Section structure
This topic is best organized around clinical context, study design, major epidemiologic findings, phenotypic differences between post-infection and non-post-infection disorders of gut-brain interaction, and implications for practice and research. The article therefore follows this structure: Highlights; Clinical background and disease burden; Study design and methods; Key findings; Clinical interpretation and expert commentary; Limitations and generalizability; Implications for practice and policy; Conclusion; Funding and trial registration; References.
Highlights
In a 26-country Rome Foundation survey, post-infection disorders of gut-brain interaction (PI-DGBI) represented 10.5% of all respondents with at least one DGBI diagnosis.
PI-DGBI showed clear geographic variation, with the highest prevalence reported in Asia and Latin America.
Younger age, male sex, urban residence, anxiety, and higher somatic symptom scores were associated with PI-DGBI, while female sex and rural residence were negatively associated.
Compared with DGBI not linked to infection, PI-DGBI was associated with greater psychological and physical health impairment and a distinctive symptom profile, including functional dyspepsia, irritable bowel syndrome, and anorectal disorders.
Clinical background and disease burden
Disorders of gut-brain interaction, formerly grouped under the term functional gastrointestinal disorders, are among the most common chronic digestive conditions encountered in primary care and gastroenterology. They include irritable bowel syndrome (IBS), functional dyspepsia, functional bowel disorders, and anorectal disorders. Although these conditions are defined symptomatically, they are not “medically unexplained” in a simplistic sense. Current models emphasize altered motility, visceral hypersensitivity, epithelial barrier dysfunction, immune activation, microbiome perturbation, and central processing abnormalities within the gut-brain axis.
One clinically important subgroup is post-infection DGBI, in which chronic gastrointestinal symptoms begin after an episode of acute infectious gastroenteritis. This phenomenon has been most extensively described in post-infectious IBS, but the syndrome extends beyond IBS to include upper gastrointestinal and anorectal manifestations. In routine practice, this history matters. It can improve diagnostic confidence, guide patient counseling, and shape expectations about prognosis. It also provides a biologically plausible bridge between an acute enteric insult and long-term symptom generation.
Despite this importance, the global epidemiology of PI-DGBI has been incompletely characterized. Most prior data come from single-country cohorts, outbreak studies, or post-infectious IBS meta-analyses. Less is known about how frequently these disorders occur across world regions, whether they differ demographically from non-post-infection DGBI, and how strongly they track with anxiety and somatic symptom burden in the general population. The Rome Foundation Global Epidemiology Study offers a rare opportunity to examine these questions at scale.
Study design and methods
Marasco and colleagues analyzed data from the Rome Foundation Global Epidemiology Study, an online survey that included 54,127 participants from 26 countries. From this global sample, 21,713 individuals were identified as having at least one DGBI. Within that subgroup, respondents were classified as having PI-DGBI if they reported gastrointestinal symptoms that began after an episode of acute gastroenteritis.
The study was observational and cross-sectional. Diagnoses were based on self-reported symptom data captured through Rome Foundation survey methods rather than physician adjudication, microbiologic confirmation, or prospective follow-up after documented infection. The principal goals were to estimate the prevalence of PI-DGBI among individuals with DGBI and to identify factors associated with PI-DGBI using multivariable logistic regression. The investigators also compared respondents with PI-DGBI against those with DGBI not associated with infection.
The outcomes of interest were therefore epidemiologic and phenotypic rather than therapeutic. Key variables included age, sex, geographic region, living environment, psychological measures such as anxiety, somatic symptom burden, and the distribution of DGBI subtypes.
Key findings
Overall prevalence
Among 21,713 respondents with at least one DGBI, 987 were classified as having PI-DGBI, corresponding to 10.5%. Clinically, that means roughly 1 in 10 people with a disorder of gut-brain interaction in this large multinational cohort linked the onset of their chronic gastrointestinal symptoms to a prior acute gastroenteritis episode.
This estimate is notable because it positions post-infectious disease as a substantial pathway into chronic gut-brain disorders, rather than a niche phenomenon confined to outbreak settings or tertiary referral centers.
Geographic variation
Prevalence varied across world regions. The highest reported rates were in Asia at 7.1% and Latin America at 6.4%. These regional differences likely reflect a combination of factors, including varying burdens of enteric infection, sanitation and food safety conditions, urbanization, healthcare access, pathogen mix, host factors, and differences in symptom reporting or survey participation. The study does not establish which of these explanations is dominant, but the geographic gradient reinforces the idea that PI-DGBI is shaped by both biological and social context.
Demographic and psychosocial associations
Multivariable analysis identified several factors positively associated with PI-DGBI. These included younger age, male sex, urban residence, anxiety, and higher somatic symptom scores. Female sex and rural residence were negatively associated.
Some of these findings are expected, while others are thought-provoking. Anxiety and somatic symptom burden fit well with current gut-brain models, in which heightened central symptom processing, autonomic arousal, and stress-related amplification interact with peripheral post-infectious changes such as low-grade mucosal inflammation or microbiome disruption. Younger age may reflect higher exposure to enteric infections, greater likelihood of symptom recall, or age-related differences in immune response and neurogastrointestinal resilience.
The male predominance is particularly interesting because many non-post-infectious DGBI, especially IBS, are more frequently reported in women in several populations. This suggests that the post-infectious pathway may not simply mirror the epidemiology of DGBI overall. It may also indicate regional sociocultural effects on reporting, different exposure patterns, or differential host-pathogen interactions. This deserves further study rather than overinterpretation.
Clinical phenotype
Participants with PI-DGBI experienced greater psychological and physical health impairment than those with DGBI not associated with infection. That finding has practical implications. A post-infectious onset should not be interpreted as a narrow bowel symptom disorder alone; it often signals a broader, more burdensome illness experience affecting mental well-being and daily functioning.
