Like the other strains of the 1x
E. coli, O157:H7 is
gram-negative and
oxidase-negative. Unlike many other strains, it does not ferment
sorbitol, which
provides a basis for clinical laboratory differentiation of the strain.
Strains of E. coli that express Shiga and Shiga-like toxins gained that ability via
infection with a prophage containing the structural gene coding for the toxin, and nonproducing strains may become infected and produce shiga-like toxins after incubation with shiga toxin positive strains. The
prophage responsible seems to have infected the strain's ancestors fairly recently, as viral particles have been observed to replicate in the host if it is stressed in some way (e.g. antibiotics). All clinical isolates of
E. coli O157:H7 possess the
plasmid pO157. The periplasmic
catalase is encoded on pO157 and may enhance the bacterium's virulence by providing additional oxidative protection when infecting the host.
E. coli O157:H7 non-hemorrhagic strains become hemorrhagic strains by lysogenic conversion after bacteriophage infection of non-hemorrhagic cells.
Natural habitat While it is relatively uncommon, the
E. coli serotype O157:H7 is found in the intestinal contents of some cattle, goats, and sheep. Cows' digestive tracts lack the Shiga toxin receptor
globotriaosylceramide, and thus can be asymptomatic carriers of the bacterium. The prevalence of
E. coli O157:H7 in North American
feedlot cattle herds ranges from 0 to 60%. Some cattle may also be so-called "super-shedders" of the bacterium. Super-shedders may be defined as cattle exhibiting rectoanal junction colonization and excreting >103 to 4 CFU g−1 feces. Super-shedders have been found to constitute a small proportion of the cattle in a feedlot (90% of all
E. coli O157:H7 excreted. ==Transmission==