Analysis of the mechanisms of fluoroquinolone resistance in clonal group ST 131 uropathogenic Escherichia coli
Abstract number: P765
Objectives: Recent studies have reported the widespread emergence of the O25:H4-ST131 clone of uropathogenic Escherichia coli (UPEC) which is characterized by CTX-M-15 ESBL production and has frequently been associated with fluoroquinolone resistance, this resistance has increasingly been traced to plasmid medicated factors such as the aac (6'')-Ib-cr gene and different Qnr genes that offer topoisomerase protection. In this study we explore the prevalence of different quinolone resistance mechanisms among ST131 strains within a defined UPEC population.
Methods: 32 E. coli isolates were examined representing the total of ST 131 found among 250 non-duplicate isolates recovered from patients with urinary tract infection, in the northwest region of England between September 2007 and December 2008. All isolates were screened for mutations in quinolone resistance determinant regions (QRDRs) of gyrA and parC genes by sequencing the respective targets. A PCR-based restriction fragment length polymorphism (PCR-RFLP) assay was used to identify the aac (6')-lb-cr variants and screening for the three known qnr genes was carried out using Multiplex PCR.
Results: Of the 32 tested ST131 isolates 20 (62%) showed resistance to quinolones (nalidixic acid) and 19 (59%) expressed additional resistance to fluoroquinolones (ciprofloxacin). All ciprofloxacin resistant isolates had multiple mutations in both gyrA and parC genes while the one nalidixic acid resistant isolate that failed to show resistance to ciprofloxacin had a single gyrA mutation at codon 83 (Ser-Leu). On the other hand only nine isolates carried the aac (6')-lb-cr gene, which represents 50% of ciprofloxacin resistant isolates. Of the 20 isolates tested, none carried any of the targeted qnr genes.
Conclusion: The strong linkage between the ST131 clone and quinolone resistance has been suggested to be the result of the high prevalence of aac (6)-lb-cr among isolates of this clone. However, our study shows that fluoroquinolone resistance occurs in ST131 UPEC as a result of accumulated point mutations in both gyrA and parC genes, irrespective of their acquisition of any plasmid mediated resistance.
|Session name:||Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases|
|Location:||Vienna, Austria, 10 - 13 April 2010|
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