July 01, 2013
2 min read

Additional research needed of post-infectious irritable bowel syndrome

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Irritable bowel syndrome affects up to 15% of the general public and is one of the forms of functional bowel diseases that are defined by having no anatomic or biochemical explanation. Studies carried out in the past decade have shown that enteric infection in apparently healthy young people can trigger events that lead to functional bowel disease and irritable bowel syndrome.

Irritable bowel syndrome (IBS) is defined by the presence of a combination of persistent or intermittent abdominal pain and discomfort coupled with change in bowel function. When a group of patients with IBS are asked when their IBS began, two answers are characteristically found. The most common response indicates that the gastrointestinal symptoms started slowly with no obvious antecedent event. However, in approximately 25% of the patients, they will respond that their chronic misery started with a bout of diarrhea or gastroenteritis on a specific date, often during international travel. That condition is referred to as post-infection (PI)-IBS. In this review we will discuss what is known about PI-IBS.

Herbert L. DuPont

Herbert L. DuPont

Travelers’ diarrhea

Some of the best studies in this area came from England, where patients with bacterial diarrhea, especially Campylobacter diarrhea, were followed for some time after their acute illness, and in Canada, where a waterborne outbreak of diarrhea was caused by a Campylobacter Shiga toxin-producing Escherichia coli strain. In travel medicine, approximately 5% of patients with travelers’ diarrhea progressed to PI-IBS. In a population of IBS patients in a large Houston gastroenterology clinic, 8% of the patients overall and 16% of the patients with PI-IBS had taken an international trip the 6 months before the onset of their IBS; nearly all had acquired diarrhea during that trip. It appears that bacterial pathogens that induce inflammatory changes in the gut are the major offenders leading to the condition. That includes strains of Campylobacter, Shigella, Salmonella and Shiga toxin-producing E. coli. Other infectious pathogens can lead to the events that result in IBS.

Risk factors for acquiring PI-IBS include age younger than 60 years; increased severity of the bout of diarrhea or gastroenteritis first experienced; and pre-existent psychological difficulties, including depression or anxiety. People who develop PI-IBS often possess genes that appear to be important in the disease development. The genes that appear to be involved include TLR9, a pattern recognition receptor; interleukin-6, a proinflammatory cytokine; CDH1, a tight junction protein; and low producers of IL-10, an anti-inflammatory cytokine.


Pathogenesis of the condition characteristically includes a genetically susceptible host, an inflammatory pathogen and stimulation of inflammation-immunological pathways. The initial intestinal inflammation leads to chronic low-grade inflammatory stimulus, presence of serotonin-containing enterochromaffin cells, release non-down-regulated cytokines and mast cells. Patients with constipation related to IBS have been shown to have delayed intestinal transit in the small bowel and colon.

PI-IBS is in its infancy of understanding. We don’t know if susceptible patients can be identified by efforts put forth to prevent the inciting events or if they are destined to develop the condition at some point. Although the prognosis appears to be better in PI-IBS compared with the idiopathic form, those affected may suffer for years.

As more studies are carried out, it is becoming clear that IBS is not truly a functional disorder. There are biochemical, inflammatory and gut motor defects seen in the condition. The first enteric infection that led to chronic gastrointestinal disease was Helicobacter pylori as the cause of gastritis, peptic ulcer disease and gastric cancer. Bacterial enteric infection has now been shown to trigger events leading to IBS. It is likely that other infectious diseases stimulate the development of chronic medical disorders.

For more information:

Herbert L. DuPont, MD, MACP, is clinical professor of medicine and vice chair of the department of medicine section of infectious diseases at Baylor College of Medicine. He also is chief of medicine at St. Luke’s Episcopal Hospital, Houston, and a member of the Infectious Disease News Editorial Board.

Disclosure: DuPont reports no relevant financial disclosures.