PATHOGENESIS OF ESCHERICHIA-COLI O157-H7 INFECTION

Escherichia coli O157:H7 has increasingly become a focus of public health attention because of its propensity to cause outbreaks of severe and sometimes fatal diarrheal disease. A recurring but not exclusive theme is its transmission by undercooked ground beef, which occurred in the western USA in early 1993 in the largest outbreak on record for this pathogen. Other vehicles of transmission, including water, and person-to-person transmission have made the design of adequate control strategies quite difficult. This emerging pathogen appears to have arisen recently from an enteropathogenic E. coli progenitor and shares certain features with enteropathogenic E. coli strains at both the phenotypic and genotypic level, for example, attaching and effacing activity and the eae gene. E. coli O157:H7 produces potent Shiga-like toxins which, after binding to surface glycolipid receptors, are internalized and inhibit cellular protein synthesis. There is differential susceptibility of human endothelial cells from different microvascular sources to the cytotoxic effects of these toxins and endothelial cell sensitivity to toxin can be modulated by both bacterial products and host-derived cytokines.