Postinfectious IBS: What to Look For

stomach pain
stomach pain, ibd, ibs, stomachache
Given the overall prevalence of irritable bowel syndrome, it is important for clinicians to be able to distinguish postinfectious irritable bowel syndrome from its other subtypes.

Irritable bowel syndrome (IBS) is one of the most common conditions encountered by a gastroenterologist. Clinically, it can present with a multitude of symptoms including constipation, diarrhea, abdominal pain, and bloating. Postinfectious IBS (PI-IBS) is a specific subtype of IBS in which an enteric infection triggers a cascade of events within the gastrointestinal tract (GIT). Up to 17% of patients believe that their IBS began after an infection and up to 36% of patients with an enteric infection can develop symptoms consistent with PI-IBS.1 Although there is no formal definition, PI-IBS can be considered when a patient experiences acute onset of IBS symptoms (fever, vomiting, diarrhea, positive stool culture) without previously being diagnosed with IBS based on the Rome criteria.1 Patients with PI-IBS can develop symptoms anywhere from days to years postinfection, which can make the clinical course challenging to predict.1-3 

An enteric infection can lead to a proinflammatory state within the GIT, causing an alteration in the gut microbiome as well as the cellular composition of the tract.2 These changes can lead to increased permeability of the GIT, alterations in the immune system, and development of a multitude of GI symptoms.2 Changes induced by an enteric infection can be self-limited for a relatively short amount of time, though some literature has proposed this leads to chronic changes and long-term development of IBS.2 Risk factors for developing the more chronic sequelae include duration of initial illness, toxicity of infectious agents, utilization of antibiotics, smoking status, inflammatory markers, sex (women > men), psychosocial stressors, and certain genetic variants.2,3 Patients with a viral gastroenteritis (VGE) are less likely to develop PI-IBS than those with a bacterial infection that causes more significant mucosal damage, such as Campylobacter jejuni and Escherichia coli (E coli).2 Therefore, patients with VGE typically have shorter duration of symptoms and are less likely to develop long-term IBS symptoms.2,3 

Patients with PI-IBS are more likely to exhibit symptoms consistent with diarrhea predominant IBS (IBS-D), which occurs in approximately 63% of patients.1 Close to 25% of patients can develop alternating constipation and diarrhea, while 13% have constipation alone.1 Additional symptoms include bloating and increased mucus in the stool. Some of the most commonly implicated bacteria include E coli, Salmonella, giardia, and Campylobacter.2 Symptoms can persist for an extended period of time, although the prevalence appears to decline after several years.3

There are multiple mechanisms through which an enteric infection can induce PI-IBS. Infections can lead to increased intestinal motility resulting in diarrhea and abdominal cramping.2 Colonic distension induced by infectious agents can lead to abdominal visceral hypersensitivity, leading to an increase in symptoms, especially pain and bloating.2 Damage to the epithelial cell barrier within the GIT predisposes patients to a proinflammatory state with persistent immune cell activation.2 Immune system components that have been implicated include mast cells, macrophages, enterochromaffin cells, and excessive cytokines (CYK).2 Certain infectious agents can cause acute villous blunting and infiltration of the mucosa with intraepithelial lymphocytes (IELs).1 Additionally, the mechanism may vary based on the area of the GIT affected by the infectious agent (eg, small intestine vs colon). An acute infection can also disrupt the gut microbiome, causing a reduction in the amount of short chain fatty acids (SCFAs) and an increase in luminal pH.2 

Klem et al conducted a large systematic review and meta-analysis to determine the prevalence of IBS 3 months or more after an initial infectious enteritis.4 This review consisted of 45 total studies including 21,421 patients. The pooled prevalence at 12 months postinfection was 10.1% (95% CI, 7.2-14.1) and 14.5% (95% CI, 7.7-25.5) at more than 12 months. Patients with infectious enteritis had a 4.2 times higher risk of developing IBS vs those without infection in the last 12 months (95% CI, 3.1-5.7). More patients with a parasite or protozoal infection developed IBS compared against those with a bacterial infection (41.9% vs 13.8%). Additional risk factors for developing PI-IBS included sex (women > men), antibiotic exposure, and anxiety and/or depression. It is important to note that there was a substantial amount of heterogeneity among studies included in this review. 

When evaluating a patient for PI-IBS it is important to also keep other conditions on the differential diagnosis, including inflammatory bowel disease, lactose intolerance, bile acid malabsorption, and microscopic colitis (eg, lymphocytic and/or collagenous colitis).1 As IBS is typically a diagnosis of exclusion, many patients undergoing evaluation for PI-IBS will have a series of tests that may include laboratory testing (complete blood count, basic metabolic panel, liver function tests, C-reactive protein, celiac panels, thyroid stimulating hormone), stool testing (infectious panel, fecal calprotectin), imaging (computed tomography, computed tomography enterography/magnetic resonance enterography) and endoscopic procedures (colonoscopy and/or endoscopy). 

Often, patients with PI-IBS can be managed conservatively. Although there are no medications formally indicated for PI-IBS, most of the treatments are aimed at symptomatic relief with medications such as loperamide or dicyclomine. Additional agents that have been reported in the literature include prebiotics, probiotics, mesalamine, alosetron and rifaximin, although there is a paucity of data supporting the routine use of any of these medications.1 


  1. Spiller R, Garsed K. Postinfectious irritable bowel syndrome. Gastroenterol. 2009;136(6):1979-88.  doi: 10.1053/j.gastro.2009.02.074
  2. Beatty JK, Bhargava A, Buret AG. Post-infectious irritable bowel syndrome: mechanistic insights into chronic disturbances following enteric infection. World J Gastroenterol. 2014;20(14):3976-3985. doi: 10.3748/wjg.v20.i14.3976
  3. Thaban M, Marshall JK. Post-infectious irritable bowel syndrome. World J Gastroenterol.  2009;15(29):3591-3596. doi: 10.3748/wjg.15.3591
  4. Klem F, Wadhwa A, Prokop L, et al. Prevalence, risk factors, and outcomes of irritable bowel syndrome after infectious enteritis: a systematic review and meta-analysis. Gastroenterol.  2017;152(5):1042-1054.e1.  doi: 10.1053/j.gastro.2016.12.039