What are infectious causes of reactive arthritis (ReA)?

Updated: Dec 24, 2020
  • Author: Carlos J Lozada, MD; Chief Editor: Herbert S Diamond, MD  more...
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Answer

ReA is usually triggered by a GU or GI infection and thus is sometimes classified as venereal or dysenteric. Such infections are mostly the result of gram-negative, obligate, or facultative intracellular pathogens. [27] Organisms that have been associated with ReA include the following:

  • C trachomatis/ C pneumoniae, [28] including  C trachomatis serovars L2 in lymphogranuloma venereum [29, 30]
  • Ureaplasma urealyticum
  • Neisseria gonorrhoeae
  • Shigella flexneri
  • Salmonella enterica serovars Typhimurium, Enteritidis, [31] and Hadar [32]
  • Mycoplasma pneumoniae
  • Mycobacterium tuberculosis  [33]
  • Cyclospora [34]
  • Yersinia enterocolitica and Y  pseudotuberculosis
  • Campylobacter jejuni [35] and  C coli
  • Clostridium difficile
  • Beta-hemolytic [21] (eg, group A [36] ) and viridans streptococci
  • Severe acute respiratory syndrome coronavirus–2 (SARS–CoV-2) [2, 3, 4, 5]

Data suggest that chlamydial ReA is underdiagnosed and that asymptomatic chlamydial infections might be a common cause. [37] An important difference between Chlamydia-induced (postvenereal) ReA and postenteric ReA is the presence of viable but aberrant chlamydial organisms in the synovial fluid [38] (so-called Chlamydia persistence [39] ). Polymerase chain reaction (PCR) assay to detect C trachomatis DNA in synovial samples may be a good method for establishing the diagnosis of Chlamydia-induced arthritis in patients with ReA. [40]

The prevalence of different serotypes of C trachomatis antibodies and the incidence of Chlamydia-induced ReA was studied in patients with early arthritis in a defined population in Finland. [17] Antibodies against C trachomatis were most common in patients with arthritis because cases with Chlamydia-induced ReA are included in this subgroup.

Ureaplasma organisms are known to be capable of causing experimental and clinical nongonococcal urethritis. Synovial mononuclear cells from arthritic joints of patients with ReA react with Ureaplasma antigens; this organism has been isolated from an ReA patient.

The enteric pathogen that most commonly results in ReA is Campylobacter (C jejuni, 90-95%; C coli, 5-10%). [41] ReA patients with arthritic symptoms are more frequently infected with C jejuni strains with sialic acid lipo-oligosaccharide. In addition, sialylation of C jejuni lipo-oligosaccharide is associated with more severe enteric disease. [42]

Group A streptococci are known to be capable of causing poststreptococcal ReA. [43] Patients with this condition demonstrate increase antistreptolysin O (ASO) antibodies and an increased erythrocyte sedimentation rate (ESR). [44] ReA can also be induced by tonsillitis. In one study, 13 of 21 patients were positive for ASO and 12 were positive for group A Streptococcus. [45]

Acute tuberculosis can sometimes cause ReA. The resulting condition is known as Poncet disease, which is a different entity from tuberculous arthritis. [46, 47, 48]

ReA following infection with C difficile has been reported. [49, 50]  Intravesical instillation of bacillus Calmette-Guérin (BCG) for bladder cancer has been associated with ReA. [51, 52, 53]  has also been shown to occur after tetanus and rabies vaccination. [54, 55]


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