Actinomycosis is uncommon, and most physicians’ personal experience with its clinical presentations is limited. Laboratory identification of the etiologic agents from the order Actinomycetales is not routine. Thus actinomycosis remains a diagnostic challenge, even for a skilled clinician. However, this infection is usually curable with medical therapy alone. Therefore, an awareness of the full spectrum of clinical syndromes can expedite diagnosis and treatment and minimize unnecessary surgical interventions, morbidity, and mortality.
Actinomycosis is an indolent, slowly progressive infection caused by anaerobic or microaerophilic bacteria, primarily of the genus Actinomyces, that colonize the mouth, colon, and vagina. Mucosal disruption may lead to infection at virtually any site in the body. In vivo growth of actinomycetes usually results in the formation of characteristic clumps called grains or sulfur granules. The clinical presentations of actinomycosis are myriad. Common in the preantibiotic era, actinomycosis has diminished in incidence, as has its timely recognition. Actinomycosis has been called the most misdiagnosed disease, and it has been said that no disease is so often missed by experienced diagnosticians.
Three “classic” clinical presentations that should prompt consideration of this unique infection are (1) the combination of chronicity, progression across tissue boundaries, and mass-like features (mimicking malignancy, with which it is often confused); (2) the development of a sinus tract, which may spontaneously resolve and recur; and (3) a refractory or relapsing infection after a short course of therapy, since cure of established actinomycosis requires prolonged treatment.
Actinomycosis is most commonly caused by A. israelii, A. naeslundii, A. odontolyticus, A. viscosus, A. meyeri, A. graevenitzii, and A. gerencseriae. Most if not all actinomycotic infections are polymicrobial. Aggregatibacter (Actinobacillus) actinomycetemcomitans, Eikenella corrodens, Enterobacteriaceae, and species of Fusobacterium, Bacteroides, Capnocytophaga, Staphylococcus, and Streptococcus are commonly isolated with actinomycetes in various combinations, depending on the site of infection. Their contribution to the pathogenesis of actinomycosis is uncertain.
Comparative 16S rRNA gene sequencing has led to the identification of an ever-expanding list of Actinomyces species and a reclassification of some species to other genera. At present, 47 species and 2 subspecies have been recognized (http://www.bacterio.net/actinomyces.html), with 25 species implicated as causes of human disease. A. europaeus, A. neuii, A. radingae, A. turicensis, A. cardiffensis, A. urogenitalis, A. hongkongensis, A. georgiae, A. massiliensis, A. timonensis, and A. funkei as well as two former Actinomyces species—Trueperella (Arcanobacterium) pyogenes and Trueperella (Arcanobacterium) bernardiae—and Propionibacterium propionicum are additional causes of human actinomycosis, albeit not always with a “classic” presentation.
Actinomycosis has no geographic boundaries and occurs throughout life, with a peak incidence in the middle decades. Males have a threefold higher incidence than females, possibly because of poorer dental hygiene and/or more frequent trauma. Improved dental hygiene and the initiation of antimicrobial treatment before actinomycosis ...