Introduction: When food poisoning is not really over
Most people think of infectious gastroenteritis as a short-lived misery: a few days of diarrhea, cramping, nausea, and then recovery. But for a meaningful minority of patients, the story does not end when the infection clears. Weeks or months later, they still feel bloated, nauseated, constipated, urgently need the bathroom, or experience abdominal pain that seems out of proportion to any visible damage. Increasingly, researchers understand that an acute gut infection can act as a trigger for long-term disorders of gut-brain interaction, or DGBI.
A newly published analysis from the Rome Foundation Global Epidemiology Study brings this issue into sharper focus. The study, published in Gut in 2026, examined more than 54,000 participants across 26 countries and found that post-infection disorders of gut-brain interaction, abbreviated PI-DGBI, represent a substantial subgroup of chronic gastrointestinal disorders. Among people with at least one DGBI, about 10.5% reported symptoms that began after acute gastroenteritis.
That finding matters because DGBI are often misunderstood. They are real disorders with measurable effects on quality of life, functioning, and mental health, even when routine scans or blood tests are unrevealing. The new study also suggests that post-infectious cases may have a somewhat distinct profile, with important implications for prevention, diagnosis, and treatment.
What are post-infection disorders of gut-brain interaction?
The term DGBI is the modern replacement for what many clinicians once called “functional gastrointestinal disorders.” These conditions arise from altered communication between the gut and the brain, involving changes in motility, intestinal permeability, immune activation, visceral sensitivity, the microbiome, and stress-response pathways. They are not imaginary and they are not simply “stress.”
Post-infection DGBI are DGBI that begin after an episode of infectious gastroenteritis. The best-known example is post-infectious irritable bowel syndrome, or PI-IBS, but the new Rome Foundation analysis shows the problem extends beyond IBS. Functional dyspepsia, bowel disorders, and anorectal disorders can also emerge after infection.
In practical terms, a patient may have a severe bout of bacterial, viral, or parasitic diarrhea and later develop chronic abdominal pain, early fullness, post-meal discomfort, bloating, altered stool frequency, or anorectal symptoms such as incomplete evacuation. The original infection may be gone, but the gut’s signaling and regulation remain altered.
What the new global study found
The Rome Foundation Global Epidemiology Study is notable for its scale and international reach. Investigators analyzed online survey data from 54,127 participants in 26 countries. Of the 21,713 people who met criteria for at least one DGBI, 987 were classified as having PI-DGBI.
Several findings stand out.
First, PI-DGBI are not rare. If roughly one in ten DGBI cases are linked to a prior acute gastroenteritis episode, that means clinicians should routinely ask about infection history when evaluating chronic digestive symptoms.
Second, prevalence varied across regions. The highest rates were reported in Asia at 7.1% and Latin America at 6.4%. Geographic variation does not automatically mean biology is different from one continent to another. It may reflect differences in infection burden, sanitation, food and water exposure, healthcare access, antibiotic use, symptom reporting, or cultural understanding of bowel symptoms.
Third, certain factors were associated with higher odds of PI-DGBI: younger age, male sex, urban residence, anxiety, and higher somatic symptom scores. Female sex and rural living were negatively associated in this particular study. That does not mean women are protected from DGBI overall; in fact, many DGBI are more common in women. Rather, this suggests that the post-infectious subgroup may differ from non-post-infectious DGBI in meaningful ways.
Fourth, people with PI-DGBI had greater psychological and physical health impairment than those without infection-linked onset. They also showed distinct gastrointestinal patterns, including relatively high rates of functional dyspepsia, irritable bowel syndrome, and anorectal disorders.
Why a gut infection can leave a long shadow
Why would a short infection trigger months or years of digestive trouble? The answer appears to involve several overlapping mechanisms rather than one single cause.
One mechanism is low-grade immune activation. Even after the pathogen is cleared, the intestinal immune system may remain in a state of increased alertness. This can alter barrier function and make the gut more reactive.
A second mechanism is microbiome disruption. Infectious diarrhea and its treatments, especially antibiotics, can shift the composition and function of gut microbes. Some patients recover their prior microbial balance; others may not, or recover differently.
A third is visceral hypersensitivity. The nerves that carry sensation from the intestine to the brain may become more responsive after inflammation or injury, so normal stretching or digestion feels painful or urgent.
A fourth involves motility changes. The coordinated muscular activity that moves food through the digestive tract can become dysregulated, leading to diarrhea, constipation, or mixed patterns.
Finally, the brain-gut axis matters. Anxiety, sleep disturbance, trauma, and hypervigilance can amplify symptoms, while chronic symptoms can worsen anxiety in return. This is a two-way biological conversation, not a one-way psychological explanation.
