Genomic analysis of the PAI ICL3 locus in pathogenic LEE-negative Shiga toxin-producing Escherichia coli and Citrobacter rodentium

Shiga toxin-producing Escherichia coli (STEC) causes a spectrum of human illnesses such as haemorrhagic colitis and haemolytic–uraemic syndrome. Although the locus of enterocyte effacement (LEE) seems to confer enhanced virulence, LEE-negative STEC strains are also associated with severe human disease, suggesting that other unknown factors enhance the virulence potential of STEC strains. A novel hybrid pathogenicity island, termed PAI ICL3, has been previously characterized in the LEE-negative O113:H21 STEC strain CL3. Screening for the presence of PAI ICL3 elements in 469 strains of E. coli, including attaching and effacing (A/E) pathogens [enteropathogenic E. coli (EPEC) and enterohaemorrhagic E. coli (EHEC)], non-A/E pathogens [LEE-negative STEC, extra-intestinal pathogenic E. coli (ExPEC), enterotoxigenic E. coli (ETEC) and enteroaggregative E. coli (EAEC)] and commensal E. coli isolates, showed that PAI ICL3 is unique to LEE-negative STEC strains linked to disease, providing a new marker for these strains. We also showed that a PAI ICL3-equivalent gene cluster is present in the genome of Citrobacter rodentium, on a 53 kb genomic island inserted into the pheV tRNA locus. While the C. rodentium PAI ICL3 shows high similarities at the nucleotide level and in organization with the E. coli PAI ICL3, the genetic context of the integration differs completely. In addition, BLAST searche