Organism: Actinomyces are slow-growing, filamentous, gram-positive non acid-fast bacteria whose cell walls contain muramic and diaminopimelic acids. Actinomyces ssp. are either facultative anaerobes or strict anaerobes. On an enriched solid medium such as brain-heart infusion agar or thioglycollate broth at 37 degrees C, they produce initial microcolonies composed of filaments that, after 24 to 48 hours, fragment into diptheroids, short chains, and coccobacilli. The filaments branch and are roughly 1 micrometer in diameter. Reproduction is by bacterial fission, never by spores or budding. Actinomyces spp. were at one time thought to be fungal organisms. This was based primarily on the branching morphology and mycelial-like appearance of the organisms in sulfur granules. Actinomyces are prokaryotic bacteria, lacking the nuclear membranes and mitochondria of eucaryotic organisms such as fungi.
Sulfur granules represent a conglomeration of microorganisms that forms only in vivo. They are usually yellow, but can be white, pinkish gray, gray or brown. Granules may be identified in draining sinus tracts or other purulent material. Identification of actinomycotic sulfur granules from clinical material other than tonsils implies a pathologic state. Because these organisms are normal inhabitants of the oral cavity and female genital tract, identification of the organisms by culture from sputum, bronchial washings, and cervicovaginal secretions is of little significance. The microbiologic identification of Actinomyces ssp. occurs only in a minority of cases. Identification is usually make on the basis of gram stain and direct immunofluorescence.
Disease: Most cases of actinomycosis occur between the ages of 15 and 35 years. The infection rate in males is two to three times the rate in females. Actinomycosis in humans is caused primarily by A. israelii. Actinomyces naeslundii, A. odontolyticus, A. viscosus, A. meyeri and Propionibacterium propionicus are less frequent causes of actinomycosis. Most are endogenous flora of mucous membranes. A. israelii can be routinely found in the oral cavity, and is often cultured from the gastrointestinal tract, bronchi and female genital tract. Most actinomycotic infections are believed to be polymicrobial [Weese 1975], Actinobacillus actinomycetemcomitans, Eikenella corrodens, Fusobacterium, Bacteroides, Capnocytophaga, Staphylococcus, Streptococcus and Enterobacteriaceae species have been isolated in actinomycotic infections [Russo 1995].
Disruption of the mucosal barrier is a pivotal step in the pathogenesis. Actinomycosis spreads contiguously in a slow but progressive manner and ignores tissue planes. Multiple pyogenic lesions become joined by interconnecting sinuses; draining sinus tracts can erupt to the skin surface. Organisms are contained in the pyogenic or granlomatous lesions and within granules in the sinus channels.
Oral-Cervicofacial Actinomycosis: Oral-cervicofacial disease is the most common type of actinomycosis. Antecedent conditions associated with oral and cervical-facial disease are neglected dental care with a history of dental decay, tooth extractions, other oral surgical procedures, jaw fracture or other nonsurgical trauma [Lerner 1988]. In many cases, no underlying antecedent condition is found. The most common presentations can involve a soft tissue swelling, abscess, or mass lesion. Pain, fever and leukocytosis may or may not be present. The skin over the affected area becomes swollen and discolored. Pyogenic abscesses may develop, with the formation of interconnecting sinuses that contain granules. The bacteria can spread to bone to produce osteomyelitis. The most common location for actinomycosis is the perimandibular region. The classic and most commonly occurring lesion occurs at the angle of the jaw. Involvement of muscles of mastication frequently occurs, resulting in trismus.
Thoracic Actinomycosis: Approximately 15 percent of actinomycosis cases involve the thorax. Aspiration of the infectious agent or extension of cervicofacial actinomycosis may lead to pulmonary infection. The symptoms are mild fever, chest pain, weight loss and less commonly hemoptysis. A cough may be present, and when cough occurs, it produces purulent sputum. The clinical presentation is an indolent, slowly progressive process. The infection typically involves some combination of pulmonary parenchyma and pleural space, any lobe may be involved. The usual radiological appearance is either a mass lesion or pneumonitis with or without pleural involvement. Cavitary disease and hilar adenopathy may be present. As the infection proceeds, lung tissue is destroyed, sinus tracts develop and invasion of the ribs or vertebrae may occur. The sinus tracts can extend to the chest wall, and draining sinuses and soft tissue masses can form. Thoracic actinomycosis can be mistaken for malignant disease or with tuberculosis, nocardiosis, histoplasmosis, blastomycosis, cryptococcosis, mixed anaerobic infection, bronchogenic carcinoma, lymphoma and mesothelioma.
Abdominal Actinomycosis: Abdominal infection is initiated by a perforation of the intestinal mucosa, most often resulting from a rupture appendix, diverticulitis, foreign body perforation of the transverse or sigmoid colon, peptic ulcer or gastrectomy. The proportion of reported cases of actinomycosis that involve the abdomen ranges greatly from study to study, with a range of 0 to 63 percent [Russo 1995]. Appendicitis, particularly with perforation, is the most common predisposing event and in one study was associated with 65 percent of the cases of abdominal actinomycosis [Deshmukh 1986]. Hematogenous dissemination, extension from the thorax or ascension from the vagina through the cervix are other portals of entry. The symptomatology is determined by the location of the lesion and the organs involved. Symptoms associated with abdominal actinomycosis include fever, weight loss, change in bowel habits, abdominal pain or sensation of mass. Abdominal actinomycosis can present as an abscess or as a mass lesion that is often fixed to the underlying tissue. Sinus tracts with drainage may develop. Perirectal or perianal disease may occur, with single or multiple perianal abscesses and sinus tract formation. The liver, gallbladder, and kidney may also be involved. Hepatic infection was reported to be present in 19 of 122 cases of abdominal disease [Putman 1950]. Single or multiple abscesses or legions suggesting neoplasia are the typical presentation. Liver enzymes may be normal.
Pelvic Actinomycosis: Pelvic actinomycosis may be associated with any type of intrauterine contraceptive device or with an intra-abdominal portal of entry. Presentation is indolent with fever, weight loss, abdominal pain, and abnormal vaginal bleeding or discharge. Pelvic masses, and tubo-ovarian abscesses may occur. The disease may involve ureters and bladder.
Disseminated Disease: Infection may spread hematogenously and involve the lungs, liver, kidneys, brain, spleen and soft tissues of the extremities. Disease can disseminate from any location.
Treatment: In the pre-antibiotic era, surgical removal of infected tissue was the only available treatment. Actinomyces spp. are sensitive to penicillin, but to avoid relapses, it is necessary to treat this disease both with high doses and for a prolonged period of time. Tetracycline, erythromycin, minocycline and clindamycin can be used for patients who are allergic to penicillin.
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