Mutations in gyrA, gyrB, parC, and parE in quinolone-resistant strains of Neisseria gonorrhoeae. - Related Documents




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597901.0000Mutations in gyrA, gyrB, parC, and parE in quinolone-resistant strains of Neisseria gonorrhoeae. Mutations in the genes for the subunits GyrA and ParC of the target enzymes DNA gyrase and topoisomerase IV are important mechanisms of resistance in quinolone-resistant bacteria, including Neisseria gonorrhoeae. The target enzymes also consist of the subunits GyrB and ParE, respectively, though their role in quinolone-resistance has not been fully investigated. We sequenced the quinolone-resistance-determining regions (QRDR) of gyrA, gyrB, parC, and parE in 25 ciprofloxacin-resistant strains from Bangladesh (MIC 4-->32 mg/l) and 5 susceptible strains of N. gonorrhoeae. All the resistant strains had three or four mutations. Two of these were at positions 91 and 95 of gyrA. Fourteen strains had an additional mutation in parC at position 91, and 17 strains had an additional mutation in parE in position 439. No alterations were found in gyrB. The five susceptible strains had identical DNA sequences. Data indicate that the mutations detected in the QRDR of gyrA and parC may be important in the development of quinolone resistance. According to transformation experiments we assume that the alteration in parE is not related to a high degree of quinolone resistance. There was no correlation between ciprofloxacin MICs and pattern or number of mutations in the target genes.200212529019
598010.9999Mutation in the gyrA gene of quinolone-resistant clinical isolates of Acinetobacter baumannii. The gyrA gene mutations associated with quinolone resistance were determined in 21 epidemiologically unrelated clinical isolates of Acinetobacter baumannii. Our studies highlight the conserved sequences in the quinolone resistance-determining region of the gyrA gene from A. baumannii and other bacteria. All 15 isolates for which the MIC of ciprofloxacin is > or = 4 micrograms/ml showed a change at Ser-83 to Leu. Six strains for which the MIC of ciprofloxacin is 1 microgram/ml did not show any change at Ser-83, although a strain for which the MIC of ciprofloxacin is 1 microgram/ml exhibited a change at Gly-81 to Val. Although it is possible that mutations in other locations of the gyrA gene, the gyrB gene, or in other genes may also contribute to the modulation of the MIC level, our results suggest that a gyrA mutation at Ser-83 is associated with quinolone resistance in A. baumannii.19957625818
598420.9998First characterization of fluoroquinolone resistance in Streptococcus suis. We have identified and sequenced the genes encoding the quinolone-resistance determining region (QRDR) of ParC and GyrA in fluoroquinolone-susceptible and -resistant Streptococcus suis clinical isolates. Resistance is the consequence of single point mutations in the QRDRs of ParC and GyrA and is not due to clonal spread of resistant strains or horizontal gene transfer with other bacteria.200717116660
598130.9998Alterations in the DNA topoisomerase IV grlA gene responsible for quinolone resistance in Staphylococcus aureus. A 4.2-kb DNA fragment conferring quinolone resistance was cloned from a quinolone-resistant clinical isolate of Staphylococcus aureus and was shown to possess a part of the grlB gene and a mutated grlA gene. S-80-->F and E-84-->K mutations in the grlA gene product were responsible for the quinolone resistance. The mutated grlA genes responsible for quinolone resistance were dominant over the wild-type allele, irrespective of gene dosage in a transformation experiment with the grlA gene alone. However, dominance by mutated grlA genes depended on gene dosage when bacteria were transformed with the grlA and grlB genes in combination. Quinolone-resistant gyrA mutants were easily isolated from a strain, S. aureus RN4220, carrying a plasmid with the mutated grlA gene, though this was not the case for other S. aureus strains lacking the plasmid. The elimination of this plasmid from such quinolone-resistant gyrA mutants resulted in marked increases in quinolone susceptibility. These results suggest that both DNA gyrase and DNA topoisomerase IV may be targets of quinolones and that the quinolone susceptibility of organisms may be determined by which of these enzymes is most quinolone sensitive.19968723458
