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Infections are suggested as one of the etiological factors or causative factors in irritable bowel syndrome (IBS).
There are a small number of patients with irritable bowel syndrome who can relate the onset of their symptoms to a bout of infectious gastroenteritis. These are termed post-infectious irritable bowel syndrome.
The prevalence of post-infective cases varies from 17% in primary care setting in United Kingdom to 6% in tertiary care setting in the United States of America. The relative risk of getting irritable bowel syndrome is around 11% in the year following a bout of gastroenteritis.
The risk factors that predispose an individual to develop irritable bowel syndrome after an infection include:-
Commonly after infections with bacteria like shigella, salmonella and campylobacter infections irritable bowel syndrome may be precipitated in the susceptible individuals.
On examining the patients some distinctive features are noted in patients with post infective irritable bowel syndrome.
The histology or microscopic studies of the inner walls of the intestines shows that there is an increase in presence of lymphocytes. This is seen throughout the colon. In the terminal ileum increased mast cells are noted on biopsy.
There is also an abnormal growth in the enterochromaffin cells of the intestines. This is dependent of immune cells called T cell functioning. Evidence shows that the inflammation within the gut fails to subside in these cases.
The rise in the number of enterochromaffin cells is associated with an increase in release of Serotonin after meals. Serotonin is a chemical messenger in the gut and mainly in the brain. Increased Serotonin release is seen both in the diarrhoea predominant irritable bowel syndrome as well as in post infective irritable bowel syndrome.
Immediately after gastroenteritis of the small bowel there may be transient lactose intolerance. This is common among young children. In adults with post infective irritable bowel syndrome symptoms of lactose malabsorption or lactose intolerance is not different from non infected individuals.
There is increased permeability of the gut in these patients as well. This allows access of bacterial products to the inner walls of the gut or the lamina propria leading to chronic inflammation.
Furthermore stress and adverse life events also lead to activation of mast cells. This may contribute to development of post infective irritable bowel syndrome.