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.