Extra-genital Chlamydia trachomatis infection as sexually-acquired reactive arthritis

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Chlamydial infection is closely associated with several forms of inflammatory arthritis in both animals and man. In man arthritis is a well-recognised complication 1 of acute genital-tract infection, lymphogranuloma venereum and psittacosis so that a direct role of chlamydial micro-organisms in the aetiology of inflammatory arthritis has long been considered. Approximately 1% of men presenting to genito-urinary medicine clinics with non-gonococcal urethritis (NGU) develop acute aseptic arthritis. This has been referred to as sexually-acquired reactive arthritis (SARA), ~ approximately one third of patients having Reiter's syndrome. Initial isolation studies indicated a prevalence of acute Chlamydia trachomatis genital-tract infection ranging from o-69 % at the onset of acute SARA, 3 findings comparable with isolation rates in uncomplicated urethritis. Prospective follow-up of patients with chlamydiapositive and chlamydia-negative urethritis failed to reveal a difference in the incidence of acute arthritis between the two groups. However, serological studies have indicated that titres of IgG chlamydial antibody in both serum 3 and synovial fluid 4 of patients with SARA are raised compared with patients with uncomplicated genital-tract infection and rheumatic disease controls. IgA class chlamydial antibody has been reported in serum by some workers 5 but not others. 4 Specificity of antibody both in serum and synovial fluid has been investigated by Inman et al. 6 and Kihlstrom et al. 7 using separation of chlamydial protein antigens on polyacrylamide gel and immunoblotting techniques. Antibody, both in serum and synovial fluid, has been shown to be of broad specificity; no antigens have been detected by this technique which are specific to synovial fluid or to patients with arthritis. Antibodies to Chlamydia pneumoniae have been detected in both serum and synovial fluid of some patients with SARA though in the absence of controlled data the significance of these findings is unclear. 4 Studies of cellular immunity to C. trachomatis in patients with SARA have shown enhanced lymphocyte proliferative responses especially in cells obtained from the joint. 8 The finding of enhanced synovial fluid cellular responses to C. trachomatis compared with peripheral blood lymphocyte responses has been interpreted by Ford et al. 8 as indicating that the stimulatory antigen is present within the joint and may therefore be intimately involved in the pathogenesis of the arthritis. Although an attractive concept which has merited further investigation, these findings are susceptible to alternative explanations so that their true significance is unclear. Attempts to isolate chlamydia from joint samples have produced results which are also difficult to interpret. Early studies using culture in embryonated