598740.9998Mutations in gyrA and parC QRDRs are not relevant for quinolone resistance in epidemiological unrelated Stenotrophomonas maltophilia clinical isolates. Clinical strains of Stenotrophomonas maltophilia are often highly resistant to multiple antibiotics and this resistance is steadily rising. Quinolones are included in the group of antimicrobial agents to which this microorganism is developing resistance. Therefore, the aim of this study was to analyze the epidemiological relationship among 22 clinical isolates of S. maltophilia as well as the molecular mechanisms responsible for the acquisition of quinolone-resistance in these strains. The results of the pulsed-field gel electrophoresis (PFGE) showed an heterogenicity of 82% among the strains used in the study. On the other hand, no amino acid changes were found in the quinolone resistance-determining region (QRDR) of either gyrA and parC genes among quinolone-susceptible and -resistant S. maltophilia strains. Besides, the amino acid of the GyrA found in the position equivalent to Ser-83 of E. coli was Gln instead of a Ser or Thr, the amino acids usually encountered in this position among Gram-negative bacteria. The results suggest that there is not a relationship between the presence of this Gln and the resistance to quinolones in S. maltophilia. We can conclude that, contrary to what has been described in other microorganisms, in these S. maltophilia isolates, the development of resistance to quinolones was not related to mutations in the QRDR of gyrA and parC genes. Thus, to our knowledge, this is the first report describing this phenomenon.200212523620
625850.9998Alterations in GyrA and ParC associated with fluoroquinolone resistance in Enterococcus faecium. High-level quinolone resistance in Enterococcus faecium was associated with mutations in both gyrA and parC genes in 10 of 11 resistant strains. On low-level resistant strain without such mutations may instead possess an efflux mechanism or alterations in the other subunits of the gyrase or topoisomerase IV genes. These findings are similar to those for other gram-positive bacteria, such as Enterococcus faecalis.199910103206
598560.9998Alternative quinolone-resistance pathway caused by simultaneous horizontal gene transfer in Haemophilus influenzae. BACKGROUND: Quinolone-resistant bacteria are known to emerge via the accumulation of mutations in a stepwise manner. Recent studies reported the emergence of quinolone low-susceptible Haemophilus influenzae ST422 isolates harbouring two relevant mutations, although ST422 isolates harbouring one mutation were never identified. OBJECTIVES: To investigate if GyrA and ParC from quinolone low-susceptible isolates can be transferred horizontally and simultaneously to susceptible isolates. METHODS: Genomic DNA was extracted from an H. influenzae isolate harbouring amino acid substitutions in both gyrA and parC and mixed with clinical isolates. The emergence of resistant isolates was compared, and WGS analysis was performed. RESULTS: By adding the genomic DNA harbouring both mutated gyrA and parC, resistant bacteria exhibiting recombination at gyrA only or both gyrA and parC loci were obtained on nalidixic acid and pipemidic acid plates, and the frequency was found to increase with the amount of DNA. Recombination events in gyrA only and in both gyrA and parC occurred with at least 1 and 1-100 ng of DNA, respectively. The genome sequence of a representative strain showed recombination events throughout the genome. The MIC of quinolone for the resulting strains was found to be similar to that of the donor. Although the recombination efficacy was different among the various strains, all strains used in this study obtained multiple genes simultaneously. CONCLUSIONS: These findings indicate that H. influenzae can simultaneously obtain more than two mutated genes. This mechanism of horizontal transfer could be an alternative pathway for attaining quinolone resistance.202236124853
45770.9997Molecular characterization of the genes encoding DNA gyrase and topoisomerase IV of Listeria monocytogenes. The genes encoding subunits A and B of DNA gyrase and subunits C and E of topoisomerase IV of Listeria monocytogenes, gyrA, gyrB, parC and parE, respectively, were cloned and sequenced. Compared with the sequences of quinolone-susceptible bacteria, such as Escherichia coli and Bacillus subtilis, the quinolone resistance-determining region (QRDR) of DNA gyrase subunit A was altered; the deduced amino acid sequences revealed the substitutions Ser-84-->Thr and Asp/Glu-88-->Phe, two amino acid variations at hot spots, commonly associated with resistance to quinolones. No relevant divergences from QRDR consensus sequences were observed in GyrB or both topoisomerase IV subunits. Thus, it could be argued that the amino acid substitutions in GyrA would explain the intrinsic resistance of L. monocytogenes to nalidixic acid. In order to analyse the actual role of the GyrA alterations, a plasmid-encoded gyrA allele was mutated and transformed into L. monocytogenes. However, these heterodiploid strains were not affected in their resistance to nalidixic acid. The effects of the mutant plasmids on ciprofloxacin and sparfloxacin susceptibility were only modest.200212039883
