“…These genetic loci characterize the pathogenicity of bacterial species by determining what toxins are produced and how the bacterium attaches to and invades host cells, modulates the host cell cycle and immune responses, survives in stressful environments, and produces biofilms. Many virulence loci have been characterized for STEC, including a number of pathogenicity islands (e.g., the locus of enterocyte effacement [LEE], the locus of proteolysis activity [LPA], the high-pathogenicity island [HPI], the E. coli type III secretion apparatus [ETT2], the urease gene cluster, the long polar fimbrial operon, O-island 36 , OI-57, OI-71, OI-122, OI-141, and OI-154), two key virulence plasmids (pO157 and pO113), and chromosomal lambdoid bacteriophage insertions that carry genes for two types of Shiga toxin (10,14,29,31,36,38,39,42,48,59,63). Variants of the genes encoding the Shiga toxins have been reported, and certain variants, including stx 2 and stx 2c , are more likely to be associated with HC and HUS (3,15).…”