Related Experiment Video
Updated: Mar 10, 2026

Chronic Salmonella Infection Induced Intestinal Fibrosis
Published on: September 22, 2019
Factors Associated with Sequelae of Campylobacter and Non-typhoidal Salmonella Infections: A Systematic Review
Oluwaseun B Esan1, Madison Pearce2, Oliver van Hecke3
1Nuffield Department of Primary Care Health Sciences, University of Oxford, United Kingdom; National Institute for Health Research, Health Protection Research Unit, Gastrointestinal Infections, University of Oxford, United Kingdom.
Abstract:
Despite the significant global burden of gastroenteritis and resulting sequelae, there is limited evidence on risk factors for sequelae development. We updated and extended previous systematic reviews by assessing the role of antibiotics, proton pump inhibitors (PPI) and symptom severity in the development of sequelae following campylobacteriosis and salmonellosis. We searched four databases, including PubMed, from 1 January 2011 to 29 April 2016. Observational studies reporting sequelae of reactive arthritis (ReA), Reiter's syndrome (RS), irritable bowel syndrome (IBS) and Guillain-Barré syndrome (GBS) following gastroenteritis were included. The primary outcome was incidence of sequelae of interest amongst cases of campylobacteriosis and salmonellosis. A narrative synthesis was conducted where heterogeneity was high. Of the 55 articles included, incidence of ReA (n=37), RS (n=5), IBS (n=12) and GBS (n=9) were reported following campylobacteriosis and salmonellosis. A pooled summary for each sequela was not estimated due to high level of heterogeneity across studies (I2>90%). PPI usage and symptoms were sparsely reported. Three out of seven studies found a statistically significant association between antibiotics usage and development of ReA. Additional primary studies investigating risk modifying factors in sequelae of GI infections are required to enable targeted interventions.
Related Concept Videos
Acute Pyelonephritis II: Diagnostic Studies and Management
Urinary Tract Infection II: Pathophysiology

