This study aimed to investigate the genetic basis for quinolones and fluoroquinolones insusceptibility in E.coli isolated from outpatients suspected with urinary tract infections (UTIs). Fifty-one nalidixic acid unsusceptible E. coli isolates were collected from adult patients with UTIs . Antimicrobial sensitivity testing was performed by disc diffusion test, and minimum inhibitory concentrations of nalidixic acid and ciprofloxacin were determined by E. test strips. PCR amplification and DNA sequencing were carried out for the detection of alterations in the quinolone resistance determining region (QRDR) of gyrA and parC genes and screening for plasmid-mediated quinolone resistance (PMQR) genes (qnr, aac(6)-ib-cr, qepA and oqxAB). Genetic analysis of the QRDR revealed amino acid substitutions in the codons 83 and 87 of the gyrA gene with or without alterations at codons 80 and 84 of the parC gene. Most of the quinolone-resistant isolates (94%) had at least one of the PMQR genes. QRDR mutations in chromosomal genes encoding gyrA and parC have the principal role in the development of quinolones and fluoroquinolnes resistance in E.coli. The accumulation of amino acid alterations in gyrA and the concurrent mutations in parC lead to the emergence of a high-level of insensitivity toward fluoroquinolones. The detected PMQR determinants are widespread in the community, and they are associated with the development of resistance to many other categories of antibiotics. This is the first report to detect oqxAB in E.coli in Egypt.
E. coli, Urinary tract infection, Egypt, oqxAB
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