625680.9997Conjugation between quinolone-susceptible bacteria can generate mutations in the quinolone resistance-determining region, inducing quinolone resistance. Quinolones are an important group of antibacterial agents that can inhibit DNA gyrase and topoisomerase IV activity. DNA gyrase is responsible for maintaining bacteria in a negatively supercoiled state, being composed of subunits A and B. Topoisomerase IV is a homologue of DNA gyrase and consists of two subunits codified by the parC and parE genes. Mutations in gyrA and gyrB of DNA gyrase may confer resistance to quinolones, and the majority of resistant strains show mutations between positions 67 and 106 of gyrA, a region denoted the quinolone resistance-determining region (QRDR). The most frequent substitutions occur at positions 83 and 87, but little is known about the mechanisms promoting appearance of mutations in the QRDR. The present study proposes that some mutations in the QRDR could be generated as a result of the natural mechanism of conjugation between bacteria in their natural habitat. This event was observed following conjugation in vitro of two different isolates of quinolone-susceptible Pseudomonas aeruginosa, which transferred plasmids of different molecular weights to a recipient strain of Escherichia coli (HB101), also quinolone-susceptible, generating two different transconjugants that presented mutations in DNA gyrase and acquisition of resistance to all quinolones tested.201525262036
598690.9997Transferable fluoroquinolone resistance in Enterobacteriaceae and Pseudomonas aeruginosa isolated from hemocultures. BACKGROUND: The main mechanisms causing high-level resistance to fluoroquinolones (FQ) are encoded chromosomally; that includes mutations in genes coding DNA-gyrase, but overexpression of efflux pumps contributes to increased minimum inhibitory concentration (MIC) of FQ as well. However, genes responsible for FQ-resistance may be harboured in transferable/conjugative plasmids. For some time, there was an assumption that resistance to FQ cannot be transferable in conjugation due to their synthetic origin, until 1998, when plasmid-mediated resistance transmission in Klebsiella pneumoniae was proved. We aimed to detect the occurrence of transferable FQ-resistance among Gram- negative bacteria isolated from patients in Czech and Slovak hospitals. METHODS: In this study, we tested 236 clinical isolates of Gram-negative bacteria for transferable resistance. Among relevant isolates we performed PCR detection of transferable fluoroquinolone genes (qnr). RESULTS: We have observed transfer of determinants of cephalosporin-resistance, aminoglycoside resistance as well as FQ-resistance (in 10 cases; 4.24%) not only intra-species but inter-species too. The presence of qnr gene was detected in two isolates of forty tested (5%). We have also observed that determinants of cephalosporin-resistance and aminoglycoside-resistance were linked to those of FQ-resistance and were transferred en block in conjugation. CONCLUSION: We have proved that resistance to fluoroquinolones can be transferred horizontally via conjugation among Gram-negative bacteria of different species and is associated with resistance to other antibiotics.201424844110
5947100.9997Fluoroquinolone-resistant Streptococcus agalactiae: epidemiology and mechanism of resistance. Quinolone-resistant Streptococcus agalactiae bacteria were recovered from single-patient isolates and found to contain mutations in the gyrase and topoisomerase IV genes. Pulsed-field gel electrophoresis demonstrated that four isolates from the same long-term care facility were closely related; in seven cases, quinolone-resistant Haemophilus influenzae and S. agalactiae bacteria were isolated from the same patient.200515917553
5854110.9997Discovery of a gene conferring multiple-aminoglycoside resistance in Escherichia coli. Bovine-origin Escherichia coli isolates were tested for resistance phenotypes using a disk diffusion assay and for resistance genotypes using a DNA microarray. An isolate with gentamicin and amikacin resistance but with no corresponding genes detected yielded a 1,056-bp DNA sequence with the closest homologues for its inferred protein sequence among a family of 16S rRNA methyltransferase enzymes. These enzymes confer high-level aminoglycoside resistance and have only recently been described in Gram-negative bacteria.201020368404
