Plasmid Mediated Quinolones Resistance ESBL-EnterobactÃÂ©riaceae in Moroccan
- *Corresponding Author:
- Barrijal Said
Faculty of Sciences and Techniques
E-mail: [email protected]
Received date: March 16, 2012; Accepted date: May 25, 2012; Published date: April 27, 2012
Citation: Malki Fatima EL, Bouraissi Meriem EL, Said B (2012) Plasmid Mediated Quinolones Resistance ESBL-Enterobactériaceae in Moroccan. Pharmaceut Anal Acta S15:006. doi: 0.4172/2153-2435.S15-006
Copyright: © 2012 Malki Fatima EL, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Multidrug Resistance (MDR) in Enterobacteriaceae including resistance to quinolones is rising worldwide. This study was conducted to assess the resistance level to antibiotics and to detect plasmid genes mediated quinolones resistance in Extended-Spectrum β-lactamase (ESBL)-producing Enterobacteriaceae collected from regional hospitals of Fes–Meknes in central Morocco. ESBL phenotype was determined according to the combination disc method recommended by the Clinical and Laboratory Standards Institute (CLSI) using double disc synergy test (DDST). The antimicrobial susceptibility patterns of isolates showed high resistance rate to most antibiotics except imipenem which showed 100% of susceptibility.
A sub-site of 27 isolates was screened for qnr genes by multiplex PCR. qnrB gene was detected in 8 ESBL isolates (2 E. coli, 4 K. pneumoniae, 01 E. aerogenes and 01 C. freundii) while no qnrA neither qnrS could be detected. aac(60)-Ib-cr gene was detected in 15 strains, 13 of them were ESBL.
Our results are in agreement with the general rule that imipenem stays the drug of choice for the treatment of infections caused by ESBL producers. Moreover, the presence of qnr determinants is closely related to ESBL phenotype while aac(60)-Ib-cr gene could be detected in isolates with or without ESBL phenotype.