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. 2005 Apr 15;40(8):1101-7.
doi: 10.1086/428727. Epub 2005 Mar 15.

Clonal groups and the spread of resistance to trimethoprim-sulfamethoxazole in uropathogenic Escherichia coli

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Clonal groups and the spread of resistance to trimethoprim-sulfamethoxazole in uropathogenic Escherichia coli

Anne Marie France et al. Clin Infect Dis. .

Abstract

Background: Antibiotic resistance is increasingly complicating the management of urinary tract infection. We investigated the extent to which a group of Escherichia coli called clonal group A (CGA), which is associated with resistance to trimethoprim-sulfamethoxazole (TMP-SMZ), accounted for TMP-SMZ resistance among a prospectively collected set of uropathogenic and rectal E. coli isolates from a university population in Michigan.

Methods: Resistant and susceptible uropathogenic E. coli isolates (45 each) and 79 randomly selected rectal E. coli isolates were evaluated for CGA status by use of 2 definitions of this group-- the enterobacterial repetitive intergenic consensus sequence 2 (ERIC2)-polymerase chain reaction (PCR) pattern A fingerprint and the C288T single nucleotide polymorphism (SNP) in the fumC gene. We compared virulence gene profiles and molecular mechanisms of resistance to TMP-SMZ between isolates classified as CGA by both approaches to better characterize the relationship between isolates.

Results: Of the 45 isolates that exhibited ERIC2-PCR pattern A, one-half (23 of 45) were resistant to TMP-SMZ, and 16 contained the C288T SNP. The pattern A isolates were diverse, exhibiting multiple mechanisms of resistance to TMP-SMZ and various combinations of virulence factors. C288T SNP isolates showed less variation, with 15 of 16 resistant to TMP-SMZ and a 1.8-kb class I integron bearing the dfrA17 gene present in 14 of 15 resistant isolates. Twelve of 16 exhibited the same combination of virulence genes. Pulsed-field gel electrophoresis patterns for these 12 isolates were unique.

Conclusion: CGA, as defined by the fumC C288T SNP, appears to be distantly clonal but is not an outbreak-related group. The widespread group has likely evolved through lateral transfer of genes conferring virulence and antibiotic resistance.

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