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Shiga toxin-producing  Escherichia coli  (STEC) are significant public health threats. Although STEC O157 are recognized foodborne pathogens, non-O157 STEC are also important causes of human disease. We characterized 10 O157:H7 and 15 non-O157 clinical STEC derived from British Columbia (BC).  Eae, hlyA,  and  stx  were more frequently observed in STEC O157, and 80 and 100% of isolates possessed  stx   1  and  stx   2 , respectively. In contrast,  stx   1  and  stx   2  occurred in 80 and 40% of non-O157 STEC, respectively. Comparative genomic fingerprinting (CGF) revealed three distinct clusters (C). STEC O157 was identified as lineage I (LI; LSPA-6 ) and clustered as a single group (C1). The  cdi  gene previously observed only in LII was seen in two LI O157 isolates. CGF C2 strains consisted of diverse non-O157 STEC while C3 included only O103:H25, O118, and O165 serogroup isolates. With the exception of O121 and O165 isolates which were similar in virulence gene complement to STEC O157, C1 O157 STEC produced more Stx2 than non-O157 STEC. Antimicrobial resistance (AMR) screening revealed resistance or reduced sensitivity in all strains, with higher levels occurring in non-O157 STEC. One STEC O157 isolate possessed a mobile  bla   CMY-2  gene transferrable across genre via conjugation.

Characteristics of Clinical Shiga Toxin-ProducingEscherichia coliIsolated from British Columbia