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Campylobacter  enterocolitis may lead to post-infection irritable bowel syndrome (PI-IBS) and while some  C. jejuni  strains are more likely than others to cause human disease, genomic and virulence characteristics promoting PI-IBS development remain uncharacterized. We combined pangenome-wide association studies and phenotypic assays to compare  C. jejuni  isolates from patients who developed PI-IBS with those who did not. We show that variation in bacterial stress response ( Cj0145_phoX ), adhesion protein ( Cj0628_CapA ), and core biosynthetic pathway genes (biotin:  Cj0308_bioD ; purine:  Cj0514_purQ ; isoprenoid:  Cj0894c_ispH ) were associated with PI-IBS development. In vitro assays demonstrated greater adhesion, invasion, IL-8 and TNFα secretion on colonocytes with PI-IBS compared to PI-no-IBS strains. A risk-score for PI-IBS development was generated using 22 genomic markers, four of which were from  Cj1631c , a putative heme oxidase gene linked to virulence. Our finding that specific  Campylobacter  genotypes confer greater in vitro virulence and increased risk of PI-IBS has potential to improve understanding of the complex host-pathogen interactions underlying this condition.

Campylobacter jejuni genotypes are associated with post-infection irritable bowel syndrome in humans