The term actinomycosis implies disease produced by endogenous, anaerobic, or microaerophile, Gram-positive, nonspore-forming bacteria, belonging to the families Actinomycetaceae and Propionibacteriaceae, of the order Actinomycetales; and Bifidobacteriaceae, of the order Bifidobacteriales.1 Their normal habitat is human or animal mucosal surfaces, with considerable host specificity, from the mouth to the upper respiratory, gastrointestinal, and female genital tract. Species known to cause disease in humans include A. israelii, Actinomyces naeslundii, Actinomyces gerencseriae, Actinomyces viscosus, Actinomyces odontolyticus, and Actinomyces meyeri, as well as Propionibacterium propionicum and Bifidobacterium dentium. The disease in most cases is mixed with other microorganisms sharing the same habitat, so it should be considered a synergistic infection, with the Actinomyces playing the role of guiding organism, defining the course, the symptoms, and the ultimate prognosis. Accompanying organisms may vary in number, from one to nine different species, and may include coagulase negative staphylococci, Staphylococcus aureus, α- and β-hemolytic streptococci, microaerophile and anaerobic streptococci, Fusarium and Bacteroides spp., and even Propionibacterium sp. other than P. propionicum.1 This concomitant flora may be in part responsible for the disease course. If pyogenic bacteria are involved, such as S. aureus or β-hemolytic streptococci, the lesion will be acutely inflammatory and painful. If, on the contrary, anaerobes predominate, the course will be subacute and insidious. A distinctive more chronic course is seen when A. israelii or A. gerencseriae is accompanied by Actinobacillus actinomycetemcomitans. In recent years, with better culturing techniques, more than one Actinomyces have been isolated from one single lesion in several patients, stressing the possibility that single bacterial isolation, common in the past, was a technical artifact.
The infection has its portal of entry at a break on a mucous membrane. Most cervical and facial cases originate from periapical abscesses or after dental procedures. Actinomyces bacteremia seems to occur quite commonly after dental procedures.2 Thoracic cases represent involvement of the chest wall by continuity either from pleural or lung disease acquired by obstruction or aspiration. The same mechanism of spreading applies to disease of the abdominal wall, secondary to gut or genital pathology, following appendicitis, diverticulitis, surgery, or trauma. Perineal disease occurs as a consequence of involvement of the internal organs of the pelvis, often secondary to use of an intravaginal device or IUD. The only exception to the endogenous origin of the infection is hand involvement that follows fist or bite trauma.3
In tissue, the bacteria cluster in filamentous aggregates, the so-called sulfur granules (grains; see Table 185-1). They are commonly surrounded by acute and chronic inflammation, usually neutrophils, granulation tissue, and fibrosis. Granuloma formation is unusual. The fistula formation may give way to drainage of granules, their presence at once should not be considered specific for this disease.