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Mohamed F El-Badawy,1,* Emad M Eed,2,* Asmaa S Sleem,3 Azza AK El-Sheikh,4 Ibrahim A Maghrabi,5 Sayed F Abdelwahab6 1Department of Microbiology and Immunology, Faculty of Pharmacy, University of Sadat City, Sadat City, Menoufia, 32897, Egypt; 2Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, Taif, 21944, Saudi Arabia; 3Department of Medical Microbiology and Immunology, Faculty of Medicine, Menoufia University, Menoufia, 32511, Egypt; 4Basic Health Sciences Department, College of Medicine, Princess Nourah bint Abdulrahman University, Riyadh, 11671, Saudi Arabia; 5Department of Clinical Pharmacy, College of Pharmacy, Taif University, Taif, 21944, Saudi Arabia; 6Department of Pharmaceutics and Industrial Pharmacy, College of Pharmacy, Taif University, Taif, 21944, Kingdom of Saudi Arabia*These authors contributed equally to this workCorrespondence: Mohamed F El-Badawy, Department of Microbiology and Immunology, Faculty of Pharmacy, University of Sadat City, Sadat City, Menoufia, 32897, Egypt, Tel +20-103-205-9964, Email Mohamed.Elbadawy@fop.usc.edu.egBackground and Aims: Reports examine quinolone resistance mechanisms among Pseudomonas spp. are sporadic in the Kingdom of Saudi Arabia (KSA). We previously examined the genetic bases of plasmid-mediated quinolone resistance among Pseudomonas spp. clinical isolates. This study investigated chromosomally mediated quinolone resistance mechanisms via investigation of the mutations in the gyrA and parC genes.Methods: The minimum inhibitory concentration (MIC) to different quinolones was determined. Twenty-nine quinolone resistant Pseudomonas spp. clinical isolates were included. The gyrA and parC genes were sequenced by Sanger capillary electrophoresis. Multiple sequence alignment for the translated gyrA and parC genes was performed to identify mutation sites.Results: Of the 29 isolates, 27 isolates were P. aeruginosa and two were P. putida. The cluster analysis of the quinolone susceptibility pattern revealed seven susceptibility phenotypes (A-G) based on susceptibility patterns rather than the MIC values. Also, 22 different susceptibility phenotypes were detected based on MIC values. All isolates exhibited a missense mutation at position 83 (S83I/T/F) of the gyrA gene in addition to six missense mutations at positions outside the QRDR of this gene. In addition, 82.8% (24/29) of the isolates harbored a missense mutation in the parC gene at position 87 (S87L), along with six novel mutations outside the QRDR of the parC gene. Haplotyping of the gyrA, parC, and the overall QRDR revealed six, 10, and 13 different haplotypes, respectively.Conclusion: This study documents the incidence of the commonly reported mutations in the gyrA and parC genes in addition to novel mutations in these genes among Pseudomonas spp. clinical isolates recovered from KSA. Together with our previous findings, these data provide an insight into the genetic background of quinolone resistance among Pseudomonas spp. clinical isolates in KSA.Keywords: minimum inhibitory concentration, Pseudomonas, quinolone resistance determining region, quinolones, haplotyping |
