See “Prevalence, risk factors, and outcomes of irritable bowel syndrome after infectious enteritis: a systematic review and meta-analysis,” by Klem F, Wadhwa A, Prokop L, et al, on page 1042

1 Mearin F.

Lacy B.E.

Chang L.

et al. Bowel disorders. Although the current literature would suggest that postinfectious irritable bowel syndrome (PI-IBS) is a new phenomenon, the prevalence of enteric infections in the ancient world renders it inevitable that this entity is far from new. All we need is the discovery of an Egyptian papyrus, Greek vase, or Roman monument that in symbol, letter, or paint depicts the development of chronic gastrointestinal symptoms after an enteric infection. That the literature on PI-IBS is so consistently modern and overwhelmingly Western is, in large part, a tribute to the recent access to accurate microbiological testing and the recognition and standardization of IBS as a diagnostic entity.

2 Hargreaves W.H. The treatment of amoebiasis; with special reference to chronic amoebic dysentery. , 3 Stewart G.T. Post-dysenteric colitis. 3 Stewart G.T. Post-dysenteric colitis. 3 Stewart G.T. Post-dysenteric colitis. 3 Stewart G.T. Post-dysenteric colitis. 4 Chaudhary N.A.

Truelove S.C. The irritable colon syndrome. A study of the clinical features, predisposing causes, and prognosis in 130 cases. In the modern era, reports of the development of chronic gastrointestinal symptoms in the aftermath of an apparently resolved enteric infection or infestation date back at least to the 1940s.The report by Stewartis especially noteworthy. He described in elegant detail the long-term outcome of cases of dysentery seen in a military hospital in Sri Lanka and at the Tropical Diseases Center in Liverpool, UK.In Sri Lanka, he noted that although persistent symptoms were rare after bacillary dysentery, diarrhea persisted in many patients after amoebiasis. The Liverpool cases were studied in more detail and, in those, he presciently differentiated 1 group whom he referred to as functional, type I, postdysenteric colitis (surely, the first description of PI-IBS) and who, despite chronic symptoms, had normal or near normal appearances on sigmoidoscopic examination.Twelve years later, in what remains a classic description of the syndrome, Chaudhary and Truelove reported that “in 34 (of 130 irritable colon) patients the symptoms dated from an attack of infective dysentery, either proven or strongly presumptive.”

5 McKendrick M.W.

Read M.W. Irritable bowel syndrome-post salmonella infection. 6 Mearin F.

Perez-Oliveras M.

Perello A.

et al. Dyspepsia and irritable bowel syndrome after a Salmonella gastroenteritis outbreak: one-year follow-up cohort study. , 7 Marshall J.K.

Thabane M.

Garg A.X.

et al. Walkerton Health Study Investigators. Incidence and epidemiology of irritable bowel syndrome after a large waterborne outbreak of bacterial dysentery. 8 Neal K.R.

Hebdon J.

Spiller R. Prevalence of gastrointestinal symptoms six months after bacterial gastroenteritis and risk factors for development of the irritable bowel syndrome. , 9 Garcia Rodriguez L.A.

Ruigomez A. Increased risk of irritable bowel syndrome after bacterial gastroenteritis: cohort study. 10 Zanini B.

Ricci C.

Bandera F.

et al. San Felice del Benaco Study Investigators

Incidence of post-infectious irritable bowel syndrome and functional intestinal disorders following a water-borne viral gastroenteritis outbreak. 11 Stark D.

van Hal S.

Marriott D.

et al. Irritable bowel syndrome: a review on the role of intestinal protozoa and the importance of their detection and diagnosis. , 12 Grazioli B.

Matera G.

Laratta C.

et al. Giardia lamblia infection in patients with irritable bowel syndrome and dyspepsia: a prospective study. 6 Mearin F.

Perez-Oliveras M.

