Culture of Chlamydia trachomatis from synovial tissues/fluids from Reiter's syndrome (RS) patients frequently yields negative results. However, we have identified chlamydial RNA at that site in such patients, suggesting that viable organisms may be present. Here we define the cellular location of chlamydia within the synovium via in situ hybridization. Using a chlamydial ribosomal RNA-directed probe, we show that synovial tissue from culture-negative RS patients gives strong hybridization which is often localized to a subsynovial cell layer, rather than to the synovial lining; in some cases, hybridizing cells are dispersed through the synovium. All hybridization signal is located within host cells, indicating that infectious extracellular elementary bodies are rare or absent. These data confirm the extensive intracellular presence of inapparent chlamydia in the synovia of RS patients and provide some insight into the usual culture negativity of synovial tissues for the organism.
SUMMARYReactive arthritis (ReA) is one of the most common arthritides affecting young adults. In most cases it follows urogenital or enteric bacterial infection, but its pathogenesis is not fully understood. It is generally considered a sterile arthritis which appears to involve immune response to bacterial organisms and genetic host susceptibility associated with the presence of HLA‐B27 antigen. New findings suggest that in some ReA cases, viable bacteria are present inside the joints, and these organisms may cause the disease and trigger the inflammatory response. ReA manifests clinically as a rheumatoid factor negative oligoarthritis associated with enthesopathy and certain mucosal and skin lesions. Laboratory findings in ReA are non‐specific. Although concepts of its pathogenesis are still evolving, so‐called ReA remains an important condition to be distinguished from rheumatoid arthritis. Prognosis is generally better. Treatments with known effects in some cases include non‐steroidal antiinflammatory drugs, intra‐articular corticosteroids, oral tetracyclines and sulphasalazine. The occasional chronic and severe ReA may be very difficult to treat.
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