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JAC Advance Access originally published online on January 3, 2006
Journal of Antimicrobial Chemotherapy 2006 57(2):204-211; doi:10.1093/jac/dki468
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© The Author 2006. 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

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

Eva Moreno1, Guillem Prats1, Montserrat Sabaté1, Teresa Pérez1, James R. Johnson2 and Antonia Andreu1,*

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

Received 30 July 2005; returned 10 October 2005; revised 19 October 2005; accepted 1 December 2005

* Corresponding author. Tel: +34-93-274-6867; Fax: +34-93-274-6801; E-mail: anandreu{at}vhebron.net

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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