Post-infectious gut urgency — the persistence of bowel hypersensitivity and urgency to defecate following resolution of an acute gastrointestinal infection or travelers' diarrhea — represents a clinically underappreciated sequela affecting a meaningful subset of travelers and individuals recovering from GI illness. While the acute infectious episode typically resolves spontaneously or with antimicrobial therapy, transient dysbiosis induced by the infection itself, or by the antibiotics used to treat it, may sustain altered gut motility and fermentation dynamics beyond the acute phase. Three mechanistic patterns are described in the literature that may contribute to this persistence: overrepresentation of hydrogen sulfide–producing bacteria, depletion of beneficial obligate anaerobes and the short-chain fatty acids they produce, and bloom of opportunistic pathobionts that metabolize fermentable substrates differently from commensal species. Collectively, these shifts increase sensitivity to rapidly fermentable carbohydrates (FODMAPs) even in individuals who were previously tolerant. We hypothesize that substrate-level intervention using FODZYME®, an enzymatic formulation targeting fructans, GOS, and lactose, may offer a pragmatic approach to managing post-infectious urgency by reducing the fermentable carbohydrate load reaching the colon, thereby limiting osmotic fluid shifts, gas production, and fermentable substrate availability for dysbiosis-associated taxa during the transient recovery window.
Some people experience increased digestive sensitivity after travel or a short-lived stomach upset. Even after the acute episode resolves, they may notice annoying, occasional urgency with their usual diet. We hypothesize here why this might be the case and how this post-travel urgency might be addressed with FODZYME®.
Gastrointestinal infections are one of the most frequent medical conditions diagnosed in patients who travel to tropical or subtropical destinations. For example, Travelers’ diarrhea affects 10–70% of travelers from low infectious disease-risk countries visiting middle- and high-risk destinations. Typically, travel-related GI infections resolve spontaneously or upon self-administered empirical antimicrobial therapy.
However, in some patients the symptoms of increased bowel sensitivity and urgency to defecate following meals can persist. After infectious gastroenteritis/traveler’s diarrhea, a subset develops ongoing bowel sensitivity. The gut remains more reactive following infection and can even lead to long-term health consequences such as post-infectious IBS. Reports suggest that >10% of patients with infectious enteritis develop IBS later.
Increased urgency to defecate following travel or gastrointestinal infections may reflect transient alterations in the gut microbial ecosystem. The gut microbiota composition after international travel has been observed to show reduced diversity and a richness in pathogenic species such as E. coli and Shigella. Any infectious episode whether self-limited or treated with antibiotics, can potentially perturb the normal composition of the gut microbiome.
Even short-term infections can create subtle but meaningful shifts in microbial balance. Further, use of antimicrobials to resolve the infectious episode can represent another microbiome destabilizing event. These imbalances in the equilibrium of the gut microbial community are commonly referred to as dysbiosis. Perturbations in the gut microbial communities may contribute to increased gut motility and altered fermentation dynamics. Several dysbiosis patterns are described in the literature:
An overrepresentation of sulfate-reducing or other hydrogen sulfide–producing bacteria has been associated with increased intestinal motility and epithelial irritation. H₂S is a biologically active gasotransmitter that, in higher concentrations, may:
Experimental and human studies have linked increased luminal H₂S production to altered motility patterns and diarrheal phenotypes in susceptible individuals.
Acute infection or antibiotic exposure can reduce populations of beneficial obligate anaerobes (e.g., butyrate-producing Firmicutes). Loss of these taxa may:
Reduced microbial diversity and depletion of SCFA–producing commensals such as Faecalibacterium prausnitzii, and Bifidobacterium spp. often occur with expansion of pro-inflammatory taxa.
During an infection, pathogens such as Salmonella and Campylobacter can re-engineer the host environment to facilitate their proliferation. These opportunistic organisms produce metabolites (e.g., certain organic acids, toxins, or inflammatory mediators) that may increase motility and fluid secretion, contributing to urgency. Concurrently, the flourishing pathogen population can metabolize fermentable substrates differently compared to commensal species, generating fermentation byproducts that further perturb gut motility. Antibiotic exposure can additionally reduce microbial diversity, potentially increasing gut sensitivity to fermentable substrates during recovery.
These shifts have been documented following antibiotic exposure and gastrointestinal infection, often resulting in increased microbial instability and altered fermentation dynamics.
Transient dysbiosis, whether driven by infection, antibiotic use, or environmental microbial exposure during travel, can disrupt the obligate anaerobe compartment that underpins colonic SCFA production from fermentable substrates. Even short-lived perturbations in this compartment may be sufficient to alter fermentation balance and increase colonic sensitivity to fermentable substrates like FODMAPs (Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols).
FODZYME®’s enzyme formulation targeting fructans, GOS, and lactose is designed to effectively break down select fermentable carbohydrates (FODMAPs) before they reach the colon. By reducing this rapidly fermentable substrate load, we aim to:
Reducing the fermentable carbohydrate load reaching the colon may limit the downstream consequences of dysbiosis-associated fermentation shifts. This is the mechanistic basis for evaluating FODMAP-targeted enzymatic supplementation in individuals experiencing post-infectious bowel urgency.
It should be noted that the mechanistic framework presented here represents a hypothesis based on existing literature and plausible biological reasoning. The role of FODMAP-targeted enzymatic supplementation in post-infectious gut urgency has not yet been evaluated in controlled clinical studies, and the proposed mechanisms require prospective investigation before clinical recommendations can be made.