PATHOGENESIS OF ESCHERICHIA-COLI O157-H7 INFECTION

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