Evolution, Clonality and Some Virulence Characteristics of Enterohaemorrhagic <i>Escherichia coli</i> (EHEC): An Update

Abstract

The evolution of Escherichia coli O157 was thought probably to be due to its ability to produce verotoxin. Thus, it appears that non-O157:H7 E. coli strains producing stx have been around for several decades but it was only with the emergence in the early 1980s of the O157:H7 clone that this pathogenic class of E. coli was recognized. The major and the most essentially suggested cardinal feature of EHEC strains is the production of shiga toxins (stx1 and stx2), which comprise a family of structurally related
cytotoxins with similar biological activity and distinct antigenic structures. The colonization of the intestinal mucosa by most of the EHEC is associated with a mechanism that subverts the function of the epithelial cells. The effect of this interaction is the inducement of a characteristic “attaching and effacing” (A/E) lesion, a complex mechanism genetically controlled by a locus of large pathogenicity island (PAI) called the “locus of enterocyte effacement (LEE)”. Intimin mediates the intimate attachment
of EHEC by binding to β1-integrins and to cell-surface localized nucleolin. All these changes together with other factors which may be genetic in origin have resulted in evolution, the existence of clones and the occurrence and acquisition of virulence characteristics of enterohaemorrhagic Escherichia coli.

Keywords: Evolution, clonality, enterohaemorrhagic E. coli, virulence characteristics.