Certain strains of E. coli, such as O157:H7, O121 and O104:H21, produce toxins. Food poisoning caused by E. coli are usually associated with eating unwashed vegetables and meat contaminated post-slaughter. O157:H7 is further notorious for causing serious and even life-threatening complications like hemolytic-uremic syndrome (HUS). This particular strain is linked to the 2006 United States E. coli outbreak of fresh spinach. Severity of the illness varies considerably; it can be fatal, particularly to young children, the elderly or the immunocompromised, but is more often mild. E. coli can harbor both heat-stable and heat-labile enterotoxins. The latter, termed LT, contains one 'A' subunit and five 'B' subunits arranged into one holotoxin, and is highly similar in structure and function to Cholera toxins. The B subunits assist in adherence and entry of the toxin into host intestinal cells, while the A subunit is cleaved and prevents cells from absorbing water, causing diarrhea. LT is secreted by the Type 2 secretion pathway.
If E. coli bacteria escape the intestinal tract through a perforation (for example from an ulcer, a ruptured appendix, or a surgical error) and enter the abdomen, they usually cause peritonitis that can be fatal without prompt treatment. However, E. coli are extremely sensitive to such antibiotics as streptomycin or gentamicin. This could change since, as noted below, E. coli quickly acquires drug resistance. Recent research suggests that treatment with antibiotics does not improve the outcome of the disease, and may in fact significantly increase the chance of developing haemolytic uraemic syndrome.
Intestinal mucosa-associated E. coli are observed in increased numbers in the inflammatory bowel diseases, Crohn's disease and ulcerative colitis. Invasive strains of E. coli exist in high numbers in the inflamed tissue, and the number of bacteria in the inflamed regions correlates to the severity of the bowel inflammation.
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