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IBS-D: Post-infectious IBS, causes and treatment options

Understanding IBS-D

IBS is a functional disorder of the gastrointestinal tract, presenting with chronic abdominal pain and altered bowel habits. In the case of IBS-D, diarrhea is the predominant symptom, often accompanied by abdominal pain, bloating, and increased flatulence.

Diagnosis and Prevalence

Diagnosing IBS-D relies on the Rome IV criteria, which include recurrent abdominal pain associated with changes in stool frequency and form. There's no specific test for IBS, making its diagnosis challenging. Approximately 40 percent of people living with IBS-D are not receiving formal diagnosis [1]. Despite its prevalence—accounting for 25 to 50 percent of gastroenterologist referrals in the US—many individuals remain undiagnosed [2].

What are things that are NOT common in IBS?

Some alarm features that are NOT common in IBS and should lead someone to talk to a doctor include large volume diarrhea, rectal bleeding, unexplained weight loss, and progressive abdominal pain, which may signify conditions beyond IBS.

Exploring Potential Causes

The causes of IBS-D are multifaceted, involving a complex interplay of genetic, environmental, and psychosocial factors.

Alterations in gut motility, visceral hypersensitivity, inflammation, microbiota composition, and post-infectious triggers like bacterial or viral gastroenteritis are among the leading contributors.

Emerging data suggest that the fecal microbiota in individuals with IBS differ from healthy controls and vary with the predominant symptom [4].

In support of an association between SIBO and IBS are studies demonstrating abnormal breath hydrogen levels in IBS patients after receiving a test dose of a carbohydrate, as well as improvement in symptoms after eradication of the overgrowth. In these studies, 78-84% of IBS patients had SIBO, and in one of the studies 48% resolved IBS when SIBO was eradicated [6,7].

Post-Infectious IBS

Post-infectious IBS (PI-IBS) occurs following acute gastroenteritis, for example after an infection with organisms like campylobacter, e. coli, or giardia. It is characterized by ongoing gastrointestinal symptoms, typically diarrhea. Studies suggest that around 11% of individuals develop IBS after an infection, with certain pathogens posing higher risks than others [11]. Antibiotic use during acute gastroenteritis is also associated with an increased likelihood of developing PI-IBS.

6% to 17% of patients with IBS believe their symptoms began with an infective illness [12]. Possible mechanisms underlying PI-IBS include: development of anti-CDTB and anti-vinculin antibodies leading to gut nerve damage, bile acid malabsorption, and increases in lymphocytes and serotonin enteroendocrine cells [12,14,15].

Mechanisms and Testing

Testing to evaluate diarrhea typically includes assessing for anemia, inflammatory markers, stool pathogens, lactulose breath test for SIBO, celiac panel. Anti-CDTB and anti-vinculin antibodies can be tested but aren’t routinely run due to limitations in sensitivity.

Treatment Strategies

Soluble fiber should be offered to patients with IBS. Studies suggest that soluble, like psyllium, has a significant effect for the treatment of IBS symptoms. In a meta-analysis of 15 trials that included 946 patients, fiber was associated with an improvement in IBS symptoms [18]. Psyllium has been shown to improve both constipation and diarrhea.

Managing IBS-D often involves a multidisciplinary approach. Gut-brain support through GI-CBT and gut directed hypnotherapy are often recommended.

Dietary modifications, such as low-FODMAP diets and fiber supplementation, can help alleviate symptoms.

Additionally, medications like antibiotics, antidiarrheals, bile acid sequestrants, and antispasmodics may provide relief, depending on individual needs.

Questions? Let us know below.


  1. Sayuk, Gregory S et al. “Comparison of Symptoms, Healthcare Utilization, and Treatment in Diagnosed and Undiagnosed Individuals With Diarrhea-Predominant Irritable Bowel Syndrome.” The American journal of gastroenterology vol. 112,6 (2017): 892-899. doi:10.1038/ajg.2016.574

  2. Everhart, J E, and P F Renault. “Irritable bowel syndrome in office-based practice in the United States.” Gastroenterology vol. 100,4 (1991): 998-1005. doi:10.1016/0016-5085(91)90275-p

