Abstract

Enteropathogenic Escherichia coli (EPEC) strains of classical serotypes were the first E. coli strains to be identified as intestinal pathogens in association with outbreaks of infantile diarrhoea in the 1940’s and 1950’s. EPEC remain a significant cause of severe and persistant disease in infants, particularly in developing countries. The pathogenesis of EPEC diarrhoea has remained elucive since EPEC do not possess any of the well-defined virulence characteristics of other diarrhoea-causing E. coli such as enterotoxins or epithelial invasiveness. A major breakthrough in EPEC pathogenesis came with the observation that EPEC adhere to the small intestine and produce an ‘attaching and effacing’ (AE) lesion in the enterocyte brush border membrane (Ulshen and Rollo, 1980). The lesion (visible by electron microscopy) is characterised by localised destruction of brush border microvilli and intimate attachment of bacteria to the apical enterocyte membrane, often in a cup-like pedestal structure. In another important study Cravioto et al. (1979) showed that most EPEC strains adhered to cultured HEp-2 cells whereas non-EPEC strains rarely adhered.

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