Document 0461 DOCN M9490461 TI Nocardia species: host-parasite relationships. DT 9411 AU Beaman BL; Beaman L; Department of Medical Microbiology and Immunology, University of; California, Davis 95616. SO Clin Microbiol Rev. 1994 Apr;7(2):213-64. Unique Identifier : AIDSLINE MED/94332802 AB The nocardiae are bacteria belonging to the aerobic actinomycetes. They are an important part of the normal soil microflora worldwide. The type species, Nocardia asteroides, and N. brasiliensis, N. farcinica, N. otitidiscaviarum, N. nova, and N. transvalensis cause a variety of diseases in both normal and immunocompromised humans and animals. The mechanisms of pathogenesis are complex, not fully understood, and include the capacity to evade or neutralize the myriad microbicidal activities of the host. The relative virulence of N. asteroides correlates with the ability to inhibit phagosome-lysosome fusion in phagocytes; to neutralize phagosomal acidification; to detoxify the microbicidal products of oxidative metabolism; to modify phagocyte function; to grow within phagocytic cells; and to attach to, penetrate, and grow within host cells. Both activated macrophages and immunologically specific T lymphocytes constitute the major mechanisms for host resistance to nocardial infection, whereas B lymphocytes and humoral immunity do not appear to be as important in protecting the host. Thus, the nocardiae are facultative intracellular pathogens that can persist within the host, probably in a cryptic form (L-form), for life. Silent invasion of brain cells by some Nocardia strains can induce neurodegeneration in experimental animals; however, the role of nocardiae in neurodegenerative diseases in humans needs to be investigated. DE Animal AIDS-Related Opportunistic Infections/MICROBIOLOGY Brain Diseases/MICROBIOLOGY Human Nocardia/*PHYSIOLOGY Nocardia Infections/COMPLICATIONS/DIAGNOSIS/IMMUNOLOGY/ *MICROBIOLOGY Phagocytosis Support, U.S. Gov't, P.H.S. JOURNAL ARTICLE REVIEW REVIEW, ACADEMIC SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).