Quinolone, Fluoroquinolone and trimethoprim/sulfamethoxazole Resistance in Relation to Virulence Determinants and Phylogenetic Background Among Uropathogenic Escherichia Coli

J Antimicrob Chemother. 2006 Feb;57(2):204-11. doi: 10.1093/jac/dki468. Epub 2006 Jan 3.


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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Adult
  • Anti-Bacterial Agents / pharmacology*
  • Data Interpretation, Statistical
  • Escherichia coli / drug effects
  • Escherichia coli / genetics*
  • Escherichia coli / pathogenicity*
  • Escherichia coli Infections / microbiology
  • Female
  • Fluoroquinolones / pharmacology*
  • Genotype
  • Humans
  • O Antigens / immunology
  • Quinolones / pharmacology*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Trimethoprim Resistance*
  • Trimethoprim, Sulfamethoxazole Drug Combination / pharmacology*
  • Urinary Tract Infections / microbiology*
  • Virulence Factors / physiology*


  • Anti-Bacterial Agents
  • Fluoroquinolones
  • O Antigens
  • Quinolones
  • Virulence Factors
  • Trimethoprim, Sulfamethoxazole Drug Combination