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JAC Advance Access published online on January 3, 2006
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dki468
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Received July 30, 2005
Revised October 19, 2005
Accepted December 1, 2005

Original article

Quinolone, fluoroquinolone and trimethoprim/sulfamethoxazole resistance in relation to virulence determinants and phylogenetic background among uropathogenic Escherichia coli

Eva Moreno 1, Guillem Prats 1, Montserrat Sabaté 1, Teresa Pérez 1, James R. Johnson 2, and Antonia Andreu 1 *

1 Microbiology Department, Hospital Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain
2 Mucosal and Vaccine Research Center, VA Medical Center; Department of Medicine, University of Minnesota, Minneapolis, MN, USA

* To whom correspondence should be addressed.
Antonia Andreu, E-mail: anandreu{at}vhebron.net


  Abstract

Introduction: The goal of this study was to assess how resistance to quinolones, fluoroquinolones and trimethoprim/sulfamethoxazole relates to the virulence potential and phylogenetic background of clinical Escherichia coli isolates.

Methods: Among 150 uropathogens (21% resistant to quinolones, 12% resistant to fluoroquinolones and 29.3% resistant to trimethoprim/sulfamethoxazole), E. coli phylogenetic group, 15 virulence-associated genes and 7 O antigens were analysed. Clonal group A (CGA) and genomic PCR profiles were studied among trimethoprim/sulfamethoxazole-resistant isolates.

Results: Isolates susceptible to the three antimicrobial agents were significantly associated with phylogenetic group B2, whereas resistant isolates exhibited shifts to non-B2 groups (quinolone and fluoroquinolone-resistant isolates to group A; trimethoprim/sulfamethoxazole-resistant isolates to group D). Diverse virulence traits, including UTI-associated O antigens, were significantly less frequent among resistant isolates, particularly those resistant to fluoroquinolones (median score, 3.9 virulence factors/strain) and also to quinolones (5.2) or trimethoprim/sulfamethoxazole (6.4), as compared with the corresponding drug-susceptible isolates (median scores of 7.9, 8.6 and 7.9, respectively). Among 44 trimethoprim/sulfamethoxazole-resistant isolates, 3 (6.8%) belonged to CGA. All these 3 CGA strains caused pyelonephritis (P = 0.02) and exhibited the consensus virulence profile of previously described CGA strains from abroad.

Conclusions: E. coli isolates resistant to quinolones, trimethoprim/sulfamethoxazole and especially fluoroquinolones were associated with reductions in virulence traits and shifts to non-B2 phylogenetic groups. Moreover, fluoroquinolone resistance usually occurred in low-virulence E. coli group A isolates rather than in isolates from groups B2 and D which had lost virulence traits. CGA accounted for 23% of trimethoprim/sulfamethoxazole-resistant E. coli producing pyelonephritis.

Keywords: E. coli; virulence traits; urinary tract infections.
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