Editorial
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 28, 2016; 22(4): 1331-1334
Published online Jan 28, 2016. doi: 10.3748/wjg.v22.i4.1331
Is irritable bowel syndrome an infectious disease?
John Richard Thompson
John Richard Thompson, Department of Pharmacy Practice, Lipscomb University College of Pharmacy, One University Park Drive, Nashville, TN 37204, United States
Author contributions: Thompson JR contributed solely to the literature analysis and writing of the manuscript.
Conflict-of-interest statement: Dr. Thompson serves on the Speakers’ Bureau for GlaxoSmithKline and Salix Pharmaceuticals.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: John Richard Thompson, PharmD, MBA, Professor, Chair, Department of Pharmacy Practice, Lipscomb University College of Pharmacy, One University Park Drive, Nashville, TN 37204, United States. richard.thompson@lipscomb.edu
Telephone: +1-615- 9667172 Fax: +1-615-9667163
Received: April 29, 2015
Peer-review started: May 12, 2015
First decision: August 26, 2015
Revised: October 6, 2015
Accepted: November 24, 2015
Article in press: November 24, 2015
Published online: January 28, 2016
Processing time: 266 Days and 14.5 Hours
Abstract

Irritable bowel syndrome (IBS) is the most common of all gastroenterological diseases. While many mechanisms have been postulated to explain its etiology, no single mechanism entirely explains the heterogeneity of symptoms seen with the various phenotypes of the disease. Recent data from both basic and clinical sciences suggest that underlying infectious disease may provide a unifying hypothesis that better explains the overall symptomatology. The presence of small intestinal bowel overgrowth (SIBO) has been documented in patients with IBS and reductions in SIBO as determined by breath testing correlate with IBS symptom improvement in clinical trials. The incidence of new onset IBS symptoms following acute infectious gastroenteritis also suggests an infectious cause. Alterations in microbiota-host interactions may compromise epithelial barrier integrity, immune function, and the development and function of both central and enteric nervous systems explaining alterations in the brain-gut axis. Clinical evidence from treatment trials with both probiotics and antibiotics also support this etiology. Probiotics appear to restore the imbalance in the microflora and improve IBS-specific quality of life. Antibiotic trials with both neomycin and rifaximin show improvement in global IBS symptoms that correlates with breath test normalization in diarrhea-predominant patients. The treatment response to two weeks of rifaximin is sustained for up to ten weeks and comparable results are seen in symptom reduction with retreatment in patients who develop recurrent symptoms.

Keywords: Irritable bowel syndrome; Pathopohysiology; Etiology; Probiotics; Antibiotics; Infectious disease

Core tip: Recent evidence from both basic and clinical science supports the hypothesis of infectious disease as an etiological agent in irritable bowel syndrome (IBS). The presence of small intestinal bowel overgrowth and its treatment as reflected in reductions of lactulose hydrogen breath tests correlates with improvement in IBS symptoms. Clinical trials with both probiotics and antibiotics also appear to relieve symptoms of IBS and have a sustained effect post-treatment. Recurrences of symptoms post-treatment appear to respond similarly with no loss of effect. An infectious disease etiology of IBS may explain the heterogeneous symptoms of the disease and varying responses seen with different symptom phenotypes.