Is functional abdominal pain a sequela of gastrointestinal (GI) infections?

Article Outline

• Copyright

When this question was raised at a conference, a wag, perhaps referring to work-related stress, commented, “Of course abdominal pain is infectious—I get it everyday from my co-workers.” Sarcasm aside, there is increasing evidence that exposure to bacterial pathogens may lead to post-infective GI dysfunction or manifest as chronic abdominal pain or other components of Irritable Bowel Syndrome (IBS).

In this issue of The Journal, Saps et al report a significant increase in IBS-like symptoms in children following a documented episode of acute infectious gastroenteritis. Children were evaluated six months after the acute bacterial infection. They found that 36% of the patients who had documented infection subsequently complained of abdominal pain, consistent with IBS. This contrasted with a rate of 11% in the controls.

We are learning more about the role of the endogenous and acquired GI microflora, the so-called “microbiome,” in determining health or disease. This was most dramatically illustrated by the recent observation of increased numbers of Bacteroidetes bacteria in the gut of obese individuals; in genetically obese mice, this gut microbial community was found to have a “great capacity to harvest energy from diet” (Nature 2006;444:1027-31). Thus, the “obese microbiome” seems to directly contribute to excess weight gain.

A spate of recent studies suggests that the bacterial flora in the human gut interact with the bowel in a complex and dynamic relationship which may lead to the induction and progression of IBS. Viral and bacterial GI infections can trigger post-infectious IBS. Studies done in adults have indicated that acute bacterial gastroenteritis due to Salmonella, Shigella, and Campylobacter species may precede changes in the perception of GI symptoms, such as abdominal pain. Infection by pathogenic organisms leads to mucosal damage and disruption of the extensive commensal flora of the gut (J Gastroenterol 2007;42 Suppl 17:41-7). Inflammatory changes, consistent with the pro-inflammatory role of bacteria, have been demonstrated. Acute injury may then trigger any of the postulated mechanisms underlying IBS—such as altered intestinal motility, visceral hypersensitivity, serotonin system abnormalities, and neuropsychiatric disturbances. In fact, patients with high stress and anxiety levels are more prone to develop IBS after a bout of gastroenteritis (Gut 2007;56:1066-71).

Short-term therapy with either broad-spectrum antibiotics or various probiotics reduces symptoms among patients with IBS. The benefits of such therapy may be mediated through quantitative and/or qualitative changes in the colonic flora. An anti-inflammatory effect seems likely (J Dig Dis 2007;8:2-7).

Although there may be other environmental and genetic factors which predispose children to functional abdominal pain, this study should be a stimulus to further explore the postulated link, and, if confirmed, the underlying mechanism. These studies, in turn, could lead to the development of intervention strategies to reduce the risk of long-term consequences of GI infection.