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JAC Advance Access published online on May 23, 2006

Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkl207
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Received February 28, 2006
Revised April 26, 2006
Accepted April 27, 2006

Brief report

Chloramphenicol and kanamycin resistance among porcine Escherichia coli in Ontario

Rebeccah M. Travis 1, Carlton L. Gyles 1, Richard Reid-Smith 2, Cornelis Poppe 3, Scott A. McEwen 4, Robert Friendship 4, Nicol Janecko 4, and Patrick Boerlin 1 *

1 Department of Pathobiology, University of Guelph, Ontario, N1G 2W1, Canada
2 Department of Population Medicine, University of Guelph, Ontario, N1G 2W1, Canada; Laboratory for Foodborne Zoonoses, Public Health Agency of Canada, 110 Stone Road West, Guelph, Ontario, N1G 3W4, Canada
3 Laboratory for Foodborne Zoonoses, Public Health Agency of Canada, 110 Stone Road West, Guelph, Ontario, N1G 3W4, Canada
4 Department of Population Medicine, University of Guelph, Ontario, N1G 2W1, Canada

* To whom correspondence should be addressed.
Patrick Boerlin, E-mail: pboerlin{at}uoguelph.ca


   Abstract

Objectives: The purpose of this study was to compare the distribution of chloramphenicol and kanamycin resistance genes across three populations of porcine Escherichia coli.

Methods: PCR was used to assess the distribution of the major chloramphenicol and kanamycin resistance genes catA1, cmlA and floR, and aphA1, aphA2 and aadB in enterotoxigenic E. coli (ETEC), non-ETEC isolates from cases of diarrhoea and commensal E. coli from healthy pigs. Associations between these genes and resistance genes for other antimicrobials or virulence genes were assessed.

Results: The chloramphenicol and kanamycin resistance genes were distributed differently among the three E. coli populations. While aphA1, aphA2 and aadB were evenly distributed among resistant ETEC, non-ETEC and commensals, the catA1 gene was significantly more frequent in ETEC than in non-ETEC and commensals. Transformation experiments confirmed statistical associations by demonstrating that elt, estB, astA, aadA and sul1 were located with catA1 on a large ETEC plasmid. Plasmids carrying cmlA also carried sul3 and aadA. Other plasmids carrying floR and aadB also carried tet(A), sul2, strA/strB, blaCMY-2 and occasionally aac(3)IV.

Conclusions: The clustering of genes observed is a likely cause for chloramphenicol resistance persistence. Similar to tetracycline, chloramphenicol resistance genes are physically linked to virulence genes. This is not the case for kanamycin resistance determinants, which were linked to other resistance genes only.

Keywords: chloramphenicol resistance; kanamycin resistance; E. coli; swine; genotyping; plasmids.
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