Perello A.

et al. Dyspepsia and irritable bowel syndrome after a Salmonella gastroenteritis outbreak: one-year follow-up cohort study. , 11 Stark D.

van Hal S.

Marriott D.

et al. Irritable bowel syndrome: a review on the role of intestinal protozoa and the importance of their detection and diagnosis. Real and sustained interest in PI-IBS did not resurface until the 1990s; since then, several series of varying size, design, and geographic origin have delineated the prevalence, risk factors, and natural history of PI-IBS. Some followed the outcome of large, single-source outbreaks resulting from food- or water-borne pathogens,whereas others calculated occurrence rates among those infections that had been catalogued by a central reference laboratory or primary care database.Although many of these reports focused on bacterial infections, reports of PI-IBS after viral,protozoal, and parasitic infectionsalso began to appear and it became clear that dyspeptic as well as IBS-type symptoms could ensue.

13 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. 14 Schwille-Kiuntke J.

Mazurak N. Systematic review with meta-analysis: post-infectious irritable bowel syndrome after travellers' diarrhoea. , 15 Halvorson H.A.

Schlett C.D.

Riddle M.S. Postinfectious irritable bowel syndrome–a meta-analysis. 16 Neal K.R.

Barker L.

Spiller R.C. Prognosis in post-infective irritable bowel syndrome: a six year follow up study. 17 Paula H.

Grover M.

Halder S.L.

et al. Non-enteric infections, antibiotic use, and risk of development of functional gastrointestinal disorders. In this issue of Gastroenterology, Klem et alprovide an up-to-date systematic review of PI-IBS including 45 studies and more than 21,000 individual cases. They calculated an overall pooled prevalence of IBS after an episode of infectious enteritis of 11.5%, very much in line with prior estimates.PI-IBS was most likely to follow a protozoan or parasitic infection (event rate 41.9%) and least likely after a viral infection (6.4%), with rates after a bacterial infection being intermediate between these extremes at 13.8%. In general, and contrary to earlier perceptions, PI-IBS was not a short-lived disturbance of bowel function with rates remaining high well beyond 12 months (and up to 6 years in 1 study). In this regard, postviral PI-IBS was an exception with rates dropping from 19.4% within 12 months of infection to as low as 4.4% beyond 12 months. Although cautioning that heterogeneity between studies may have complicated their analysis of risk factors, the authors found that females, those who suffered a severe index attack of enteritis, those who received antibiotic therapy, and those who experienced psychological distress at the time of the infection were at greatest risk for the development of PI-IBS, findings that are consistent with most individual studies. Whether antibiotic use is a mere surrogate for a more severe and presumed bacterial infection or, as has been suggested by other data,represents an independent risk factor remains unclear.

Although none of these findings are new to those who have followed this literature, 1 deduction made from their analyses will truly shock the reader: a proposal that PI-IBS may contribute to the majority of IBS cases! Is enteric infection indeed the foundation on which the edifice we now behold as IBS is built?

13 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. 18 Center for Disease Control and Prevention. Estimates of foodborne illness in the United States. Available at: www.cdc.gov/foodborneburden/. Accessed February 4, 2017. 19 Shah E.D.

Riddle M.S.

Chang C.

et al. Estimating the contribution of acute gastroenteritis to the overall prevalence of irritable bowel syndrome. 19 Shah E.D.

Riddle M.S.

Chang C.

et al. Estimating the contribution of acute gastroenteritis to the overall prevalence of irritable bowel syndrome. 20 Lovell R.M.

Ford A.C. Global prevalence of and risk factors for irritable bowel syndrome: a meta-analysis. 19 Shah E.D.

Riddle M.S.

