1887

Abstract

Shiga toxin-producing (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 I, has been previously characterized in the LEE-negative O113 : H21 STEC strain CL3. Screening for the presence of PAI I elements in 469 strains of , including attaching and effacing (A/E) pathogens [enteropathogenic (EPEC) and enterohaemorrhagic (EHEC)], non-A/E pathogens [LEE-negative STEC, extra-intestinal pathogenic (ExPEC), enterotoxigenic (ETEC) and enteroaggregative (EAEC)] and commensal isolates, showed that PAI I is unique to LEE-negative STEC strains linked to disease, providing a new marker for these strains. We also showed that a PAI I-equivalent gene cluster is present in the genome of , on a 53 kb genomic island inserted into the tRNA locus. While the PAI I shows high similarities at the nucleotide level and in organization with the PAI I, the genetic context of the integration differs completely. In addition, searches revealed that other pathotypes (O157 : H7 EHEC, ExPEC, EPEC and EAEC) possess incomplete PAI I elements that contain only the genes located at the extremities of the island. Six of the 16 sequenced genomes showed deleted PAI I gene clusters which are carried on mobile genetic elements inserted into , or tRNA loci, which is compatible with the idea that the PAI I gene cluster entered and at multiple times through independent events. The phylogenetic distribution of the PAI I variants suggests that a B1 genetic background is necessary for the maintenance of the full complement of PAI I genes in .

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2009-04-01
2024-04-19
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