Persistent Chlamydia trachomatis infection in the joint of patients with Chlamydia-induced arthritis - Implications for pathogenesis and treatment

After an urogenital infection with Chlamydia trachomatis, 1-3% of all persons develop reactive arthritis. Although Chlamydia trachomatis cannot be cultured from the synovial fluid and membrane by microbiological techniques, Chlamydia trachomatis was identified by molecular biological and immunological methods in the joints of patients with reactive arthritis. Moreover, new studies demonstrated Chlamydia trachomatis as a viable and metabolically active bacterium in the joint. Chlamydial antigens are produced and infected macrophages are stimulated to produce monokines. By these means the persistent chlamydial infection can initiate and perpetuate the synovial inflammatory process. According to this pathogenetic concept the elimination of Chlamydia trachomatis in the joint should ameliorate the arthritis. However, studies with antibiotics (tetracycline, ciprofloxacine) failed to show a therapeutic value of this strategy. The failure of the antibiotics tested so far might result from the particular metabolical state of the persistent chlamydial infection in the joint. We developed an in-vitro model of a persistent infection to test new antibiotics with improved efficacy against intracellular bacteria. Moreover, clinical studies with these new antibiotics are under way. These results will show whether reactive arthritis can be treated by antibiotics and whether the elimination of Chlamydia trachomatis in the joint leads to an amelioration of the arthritis.