Abstract

Background: Quinolone resistant Salmonella serotypes have been reported in recent years and have become increasingly widespread worldwide. Objectives: We evaluated the molecular mechanism of quinolone resistance in non-typhoidal Salmonella strains isolated from clinical samples in Tehran, Iran. Methods: The present study included the Salmonella isolates originated from hospitalized individuals and outpatients in Tehran, Iran. Serotyping of nalidixic acid-resistant Salmonella isolates was done by slide agglutination method. Then, the quinolone resistance-determining region (QRDR) of topoisomerase gene gyrA and the plasmid-mediated quinolone resistance (PMQR) determinants were detected using the polymerase chain reaction (PCR) method. Restriction fragment length polymorphism (RFLP) analysis was also employed to determine the possible mutation in the gyrA gene of those strains. Mutant strains were detected by enzymatic digestion, and their PCR products were sequenced immediately. Results: Amongst 141 isolates, 60% showed nalidixic acid resistance, whereas none of them were ciprofloxacin-resistant. The commonly prevalent serotypes were S. Enteritidis and S. Infantis. Of 85 nalidixic acid-resistant strains, 17 (20%) isolates harbored the qnrS gene. However, PCR analysis of the quinolone-resistant strains did not detect qnrA and qnrB genes. PCR-RFLP and sequencing analysis of the QRDRs of the gyrA gene indicated that 16 (18.8%) isolates had mutant patterns, and the most common point mutation was serine to phenylalanine at position 83. Conclusions: Our results demonstrated that point mutations in gyrA and the existence of plasmid-mediated gene qnrS were important mechanisms of quinolone resistance in non-typhoidal Salmonella strains isolated from human origin. Other alternative mechanisms of resistance, such as alterations in the expression of efflux pumps, should be studied to provide greater insight into the molecular mechanism of quinolone-resistant non-typhoidal Salmonella isolates.

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