Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: June 1, 2011
Publication Date: July 1, 2011
Citation: Clawson, M.L., Bono, J.L. 2011. Evolution of Shiga toxin-producing Escherichia coli O157: eight major lineages of human and cattle origin strain signature genotypes [abstract]. Proceedings of the BIT's 1st Annual World Congress of Microbes - 2011, July 30 - August 1, 2011, Beijing, China. p. 195.
Cattle are a major reservoir for Shiga toxin-producing Escherichia coli O157 (STEC O157) and harbor genetic subtypes that do not all associate with human disease. STEC O157 evolved from an E. coli O55:H7 progenitor, however, depauperate nucleotide polymorphism discovery from cattle and human origin STEC O157 strains has precluded high-resolution detection and analyses on the emergence of human and/or cattle associated subtypes. Our goals were to identify nucleotide polymorphisms for STEC O157 genetic subtype detection and to determine the phylogeny of STEC O157 genetic subtypes originating from either human and/or cattle strains using polymorphism-derived genotypes. Accordingly, we genotyped 762 nucleotide polymorphisms that were identified through 1X genome sequencing coverage of 193 STEC O157 strains (91 and 102 human and cattle origin, respectively) in 427 STEC O157 strains (158 and 269 human and cattle origin, respectively). Concatenated alleles from the 762 polymorphisms defined 175 polymorphism-derived genotypes that were tagged by a minimal set of 138 polymorphisms. Phylogenetic analyses of the polymorphism-derived genotypes identified eight major lineages of STEC O157, and indicate that cattle were not initially a major reservoir for STEC O157. Rather, after STEC O157 diverged from E. coli O55:H7, cattle became a reservoir for STEC O157 subtypes that had a propensity to cause human disease. Since then, cattle have come to harbor seven major lineages of STEC O157. Of these, two account for the majority of human disease, whereas, one other lineage is rarely represented in clinically ill humans and may have evolved towards reduced human virulence. These results indicate that STEC O157 genetic subtypes of variable predilection to associate with human disease are detectable with nucleotide polymorphism-derived genotypes, and that the set developed here may be useful in assessing the evolutionary relatedness of STEC O157 genetic subtypes comprising epidemiological investigations.
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