5982120.9997Genetic diversity of penicillin-binding protein 2B and 2X genes from Streptococcus pneumoniae in South Africa. Streptococcus pneumoniae (the pneumococcus) is believed to have developed resistance to penicillin by the production of altered forms of penicillin-binding proteins (PBPs) that have decreased affinity for penicillin. Sixty-eight clinical isolates of serogroup 6 and 19 pneumococci (MICs, < 0.015 to 8 micrograms/ml) were randomly selected from hospitals across South Africa which are at substantial geographic distance from each other. The polymerase chain reaction was used to isolate the penicillin-binding domain of PBPs 2B and 2X from the chromosomal DNAs of the bacteria; the purified PBP DNA was digested with restriction enzymes, the fragments were end-labelled and separated on polyacrylamide gels, and the DNA fingerprints were visualized following autoradiography. Fingerprint analysis revealed that at least 19 PBP 2B gene variants occur in the serogroup 6 and 19 pneumococci. The PBP 2B gene revealed a uniform profile among penicillin-susceptible isolates, with variation from this profile occurring only in isolates for which MICs were > or = 0.06 micrograms/ml. Analysis of the PBP 2X gene revealed a greater diversity in the population with 26 variant genes, including some diversity among susceptible isolates. Discrete profiles of both genes were found only within narrow bands of the penicillin MIC, so that the gene pattern predicted the MIC. PBP 2X gene variation and the lack of variability among PBP 2B genes in pneumococci inhibited at low MICs confirm that PBP 2X alteration may be responsible for low-level penicillin resistance, while alterations in both PBP 2B and PBP 2X are required for high-level resistance. The extensive diversity of PBP genes in South African serogroup 6 and 19 strains suggests that altered PBP genes have arisen frequently in this population.19938239609
5937130.9997Association of mutation patterns in GyrA and ParC genes with quinolone resistance levels in lactic acid bacteria. The quinolone resistance of 19 lactic acid bacterial strains belonging to the genera Enterococcus and Lactobacillus isolated from the natural fermented koumiss and yoghurt were investigated. The objective of this study was to determine the quinolone resistance levels and to explore the association of the resistance with the mutation patterns in gyrA and parC genes, as is currently recommended by the Food and Agriculture Organization/World Health Organization Joint Expert Committee in Guidelines for Evaluation of Probiotics in Food for probiotic lactic acid bacteria drug resistance in 2001. The Oxford Cup method and double-tube dilution method were used to determine the quinolone resistance levels of the isolated strains. Generally, all of the 19 strains showed resistance towards norfloxacin and ciprofloxacin when the Oxford cup method was used, whereas the incidence was lower (to norfloxacin 89.5% and to ciprofloxacin 68.4%) when minimum inhibitory concentration breakpoints (CLSI M100-S23) were tested. Furthermore, gene sequencing was conducted on gyrA and parC of topoisomerase II of these isolated strains. The genetic basis for quinolone resistance may be closely related to mutations in gyrA genes as there were 10 mutation sites in amino-acid sequences encoded by gyrA genes in 10 quinolone resistance strains and 14 mutation sites in Enterococcus durans HZ28, whereas no typical mutations were detected in parC genes.201525204345
6259140.9997Evidence of an efflux pump in Serratia marcescens. Spontaneous mutants resistant to fluoroquinolones were obtained by exposing Serratia marcescens NIMA (wild-type strain) to increasing concentrations of ciprofloxacin both in liquid and on solid media. Frequencies of mutation ranged from 10(-7) to 10(-9). Active expulsion of antibiotic was explored as a possible mechanism of resistance in mutants as well as changes in topoisomerase target genes. The role of extrusion mechanisms in determining the emergence of multidrug-resistant bacteria was also examined. Mutants resistant to high concentrations of fluoroquinolones had a single mutation in their gyrA QRDR sequences, whereas the moderate resistance in the rest of mutants was due to extrusion of the drug.200010990265
