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Antimicrobial Agents and Chemotherapy, January 2009, p. 235-241, Vol. 53, No. 1
0066-4804/09/$08.00+0     doi:10.1128/AAC.00665-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Mechanisms Accounting for Fluoroquinolone Resistance in Escherichia coli Clinical Isolates{triangledown}

Sonia K. Morgan-Linnell,1,{dagger} Lauren Becnel Boyd,1,{dagger} David Steffen,2 and Lynn Zechiedrich1*

Department of Molecular Virology and Microbiology,1 Bioinformatics Research Center, Baylor College of Medicine, Houston, Texas 770302

Received 20 May 2008/ Returned for modification 25 July 2008/ Accepted 28 September 2008

Fluoroquinolone MICs are increased through the acquisition of chromosomal mutations in the genes encoding gyrase (gyrA and gyrB) and topoisomerase IV (parC and parE), increased levels of the multidrug efflux pump AcrAB, and the plasmid-borne genes aac(6')-Ib-cr and the qnr variants in Escherichia coli. In the accompanying report, we found that ciprofloxacin, gatifloxacin, levofloxacin, and norfloxacin MICs for fluoroquinolone-resistant E. coli clinical isolates were very high and widely varied (L. Becnel Boyd, M. J. Maynard, S. K. Morgan-Linnell, L. B. Horton, R. Sucgang, R. J. Hamill, J. Rojo Jimenez, J. Versalovic, D. Steffen, and L. Zechiedrich, Antimicrob. Agents Chemother. 53:229-234, 2009). Here, we sequenced gyrA, gyrB, parC, and parE; screened for aac(6')-Ib-cr and qnrA; and quantified AcrA levels in E. coli isolates for which patient sex, age, location, and site of infection were known. We found that (i) all fluoroquinolone-resistant isolates had gyrA mutations; (ii) ~85% of gyrA mutants also had parC mutations; (iii) the ciprofloxacin and norfloxacin MICs for isolates harboring aac(6')-Ib-cr (~23%) were significantly higher, but the gatifloxacin and levofloxacin MICs were not; (iv) no isolate had qnrA; and (v) ~33% of the fluoroquinolone-resistant isolates had increased AcrA levels. Increased AcrA correlated with nonsusceptibility to the fluoroquinolones but did not correlate with nonsusceptibility to any other antimicrobial agents reported from hospital antibiograms. Known mechanisms accounted for the fluoroquinolone MICs of 50 to 70% of the isolates; the remaining included isolates for which the MICs were up to 1,500-fold higher than expected. Thus, additional, unknown fluoroquinolone resistance mechanisms must be present in some clinical isolates.

* Corresponding author. Mailing address: Department of Molecular Virology and Microbiology, Baylor College of Medicine, One Baylor Plaza, mail stop BCM-280, Houston, TX 77030-3411. Phone: (713) 798-5126. Fax: (713) 798-7375. E-mail: elz{at}bcm.edu

{triangledown} Published ahead of print on 6 October 2008.

{dagger} These authors contributed equally to this work.

Antimicrobial Agents and Chemotherapy, January 2009, p. 235-241, Vol. 53, No. 1
0066-4804/09/$08.00+0     doi:10.1128/AAC.00665-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



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