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

Eva Moreno, Guillem Prats, Montserrat Sabaté, Teresa Pérez, James R. Johnson, Antonia Andreu

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120 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)204-211
Number of pages8
JournalJournal of Antimicrobial Chemotherapy
Issue number2
StatePublished - Feb 2006

Bibliographical note

Funding Information:
J. R. J. has received grants from Merck, Bayer, Ortho-McNeil, Wyeth-Ayerst and Procter and Gamble. The other authors do not have any commercial or other associations that might pose a conflict of interest (e.g. pharmaceutical stock ownership, consultancy).

Funding Information:
This work was funded by a grant from the Fondo de Investigación Sanitaria, Spain (FIS 01/1353 and FIS 02/1887), Red Española de Investigación en Patología Infecciosa-REIPI (ISCIII C03/14) (G. P. and A. A.) and Office of Research and Development, Medical Research Service, Department of Veterans Affairs (J. R. J.).


  • E. coli
  • Urinary tract infections
  • Virulence traits


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