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Actinomycosis

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

1 Scopus citations

Abstract

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, Actinomyces gerencseriae, and Propionibacterium propionicum are less common causes of infection. Nearly all of actinomycotic infections are polymicrobial in nature. Actinobacillus actinomy-cetemcomitans, Eikenella corrodens, Fusobacterium, Bacteroides, Capnocytopaga, Staphylococcus, Streptococcus, and Enterobacteriaceae are commonly coisolated (“companion organisms”) with the agents of actinomycosis in various combinations depending on the site of the infection. Recently a variety of bacterial species isolated from human clinical specimens have been reclassified as Actinomyces. Increasing data support that Actinomyces europaeus, Actinomyces neuii, Actinomyces radingae, Actinomyces graevenitzii, Actinomyces turicensis, Actinomyces cardiffensis, Actinomyces houstonensis, Actinomyces hongkongensis, and Actinomyces funkei also cause human actinomycosis. 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.

Original languageEnglish
Title of host publicationClinical Infectious Disease
PublisherCambridge University Press
Pages881-886
Number of pages6
ISBN (Electronic)9780511722240
ISBN (Print)9780521871129
DOIs
StatePublished - Jan 1 2010

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