A patient story: Emily’s “food poisoning” that never really ended
Emily, a 29-year-old marketing manager, had what seemed like classic food poisoning after a summer wedding. She spent three days with severe diarrhea, fever, and abdominal cramps. Her acute illness resolved, but two months later she was still avoiding social events because she never knew when she would need a bathroom. She felt bloated after meals, had cramping several times a week, and became anxious during meetings.
Basic blood work was normal. A clinician initially reassured her that “everything looks fine,” which she heard as “nothing is wrong.” But a gastroenterologist later explained that her symptoms were consistent with post-infectious IBS, a recognized disorder of gut-brain interaction. Once she understood that the condition was real, common, and treatable, her care plan became more focused: diet review, targeted symptom therapy, stress-reduction strategies, and gradual return to feared activities.
Emily’s story is fictional, but the pattern is familiar. Many patients with PI-DGBI feel invalidated because their symptoms began after a clear physical trigger, yet persist without obvious structural abnormalities on testing.
How this study changes the conversation
This new paper does more than provide prevalence estimates. It challenges a persistent misconception that DGBI are vague, minor, or mainly psychological. The findings support a model in which infection can act as a biologic initiating event for chronic gastrointestinal illness.
That matters clinically. A patient who develops new symptoms after gastroenteritis should not automatically be told to “just wait it out” indefinitely, nor should extensive testing be ordered reflexively without a thoughtful history. Instead, clinicians can use the infection timeline as an important clue. The key is balanced evaluation: rule out red flags, but recognize that normal structural tests do not exclude significant disease.
It also matters for public health. Preventing foodborne and waterborne infections may reduce not only acute illness but a long tail of chronic suffering that often goes uncounted in traditional infection statistics.
Misconceptions that can delay recovery
Several myths still surround post-infectious gut disorders.
The first is that if scans and blood tests are normal, the symptoms must be psychological. This is false. PI-DGBI involve measurable physiologic changes, even if routine tests do not capture them.
The second is that the problem is always IBS. IBS is common, but post-infectious syndromes can include functional dyspepsia and anorectal disorders too. Some patients have overlap syndromes.
The third is that one restrictive diet fits everyone. Many patients experiment with broad elimination diets they find online, sometimes worsening nutrition, food fear, and social isolation. Dietary therapy can help, but it should be individualized.
The fourth is that antibiotics are a cure for lingering symptoms. Unless there is evidence of ongoing infection or a specific indication, repeated antibiotics may do harm by further disturbing the microbiome.
The fifth is that anxiety means the symptoms are not physical. Anxiety can increase symptom severity and is associated with PI-DGBI, but it is part of the illness experience, not proof that the condition is imagined.
What patients and clinicians should do in practice
A sensible approach starts with careful history-taking. Ask whether chronic digestive symptoms began after a discrete episode of vomiting, diarrhea, fever, traveler’s diarrhea, food poisoning, or a diagnosed enteric infection.
Next, look for red flags that warrant broader evaluation: gastrointestinal bleeding, significant unintentional weight loss, persistent fever, nocturnal symptoms, anemia, progressive swallowing difficulty, family history of inflammatory bowel disease or colorectal cancer, or onset at an older age without prior explanation.
If red flags are absent and symptoms fit Rome criteria, clinicians can often make a positive diagnosis of a DGBI rather than using it as a diagnosis of exclusion after endless testing.
Treatment is usually multimodal. Depending on the symptom pattern, options may include dietary counseling, soluble fiber, antidiarrheals, osmotic laxatives, antispasmodics, gut-directed neuromodulators, pelvic floor therapy for anorectal dysfunction, and psychological therapies such as cognitive behavioral therapy or gut-directed hypnotherapy.
Patients also benefit from validation. One of the most therapeutic moments in a clinic visit is often when a patient hears, “Your symptoms are real, and we have a framework to understand them.”
