Abstract

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 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 bla CMY-2 gene transferrable across genre via conjugation.

Highlights

  • Escherichia coli are Gram negative, facultative anaerobic bacteria found in mammalian gastrointestinal tracts

  • We examined clinical Shiga toxin-producing Escherichia coli (STEC) originating from British Columbia (BC) using molecular and phenotypic methods to examine lineage, stx subtype, toxin production, presence of other virulence loci and plasmids, and Antimicrobial resistance (AMR)

  • Based on Comparative genomic fingerprinting (CGF), increased genomic variation was observed in non-O157 STEC strains, with isolates clustering into two distinct groups

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Summary

Introduction

Escherichia coli are Gram negative, facultative anaerobic bacteria found in mammalian gastrointestinal tracts. Escherichia coli possessing Shiga toxin genes (stx) (i.e., Shiga toxinproducing E. coli [STEC]) pose serious health risks through consumption of contaminated food [1,2,3,4]. In 2003, Karmali et al [6] grouped STEC into seropathotypes based on serogroup occurrence in human disease, the capacity to cause outbreaks, and the association with hemolytic uremic syndrome (HUS). STEC O157:H7 and O157:NM were identified as the most significant public health risk (seropathotype A), whereas non-O157 STEC are progressively of lower risk from groups B to E. A US study examining high-risk non-O157 STEC in beef revealed that 1006 of 4133 samples were positive for STEC by PCR, though only 10 isolates possessed virulence gene combinations of known pathogens [11].

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