannels creating a favorable
environment for snails.
The highest Schistosoma
prevalence is in:
- Al-Jazeera state.
- White Nile state.
- River Nile state specially
after Marawi dam.

Transmission also occurs in the Nile
River valley in Sudan, Egypt & the
Maghreb region of North Africa.
South America: including Brazil,
Suriname, Venezuela Caribbean.
In areas of East of Asia:
S. japonicum found in Indonesia,
parts of China & Southeast Asia.
S.Mekongi found in
Cambodia & Laoss.
Intercalatum found in parts
of Central & West Africa.

.. Main types that affect humans ..

Schistosoma Haematobium:
- Causes urogenital Schistosomiasis.
- It is scattered throughout Africa, parts of Arabia,
the Near East, Madagascar and Mauritius.
Schistosoma Mansoni:
- Is mainly found in Africa & Madagascar.
- It was exported by the slave trade to parts of South
America, the Caribbean & Arabia, where permissive
snail intermediate hosts were present.

First discovered in JAPAN, Nowadays is found
in China, the Philippines & Sulawesi.
There’s also a small focus in the Mekong river on
the east border of Thailand caused by Schistosoma
Mekongi.
Schistosoma Mansoni & S. japonicum
cause disease of the bowel & liver.
Schistosoma Intercalatum.

Adult worms in humans reside in the mesenteric venules
in various locations, which are specific for each species:
S. Japonicum is more often in small intestine.
S. Mansoni occurs more often in the superior
mesenteric veins draining the large intestine.
S.Haematobium most often occurs in the venous plexus
of bladder & uterus, but it can also be found in the rectal
venules.

S.Intercalatum: which found in urine & it’s
related to S.Haematobium.
S.Bovis: which infects cattle.
S.Makongi: similar to S.japonicum.

Adult schistosomes are white
greyish worms.
( 6 – 28 ) mm long & in breadth
of ( 0.25 – 1 ) mm.
Schistosomes have separate
sexes ( male & female ).
Both have an oral sucker
opening into the alimentary tract,
& a posteriorly situated sucker.

Flat in shape.
It has a large ventral groove
( gynaecophoric canal ), encloses
the female during pairing.
The digestive system consists of
short esophagus opening into an
intestine.
The male reproductive system
comprises 4 or 5 pairs of testes.

Cylindrical in shape.
More longer, slender &
much darker color than
male.
The digestive system is
similar to that of male.
The reproductive system
consist of a pear shaped
ovary in the mid body line.

The different schistosomes spices use different
spices of snails as intermediate host:

Stages of life cycle & their time frames:
(1) Cercarial invasion & Schistosomular migration.
(2) Maturation of schistosomes, pairing
& commencement of egg-laying.
(3) Established infection with continuous egg-laying.
(4) Late stages & complications.

The clinical complement
of cercarial dermal invasion
is a schistosome ( cercarial
or allergic ) dermatitis
lasting for 24 - 48 hours.
The pathophysiological
response is the initiation
of the 1st mechanisms of the immune response
with marked eosinophilia & an antibody-dependent
cell mediated cytotoxic response involving IgG.

After 2 to 16 weeks after cercarial invasion,
during the migration of schistosomulae, their
maturation, pairing & initiation of egg-laying,
the clinical manifestations of acute toxemic
Schistosomiasis ( katayama syndrome ) may arise.
Worm or egg antigens produce a marked antigenic
stimulus with rapidly rising antibody levels & an
increase in serum IgG, IgA & IgM levels.

Then circulating antigen antibody complexes are
found & may be deposited in glomeruli, producing
immune complex glomerulopathy.
The whole clinical picture is one resembling
the acute serum sickness syndrome.
From 2 months onwards the stage of established
infection occurs, with continuous egg-laying
associated with the classical symptoms &
signs of established Schistosomiasis.

SEAs from miracidia in the eggs provoke a T
lymphocyte-mediated host response which
in time result in the characteristic granuloma
with eosinophils prominent in the destruction
of the eggs.
After some years, change in clinical symptoms
& physical sign appear, & there is superimposi-
tion of late stage complication such as:
Obstructive Uropathy, Hydronephrosis
& Pyelonephritic renal failure.