Table: Key takeaways from the Rome Foundation Global Epidemiology Study
| Study element | Main finding | Why it matters |
|---|---|---|
| Population | 54,127 participants across 26 countries | Provides rare global insight rather than a single-country snapshot |
| DGBI subgroup analyzed | 21,713 had at least one DGBI | Shows how common gut-brain disorders are overall |
| PI-DGBI cases | 987 participants; 10.5% of those with DGBI | Suggests infection-triggered disorders are a substantial subgroup |
| Geographic pattern | Highest reported rates in Asia and Latin America | Points to possible differences in infection exposure, healthcare access, and reporting |
| Associated factors | Younger age, male sex, urban living, anxiety, higher somatic symptom scores | Helps identify who may be at higher risk after gastroenteritis |
| Common symptom profiles | Functional dyspepsia, IBS, and anorectal disorders were frequent | Clinicians should think beyond IBS alone |
| Health impact | Greater psychological and physical impairment than non-post-infectious DGBI | Highlights the seriousness of these conditions |
What remains uncertain
Like all large epidemiologic surveys, this study has limitations. Diagnoses and infection histories were based on self-report rather than confirmed microbiology or longitudinal clinical follow-up. Online surveys may miss people with limited internet access or different symptom-reporting habits. The study also identifies associations, not direct causation.
Even so, the findings fit with a larger body of evidence built over two decades. Prior studies have shown increased risk of IBS after bacterial enteritis caused by organisms such as Campylobacter, Salmonella, and Shigella, as well as after traveler’s diarrhea and some viral infections. The new work expands that picture on a global scale and underscores that the consequences are broader than one syndrome.
Future research will likely focus on who is most vulnerable, whether specific pathogens carry greater long-term risk, how the microbiome changes over time, and whether early interventions after gastroenteritis can prevent chronic symptoms from becoming established.
Expert perspective: prevention and early recognition matter
One important implication of this research is that the cost of gastroenteritis is often underestimated. Public health discussions usually focus on acute dehydration, missed workdays, or outbreak control. But if a fraction of infected individuals go on to develop chronic gut-brain disorders, then the burden of foodborne and waterborne illness is much larger than acute case counts suggest.
For clinicians, early recognition may help reduce unnecessary testing and months of confusion. For patients, understanding the diagnosis may reduce fear of hidden catastrophic disease. And for researchers, PI-DGBI may provide a useful model for studying how an external trigger reshapes gut-brain biology.
As the Rome Foundation and many gastroenterology experts have emphasized, DGBI deserve the same seriousness as other chronic conditions. Their impact on daily function, work productivity, nutrition, mood, and social life can be profound.
Conclusion
The 2026 Rome Foundation Global Epidemiology Study offers a timely reminder that an ordinary stomach infection can have extraordinary aftereffects. Post-infection disorders of gut-brain interaction are common enough to matter, serious enough to impair quality of life, and biologically plausible enough to demand more than dismissal.
The study’s message is straightforward: acute gastroenteritis is not always an isolated event. For some people, it is the starting point of a chronic disorder shaped by immunity, nerves, microbes, motility, and the brain-gut axis. Better prevention of enteric infections, faster recognition of post-infectious symptoms, and more integrated treatment could reduce a burden that is currently hidden in plain sight.
For patients still struggling months after “just a stomach bug,” the most important message may be the simplest one: you are not imagining it, and you are not alone.
References
1. Marasco G, Schmulson M, Ghoshal UC, et al. Post-infection disorders of gut-brain interaction: results of the Rome Foundation Global Epidemiology Study. Gut. 2026;75(7):1297-1306. doi:10.1136/gutjnl-2025-334731.
2. Drossman DA, Tack J, Ford AC, et al. Neuromodulators for functional gastrointestinal disorders (disorders of gut-brain interaction): A Rome Foundation working team report. Gastroenterology. 2018;154(4):1140-1171.e1. doi:10.1053/j.gastro.2017.11.279.
3. Sperber AD, Bangdiwala SI, Drossman DA, et al. Worldwide prevalence and burden of functional gastrointestinal disorders, results of Rome Foundation Global Study. Gastroenterology. 2021;160(1):99-114.e3. doi:10.1053/j.gastro.2020.04.014.
4. Schmulson M, Ghoshal UC, Barbara G. Managing the inevitable surge of post-COVID-19 functional gastrointestinal disorders. Am J Gastroenterol. 2021;116(1):4-7. doi:10.14309/ajg.0000000000001082.
5. Thabane M, Kottachchi DT, Marshall JK. Systematic review and meta-analysis: The incidence and prognosis of post-infectious irritable bowel syndrome. Aliment Pharmacol Ther. 2007;26(4):535-544. doi:10.1111/j.1365-2036.2007.03399.x.
6. Spiller R, Garsed K. Postinfectious irritable bowel syndrome. Gastroenterology. 2009;136(6):1979-1988. doi:10.1053/j.gastro.2009.02.074.
7. Black CJ, Drossman DA, Talley NJ, Ruddy J, Ford AC. Functional gastrointestinal disorders: Advances in understanding and management. Lancet. 2020;396(10263):1664-1674. doi:10.1016/S0140-6736(20)32115-2.