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Antimicrobial Agents and Chemotherapy, May 2000, p. 1404-1406, Vol. 44, No. 5
0066-4804/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Evidence for the Existence of a Multidrug Efflux Transporter Distinct from NorA in Staphylococcus aureus

Glenn W. Kaatz,1,2,* Susan M. Seo,2 Louise O'Brien,3 Mohammad Wahiduzzaman,2 and Timothy J. Foster3

The John D. Dingell Department of Veteran's Affairs Medical Center1 and Department of Internal Medicine, Division of Infectious Diseases,2 Wayne State University School of Medicine, Detroit, Michigan 48201, and Microbiology Department, Moyne Institute of Preventive Medicine, Trinity College, Dublin 2, Ireland3

Received 13 October 1999/Returned for modification 10 December 1999/Accepted 15 February 2000

A Staphylococcus aureus norA disruption mutant was created by allelic replacement. Exposure of this mutant to norfloxacin produced SA K1748, a derivative with raised fluoroquinolone MICs, found to be the result of a grlA mutation, and raised organic cation MICs. Ethidium and enoxacin uptake was identical in SA K1748 and its parent, but pre-exposure of SA K1748 to organic cations caused a reduction in ethidium uptake as a result of increased efflux. Altered ethidium uptake and efflux, as well as increased MICs of other organic cations, suggest that SA K1748 possesses a non-NorA multidrug efflux transporter that is inducible by its substrates.

* Corresponding author. Mailing address: Department of Internal Medicine, Division of Infectious Diseases, Wayne State University School of Medicine, B4333 John D. Dingell VA Medical Center, 4646 John R, Detroit, MI 48201. Phone: (313) 576-4487. Fax: (313) 576-1112. E-mail: gkaatz{at}juno.com.

Antimicrobial Agents and Chemotherapy, May 2000, p. 1404-1406, Vol. 44, No. 5
0066-4804/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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