Increased visceral sensitivity in Giardia‐induced postinfectious irritable bowel syndrome and functional dyspepsia. Effect of the 5HT₃‐antagonist ondansetron

Abstract

In an outbreak of waterborne giardiasis where 1300 subjects were diagnosed, with Giardia lamblia, 139 continued to have abdominal symptoms of whom two of three had negative stool culture and microscopy. These were considered to have a postinfectious functional gastrointestinal disorder. We investigated visceral hypersensitivity in patients with persisting abdominal symptoms after Giardia infection and assessed the effect of 5HT(3)-antagonist ondansetron. Twenty-two patients with Giardia negative stools and 19 controls were included. A subset of patients (n = 15) had both irritable bowel syndrome (IBS) and functional dyspepsia (FD). All subjects underwent a satiety test with a soup combined with three-dimensional ultrasound. Fifteen of 22 patients underwent double-blind, randomized, placebo-controlled study with the 5-HT(3) antagonist ondansetron given orally. Drinking capacity was lower in patients than in controls (P < 0.01) and gastric emptying was reduced (P < 0.05). Patients had more symptoms both fasting and postprandially (P < 0.001) compared to controls. Ondansetron had no effect on these parameters except from less nausea postprandially (P < 0.05). In conclusion, patients with Giardia-induced gastrointestinal symptoms developed both IBS and FD. They exhibited gastric hypersensitivity with lower drinking capacity and delayed gastric emptying. The 5-HT(3) antagonist ondansetron did not improve drinking capacity, gastric emptying or symptoms except nausea.

Long-term Clinical Course of Post-infectious Irritable Bowel Syndrome After Shigellosis: A 10-year Follow-up Study

“…Several studies have established the causative pathogens of PI-IBS, including Shigella spp., 16,23 pathogenic E. coli, 22 Salmonella spp., 13,18 C. jejuni, 15 G. duodenali, 19 Trichinella britovi, 25 norovirus, 26 or combinations of the preceding pathogens. 14,22 The reported incidence of PI-IBS varies from about 5-30%, 11 and PI-IBS is now a well-recognized consequence of acute infectious gastroenteritis.…”

“…12 Post-infectious IBS (PI-IBS) is defined as the acute onset of new IBS symptoms in an individual who has not previously met the criteria for IBS immediately following an acute illness characterized by 2 or more of the following: fever, vomiting, diarrhea, or positive bacterial stool culture. 12 Although there have been many reports regarding PI-IBS associated with pathogens such as Shigella spp., pathogenic Escherichia coli, Salmonella, Campylobacter jejuni, and Giardia duodenalis in the past 20 years, [13][14][15][16][17][18][19] most of these reports address the shortterm clinical course of PI-IBS, and only few examined the longterm course (≥ 5 years) of PI-IBS. [20][21][22][23] We previously reported on the clinical course of PI-IBS in a homogenous cohort comprised of patients recovered from shigellosis.…”

Clostridium difficile-related postinfectious IBS: a case of enteroglial microbiological stalking and/or the solution of a conundrum?

“…For instance, mucosal cellular changes (enterochromaffin cells hyperplasia) [14], abnormal intestinal permeability and cytokine increase [15] have been reported in PI-IBS related to Campylobacter species; abnormalities of immunoendocrine cells [16] have been described in PI-IBS related to Shigella infection; and mucosal cellular changes (enterochromaffin cells decrease and cholecystokinin-containing cell increase) [17] and visceral hypersensitivity [18] have been documented in Giardia infested patients.…”

Postinfectious Chronic Gut Dysfunction: From Bench to Bedside

“…Giardia infection has been associated with an increased risk for IBS ( 14 ). In 2007, Marshall et al ( 8 ) published a report of a prospective study conducted aft er a large outbreak of acute gastroenteritis at a medical meeting attributable to food-borne norovirus.…”

“…Most previous studies of postinfectious functional gastrointestinal diseases have focused on bacterial causes of gastroenteritis, which are characterized by infl ammation and mucosal tissue destruction. However, they may occur also aft er Giardia lamblia infection ( 14 ) and viral gastroenteritis ( 8 ) where infl ammation is mild or absent. Another controversial issue is how an infection involving a given segment of the gut (i.e., the colon) is able to induce chronic symptoms that seem to correspond to another part of the digestive system (i.e., dyspepsia).…”