Use of comparative genomics as a tool to assess the clinical and public health significance of emerging Shiga toxin-producing Escherichia coli serotypes

Abstract

Shiga toxin (Stx)-producing Escherichia coli (STEC) cause sporadic or epidemic food- or water-borne illness whose clinical spectrum includes diarrhea, hemorrhagic colitis, and the potentially fatal hemolytic uremic syndrome (HUS). Over 200 STEC serotypes have now been implicated in human disease. Serotype O157:H7 is associated most outbreaks and most cases of HUS. Other serotypes are also associated with outbreaks and HUS but less commonly than serotype O157:H7, and some cause HUS but are typically non-epidemic. Many STEC serotypes have been associated with diarrhea, but not with outbreaks or HUS, while others, isolated from cattle, have never been linked to human disease. The only proven virulence strategies for STEC are Stx production and, in some strains, a characteristic attaching and effacing cytopathology on enterocyte that is mediated by factors encoded on a pathogenicity island (PAI) known as the locus of enterocyte effacement (LEE). But Stx subtypes and LEE cannot fully explain the apparent differences in virulence between STEC subgroups. However, publication of the genome sequences of two E. coli O157:H7 strains has revealed new candidate PAIs and has stimulated the use of novel approaches for assessing differences in virulence potential between groups of strains. This paper highlights the clinico-pathological features and pathogenesis of STEC infection, new information arising from E. coli O157:H7 genome sequences, and progress in the use of of comparative genomics for assessing potential differences in virulence and public health significance between STEC subgroups.