2063150.9996Nalidixic acid-a good marker of fluoroquinolone resistance mechanisms in Escherichia coli. The purpose of this study was to evaluate how ciprofloxacin, pefloxacin, and nalidixic acid disks perform in screening fluoroquinolone resistance mechanisms in 278 Escherichia coli isolates collected from a prospective clinical material. Antimicrobial susceptibility testing of ciprofloxacin, pefloxacin, and nalidixic acid was performed with the disk diffusion method. PCR-based and sequencing methods were used to detect chromosomal mutations in the gyrA and parC genes and the presence of plasmid-mediated qnr and aac(6')-1b-cr genes. In addition, whole-genome sequencing was used to confirm these results. Our results show that fluoroquinolone resistance mechanisms were discovered, even in ciprofloxacin-susceptible isolates, and plasmid-mediated low-level fluoroquinolone resistance is easily missed if only ciprofloxacin disk is used. E. coli strains with chromosomal gyrA and/or parC mutations were well detected with pefloxacin disk. However, nalidixic acid was a superior tool to detect and differentiate between low- (plasmid-mediated) and high-level (chromosomal mutations) fluoroquinolone resistance in E. coli. Thus, more clinical studies are needed to evaluate the clinical relevance of fluoroquinolone resistance mechanisms in enteric bacteria and pathogens that show potential but are not yet phenotypically fluoroquinolone-resistant. IMPORTANCE: We show in our clinical setting that fluoroquinolone resistance mechanisms are discovered, even among phenotypically fluoroquinolone-susceptible Escherichia coli isolates. When plasmid-mediated quinolone-resistance determinants are present, they are a potential risk for treatment failures due to accumulation of resistance mechanisms during the antimicrobial treatment. Therefore, when it is clinically relevant, fluoroquinolone resistance mechanisms in E. coli should be monitored more closely, and we also recommend testing nalidixic acid susceptibility.202540401973
5933160.9996Novel macrolide-resistance genes, mef(C) and mph(G), carried by plasmids from Vibrio and Photobacterium isolated from sediment and seawater of a coastal aquaculture site. The aim of this study was to determine whether mef(C) and mph(G), originally found on the transferable multi-drug plasmid pAQU1 from Photobacterium damselae subsp. damselae isolated from seawater of a fish farm, are responsible for conferring macrolide resistance. Since these genes are localized head-to-tail on pAQU1 and only four nucleotides exist between them, the single- and combination-effect of these genes was examined. When mph(G) alone was introduced to Escherichia coli, the minimum inhibitory concentrations (MICs) against erythromycin, clarithromycin and azithromycin increased, whereas introduction of mef(C) alone did not influence macrolide susceptibility. Introduction of both mef(C) and mph(G) dramatically increased the MICs to the same three macrolides, i.e. >512 μg ml(-1) , >512 μg ml(-1) and 128 μg ml(-1) respectively. These results suggest that the macrolide phosphotransferase encoded by mph(G) is essential for macrolide resistance, while the efflux pump encoded by mef(C) is required for high-level macrolide resistance. The tandem-pair arrangements of the mef(C) and mph(G) genes were conserved on plasmids ranging in size from 240 to 350 kb of the 22 erythromycin-resistant strains belonging to Vibrio and Photobacterium obtained from the fish farm. Sixteen of 22 plasmids ranged in size from 300 to 350 kb. This is the first report of novel macrolide resistance genes originating from a marine bacterium. SIGNIFICANCE AND IMPACT OF THE STUDY: In this study, mef(C) and mph(G) were found to be novel macrolide-resistance genes, and this is the first report of macrolide-resistance genes originating from a marine bacterium. These genes may be responsible for previously reported cases of the emergence of erythromycin-resistant bacteria in aquaculture sites by an unknown mechanism. The introduction of the tandem arrangement of the mef(C) and mph(G) genes in Escherichia coli increased the MICs to erythromycin, clarithromycin and azithromycin, suggesting a novel mechanism conferring high-level macrolide resistance via combined expression of the efflux pump and macrolide phosphotransferase.201525765542
5983170.9996Analysis of mutational patterns in quinolone resistance-determining regions of GyrA and ParC of clinical isolates. Fluoroquinolone (FQ)-resistant bacteria pose a major global health threat. Unanalysed genomic data from thousands of sequenced microbes likely contain important hints regarding the evolution of FQ resistance, yet this information lies fallow. Here we analysed the co-occurrence patterns of quinolone resistance mutations in genes encoding the FQ drug targets DNA gyrase (gyrase) and topoisomerase IV (topo-IV) from 36,402 bacterial genomes, representing 10 Gram-positive and 10 Gram-negative species. For 19 species, the likeliest routes toward resistance mutations in both targets were determined, and for 5 species those mutations necessary and sufficient to predict FQ resistance were also determined. Target mutation hierarchy was fixed in all examined Gram-negative species, with gyrase being the primary and topo-IV the secondary quinolone target, as well as in six of