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Antimicrobial Agents and Chemotherapy, November 2005, p. 4739-4744, Vol. 49, No. 11
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.11.4739-4744.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Spontaneous Conversion to Quinolone and Fluoroquinolone Resistance among Wild-Type Escherichia coli Isolates in Relation to Phylogenetic Background and Virulence Genotype

James R. Johnson,1,2* Brian Johnston,1,2 Michael A. Kuskowski,3,4 Raul Colodner,5 and Raul Raz6,7

Medical Service,1 Geriatric Research, Education, and Clinical Center, VA Medical Center, Minneapolis, Minnesota,2 Departments of Medicine,3 Psychiatry, University of Minnesota, Minneapolis, Minnesota,4 Microbiology Laboratory,5 Infectious Diseases Unit, HaEmek Medical Center, Afula, Israel,6 Technion School of Medicine, Afula, Israel7

Received 17 June 2005/ Returned for modification 1 August 2005/ Accepted 23 August 2005

Human clinical isolates of Escherichia coli that are resistant to quinolone or fluoroquinolone agents typically exhibit fewer extraintestinal virulence factors (VFs) than susceptible isolates, along with a different phylogenetic background. To experimentally assess the basis for this as-yet-unexplained phenomenon, 40 E. coli strains (20 E. coli Reference collection members and 20 Israeli cystitis isolates) were subjected to serial selective passaging to obtain derivatives resistant to nalidixic acid (NA) and ciprofloxacin (C). PCR-based VF profiling and phylotyping were performed on the parents and their respective resistant derivatives. All 40 susceptible parent strains yielded NA- and C-resistant derivatives after a median of 6 (range, 4 to 12) serial selective passages on agar plates containing increasing concentrations of NA and C. The numbers of passages required for resistance did not differ by collection origin, phylogenetic group, basal VF profile, source (urine versus fecal), or host group (human versus animal). With the development of C resistance, only one VF was lost in a single strain. Resistant derivatives exhibited the same phylotype as their susceptible parents. These findings suggest that the sparse VF profiles and the low-virulence phylogenetic background of NA- and C-resistant E. coli clinical isolates probably are not attributable to the loss of VFs from intrinsically high-virulence strains during conversion to resistance or to enhanced emergence of drug resistance among intrinsically low-virulence strains. A more likely explanation is the importation of resistant strains from an as-yet-undefined low-virulence external selection reservoir.

* Corresponding author. Mailing address: Infectious Diseases (111F), Minneapolis VA Medical Center, 1 Veterans Drive, Minneapolis, MN 55417. Phone: (612) 467-4185. Fax: (612) 727-5995. E-mail: johns007{at}umn.edu.

Antimicrobial Agents and Chemotherapy, November 2005, p. 4739-4744, Vol. 49, No. 11
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.11.4739-4744.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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