From Infection to Dysbiosis: Pathogenesis of Post-Infectious Irritable Bowel Syndrome - Diagnostic and Therapeutic Implications

Introduction: Post-infectious irritable bowel syndrome (PI-IBS) develops in approximately 14.5% of individuals after acute gastroenteritis and persists long-term, with emerging evidence suggesting an autoimmune component linking infection to chronic gastrointestinal dysfunction. This review aims to synthesize current literature on the proposed pathogenesis of PI-IBS, focusing on molecular mechanisms, the development of small intestinal bacterial overgrowth (SIBO), and resulting diagnostic and therapeutic implications. Materials and methods: A narrative review of PubMed literature was performed, focusing on autoantibody-mediated disruption of gut motility, candidate diagnostic biomarkers, and emerging therapeutic approaches. Studies were selected based on relevance and methodological quality, without formal inclusion or exclusion criteria. Results: Infection by cytolethal distending toxin (CDT)-producing bacteria triggers anti-CdtB antibody production, which through molecular mimicry may cross-react with human vinculin in the interstitial cells of Cajal, causing enteric neuropathy and impaired migrating motor complex function. The resulting dysmotility may facilitate SIBO development. Combined anti-CdtB and anti-vinculin serum biomarkers can offer post-test probability exceeding 98% for diarrhea-predominant IBS. Antibody-depleting therapies, such as plasmapheresis and intravenous immunoglobulin, may reduce autoantibody burden and correlate with symptomatic improvement. Conclusions: PI-IBS may represent an immune-mediated consequence of acute bacterial gastroenteritis, in which CdtB-induced autoimmunity drives dysmotility and microbial dysbiosis. This mechanistic framework offers potential biomarkers and therapeutic targets. Further prospective studies are needed to validate these findings.