Feb 4, 2026
For many people, food poisoning is a short-lived illness. You eat something contaminated, feel miserable for a few days, and then recover.
But for some, food poisoning is not the end of the story. In certain cases, the initial infection can set off a series of biological events that disrupt how the gut moves and clears bacteria, eventually creating the conditions for small intestinal bacterial overgrowth (SIBO).
Understanding how a brief infection can lead to long-term changes in gut function helps explain why SIBO often develops slowly, why symptoms may appear months later, and why it can take time for people—and their doctors—to recognize what’s really going on.
What is Food Poisoning
Food poisoning is an illness caused by eating or drinking something contaminated with harmful bacteria, viruses, or parasites. Common symptoms include nausea, vomiting, diarrhea, stomach cramps, fever, and weakness, and most cases resolve within a few days.
In the United States, food poisoning affects tens of millions of people each year. Common bacterial causes include Campylobacter, Salmonella, E. coli, and Shigella. Viral infections such as norovirus and parasitic infections such as Giardia are also common.
How a Foodborne Infection Can Change Gut Function
When food poisoning occurs, the immune system responds to help eliminate the infection. This response is essential for recovery—but in some cases, it also plays a role in longer-term gut changes.
Certain bacteria that commonly cause food poisoning, especially Campylobacter and Shigella, release toxins that trigger an immune response, including a toxin called cytolethal distending toxin B (CdtB). The immune system produces antibodies to neutralize this toxin and clear the infection. For most people, this response resolves once the infection is gone.
But in some individuals, the immune response persists and begins to affect how the gut functions. Research shows that the toxin CdTB closely resembles a protein made by the human body, called vinculin. As a result, the immune system can mistakenly target its own gut-related proteins—a process known as molecular mimicry.
Vinculin plays an important role in coordinating intestinal movement. When vinculin is attacked, this system is disrupted, and the gut may not move as effectively as it once did. This change doesn’t usually happen all at once. Instead, it can gradually weaken the gut’s ability to clear food and bacteria over time.
How This Creates the Conditions for SIBO
The small intestine is designed to contain relatively few bacteria. Its primary job is digestion and nutrient absorption—not hosting large bacterial populations.
When the system for moving food out of the small intestine isn’t working effectively, that balance can change. Food moves more slowly, bacteria aren’t cleared as efficiently, leaving a nutritional source for bacteria in the small intestine to ferment, reproduce, and overpopulate in what is normally a low-bacteria area of the gut.
This buildup is what defines small intestinal bacterial overgrowth.
One reason SIBO is often difficult to recognize is timing. These changes usually don’t happen right away. Research shows that bacterial overgrowth can develop weeks or months after the original food poisoning, long after the infection itself has resolved. By then, many people no longer connect their symptoms to the earlier illness.
Who Is More Likely to Develop SIBO After Food Poisoning?
Not everyone who gets food poisoning goes on to develop SIBO. In fact, most people don’t. But research suggests that certain factors can increase vulnerability after an infection.
Being female
Having a more severe or prolonged bout of food poisoning
Using antibiotics during the infection
Experiencing repeated gastrointestinal infections
High levels of stress around the time of illness
Differences in genetics and in the gut microbiome may also play a role, although researchers are still working to understand how these factors interact.
These are risk factors, not guarantees. Having one or more does not mean SIBO is inevitable—it simply means the gut may be more vulnerable to disruption after infection.
Understanding the Path Forward
For most people, food poisoning is an unpleasant but temporary experience. But for some, it can quietly change how the gut functions long after the infection itself has passed.
As research continues to uncover how post-infectious gut conditions develop, awareness becomes an important first step. Knowing that a brief infection can have lasting effects empowers people to ask better questions, seek informed care, and move forward with clarity and confidence.
Key References
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Chen, H., et al. (2023). Revisiting bacterial cytolethal distending toxin structure and function. Frontiers in Cellular and Infection Microbiology, 13, 1289359. https://doi.org/10.3389/fcimb.2023.1289359
Deloose, E., Janssen, P., Depoortere, I., & Tack, J. (2012). The migrating motor complex: Control mechanisms and its role in health and disease. Nature Reviews Gastroenterology & Hepatology, 9(5), 271–285. https://doi.org/10.1038/nrgastro.2012.57
DiRienzo, J. M. (2014). Uptake and processing of the cytolethal distending toxin by mammalian cells. Toxins, 6(11), 3098–3116. https://doi.org/10.3390/toxins6113098
Fischer, G. H., Hashmi, M. F., & Paterek, E. (2024). Campylobacter infection. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK537033/
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Kim, J. H., et al. (2020). Association between interstitial cells of Cajal and anti-vinculin antibody in human stomach. Korean Journal of Physiology & Pharmacology, 24(2), 185–191. https://doi.org/10.4196/kjpp.2020.24.2.185
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Morales, W., Weitsman, S., Kim, G., Marsh, E., Chang, C., & Pimentel, M. (2013). Circulating antibodies to cytolethal distending toxin B correlate with the development of small intestinal bacterial overgrowth in a rat model of post-infectious IBS. Gastroenterology, 144(5), S-931.
Pimentel, M., et al. (2015). Autoimmunity links vinculin to the pathophysiology of chronic functional bowel changes following Campylobacter jejuni infection in a rat model. Digestive Diseases and Sciences, 60, 1195–1205. https://doi.org/10.1007/s10620-014-3435-5
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Scuron, M. D., Boesze-Battaglia, K., Dlakić, M., & Shenker, B. J. (2016). The cytolethal distending toxin contributes to microbial virulence and disease pathogenesis by acting as a tri-perditious toxin. Frontiers in Cellular and Infection Microbiology, 6, 168. https://doi.org/10.3389/fcimb.2016.00168
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