E scherichia coli is both the most abundant facultative commensal of the human gastrointestinal tract and the most common bacterial cause of human diarrhea (1). However, precise recognition of E. coli pathotypes remains problematic. Enteropathogenic E. coli (EPEC), classically associated with outbreaks of infant diarrhea, harbors distinctive chromosomal (the locus of enterocyte effacement, or LEE island) and plasmidborne (residing on the EPEC adherence factor, or EAF, plasmid) virulence factors, which are linked by common gene regulators (1). At the Second International Conference on EPEC, held in So Paulo, Brazil, in 1995, the foremost authorities in the field proclaimed the global importance of such "typical" EPEC (tEPEC) but pondered the clinical relevance of strains carrying only the LEE island (dubbed at that conference "atypical EPEC," or aEPEC) (2). Had aEPEC lost the EAF plasmid? Had it incidentally acquired only fragments or incomplete packages of virulence-associated genes? Or were some aEPEC true pathogens of humans or animals?
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James P. Nataro (2006) studied this question.
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