Association of Phenotypic and Genotypic Fluoroquinolone Susceptibility among Non-Typhoidal Salmonella Isolates from Jeddah, KSA

Abstract

Non-typhoid Salmonella (NTS) infects 250 to 3200 per 100,000 individuals from all over the world. NTS infection is relatively high in Jeddah (ranges between 44-132/100,000 population) as compared to other cities of Saudi Arabia. NTS isolates have also shown increasing resistance to conventional antibiotics. Therefore, fluoroquinolone (FQ) is considered drug of choice for the treatment of invasive NTS infections. A rapid detection of FQ resistance may greatly assist in appropriate therapy and containment of resistant NTS strains. Thus, molecular detection of mutations in FQ resistance genes (gyrA and parC) may play a promising role. Since limited data were available about FQ resistance among NTS isolates, therefore, this study primarily explored the occurrence of phenotypic and genotypic FQ resistance among NTS isolates from Jeddah, Saudi Arabia. Study also explored any correlation between phenotypic and genotypic FQ resistance. Fifty NTS isolates were collected from a public sector hospital of Jeddah from January to December, 2014. FQ susceptibility was determined for 48 NTS isolates using Kirby-bauer disk diffusion method and results were interpreted according to Clinical and Laboratory Standards Institute (CLSI) methodology. Genotypic resistance to FQ was determined by exploring mutations in gyrA and parC genes using PCR- based gene-sequencing method. Results were statistically analyzed using Social Package of Statistical Science (SPSS) version 22. Phenotypic antibiogram revealed that 38% (18/48) NTS isolates were FQ resistant, that 23% (11/48) were intermediately susceptible and that 39% (19/48) were susceptible. Genotypic resistance revealed mutations in only four codons of gyrA and parC genes among 39% (7/18) of FQ resistant isolates. 43% (3/7) of FQ resistant isolates showed mutations at two codons 83 (S83F, S83Y) and 87, (D87G, D87Y, D87W) of gyrA gene. Two resistant isolates showed triple mutations i.e. at codons 83 and 87 of gyrA and codon 80 (S80I and S80W) of parC gene, while one resistant isolate revealed mutation at codon 87 of gyrA and 57 (S57T) of parC gene. Moreover, 55% (6/11) intermediately susceptible isolates for FQ also revealed mutation at codon 83 of gyrA gene whereas; one intermediately susceptible isolate (1/6) also revealed additional mutation at codon 57 of parC gene. None of the FQ susceptible NTS isolates showed any mutations in gyrA or parC genes. Occurrence of mutations at only four codons in gyrA and parC genes among FQ resistant isolates may assist in development of rapid molecular method for FQ resistance detection. Presence of mutations among more than fifty percent of intermediately susceptible FQ isolates is alarming and may serve as a predictor for pre-resistant isolates for FQ. Moreover, absence of mutation in about sixty percent of phenotypically FQ resistant NTS isolates shows existence of an alternate resistance mechanism requiring further investigations.