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Rheum Dis Clin North Am. 2009 Feb;35(1):1-19. doi: 10.1016/j.rdc.2009.03.011.

Molecular biology of infectious agents in chronic arthritis.

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  • 1Department of Immunology and Microbiology, Wayne State University School of Medicine, 540 East Canfield Avenue, Detroit, MI 48201, USA. ahudson@med.wayne.edu

Abstract

Severe and chronic inflammatory arthritis sometimes follows urogenital infection with Chlamydia trachomatis or gastrointestinal infection with enteric bacterial pathogens. A similar clinical entity can be elicited by the respiratory pathogen Chlamydophila (Chlamydia) pneumoniae. Arthritogenesis does not universally require viable enteric bacteria in the joint. In arthritis induced by either of the chlamydial species, organisms are viable and metabolically active in the synovium. They exist in a "persistent" state of infection. Conventional antibiotic treatment of patients with Chlamydia-induced arthritis is largely ineffective. The authors outline the current understanding of the molecular genetic and biologic aspects underlying bacterially-induced joint pathogenesis, available information regarding host-pathogen interaction at that site, and several directions for future study to inform development of more effective therapies.

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