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JAC Advance Access originally published online on November 1, 2002
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Journal of Antimicrobial Chemotherapy (2002) 50, 833-838
© 2002 The British Society for Antimicrobial Chemotherapy

Identification and characterization of a novel efflux-related multidrug resistance phenotype in Staphylococcus aureus

Glenn W. Kaatz1,2,*, Varsha V. Moudgal2 and Susan M. Seo2

1 The John D. Dingell Department of Veteran’s Affairs Medical Center and 2 Department of Internal Medicine, Division of Infectious Diseases, Wayne State University School of Medicine, Detroit, MI 48201, USA

Received 12 June 2002; returned 19 July 2002; revised 22 July 2002; accepted 20 August 2002

Moxifloxacin is a C8-methoxy (C8-OMe) fluoroquinolone that is highly active against Staphylococcus aureus, including many strains resistant to older fluoroquinolones such as ciprofloxacin. Available data indicate that it is a poor substrate for the NorA multidrug efflux pump. We produced a mutant of S. aureus in vitro (SA-K2068) with a novel non-NorA-mediated multidrug resistance phenotype characterized by raised MICs of several fluoroquinolones, including the C8-OMe fluoroquinolones, moxifloxacin and gatifloxacin, and the organic cations ethidium and tetraphenylphosphonium. Reserpine reduced MIC increases by two- to eight-fold. SA-K2068 also demonstrated reduced accumulation of moxifloxacin, gatifloxacin and enoxacin, and increased efflux of ethidium, activities that were completely blocked by carbonyl cyanide m-chlorophenyl hydrazone (CCCP); competition experiments indicated that a single pump was responsible for the phenotype. The effect of CCCP and ionophores identified the proton motive force as the source of energy for efflux. These data, combined with previous work from our laboratory and genome sequence data, indicate that S. aureus possesses several multidrug efflux pump proteins and it is apparent that C8-OMe fluoroquinolones can be substrates for such pumps.

Keywords: Staphylococcus aureus, multidrug efflux

* Corresponding author. Tel: +1-313-576-4487; Fax: +1-313-576-1112; E-mail: gkaatz{at}juno.com


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