Purpose of review: Topics relating to the spondyloarthropathies have been reviewed recently, but the detailed roles of Chlamydia trachomatis and C. pneumoniae in induction of spondyloarthritis have not been discussed. This review focuses on new information regarding how these pathogens elicit joint disease, with emphasis on C. trachomatis in its role in Chlamydia-induced reactive arthritis.
Recent findings: Molecular methods continue to provide insights into the molecular genetic and cell biologic basis for chlamydial pathogenesis. For chlamydiae, residence in the synovium in patients with acute or chronic Chlamydia-induced arthritis involves organisms in an unusual infection state designated persistence. The profiles of overall metabolism and gene expression characteristic of chlamydial persistence have been assessed and unusual aspects noted, including transcriptional attenuation of one hsp60 paralog and upregulation of expression for another. Strain determinations have demonstrated that genital serotypes of C. trachomatis are not present in the joint; rather, inflammation at that site is elicited by ocular serotypes of the organism. This indicates that much remains to be learned concerning the biology of chlamydial dissemination from the urogenital tract. Analyses of undifferentiated spondyloarthritis continue to suggest that chlamydiae, and perhaps other pathogens function in the etiology of the disease. Progress has been made in developing effective treatment for patients with Chlamydia-induced arthritis.
Summary: Molecular genetic analyses regarding the role of chlamydiae in induction of inflammatory arthritis have increased our detailed understanding of the pathogenic mechanisms utilized by these organisms in the joint. Importantly, progress has been made in developing effective therapies for treatment of Chlamydia-induced arthritis.