Overtime T suppressor lymphocyte & antibody
blockade diminish the host immune response
fibroblasts stimulate collagen production and
fibrotic complications involving a variety of
anatomical sites will developed ( e.g. periportal
hepatic fibrosis and obstructive Uropathy ).

Acute Schistosomiasis
It is a systemic hypersensitivity reaction against the
migrating schistosomulae and/or the onset of egg
production, occurring within a few weeks to months
after a primary infection.
The onset is sudden, with:
- Fever & Myalgia.
- Fatigue & Malaise.
- Nonproductive cough.
- Elevated IgE.
- Patchy infiltrates on chest X-Ray.

Most patients recover spontaneously after 2-10
weeks but some develop a persistent & serious
illness with:
Weight loss.
Dyspnea.
Diarrhea.
Diffuse abdominal pain.
Toxemia.
Hepatosplenomegaly.
Generalized rash.
Intense infections are occasionally fatal.

Katayama fever caused by S.japonicum infections can
present as serious & sometimes fatal, serum sickness-
like disease which possibly results from the early
release of large quantities of egg antigens that cross-
reacts with antibodies to schistosomulae, resulting in
immune complexes that cause hypertrophy of lymph
reticular tissue characterized by:
Fever.
Hepatosplenomegaly.
Cachexia.
Which may evolve directly to severe hepatosplenic
fibrosis & portal hypertension.

Chronic Schistosomiasis:
It is largely associated with the granulomatous
& fibrotic responses to Schistosoma ova during
mature infections and mainly include:
A- Urinary Schistosomiasis.
B- Intestinal Schistosomiasis.

Urinary Schistosomiasis:
The eggs of S. haematobium provoke granulomatous
inflammation, ulceration and pseudopolyposis of the
mucosa & sub mucosa of the bladder and the ureters
Common early symptoms include Dysuria, Urinary
frequency & urgency, Terminal hematuria.
In endemic areas ( Terminal hematuria ) is the “red
flag of Schistosomiasis” in children between the age
of 5 and 10 years old.

Chronic infection may lead to:
- Obstructive Uropathy.
- Renal failure.
- Bladder cancer ( SCC ).
Intestinal Schistosomiasis:
The eggs of S. Mansoni, S. japonicum & other species
migrate through the intestinal wall where they provoke
mucosal granulomatous inflammation, pseudopolyposis,
micro-ulcerations & superficial bleeding.
Most lesions are situated in the large bowel
& the rectum.. small bowel pathology is rare.

The human immune response in
Schistosomiasis is primarily due to
antibody-dependent cell-
mediated cytotoxicity.
So based on the mixture of preformed
circulating antibodies, cytokines & the
responsiveness of lymphoid cells in
the peripheral blood.

4 to 6 weeks after a primary infection, schistosome-
specific immunoglobulin is produced that, together
with complement, eosinophils, macrophages,
platelets & mast cells is able to
form complexes & attack
schistosomules.
Acute Schistosomiasis:
It occurs in individuals who
have no previous history of
exposure & become infected
after travelling into an endemic area.

There is a remarkable level of peripheral-
blood mononuclear cells (PBMCs) produce large
quantities of tumor-necrosis factor (TNF),
interleukin-1 (IL-1) and IL-6, reflects a dominant
T helper 1 (TH1), rather than TH2 response.

There was a correlation
between elevated levels
of nitric oxide ( NO ) &
disease severity, which
indicates that a combination
of reactive oxygen & nitrogen
intermediates might have a
role in acute disease.

TH2 responses seem to have
a crucial role in modulating
potentially fibrosis life-
threatening chronic disease.
The main TH2 cytokine that
is responsible for fibrosis
is IL-13.
Chronic Schistosomiasis:

It has been recognized that the egg stage of
the schistosome is responsible for inducing
the TH2 response.
TH2 induces CD4+ T-cell response that
initiates the development of granulomatous
lesions, which are composed of collagen fibers
& cells, including macrophages, eosinophils
& CD4+ T cells around the individual eggs.

Physical Examination:
Physical findings vary with the stage of illness, worm
burden, worm location, and end organ involvement.