Chang C.

et al. Estimating the contribution of acute gastroenteritis to the overall prevalence of irritable bowel syndrome. This proposal is based on the application of their calculated pooled prevalence rate for new onset of IBS after an enteric infection (10%)to the estimated 15% of individuals who acquire an enteric infection annually in the United States (a total of >37 million cases annually).Given the chronicity of IBS symptoms the accumulation of new PI-IBS cases over time, as modeled by others,would indeed lead to enteric infection as being the major trigger for the development of IBS. In 1 model, which assumed that a majority of subjects who suffered an enteric infection were resistant to the development of PI-IBS, the prevalence of IBS attributable to PI-IBS alone would reach a steady state of 9.1% after 10 years,a figure remarkably close to that reported for IBS, in general, in the United States.In another model involving a group at high risk for the development of PI-IBS, this prevalence rate was achieved within 1 year of exposure.

4 Chaudhary N.A.

Truelove S.C. The irritable colon syndrome. A study of the clinical features, predisposing causes, and prognosis in 130 cases. Why will clinicians be so taken aback? Despite their conscientious attempts to enquire about the onset of a given sufferer’s IBS symptoms and accepting the mere description of a sudden onset of symptoms as an indication of a likely infectious trigger, clinicians find it singularly uncommon to obtain such a history and would tend to agree with the estimate of Chaudhary and Truelovethat PI-IBS, as currently defined, represents a minority of the total IBS population. One could argue that enteric infections may be asymptomatic and that surveys confined to symptomatic individuals underestimate their impact; only prospective studies of the true impact of all enteric infections on IBS prevalence will answer this question.

13 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. 21 Löwe B.

Lohse A.

Andresen V.

et al. The development of irritable bowel syndrome: a prospective community-based cohort study. 13 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. 20 Lovell R.M.

Ford A.C. Global prevalence of and risk factors for irritable bowel syndrome: a meta-analysis. 22 Cremon C.

Stanghellini V.

Pallotti F.

et al. Salmonella gastroenteritis during childhood is a risk factor for irritable bowel syndrome in adulthood. Other observations mitigate against the proposal that PI-IBS is the dominant form of IBS. Klem et alnoted, for example, that studies with lower response rates yielded higher prevalence rates suggesting responder bias; prospective studies encompassing at-risk populations also report lower rates.There is also the suggestion, again noted by Klem et al,that, in terms of symptomatology at least, PI-IBS may not be identical to IBS, in general. Then there is the global issue. If IBS was primarily caused by enteric infections, one would predict astronomical rates of IBS in emerging nations; what we know of the global epidemiology of IBS, its glaring shortcomings notwithstanding, fails to confirm this or even to reveal a clear relationship between IBS prevalence and socioeconomic status.Perhaps exposure in early childhood to multiple enteric pathogens protects the individual in the developing world from IBS in adulthood; available data from the West suggest that childhood exposure to enteric pathogens actually predisposes to IBS in adolescence and adulthood.

13 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. 23 Villani A.C.

Lemire M.

Thabane M.

et al. Genetic risk factors for post-infectious irritable bowel syndrome following a waterborne outbreak of gastroenteritis. 24 Grover M.

Camilleri M.

Smith K.

et al. On the fiftieth anniversary. Postinfectious irritable bowel syndrome: mechanisms related to pathogens. Although many issues relating to the epidemiology of PI-IBS remain to be clarified, this IBS phenotype, regardless of its true prevalence, provides us with an invaluable model within which we can explore pathophysiology. What emerges from the work of Klem et aland many others provides us with our best working hypothesis for the development of IBS: a susceptible individual (based on gender, psychological profile, and perhaps genetic makeup) exposed to environmental triggers (eg, an enteric pathogen) incurs a series of host–microbe interactions that ultimately impact on the enteric neuromuscular apparatus and the central nervous system to initiate and perpetuate the symptoms that we recognize as IBS; the microbiome–gut–brain axis in action.

Article Info Publication History Footnotes Conflicts of interest The authors discloses no conflicts. Identification DOI: https://doi.org/10.1053/j.gastro.2017.02.028 Copyright © 2017 by the AGA Institute ScienceDirect Access this article on ScienceDirect