Contrary to the classical concept that quinolone resistance mostly originates from chromosomal mutations, plasmid-mediated quinolone resistance (PMQR) has been recently reported in several parts of the world. Three different mechanisms have been identified to date: target protection by Qnr proteins, enzymatic inactivation by the aminoglycoside acetyltransferase AAC(6â��)-Ib-cr and, more recently, active efflux by the QepA pump. We screened qnrA, qnrB, and qnrS among nalidixic acid resistant Escherichia coli and Klebsiella pneumonia isolates. The plasmid-mediated quinolone determinants (qnr genes) were detected in 14 isolates out of 26 nalidixic acid resistant isolates with a percentage of 54%. Out of 14 qnr positive isolates, 9 (64%) were K. pneumoniae and 5 (36%) were E. coli. The qnrA and qnrB genes were detected, alone or in combination, in 4(15%) and 12 (46%) isolates respectively from 26 nalidixic acid resistant isolates that were chosen for PCR studies. In 2 isolates (K33 and E16), both qnrA and qnrB were simultaneously detected whereas qnrS gene wasnâ��t detected in any qnr positive isolates. In our study, Extended-Spectrum �Ÿ-Lactamases (ESBLs), AmpC �Ÿ-lactamases and carbapenemases were detected using double disc diffusion test, AmpC disk test and Modified Hodge Test respectively and it was found that 43% (6/14), 57% (8/14) and 21% (3/14) of qnr positive isolates produced ESBLs, AmpC �Ÿ-lactamases and carbapenemases respectively. According to our results, there is a strong correlation between PMQR determinants (qnr genes) and �Ÿ-lactamases whether ESBLs or AmpC �Ÿ-lactamases or even carbapenemases.
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