  3. Talley, N J et al. “Epidemiology of colonic symptoms and the irritable bowel syndrome.” Gastroenterology vol. 101,4 (1991): 927-34. doi:10.1016/0016-5085(91)90717-y

  4. Kassinen, Anna et al. “The fecal microbiota of irritable bowel syndrome patients differs significantly from that of healthy subjects.” Gastroenterology vol. 133,1 (2007): 24-33. doi:10.1053/j.gastro.2007.04.005

  5. Crouzet, L et al. “The hypersensitivity to colonic distension of IBS patients can be transferred to rats through their fecal microbiota.” Neurogastroenterology and motility vol. 25,4 (2013): e272-82. doi:10.1111/nmo.12103

  6. Pimentel, Mark et al. “Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome. a double-blind, randomized, placebo-controlled study.” The American journal of gastroenterology vol. 98,2 (2003): 412-9. doi:10.1111/j.1572-0241.2003.07234.x

  7. Pimentel, M et al. “Eradication of small intestinal bacterial overgrowth reduces symptoms of irritable bowel syndrome.” The American journal of gastroenterology vol. 95,12 (2000): 3503-6. doi:10.1111/j.1572-0241.2000.03368.x

  8. Gibson, P R, and S J Shepherd. “Personal view: food for thought--western lifestyle and susceptibility to Crohn's disease. The FODMAP hypothesis.” Alimentary pharmacology & therapeutics vol. 21,12 (2005): 1399-409. doi:10.1111/j.1365-2036.2005.02506.x

  9. Saito, Yuri A et al. “The genetics of irritable bowel syndrome.” Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association vol. 3,11 (2005): 1057-65. doi:10.1016/s1542-3565(05)00184-9

  10. Levy, R L et al. “Irritable bowel syndrome in twins: heredity and social learning both contribute to etiology.” Gastroenterology vol. 121,4 (2001): 799-804. doi:10.1053/gast.2001.27995

  11. Klem, Fabian et al. “Prevalence, Risk Factors and Outcomes of Irritable Bowel Syndrome After Infectious Enteritis: A Systematic Review and Meta-analysis” Gastroenterology vol. 152, Issue 5. P1042-1054. April 2017. DOI:

  12. Spiller, Robin et al. “Postinfectious Irritable Bowel Syndrome” Gastroenterology vol. 136, issue 6. P1979-1988. May 2009. DOI:

  13. Maxwell, P R et al. “Antibiotics increase functional abdominal symptoms.” The American journal of gastroenterology vol. 97,1 (2002): 104-8. doi:10.1111/j.1572-0241.2002.05428.x

  14. Sinha, L et al. “Idiopathic bile acid malabsorption: qualitative and quantitative clinical features and response to cholestyramine.” Alimentary pharmacology & therapeutics vol. 12,9 (1998): 839-44. doi:10.1046/j.1365-2036.1998.00388.x

  15. Spiller, R C et al. “Increased rectal mucosal enteroendocrine cells, T lymphocytes, and increased gut permeability following acute Campylobacter enteritis and in post-dysenteric irritable bowel syndrome.” Gut vol. 47,6 (2000): 804-11. doi:10.1136/gut.47.6.804

  16. Pimentel, Mark et al. “Development and validation of a biomarker for diarrhea-predominant irritable bowel syndrome in human subjects.” PloS one vol. 10,5 e0126438. 13 May. 2015, doi:10.1371/journal.pone.0126438

  17. Ong, Derrick K et al. “Manipulation of dietary short chain carbohydrates alters the pattern of gas production and genesis of symptoms in irritable bowel syndrome.” Journal of gastroenterology and hepatology vol. 25,8 (2010): 1366-73. doi:10.1111/j.1440-1746.2010.06370.x

  18. Moayyedi, Paul et al. “Canadian Association of Gastroenterology Clinical Practice Guideline for the Management of Irritable Bowel Syndrome (IBS).” Journal of the Canadian Association of Gastroenterology vol. 2,1 (2019): 6-29. doi:10.1093/jcag/gwy071

  19. Giannini, Edoardo G et al. “Role of partially hydrolyzed guar gum in the treatment of irritable bowel syndrome.” Nutrition (Burbank, Los Angeles County, Calif.) vol. 22,3 (2006): 334-42. doi:10.1016/j.nut.2005.10.003


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