The rise and rise of enteropathogenic Escherichia coli.

First described in 1885, Escherichia coli gradually achieved recognition as a cause of diarrhoea. Strains of E. coli which belonged to a limited number of O-serogroups and had been associated with outbreaks of diarrhoea in hospitalised children were designated 'enteropathogenic' E. coli (EPEC) to distinguish them from E. coli strains that cause other types of infection. The discovery that some strains of E. coli can produce toxins or invade epithelial cells in a similar fashion to established pathogens, such as Vibrio cholerae and Shigella species, shed new light on E. coli virulence. As EPEC do not exhibit either of these properties, however, their pathogenicity was brought into question. Further studies revealed that EPEC constitute a distinctive group of pathogenic bacteria that display characteristic adherence to cultured epithelial cells and produce distinctive histopathological changes, termed 'attaching-effacing lesions', in the intestinal epithelium. The ability to evoke these lesions, which are essential for virulence, is associated with a series of linked genes, known as the locus for enterocyte effacement, on the bacterial chromosome. In addition, the pathogenicity of some EPEC strains is associated with the presence of a plasmid-encoded, bundle-forming pilus. Naturally occurring strains of EPEC which lack this pilus are known as atypical EPEC and are an emerging cause of diarrhoea throughout the world.