ACTINOMYCOSIS

DR AMITHA G, BDS, MDS
ORAL AND MAXILLOFACIAL PATHOLOGY
 Actinomyces species are classified as anaerobic, gram positive and
filamentous bacteria.
 It is a chronic granulomatous suppurative and fibrosing disease
caused by anaerobic or microaerophilic gram-positive nonacid fast,
branched filamentous bacteria.
 Most of the species isolated from actinomycotic lesions have been
identified as A. israelii, A. viscosus, A. odontolyticus, A.naeslundii
or A. meyeri.
 These microorganisms have been identified in dental plaque, dental
calculus, necrotic pulp, and tonsils.
 The usual pattern of this disease is one characterized chiefly by the
formation of abscesses that tend to drain by the formation of sinus
tracts.
 pus from the abscesses is examined on a clean glass slide, it shows
the typical ‘sulfur granules’ or colonies of organisms, which appear
in the suppurative material as tiny, yellow grains.
 Another infection that produces this type of sulfur granules is
botryomycosis.
 Actinomycosis is classified anatomically according to the location
of the lesions:
1. Cervicofacial
2. Abdominal
3. Pulmonary forms.
 Actinomycete is a common inhabitant of the oral cavity

 Thus, the organisms may be cultured from carious teeth, nonvital
root canals, tonsillar crypts, dental plaque, calculus, gingival sulcus,
and periodontal pockets.
 The pathogenesis of actinomycosis is not entirely known.
 lt an endogenous infection and not communicable.
 It does not appear to be an opportunistic infection in a situation of
depressed cell-mediated immunity.
 Trauma seems to play a role in some cases by initiating a portal of
entry for the organisms, since they are not highly invasive.
 Thus the extracted socket, periodontal pocket, nonvital tooth, or
mucosal abrasion may act as the portal of entry for the infection.
Epidemiology
Infection occurs throughout the lifetime with peak incidence in the
middle age.
 Males > females.
 Incidence has decreased presently due to improved oral hygiene and
antibiotics.
Pathogenesis.
 The disruption of the mucosal barrier is the main step in the invasion
of bacteria.
 Initial acute inflammation is followed by a chronic indolent phase.
Lesions usually appear as single or multiple indurations.
 Central fluctuance with pus containing neutrophils and sulphur
granules is diagnostic of the disease.
 The fibrous walls are typically described as woody.
 It occurs in association with HIV infection, transplantation,
chemotherapy, herpes, and cytomegaloviral ulcerative mucosal
lesions. Reported in osteoradionecrosis and in patients with systemic
illness.
Clinical Features.

 Cervicofacial actinomycosis is the most common form of this
disease
The organisms may enter the tissues through the oral mucous
membranes and may either remain localized in the subjacent soft
tissues or spread to involve the salivary glands, tongue, very rarely
gingiva, bone or even the skin of the face and neck, producing
swelling and induration of the tissue.
These soft tissue swellings eventually develop into one or more
abscesses, which tend to discharge on skin surface, rarely a mucosal
surface, liberating pus containing ‘sulfur granules’.
The skin overlying the abscess is purplish red, indurated and has the
feel of wood or often fluctuant.
It is common for the sinus through which the abscess has drained to
heal, but because of the chronicity of the disease, new abscess
develope and perforate the skin surface. Thus the patient, over a
period of time, may show a great deal of scarring and disfigurement
of the skin.
The infection of the soft tissues may extend to involve the mandible,
or less commonly, the maxilla which results in actinomycotic
osteomyelitis.
If the bone of the maxilla is invaded, the ensuing specific
osteomyelitis may eventually involve the cranium, meninges, or the
brain itself. Once the infection reaches the bone, the destruction of
the tissue may be extensive.
Such destructive lesions within the bone may occur or localize at the
apex of one or more teeth and simulate a pulp related infection such
as a periapical granuloma or cyst.
Abdominal actinomycosis
 Its an extremely serious form of the disease and carries a high
mortality rate.
 Generalized signs and symptoms of fever, chills, nausea and
vomiting, intestinal manifestations develop, followed by symptoms
of the involvement of other organs such as the liver and spleen.

Pulmonary actinomycosis
 Produces similar findings of fever and chills accompanied by a
productive cough and pleural pain.
 The organisms may spread beyond the lungs to involve adjacent
structures.
Histologic Features.
 lesion of actinomycosis, either in soft tissue or in bone, is
essentially a granulomatous showing central abscess formation
within which may be seen the characteristic colonies of
microorganisms.
 These colonies appear to be floating in a sea of polymorphonuclear
leukocytes, often associated with multinucleated giant cells and
macrophages particularly around the periphery of the lesion.
 The individual colony, which may appear round or lobulated, is
made up of a meshwork of filaments that stains with hematoxylin,
but shows eosinophilia of the peripheral club shaped ends of the
filaments.
 This peculiar appearance of the colonies, with the peripheral
radiating filaments, is the basis for the often-used term ‘ray fungus.’
 The tissue surrounding the lesion exhibits fibrosis.
 Methenamine silver stain can demonstrate the organisms better.
Diagnosis.
 It should be differentiated from osteomyelitis caused by other
bacterial and fungal organisms and soft tissue infections caused by
staphylococcus.
 The diagnosis of actinomycosis depends not only upon clinical
findings in the patient and the demonstration of the organisms in the
tissue section or smear, but also upon their culture.
Brown review of 181 cases of actinomycosis, the organisms are difficult to culture.

Of the 67 cases in which culture was attempted, the organism was isolated in only
16 instances. Various organisms isolated are A israelii, A.naeslundii, A.
odontolyticus, A. viscosus, A. meyeri, A. gerencseriae, and Propionibacterium
propionicum.
They are established but are a less common cause of the disease. Most
actinomycosis is polymicrobial.
Actinobacillus actinomycetemcomitans, Eikenella corrodens, Enterobacteriaceae
and species of Fusobacterium, Bacteroides, Capnocytophaga, Staphylococcus and
Streptococcus are commonly isolated depending upon the site of infection.
Treatment and Prognosis.
 The treatment of this disease is difficult and has not been uniformly
successful.
 Long standing fibrosis cases are treated by draining the abscess,
excising the sinus tract with high doses of antibiotics.
 Long term high dose penicillin, tetracycline and erythromycin
have been used most frequently, but the course of the disease is still
often prolonged,
 In addition to this surgical drainage of the abscesses and excision
of sinus tract is necessary to accelerate healing
Neville:
Histopathologic Features
 The tissue removed from areas of active infection demonstrates a
peripheral band of fibrosis encasing a zone of chronically inflamed
granulation tissue surrounding large collections of
polymorphonuclear leukocytes and, with luck, colonies of
organisms.
 The colonies consist of club-shaped filaments that form a radiating
rosette pattern.
 With hematoxylin and eosin (H&E) stains, the central core stains
basophilic and the peripheral portion is eosinophilic.
 Methenamine silver stains demonstrate the organisms well.

 If the colonies of actinomycetes become displaced from the exudate,
then a rim of neutrophils typically clings to the periphery of the
organisms.

ACTINOMYCOSIS

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ACTINOMYCOSIS