nine Gram-positive species, with topo-IV being the primary and gyrase the secondary target. By contrast, in three Gram-positive species (Staphylococcus haemolyticus, Streptococcus pneumoniae and Streptococcus suis), under some conditions gyrase became the primary and topo-IV the secondary target. The path through individual resistance mutations varied by species. Both linear and branched paths were identified in Gram-positive and Gram-negative organisms alike. Finally, FQ resistance could be predicted based solely on target gene quinolone resistance mutations for Acinetobacter baumannii, Escherichia coli and Staphylococcus aureus, but not Klebsiella pneumoniae or Pseudomonas aeruginosa. These findings have important implications both for sequence-based diagnostics and for understanding the emergence of FQ resistance.201930582984
2296180.9996Multi-drug resistance profiles and the genetic features of Acinetobacter baumannii isolates from Bolivia. INTRODUCTION: Acinetobacter baumannii is opportunistic in debilitated hospitalised patients. Because information from some South American countries was previously lacking, this study examined the emergence of multi-resistant A. baumannii in three hospitals in Cochabamba, Bolivia, from 2008 to 2009. METHODOLOGY: Multiplex PCR was used to identify the main resistance genes in 15 multi-resistant A. baumannii isolates. RT-PCR was used to measure gene expression. The genetic environment of these genes was also analysed by PCR amplification and sequencing. Minimum inhibitory concentrations were determined for key antibiotics and some were determined in the presence of an efflux pump inhibitor, 1-(1-napthylmethyl) piperazine. RESULTS: Fourteen strains were found to be multi-resistant. Each strain was found to have the blaOXA-58 gene with the ISAba3-like element upstream, responsible for over-expression of the latter and subsequent carbapenem resistance. Similarly, ISAba1, upstream of the blaADC gene caused over-expression of the latter and cephalosporin resistance; mutations in the gyrA(Ser83 to Leu) and parC (Ser-80 to Phe) genes were commensurate with fluoroquinolone resistance. In addition, the adeA, adeB efflux genes were over-expressed. All 15 isolates were positive for at least two aminoglycoside resistance genes. CONCLUSIONS: This is one of the first reports analyzing the multi-drug resistance profile of A. baumannii strains isolated in Bolivia and shows that the over-expression of theblaOXA-58, blaADC and efflux genes together with aminoglycoside modifying enzymes and mutations in DNA topoisomerases are responsible for the multi-resistance of the bacteria and the subsequent difficulty in treating infections caused by them.201323592642
2056190.9996Mechanisms of resistance in nontyphoidal Salmonella enterica strains exhibiting a nonclassical quinolone resistance phenotype. Nontyphoidal Salmonella enterica strains with a nonclassical quinolone resistance phenotype were isolated from patients returning from Thailand or Malaysia to Finland. A total of 10 isolates of seven serovars were studied in detail, all of which had reduced susceptibility (MIC > or = 0.125 microg/ml) to ciprofloxacin but were either susceptible or showed only low-level resistance (MIC < or = 32 microg/ml) to nalidixic acid. Phenotypic characterization included susceptibility testing by the agar dilution method and investigation of efflux activity. Genotypic characterization included the screening of mutations in the quinolone resistance-determining regions (QRDR) of gyrA, gyrB, parC, and parE by PCR and denaturing high-pressure liquid chromatography and the amplification of plasmid-mediated quinolone resistance (PMQR) genes qnrA, qnrB, qnrS, qnrD, aac(6')-Ib-cr, and qepA by PCR. PMQR was confirmed by plasmid analysis, Southern hybridization, and plasmid transfer. No mutations in the QRDRs of gyrA, gyrB, parC, or parE were detected with the exception of a Thr57-Ser substitution within ParC seen in all but the S. enterica serovar Typhimurium strains. The qnrA and qnrS genes were the only PMQR determinants detected. Plasmids carrying qnr alleles were transferable in vitro, and the resistance phenotype was reproducible in Escherichia coli DH5alpha transformants. These data demonstrate the emergence of a highly mobile qnr genotype that, in the absence of mutation within topoisomerase genes, confers the nontypical quinolone resistance phenotype in S. enterica isolates. The qnr resistance mechanism enables bacteria to survive elevated quinolone concentrations, and therefore, strains carrying qnr alleles may be able to expand during fluoroquinolone treatment. This is of concern since nonclassical quinolone resistance is plasmid mediated and therefore mobilizable.200919596880