Chlamydia-induced arthritis is defined as arthritis following primary extra-articular infection with Chlamydia trachomatis or Chlamydophila pneumoniae. C trachomatis serovars D through K are the leading causes of sexually transmitted urogenital tract (UGT) infections, accounting for more than 50% of sexually transmitted UGT infections in western countries with an estimated incidence in the United States of approximately 4 million per year [1]. Cpneumoniae is a respiratory tract pathogen causing pharyngitis, sinusitis, bronchitis, and pneumoniae that accounts for about 10% of community-acquired pneumonia [2]. It is estimated that 1% to 10% of patients with chlamydial infection develop Chlamydia-induced arthritis. The prevalence of C trachomatis-induced arthritis (CIA) has an estimated annual incidence of about 4.6/100,000; the prevalence of Cpneumoniae-induced arthritis seems to be significantly lower [3,4]. Because of the higher prevalence of CIA and the fact that more is known about disease mechanisms in CIA, this article focuses on the pathogenesis of CIA. C trachomatis causes urethritis and cervicitis, and, because of ascending infection, adnexitis, epididymitis, orchitis, and perihepatitis. Chronic adnexitis (pelvic inflammatory disease) by C trachomatis is the leading cause of acquired female infertility caused by tubar occlusion. C trachomatis can also infect the mucosa of the rectum in men who engage in anal sex, and recently C trachomatis caused tonsillitis that triggered reactive arthritis [5]. C trachomatis infection of the UGT is often asymptomatic. In a cohort of CIA patients described by Wollenhaupt et al, more than 50% did not have UGT symptoms [6]. It is thought that from the entry site C trachomatis is disseminated within monocytes by way of the blood stream into the joints. Using C trachomatis-specific polymerase chain reaction (PCR), the authors and others have detected C trachomatis in the mononuclear cell fraction of peripheral blood from patients who have CIA [7]. In the joint, C trachomatis persists in the sublining layer of the synovial tissue and can be detected for prolonged periods of times (up to years) despite previous antibiotic treatment [8]. The arthritis is mostly asymmetric with oligoarticular involvement and predominance of the lower limbs and takes a self-limited course. HLA-1327 is associated especially with chronic forms and spinal involvement [9]. Diagnosis is based on the typical clinical picture, the exclusion of other rheumatic diseases, and the proof of previous or ongoing chlamydial infection at the entry site or (preferably) in the joint. [10]. Internationally accepted classification criteria for CIA do not exist, but Braun et al [11] and Pacheco-Tena et al [12] have suggested criteria that are useful for diagnosis. Treatment is symptomatic and involves primarily the use of nonsteroidal anti-inflammatories (NSAIDs) and eventually glucocorticosteroids locally or systemically in cases of highly active disease. Most CIA resolves spontaneously; in cases of chronic disease with peripheral joint involvement, sulphasalazine is the first-choice treatment. Antibiotic treatment has been shown to reduce the rate of recurrences but it does not alter the course of the arthritis [13]. Prognosis is usually excellent with a high rate of remission (about 60%70%) within 6 months.