The gastrointestinal symptom pattern was also distinctive. Among respondents with PI-DGBI, functional dyspepsia was present in 32.2%, irritable bowel syndrome in 23.5%, and anorectal disorders in 35.3%. These figures emphasize that post-infectious sequelae are not confined to IBS. Upper gastrointestinal symptoms and anorectal dysfunction appear common and may reflect diffuse effects on motility, sensory processing, pelvic floor behavior, or overlapping DGBI phenotypes.
This broad distribution is clinically important because many clinicians still use the shorthand term post-infectious IBS as if it captures the entire syndrome. The present data argue for a wider view: acute gastroenteritis may trigger multiple chronic gut-brain disorders, alone or in combination.
Clinical interpretation and expert commentary
The main translational message is that acute infectious gastroenteritis should be recognized as a meaningful trigger for chronic gastrointestinal morbidity at population scale. This is consistent with prior literature on post-infectious IBS, but the current study extends the concept internationally and across the broader Rome DGBI spectrum.
From a mechanistic standpoint, the findings are biologically plausible. Infectious gastroenteritis can induce epithelial injury, increase intestinal permeability, alter bile acid handling, shift microbial ecology, and leave behind low-grade mucosal immune activation. These peripheral changes may interact with altered enteric nervous system signaling and central stress-response pathways, leading to persistent symptoms after the acute pathogen has cleared. The strong associations with anxiety and somatic symptom burden do not weaken the biological model; rather, they support a bidirectional gut-brain process in which peripheral and central drivers reinforce each other.
The study also raises a public health point. If a measurable share of chronic DGBI arises after infection, then food safety, clean water, outbreak control, vaccination where relevant, and equitable access to early care for gastroenteritis may have downstream benefits beyond prevention of acute illness alone. In other words, preventing enteric infection may also prevent chronic gut-brain disease.
For clinicians, the data support several practical steps. First, ask about symptom onset after an acute diarrheal or vomiting illness when evaluating chronic dyspepsia, bowel disturbance, or anorectal symptoms. Second, recognize that PI-DGBI can be associated with substantial psychosocial distress and somatic symptom burden; management may require integrated care rather than a purely gastrointestinal approach. Third, avoid excessive diagnostic escalation once alarm features and organic mimics have been appropriately assessed. A clear post-infectious timeline can help frame explanation and reassurance.
However, clinicians should also avoid reductionism. Not every patient with chronic symptoms after gastroenteritis has PI-DGBI, and not every PI-DGBI presentation is benign. Celiac disease, inflammatory bowel disease, microscopic colitis, bile acid diarrhea, pancreatic insufficiency, and pelvic floor disorders still need to be considered when the history or testing suggests them.
Limitations and generalizability
The study’s strengths are considerable: very large sample size, multinational scope, and consistent survey methodology across 26 countries. Nevertheless, several limitations are central to interpretation.
First, the analysis is cross-sectional and based on self-report. Respondents identified prior acute gastroenteritis and linked it temporally to chronic symptom onset, but infection was not microbiologically confirmed and timing was not prospectively tracked. Recall bias is therefore a major concern.
Second, online survey methods can introduce selection bias. Individuals with internet access, health awareness, or symptom salience may be overrepresented. This may affect prevalence estimates and potentially distort regional comparisons.
Third, DGBI diagnoses in epidemiologic surveys are useful but not equivalent to clinician-confirmed diagnoses after structured exclusion of alternative disease. The same applies to psychological and somatic symptom measures, which are informative but not diagnostic psychiatric assessments.
Fourth, the abstract provides associations rather than causal inference. Anxiety and somatic symptoms may predispose to PI-DGBI, result from PI-DGBI, or both. A bidirectional relationship is most likely.
Finally, region-level differences should be interpreted carefully. Cross-national variation may reflect true differences in infectious burden, but also cultural norms in symptom interpretation, language effects in questionnaires, and differing thresholds for recalling or labeling an episode as gastroenteritis.
Implications for practice and policy
This study supports the idea that PI-DGBI should be more explicitly recognized in clinical pathways, epidemiologic surveillance, and research frameworks. For gastroenterologists and primary care clinicians, a post-infectious history can help identify a distinct phenotype with potentially greater symptom burden and overlapping upper, lower, and anorectal manifestations.
For health systems, the findings suggest that the burden of enteric infection extends into chronic care utilization, work productivity loss, and mental health effects. Regions with higher acute infectious gastroenteritis burden may carry a hidden long-term gastrointestinal morbidity load that is underappreciated in policy planning.
For researchers, the priorities are clear: prospective cohort studies after microbiologically defined enteric infection; biomarker discovery linking acute inflammation to chronic symptom persistence; better phenotyping of overlap syndromes; and intervention trials targeting microbiome restoration, mucosal immune pathways, neuromodulation, and integrated psychological care.
Conclusion
The Rome Foundation Global Epidemiology Study shows that post-infection disorders of gut-brain interaction account for 10.5% of DGBI cases in a large multinational sample and are associated with younger age, male sex, urban residence, anxiety, and greater somatic symptom burden. These disorders are not limited to post-infectious IBS; they include functional dyspepsia and anorectal disorders and are linked to more severe physical and psychological impairment. The study strengthens the case that acute gastroenteritis is an important gateway to chronic gut-brain disease worldwide. It also highlights an actionable clinical message: prevention of enteric infection and early recognition of post-infectious symptom trajectories may have long-term benefits for gastrointestinal health.
Funding and trial registration
Funding details were not provided in the source abstract supplied here. No ClinicalTrials.gov registration number is applicable based on the available information for this observational survey analysis.
References
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