Introduction: Pathophysiology of irritable bowel syndrome (IBS) is multifactorial. Recent investigations have associated episodes of infectious gastroenteritis with development of IBS. This condition is named post-infectious IBS (PI-IBS). The role of inflammation-infection in IBS pathogenesis is not well understood.

Aim: To review published scientific evidence on PI-IBS regarding risk factors, causal agents, histopathological changes, and treatment.

Materials and methods: An electronic search in MEDLINE and abstracts presented at national and international GI meetings was performed, looking for information published in the past 50 years including animal studies, cohort studies, case-control studies, and series of cases and case reports, using the key words post-infectious enteritis, post-dysenteric or post-infectious irritable bowel syndrome (PI-IBS), and post-infectious colitis.

Results: Fifty one papers were included. These studies were classified according to pathophysiologic mechanisms, infectious agents involved, animal or human studies, and treatment.

Conclusions: Current evidence shows a strong association between colonic infection and inflammation with development of IBS. Approximately 25% of patients with IBS have a history of infectious enteritis. Microbial agents related with PI-IBS include bacteria (Campylobacter, Salmonella) and parasites (Trichinella spiralis). Increased number of enteroendocrine cells, CD3 lymphocytes and mast cells within the colonic muscle wall, release of pro-inflammatory substances, and increased number of inflammatory cells with intestinal nervous endings are the most common histopathologic findings. Patients developing PI-IBS have a higher frequency of psychological disorders and stressful events prior to the gastroenteritis episode. Therapeutic interventions with steroids, COX-2 inhibitors, antibiotics and probiotics require further investigation.