Quinolone, fluoroquinolone and trimethoprim/sulfamethoxazole resistance in relation to virulence determinants and phylogenetic background among uropathogenic Escherichia coli.
BACKGROUND
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.
Moreno
Eva
E
Microbiology Department, Hospital Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain.
Prats
Guillem
G
Sabaté
Montserrat
M
Pérez
Teresa
T
Johnson
James R
JR
Andreu
Antonia
A
D000328:Adult; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D003627:Data Interpretation, Statistical; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics* / Q000472:pathogenicity*; D004927:Escherichia coli Infections / Q000382:microbiology; D005260:Female; D024841:Fluoroquinolones / Q000494:pharmacology*; D005838:Genotype; D006801:Humans; D019081:O Antigens / Q000276:immunology; D015363:Quinolones / Q000494:pharmacology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014296:Trimethoprim Resistance; D015662:Trimethoprim, Sulfamethoxazole Drug Combination / Q000494:pharmacology*; D014552:Urinary Tract Infections / Q000382:microbiology*; D037521:Virulence Factors / Q000502:physiology*
D000900:Anti-Bacterial Agents; D024841:Fluoroquinolones; D019081:O Antigens; D015363:Quinolones; D037521:Virulence Factors; D015662:Trimethoprim, Sulfamethoxazole Drug Combination