ABSTRACT
The ability of a single species to co-exist with its host as a symbiote and to cause so many distinct diseases is a property of the genetic heterogeneity of the organism. While much of the E. coli genome is common to all strains of the species, the various clinical syndromes ascribed to E. coli are caused by pathotypes that differ from each other and from commensal strains because they have acquired distinct sets of virulence genes. These genes are carried on plasmids, on lysogenic bacteriophages, or on large chromosomal insertions known as pathogenicity islands. The distinctive clinical syndromes recognized in patients infected with different pathotypes of E. coli are a direct result of the interactions with the host encoded by the various combinations of gene sets. Presumably, these combinations of virulence genes were not selected by virtue of their ability to harm humans, rather these genes endow the organism with the ability to occupy distinctive niches within (or between) hosts. Unfortunately, little is known about the precise selective advantage provided to the organism by the various sets of virulence genes.
