Etiologic agents

Actinomycosis is an infectious syndrome caused by anaerobic or microaerophilic bacteria, primarily from the genus Actinomyces. It is most commonly caused by Actinomyces israelii. However, Actinomyces naeslundii, Actinomyces odontolyticus, Actinomyces viscosus, Actinomyces meyeri, and Actinomyces gerencseriae are less common causes of infection. Advances in microbiologic taxonomy, using genotypic methods such as comparative 16S ribosomal RNA (rRNA) or sequencing of alternative genes, have led to the identification of many new Actinomyces species from both human and animal specimens. Presently 46 species and 2 subspecies have been recognized (http://www.bacterio.cict.fr/a/actinomyces.html). Although the syndrome of actinomycosis can be caused by these more recently described agents, most of the infections are not “classic” actinomycosis. Infections due to Actinomyces neuii have been increasingly recognized. Nearly all of actinomycotic infections are polymicrobial in nature. Aggregatibacter (formerly Actinobacillus) actinomycetemcomitans, Eikenella corrodens, Fusobacterium, Bacteroides, Capnocytophaga, Staphylococcus, Streptococcus, and Enterobacteriaceae are commonly co-isolated (“companion organisms”) with the agents of actinomycosis in various combinations depending on the site of the infection.

Epidemiology and pathogenesis

The etiologic agents of actinomycosis are members of the normal oral flora and are often present in bronchi and the gastrointestinal and female genital tracts. Although males have a higher incidence of infection (perhaps due to more frequent trauma and poorer dental hygiene), actinomycosis occurs in all age groups and geographic locations. Disruption of the mucosal barrier is the critical step for the development of actinomycosis. Subsequently, local infection may ensue and once established, if untreated, spreads contiguously ignoring tissue planes in a slow, progressive manner. Although acute inflammation may initially occur at the site of infection, the hallmark of actinomycosis is the characteristic chronic, indolent phase. This stage is manifested by lesions that usually appear as single or multiple indurations. Central necrosis develops that consists of neutrophils and sulfur granules (a finding virtually diagnostic of this disease). The walls of the mass are fibrotic and characteristically described as “wooden.” Over time sinus tracts to the skin, adjacent organs, or bone may develop. Rarely distant hematogenous seeding occurs. Foreign bodies appear to facilitate infection. This occurs most frequently with intrauterine contraceptive devices (IUCDs). Although actinomycosis has been described in the setting of various immunosuppressive therapies or states of host compromise, it remains unclear which arm(s) of host defense prevents/control infection. The contribution of the non-Actinomyces co-isolates or companion organisms to the pathogenesis of actinomycosis is also uncertain.