Ann Rheum Dis 65:281-284 doi:10.1136/ard.2005.044966
  • Editorial

Persistent infection of Chlamydia in reactive arthritis

  1. M Rihl1,
  2. L Köhler1,
  3. A Klos2,
  4. H Zeidler1
  1. 1Division of Rheumatology, Hannover Medical School (MHH), Carl-Neuberg-Str 1, 30625 Hannover, Germany
  2. 2Department of Medical Microbiology and Hospital Epidemiology, Hannover Medical School (MHH), Carl-Neuberg-Str 1, 30625 Hannover, Germany
  1. Correspondence to:
    Professor H Zeidler
  • Accepted 17 December 2005

Unravelling the molecular mechanisms

A number of bacteria have been implicated as causing reactive arthritis. In epidemiological studies Chlamydia have been identified as the most common bacteria triggering reactive arthritis in Western countries.1 Only 1–3% of patients acquiring infection at the urogenital tract as the primary site of infection develop Chlamydia-induced arthritis.

It has been shown that C trachomatis reaches the joint from the urogenital system through circulating monocytes and that monocytes/macrophages are the common host cells for persistent organisms during long term infection, with a major role in the induction of inflammation (fig 1). Most patients will achieve clinical remission within 6 months after infection. However, a chronic disease course occurs with intermittent relapses and periods of remission despite the presence of persistent bacteria in the joint. To date, there is no explanation for this clinical heterogeneity, but it is probably related to the genetic background of the host as well as to bacterial factors, such as the ability of C trachomatis to modify its life cycle.

Figure 1

 Pathogenetic concept of Chlamydia-induced arthritis. (1) Primary urogenital infection; (2) dissemination of the bacteria into the joint; (3) intracellular persistence of the bacteria (a) and subsequent synthesis of antigens (AG) out of phagosomes or antigens (b) detected by T cells, which in turn activate monocytes through multiple cytokines; (4) production and release of proinflammatory mediators by the activated monocytes establishing and sustaining the actual inflammation.


During the past decade, significant progress has been made in understanding the aetiopathogenesis of reactive arthritis. Convincing evidence suggests that bacteria and microbial antigens triggering reactive arthritis persist in the joints and other reservoirs such as the entry site of the infection. Owing to intensive immunological and immunogenetic research into reactive arthritis over past decades, the present view of the disease mechanisms is mainly …

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