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Chapter 11.8 : Immunoassay Detection of Shiga Toxin-Producing Escherichia coli
Shiga toxin-producing Escherichia coli (STEC) organisms are responsible for a broad range of gastrointestinal illnesses, from mild watery diarrhea to severe hemorrhagic colitis associated with hemolyticuremic syndrome (HUS) ( 1 , 5 , 21 , 30 , 34 , 36 ). These organisms cause disease primarily through elaboration of one or more Shiga toxins (Stx1, Stx1 variants, Stx2, and Stx2 variants) encoded by genes carried on lambda bacteriophages ( 10 , 14 , 34 , 36 ). Research supports the fact that hemorrhagic colitis and HUS likely result from the action of these toxins on vascular endothelium since Stx targets digalactosyl receptors on microvascular endothelial cells in the gut, kidneys, and brain ( 30 , 34 , 36 ). E. coli organisms that produce Stx2 alone have been found to be more virulent than isolates that have Stx1 alone or that produce Stx1 and Stx2 in combination ( 34 ). Enhanced virulence may also be related to host factors and genetic differences among strains. Some investigators have reported differences in the frequency and distribution of Stx genes in the type of clinical disease reported ( 24 , 30 ). Hence, genotyping may be important not only in characterizing particular outbreaks but also in predicting disease severity and treatment ( 18 , 24 , 30 ). Among other organism virulence factors important for pathogenesis are an adhesin, intimin, encoded by an eae gene, and enterohemorrhagic E. coli (EHEC) hemolysin (ehxA gene), a potent cytolysin ( 34 , 36 ).