Clinical Features:
swimmer’s itch
Acute manifestations:
Generalized lymphadenopathy.
Pruritic rach ( swimmer’s itch ).
Mild Fever & Headache.
Hepatosplenomegaly.
Katayama syndrome ( ).
Diarrhea.
Urticaria.
Cough.

Continue Acute manifestations:
- Right upper quadrant tenderness.
- Decreased physical performance.
- Growth retardation.
- Anorexia.
- Malaise.
- Myalgia. Chronic manifestations:
- Pedal Edema.
- Portal HTN.
- Anemia.
- HTN.
- Renal Failure.
- Easy fatigability.
Pedal Edema

Abdominal pain.
Abdominal distention.
Signs of malnutrition.
Hepatosplenomegaly.
Distended abdominal veins.
Ascites, Pallor, & Dysentery.
Intestinal Schistosomiasis:

Cardiopulmonary
Schistosomiasis:
Cor pulmonale with signs of right HF.
Larval pneumonitis with cough.
Mild wheezing.
Low grade fever.
Palpitations.
Dyspnea on exertion.
Hemoptysis.

Focal & generalized seizures.
Headache.
Spinal cord lesions.
Symptoms of increased
intracranial pressure ( ICP ).
CNS Schistosomiasis:
Focal
Seizure
Generalized Seizures

Dysuria.
Urinary frequency.
Terminal Hematuria.
Burning in micturition.
Urinary frequencyHematuria

Genital Schistosomiasis:
- Postcoital bleeding.
- Genital ulcerations.
- Nodular lesions of the cervix & vagina.
- Hypertrophic lesions.
- Pelvic pain.

Laboratory Diagnosis & Imaging
Samples:
- Stool.
- Urine.
- Serum.
Macroscopic:
- Stool speciment ( may be dysenteric ).
- Urine speciment ( may be terminal hematuria ).

Microscopically:
1- Demonstration of parasite eggs in stool or urine is
gold standard test for diagnosing Schistosomiasis.
2- The sensitivity my be low especially with light
infection & take 6 weeks for eggs to be detect
after the initial infection.
3- S.Haematobium eggs are usually found in urine
but my also be present in stool.
4- S.Mansoni & the other intestinal schistosomes,
S.japonicum, S.Merangi & S.Intercalatum are
found in stool.

URINE DIPSTICK:
S.Haematobium infections are usually associated
with hematuria on dipstick testing.

Full blood count:
1- May show an eosinophilia which is frequently
marked during the acute stage of infection.
2- Anemia patient may also be seen due to chronic
blood loss from the urinary or intestinal tract.
3- Pation with hepatosplenic Schistosomiasis my have
thrombocytopenia secondary to splenic sequestration.
Diagnosis can also be made by demonstrating eggs in
tissue biopsy specimens from the rectum, liver, bladder
or cervix depending on the site of infection.

Antigen detection:
 Schistosoma the antigen weaks are present in
the serum & urine.
 To antigen referred to as circulating anodic antigens
(CCA) & circulating cathodic antigens ( CCA ) can be
detected in laboratory sensitivity of these test
depend on largely & intensity of infection.
Antibody test:
 Schistosoma antibodies can be detected by enzyme
linked lmmunosorbent assay ( ELISA ).
 it is application is limited as these antibodies
will only appear after 4-6 weeks.
 present of IgE antibody is marked of chronic active
disease.

Polymerase chain reaction PCR:
Specific & highly sensitive detection of Schistosoma.
DNA in urine, stool & serum.
Advantage able to diagnosis Schistosomiasis in all
stage of infection.

( For S.Haematobium )
look for signs of hematuria, Dysuria, & Eosinophilia.
These should be enough to suggest a diagnosis
for those living in endemic regions.
A plain X-ray for the abdomen may show
the calcification of the urinary bladder.
An I.V.P should be done to determine the extent
of the disease in the kidneys & ureters.
The changes in the urinary system are usually
reversible on treatment.

Fatigue.
Abdominal pain even without dysenteric symptoms
in endemic regions should suggest a diagnosis.
Dysenteric symptoms.
A chest x-ray is indicated in a patient who comes in
with signs of pulmonary hypertension ( mottling of
the lungs is seen ).
( For S.Mansoni )

A Barium meal or endoscopy is used to detect any
varices.
A liver biopsy is indicated to show periportal fibrosis.
splenic-venoprtography may be done to outline the
portal system.

