SUMMARY Escherichia coli is the predominant nonpathogenic facultative flora of the human intestine. Some E. coli strains, however, have developed the ability to cause disease of the gastrointestinal, urinary, or central nervous system in even the most robust human hosts. Diarrheagenic strains of E. coli can be divided into at least six different categories with corresponding distinct pathogenic schemes. Taken together, these organisms probably represent the most common cause of pediatric diarrhea worldwide. Several distinct clinical syndromes accompany infection with diarrheagenic E. coli categories, including traveler’s diarrhea (enterotoxigenic E. coli), hemorrhagic colitis and hemolytic-uremic syndrome (enterohemorrhagic E. coli), persistent diarrhea (enteroaggregative E. coli), and watery diarrhea of infants (enteropathogenic E. coli). This review discusses the current level of understanding of the pathogenesis of the diarrheagenic E. coli strains and describes how their pathogenic schemes underlie the clinical manifestations, diagnostic approach, and epidemiologic investigation of these important pathogens.

The ability of enteropathogenic Escherichia coli (EPEC) to form attaching and effacing intestinal lesions is a major characteristic of EPEC pathogenesis. Using TnphoA mutagenesis we have identified a chromosomal gene (eae, for E. coli attaching and effacing) that is necessary for this activity. A DNA probe derived from this gene hybridizes to 100% ofE. coli of EPEC serogroups that demonstrate attaching and effacing activity on tissue culture cells as well as other pathogenic E. coli that produce attaching and effacing intestinal lesions, such as RDEC-1 (an EPEC of weanling rabbits) and enterohemorrhagic E. coli. The predicted amino acid sequence derived from the nucleotide sequence of eae shows significant homology to that of the invasin of Yersinia pseudotuberculosis.Enteropathogenic Escherichia coli (EPEC) are an important cause of infant diarrhea in the developing world (1-5). Diarrhea caused by EPEC can be severe, as evidenced by a 30% fatality rate in a recent nursery outbreak (5). Once a serious cause of "summer diarrhea" and nursery outbreaks in industrialized countries, diarrhea due to EPEC now occurs less frequently in these areas, although outbreaks in nurseries and day-care centers are reported occasionally (6, 7).Although EPEC were the first E. coli to be recognized as a diarrheal pathogen, the elucidation of EPEC virulence factors has lagged behind that of enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), and enterohemorrhagic E. coli (EHEC). Unlike that of ETEC and EHEC, the pathogenesis of EPEC does not appear to involve a toxin and no fimbrial colonization factors have been described. A major advance in the understanding of EPEC pathogenesis was the demonstration that EPEC possess a high molecular weight plasmid which is required for full virulence in volunteers (8) and is associated with the ability to adhere to HEp-2 epidermoid carcinoma cells in a pattern described as localized adherence (9, 10). This adherence phenotype is a characteristic of E. coli of the major EPEC serotypes (11) and is detectable with a DNA probe derived from one such plasmid called the EAF probe (EPEC adherence factor).Perhaps the most important feature of EPEC pathogenesis is the ability of EPEC to produce characteristic histopathological intestinal lesions in humans or experimental animal models. This lesion has been described by Moon et al. (12) as an "attaching and effacing" (A/E) lesion and is characterized by the intimate adherence of bacteria to the enterocyte, dissolution of the brush border at the site of bacterial attachment, and disruption of the cellular cytoskeleton. Within the enterocyte, high concentrations of filamentous actin are present at the site of bacterial attachment and the enterocyte membrane is frequently seen cupping the bacteria, often forming a pedestal-like structure. The production of this lesion can occur in the absence of the EAF plasmid, as evidenced by the observation that A/E lesions are produced by EAF plasmid-cured derivatives of EPEC isolates in experimental an...

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