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JAC Advance Access published online on February 21, 2006
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkl025
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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 December 7, 2005
Revised January 13, 2006
Accepted January 19, 2006

Original article

Overexpression of marA, soxS and acrB in veterinary isolates of Salmonella enterica rarely correlates with cyclohexane tolerance

Mark Webber 1, Anthony M. Buckley 1, Luke P. Randall 2, Martin J. Woodward 2, and Laura J. V. Piddock 1 *

1 Antimicrobial Agents Research Group, Division of Immunity and Infection, University of Birmingham, Birmingham, B15 2TT, UK
2 Veterinary Laboratories Agency (Weybridge), New Haw, Addlestone, Surrey, KT15 3NB, UK

* To whom correspondence should be addressed.
Laura J. V. Piddock, E-mail: l.j.v.piddock{at}bham.ac.uk


  Abstract

Objectives: To determine the contribution of the AcrAB efflux system to cyclohexane tolerance in Salmonella enterica.

Methods: The expression of the efflux pump gene, acrB, and regulators marA and soxS from 46 isolates of S. enterica of 14 different serovars was determined by comparative RT-PCR and denaturing HPLC analysis.

Results: Twenty-one of the 46 isolates were cyclohexane tolerant, a phenotype associated with multiple antibiotic resistance (MAR) and overexpression of efflux pumps. Of the cyclohexane-tolerant isolates 81% were MAR, whereas only 44% of the cyclohexane-susceptible isolates were MAR, confirming the association between cyclohexane tolerance and MAR. However, there was no correlation between cyclohexane tolerance or MAR and overexpression of acrB, soxS or marA.

Conclusions: These data suggest that cyclohexane tolerance in S. enterica can be mediated by an acrB-independent mechanism.

Keywords: multiple antibiotic resistance; efflux; AcrAB; organic solvents.
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