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SAT0003 Intestinal colonisation with sulphate-reducing bacteria: a co-factor in the aetiopathogenesis of ankylosing spondylitis?
  1. SM Stebbings1,
  2. J Highton1,
  3. G Tannock2
  1. 1Rheumatology
  2. 2Microbiology, University of Otago School of Medicine, Dunedin, New Zealand

Abstract

Background Sulphate-reducing bacteria (SRB) have only recently been identified as a constituent of the normal colonic microflora humans. Such colonisation however is far from universal. Small studies in patients with ulcerative colitis (UC) have found SRB to be present in up to 92% of patients and a pathogenic role has been speculated. Approximately 65% of patients with ankylosing spondylitis (AS) have colonic inflammation, and this is now recognised as an independent risk factor for the disease. Furthermore, studies in germfree HLA-B27 transgenic rats have shown that the normal intestinal microflora is essential to the development of spondyloarthritis in these animals.

Objectives We aimed to discover whether intestinal colonisation with SRB was more common in AS patients than controls, and thus whether SRB may play a role in the aetiology of AS.

Methods Fifteen patients fulfilling the Modified New York criteria for AS and 15 age and gender matched controls were recruited. Each subject provided 3 faecal specimens at monthly intervals. Bacterial DNA extracts were obtained from 3 faecal samples from 14 patients and 14 controls, and one each from the remaining patient and control. PCR was performed using primers targeting a conserved region of subunit A of the adenosine-5?-phosphosulphate (APS) reductase gene a gene conserved across all SRB species.

Results (See Table 1)

Chi-square with Yates? correction demonstrated a highly significant association between AS and colonisation with SRB (p = 0.003).

Abstract SAT0003 Table 1

Conclusion We have discovered a much higher prevalence of faecal carriage of SRB in patients with AS compared with healthy controls. This raises the possibility that these organisms may play a role in the aetiopathogenesis of AS. An alternative possibility is that SRB reflect the presence of colonic inflammation in these individuals.

References

  1. Gibson GR, Cummings JH, Macfarlane GT. Growth and activities of sulphate-reducing bacteria in gut contents of healthy subjects and patients with ulcerative colitis. FEMS Microbiol Ecol. 1991;86:103–12

  2. Veys EM, Mielants H, De Vos M, Cuvelier C. Spondylarthropathies: from gut to target organs. Baillieres Clin Rheumatol. 1996;10(1):123–46

  3. Taurog JD, Richardson JA, Croft JT, et al. The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats. J Exp Med. 1994;180(6):2359–64

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