Prevalence and characterization of plasmid-mediated quinolone resistance genes inSalmonellaisolated from poultry in Korea

Abstract

The purpose of this study was to investigate the prevalence and characteristics of plasmid-mediated quinolone resistance (PMQR) genes qnr, aac(6?)-Ib-cr, and qepA in a total of 185 non-duplicate Salmonella spp. isolated from hatcheries, poultry farms, and poultry slaughterhouses during the period 2001 to 2010 in Korea. Additionally, mutation analysis of quinolone resistance determining regions (QRDRs), conjugation experiments, and plasmid analysis were performed in the PMQR-positive isolates. Among the 185 isolates, six (3.2%) contained qnr genes (two qnrB4 and four qnrS1) but none carried the aac(6?)-Ib-cr or qepA genes. Among the six PMQR-positive isolates, one showed a single mutation (Ser83-Phe substitution) in the QRDRs of gyrA. Among them, three were non-susceptible (intermediate or resistant) to nalidixic acid (minimum inhibitory concentration [MIC] ]256 mg/ml), ciprofloxacin (MIC 2 mg/ml), and levofloxacin (MIC 4 mg/ml), but others were susceptible to all of the three fluoroquinolones. They were resistant to six or more antimicrobial agents tested and were able to transfer quinolone resistance to recipient Escherichia coli J53 by conjugation. By performing a hybridization test, plasmids harbouring qnrB4 and qnrS1 genes were less than 8 kb and about 70 kb in size, respectively. The horizontal dissemination of qnrS1 gene was mediated by IncN plasmid. Compared with the recipient strain, MICs of the transconjugants increased twofold to four-fold for nalidixic acid, and eight-fold to 16-fold for ciprofloxacin and levofloxacin. This report is the first to describe the detection of qnr genes in Salmonella spp. isolated from poultry in Korea. Widespread horizontal transfer of these genes among bacteria may be a serious public health concern because these can rapidly increase fluoroquinolone resistance. To ensure the public health, it is essential to continuously survey and carefully monitor the spread of PMQR genes in Salmonella from poultry.

Characteristics of Quinolone Resistance in Salmonella spp. Isolates from the Food Chain in Brazil

“…A similar association has been reported by Park et al (2006) in the United States, Xiong et al (2011) while investigating the aac (6′)-Ib and qnr genes in Enterobacter cloacae “in China, and” Kim et al (2013) in enterobacteria isolated from clinical samples in Korea. Not sequencing the aac (6′)-Ib gene to determine the cr variant was one limitation in the present study.…”

“…Regardless that some authors recognize the location of the aac (6′)-Ib gene mostly in class 1 integrons, our results show the absence of this gene in all analyzed strains [12 aac (6′)-Ib positive isolates without the integron region] (Rodríguez-Martínez et al, 2011; Kim et al, 2013). …”

Clonal relatedness and resistance patterns of Salmonella Corvallis from poultry carcasses in a Brazilian slaughterhouse

“…Nalidixic acid resistance is predictive of fluoroquinolone resistance, as observed in this study: all of the nalidixic acidresistant strains presented reduced ciprofloxacin susceptibility. Fluoroquinolone resistance is an important concern that is less frequently reported in Salmonella than in other food-borne pathogens [27]; however, Salmonella with reduced susceptibility to fluoroquinolone has been reported worldwide [28,29] and in Brazil [30,31]. In fact, to the best of our knowledge, this study is the first to report ESBLproducing strains of S. Corvallis with reduced ciprofloxacin susceptibility in Brazil.…”

Antimicrobial Resistance of Salmonella enterica Serovar Typhimurium in Shanghai, China

“…The main mechanisms of quinolone-resistance in Salmonella have been attributed to several point mutations in the QRDRs of the gyrA and parC genes and the PMQR genes (Hopkins et al, 2007; Kim et al, 2013). Mutations at different sites contribute to different levels of resistance to ciprofloxacin, and simultaneous mutations in both gyrA and parC genes produce high levels of ciprofloxacin resistance.…”