JAC Advance Access originally published online on April 3, 2008
Journal of Antimicrobial Chemotherapy 2008 62(1):83-91; doi:10.1093/jac/dkn137
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Original research |
Triclosan resistance in Salmonella enterica serovar Typhimurium
1 Antimicrobial Agents Research Group, Division of Immunity and Infection, The University of Birmingham, Edgbaston, Birmingham B15 2TT, UK 2 Veterinary Laboratories Agency (Weybridge), New Haw, Addlestone, Surrey KT15 3NB, UK
Received 14 January 2008; returned 12 February 2008; revised 6 March 2008; accepted 9 March 2008
* Corresponding author. Tel: +44-121-414-2859; Fax: +44-121-414-6815; E-mail: m.a.webber{at}bham.ac.uk
Objectives: The aim of this study was to characterize the mechanisms of resistance to triclosan in Salmonella enterica serovar Typhimurium.
Methods: Mutants resistant to triclosan were selected from nine S. enterica serovar Typhimurium strains. Mutants were characterized by genotyping, mutagenesis and complementation of fabI and analysis of efflux activity. Fitness of triclosan-resistant mutants was determined in vitro and in vivo.
Results: Three distinct resistance phenotypes were observed: low- (LoT), medium- (MeT) and high-level (HiT) with MICs of 4–8, 16–32 and >32 mg/L of triclosan, respectively, for inhibition. The genotype of fabI did not correlate with triclosan MIC. Artificial overexpression and mutagenesis of fabI in SL1344 each resulted in low-level triclosan resistance, indicating that FabI alone does not mediate high-level triclosan resistance in Salmonella Typhimurium. Active efflux of triclosan via AcrAB–TolC confers intrinsic resistance to triclosan as inactivation of acrB and tolC in wild-type strains and the triclosan-resistant mutants led to large decreases in triclosan resistance, which were reversed by complementation. Exemplars of each phenotype were evaluated for fitness in vivo; no fitness cost was seen and mutants colonized and persisted in chickens throughout a 28 day competitive index experiment.
Conclusions: These data show that triclosan resistance can occur via distinct pathways in salmonella and that mutants selected after single exposure to triclosan are fit enough to compete with wild-type strains.
Keywords: biocides , efflux , fitness
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