E. coli O157:H7 is one of thousands of serotypes of Escherichia coli.
E. coli O157:H7 was first recognized as a pathogen in 1982 during an investigation into an outbreak of haemorrhagic colitis associated with consumption of hamburgers from a fast-food chain restaurant. Retrospective examination of more than three thousand E. coli cultures obtained between 1973 and 1982 found only one isolate with serotype O157:H7, and that was a case in 1975. In the ten years that followed, there were approximately thirty outbreaks recorded in the United States. This number is likely misleading, however, because E. coli O157:H7 infections did not become a reportable disease in any state until 1987, when Washington became the first state to mandate its reporting to public health authorities. Consequently, an outbreak would not be detected if it was not large enough to prompt investigation.
E. coli O157:H7’s ability to induce injury in humans is a result of its ability to produce numerous virulence factors, most notably Shiga toxin (Stx), which is one of the most potent toxins known to man. Shiga toxin has multiple variants (e.g., Stx1, Stx2, Stx2c), and acts like the plant toxin ricin by inhibiting protein synthesis in endothelial and other cells. Endothelial cells line the interior surface of blood vessels and are known to be extremely sensitive to E. coli O157:H7, which is cytotoxigenic to these cells.
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