food poisoning

Canadian researchers have discovered that exposure to food-borne pathogens that produce acute infectious gastroenteritis, more often known as food poisoning, may enhance the growth of the bacterium adherent-invasive E. coli, which has been associated with Crohn’s disease.


Crohn’s disease is an inflammatory bowel disease characterized by chronic inflammation of the intestines. Patients with the disease experience several symptoms, including cramping, diarrhea, abdominal pain, vomiting, weight loss and fatigue, and have an increased risk of premature death and an increased risk of colorectal cancer. The rate of Crohn’s disease in Canada is 1 in every 150 people, and ranks in the highest globally.

A growing body of evidence suggests that bacteria in the gut are involved in the pathophysiology of Crohn’s disease. Exposure to foodborne pathogens (e.g. Salmonella) causing acute gastroenteritis (inflammation of the gastrointestinal tract), or more commonly known as food poisoning, has shown to create a lasting risk of Crohn’s disease even after the infection has cleared. However, the mechanisms involved in this ongoing link to disease onset are not known. Furthermore, several studies have supported the idea that adherent-invasive Escherichia coli, a bacterial species, which is linked to Crohn’s disease, has an important part in maintaining chronic inflammation in the presence of other risk factors for Crohn’s disease, particularly acute gastroenteritis.

food poisoning
E. coli under a microscope

A team of researchers in Canada conducted a study on mice in which they exposed mice colonized with adherent-invasive E. coli to Citrobacter rodentium or Salmonella enterica serovar Typhimurium, both bacteria of which cause acute infectious gastroenteritis. The findings, published in the journal PLOS Pathogens, revealed that mice colonized with adherent-invasive E. coli that developed infectious gastroenteritis due to either S. Typhimurium or Citrobacter rodentium had an increased and enhanced growth of adherent-invasive E. coli, which is associated with Crohn’s disease onset. The group also observed that even after the mice had recovered from acute gastroenteritis and the bacteria that caused it was cleared from the body, increased concentrations of adherent-invasive E. coli remained in the intestines of the mice, resulting in worse symptoms over time.

The overall findings suggest that exposure to pathogens that causes acute gastroenteritis produces an environment that favors colonization by adherent-invasive E. coli. Furthermore, individuals who are colonized by adherent-invasive E. coli during an episode of acute infectious gastroenteritis may be at an increased risk for onset of Crohn’s disease later in life. These findings of this study give justification for the development of new diagnostic tools that can detect individuals colonized by adherent-invasive E. coli who may be at greater risk for Crohn’s disease after a bout of acute gastroenteritis. Moreover, the extended time period between recovery from acute gastroenteritis and development of Crohn’s disease may create opportunities for interventions to alleviate the risk of Crohn’s disease in people who are positive for adherent-invasive E. coli.




Written By: Nigar Celep, BASc

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