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BioMed Research International
Volume 2013, Article ID 878956, 11 pages
Research Article

Characteristics of Clinical Shiga Toxin-Producing Escherichia coli Isolated from British Columbia

1Food, Nutrition and Health Program, Faculty of Land and Food Systems, University of British Columbia, 218-2205 East Mall, Vancouver, BC, Canada V6T 1Z4
2Laboratory for Foodborne Zoonoses, Public Health Agency of Canada, 225089 Township Road 9-1 (Box 640), Lethbridge, AB, Canada T1J 3Z4
3The State Key Laboratory of Microbial Technology, School of Life Science, Shandong University, Jinan 250100, Shandong, China
4BCCDC Public Health and Reference Microbiology Laboratory, PHSA, 655 West 12th Ave, Vancouver, BC, Canada V5Z 4R4
5Department of Pathology and Laboratory Medicine, University of British Columbia, 2211 Wesbrook Mall, Vancouver, BC, Canada V6T 2B5

Received 23 March 2013; Accepted 1 July 2013

Academic Editor: Jacek Osek

Copyright © 2013 Kevin J. Allen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 were more frequently observed in STEC O157, and 80 and 100% of isolates possessed and , respectively. In contrast, and 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 111111) 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 gene transferrable across genre via conjugation.