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Hemolytic-uremic syndrome (HUS), which is charac-terized by acute renal failure, microangiopathic he-molytic anemia, and thrombocytopenia, was first de-scribed in 1955 [1]. Although the cause of occasional cases of HUS could be ascribed [2], most cases of HUS resulting in renal failure during childhood were of un-certain etiology [3]. Its occurrence in outbreaks sug-gested an infectious etiology in at least some cases [4, 5], especially infections with Shigella dysenteriae type 1 (Shiga bacillus), a high-level producer of Shiga toxin. Between 1955 and 1983, case reports associated at least a dozen infectious agents with HUS; one prevailing notion was that HUS was a multifactorial disease (final common pathway) that could be triggered by a variety of infectious agents. In 1982, outbreaks of bloody diarrhea involved pa-trons of a large chain of fast-food restaurants in 2 widely separated parts of the United States; this illness, termed “hemorrhagic colitis, ” was found to be due to an Esch-erichia coli strain of serotype O157:H7 [6]. In the many years during which the Centers for Disease Control (CDC) kept records of E. coli strains associated with disease, this serotype was reported only once, in 1975, from a woman with the acute onset of bloody diarrhea [6]. In 1977, the Canadian microbiologists Konowalchuk et al. reported that certain E. coli strains had cytotoxic activity toward African green monkey kidney (Vero) cells unlike that produced by any of the known E. coli
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Martin J. Blaser (2004) studied this question.
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