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Updated: May 27, 2026

Chronic Salmonella Infection Induced Intestinal Fibrosis
Published on: September 22, 2019
Gastrointestinal infection as a trigger for inflammatory bowel disease
Elizabeth A Mann1, Shehzad A Saeed
1Division of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA. Elizabeth.mann@cchmc.org
Purpose Of Review:
There is accumulating evidence on the importance of microbes in the development and maintenance of both the intestinal and immune systems. This review focuses on the current findings on the role of gastrointestinal pathogens in the cause of chronic inflammatory bowel disease.
Recent Findings:
A number of intestinal pathogens including Mycobacterium avium subspecies paratuberculosis, adherent-invasive Escherichia coli, and Campylobacter species are associated at fairly high prevalence with Crohn's disease, while two recent studies found a low prevalence for cytomegalovirus. In a prospective study, M. avium subspecies paratuberculosis detection in early Crohn's disease was low and comparable to controls, while much higher in an established inflammatory bowel disease cohort. In the pediatric setting, a high prevalence of Clostridium difficile was seen in both active and inactive Crohn's disease and ulcerative colitis patients. Some studies have speculated that Salmonella or Campylobacter infection may increase the risk of inflammatory bowel disease on long-term follow-up, but detection bias was found to obscure the risk. Recent studies in mouse models have demonstrated that a combination of factors, including viral pathogens, genetic susceptibility, and commensal microflora, can lead to intestinal pathology.
Summary:
No evidence for causation of inflammatory bowel disease by a single agent has been found, whereas a number of microbes have been strongly associated with the presence of disease. The majority of recent studies support a role for the ability of intestinal pathogens to promote chronic inflammation in individuals with genetic susceptibility and/or other environmental factors which remain to be identified. These factors may include subsets of commensal microflora.
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