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Arthritis associated with enteric infection.

J S Hill Gaston1, Mark S Lillicrap

  • 1Department of Medicine, Box 157, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK. jshg2@medschl.cam.ac.uk

Best Practice & Research. Clinical Rheumatology
|June 6, 2003
PubMed
Summary

Reactive arthritis can follow infections from gut bacteria like Yersinia and Salmonella. This review covers causes, host factors like HLA-B27, and diagnosis for these inflammatory joint conditions.

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Area of Science:

  • Infectious disease
  • Immunology
  • Rheumatology

Background:

  • Reactive arthritis classically follows enteric infections (Yersinia, Salmonella, Campylobacter, Shigella).
  • Other enteric pathogens (Clostridium difficile, Giardia) and Tropheryma whippelii (Whipple's disease) can also cause inflammatory arthritis.
  • Brucella-associated arthritis is covered separately.

Purpose of the Study:

  • To review current understanding of reactive arthritis and related inflammatory arthropathies following enteric infections.
  • To discuss epidemiology, etiology, and pathogenesis, including host (HLA-B27) and organism factors.
  • To highlight recent findings on pathogen migration to joints and formulate a diagnostic and management approach.

Main Methods:

  • Literature review of epidemiology, etiology, pathogenesis, and management strategies.

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  • Focus on evidence from clinical trials where available.
  • Discussion of host susceptibility factors, particularly HLA-B27.

    • Main Results:

    • Reactive arthritis is linked to specific enteric pathogens and Tropheryma whippelii.
    • Host genetic factors, notably HLA-B27, significantly influence susceptibility.
    • Evidence suggests pathogenic organisms can traffic to the joint, contributing to arthritis.

    Conclusions:

    • A comprehensive understanding of reactive arthritis requires considering both infectious triggers and host immune responses.
    • HLA-B27 is a key genetic factor in susceptibility.
    • Diagnosis and management should be evidence-based, incorporating clinical trial data and pathogen-host interaction insights.