 Praziquantel affective against
all adult schistosome species
& it has no side effects.
 In the treatment of a
patient of S. Haematobium or
S. Mansoni or S. Intercalatum
a single oral dose ( 40 mg/kg ).
 But the S.japonicum total dose
is ( 60 mg/kg ), Best given after
food.
 Cure rate is 80% !!
With acute infection
corticosteroids may
..be given

Oxamniquine Only against S.Mansoni.
- High cure rates ( 60 - 90% ).
Side effects: dizziness, drowsiness, headache.
- Should not be given during the first 4 months
of pregnancy.
Metrifonate against S.Haematobium.
- Artemisinin.
- Hycanthone ( Etrenol ).
- Niridazole ( Ambilhar ).
- Lucanthone ( Mirasil D ).
OtherDrugs

Complications:
1- pulmonary Schistosomiasis:
Chronic S.Mansoni causing obliterative arteries
which lead to :
- Pulmonary hypertension.
- Increase right heart pressure.
- Right arterial dilatation.
- Right ventricular hypertrophy.
2- Glomerularnephritis:
Due to deposition of immune complex in the renal
glomeruli. May be asymptomatic or manifested as
nephrotic syndrome.

3- Genital:
- In female lead to infertility.
- In male causing hemospermia.
4- Neuroschistosomisis:
S.Haematobium & S.Mansoni caused spinal
cord & transverse myelitis.
Others:
- Paraplegia.
- Pain or loss of sensation.
- Skin rash.
- Personality change.
- Confusion.

Complication of Schistosomiasis in GIT :
Gastrointestinal bleeding this case in patient with
nonvariseal upper gastrointestinal bleeding induced
by gastric & duodenal involvement of Schistosoma
Mansoni which unique case sever & recurrent upper
gastrointestinal bleeding was induced by central
ulceration of gastric pseudopolypoid & duodenal
polypoid lesions.

• portal hypertension as complication are due to
mechanical obstructive pathology resulting from
periportal fibrosis where eggs are still found.
• Hepatitis due to chronic S.Mansoni infected patient
co infected with hepatitis B or C are prone to have
clinically more sever infection prior parenteral
treatment for Schistosomiasis my also have
substantially increased risk for hepatitis.

Complication of Schistosomiasis in pregnancy:
1- Associate with anemia and low birth weight.
2- High risk of ectopic pregnancy.
3- Pregnancy complication from uvular or fallopian
granuloma.
Schistosomiasis-associated Bladder Cancer:
Bladder cancer diagnosis & mortality are elevated in
affected area. Risk of bladder cancer appear to be high
in smokers due to chronic irritation of bladder lining
allowing it to be exposed to carcinogens from smoking.

Bleeding form esophageal varices
may be treated systematically with
β-blockers, endoscopy, Splenectomy,
or porta caval shaunts.
In advanced urinary Schistosomiasis
destructed & Non-functional kidneys
may have be removed.

Topical steroid & oral antihistamines can
provide symptomatic relief for adversarial
dermatitis.
katayama fever is primarily treated with
corticosteroids, for example: Prednisolone
40 mg daily, for 5-14 days, to suppress the
hypersensitivity reaction.
The treatment should be followed be
Praziquantel to eliminate the adult worms.

Neuro anastomosis requires specialized
care, again with corticosteroids and if
necessary anticonvulsants prior to
Praziquantel treatment.

Mass Drug Administration aims to:
1- Reducing morbidity & mortality rate due to the infection.
2- Prevent new infection by limiting transmission through
reduction of the overall prevalence in the population.
3- Reduction in excretion of schistosome eggs.
The administration
of drugs to whole
populations
irrespective
of disease status is
referred to as Mass
Drug Administration
( ).

Prevention:
1- Early diagnosis &Treatment.
2- Snails Control.
3- Health Education & Community Participation.
4- Water Supply & Environmental Sanitation.
5- Capacity building.
Control:
Is dominated by chemotherapy & molluscicides.

Schistosomiasis

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