|Cornick, N - IOWA STATE UNIVERSITY|
|Moon, H - IOWA STATE UNIVERSITY|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: June 15, 2002
Publication Date: N/A
Technical Abstract: E. coli O157:H7 and other serotypes of Shiga toxin-producing E. coli (STEC) are estimated to cause approximately 110,000 cases of human illness and 90 deaths each year in the U.S. Cattle are considered to be the major reservoir for E. coli O157:H7 and the prevalence of the organism in healthy animals ranges from 2-28% depending on the age of the animal, the culture methods used, and the season of sampling. STEC do not cause any apparent disease in mature animals even when given in very high doses during experimental infections. While much has been learned regarding the pathogenesis of E. coli O157:H7 infections, it is not known why these organisms colonize and persist in ruminants. Shiga toxin, the major virulence factor of STEC, is encoded by lamboid-like prophages. It seems logical that since the prophage(s) (and thus stx) continue to be maintained within the bacterial genome, those genes must confer some selective advantage to the bacterial host within its normal ecological niche, which putatively includes the ruminant gastrointestinal tract. We hypothesized that Stx and/or the stx-converting prophage increases the fitness and/or ability of STEC to colonize adult ruminants.