In Vitro
 Effect of
 qnrA1
 ,
 qnrB1
 , and
 qnrS1
 Genes on Fluoroquinolone Activity against Isogenic
 Escherichia coli
 Isolates with Mutations in
 gyrA
 and
 parC

Briales, Alejandra; Rodríguez-Martínez, José Manuel; Velasco, C.; Alba, Paula Díaz de; Domínguez-Herrera, Juan; Pachón, Jerónimo; Pascual, Álvaro

doi:10.1128/aac.00927-10

Cited by 61 publications

(41 citation statements)

References 19 publications

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“…Acquisition of qnrA also increased the MBC and MPC values of CIP by 15.8-to 79.1-fold (0.285-1.14 mg/mL) and by 2.6-to 21.1-fold (0.5-4 mg/mL), respectively, relative to those of the parent strains (Table 1). These results were consistent with those of previous reports (21,22). The MBCs and MPCs of CIP for the transformants of O25b strains were highest among the compared O-serotypes at 0.75-1.14 and 3-4 mg/mL, respectively.…”

Section: Resultssupporting

confidence: 93%

Contribution of QnrA, a Plasmid-Mediated Quinolone Resistance Peptide, to Survival of Escherichia coli Exposed to a Lethal Ciprofloxacin Concentration

2015

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SUMMARY:We evaluated the effects of qnrA on survival of bacteria exposed to a lethal ciprofloxacin (CIP) concentration and development of quinolone resistance through the accumulation of amino acid substitutions in quinolone resistance-determining regions (QRDRs) of GyrA and ParC, targets of quinolones, in Escherichia coli. CIP-susceptible E. coli strains of different O-serotypes (O1, O6, O18, O25b, O74, and O78) were transformed by a recombinant plasmid harboring qnrA, and the parent strains and their transformants were subjected to killing curve assays and adaptation tests. In the killing curve assay at 2 × the minimum inhibitory concentration of CIP, the viable bacterial cell numbers of strains O1, O6, and O25b were maintained at 10 5 -10 8 CFU/mL after 24-h incubation, while the remaining strains showed a 10 5 -fold reduction in viable cell numbers. In the adaptation test, a Ser83-Leu substitution in the QRDR of GyrA was identified earlier in the parent strains of O25b and O1 than in their transformants, suggesting that the acquisition of qnrA did not necessarily accelerate the rate of accumulation of amino acid substitutions in the QRDR. We confirmed that the presence of qnrA contributed to increased survival of the E. coli strains displaying certain O-serotypes. Further studies are necessary to evaluate the precise effects of qnrA on quinolone resistance acquisition by Enterobacteriaceae.

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Section: Resultssupporting

confidence: 93%

Contribution of QnrA, a Plasmid-Mediated Quinolone Resistance Peptide, to Survival of Escherichia coli Exposed to a Lethal Ciprofloxacin Concentration

2015

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“…Although our strains were resistant to quinolones, the prevalence of PMQR genes was relatively low, consistent with the fact that the contribution of these genes in the level of quinolone resistance is negligible. The genes have, in fact, also been found in both quinolone-resistant and -susceptible isolates; their role is to facilitate the emergence of resistance and to strengthen it [23,30,31].…”

Section: Discussionmentioning

confidence: 99%

Characteristics of ciprofloxacin-resistant Enterobacteriaceae isolates recovered from wastewater of an Algerian hospital

Anssour

Messai

Estepa

et al. 2016

J Infect Dev Ctries

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Introduction: Hospital effluents are a source of environmental pollution by drugs, antibiotic-resistant bacteria, and resistance genes. Quinolones, particularly ciprofloxacin, are commonly detected in these effluents, contributing to the emergence of antimicrobial resistance. The objective of this study was to characterize ciprofloxacin-resistant Enterobacteriaceae in hospital effluents. Methodology: Isolates were selected on Tergitol-7 agar supplemented with ciprofloxacin and genotyped by ERIC-PCR. Antibiotic susceptibility testing was done using the disk diffusion method, and minimum inhibitory concentrations were determined using the agar dilution method. Resistance genes, integrons, phylogenetic groups, and sequence types were identified by PCR and sequencing. Results: A total of 17 ciprofloxacin-resistant isolates were characterized: Escherichia coli, Escherichia vulneris, Klebsiella pneumoniae, Klebsiella oxytoca, Citrobacter freundii, and Citrobacter koseri/farmeri. Isolates presented concomitant resistance to nalidixic acid, ciprofloxacin, ofloxacin, and pefloxacin. A diversity in mutation patterns in gyrA and parC genes and new amino-acid substitutions in GyrA subunit were observed. Quinolone plasmidic resistance genes qnrB1, qnrB2, qnrB5/19, qnrS1, and aac(6')-Ib-cr were detected. Resistance to other antibiotic classes was observed. Class 1 integrons and resistance genes blaCTX- sul1, sul2, sul3, tetA, tetB, aadA1/2, aadA5, aac(3) II, dfrA1, dfrA5, dfrA7, and dfrA12 were detected. Bacterial tolerance to cadmium, zinc, and mercury was observed with the presence of the merA gene. E. coli isolates belonged to phylogenetic groups A, B1, and D and to sequence types ST405, ST443, ST101, ST10, and ST347. Conclusions: This study highlighted bacterial multidrug resistance linked to ciprofloxacin and, consequently, the risk of bacterial exposure to this antibiotic.

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“…The same augmentation of resistance selection has been found in clinical isolates of E. cloacae (147). Surprisingly, in qnr-harboring E. coli gyrA resistance mutants are rarely selected (217), although resistance produced by qnr and gyrA is additive (218)(219)(220), clinical isolates with qnr alleles or aac(6′)-Ib-cr and gyrA, parC, and other resistance mutations are common (221), and gyrA mutants have developed in qnr positive isolates from patients treated with quinolone for E. coli (222) or S. enterica (223) infections.…”

Section: Resistance Produced By Pmqr Determinantsmentioning

confidence: 99%

Plasmid-Mediated Quinolone Resistance

Jacoby

2009

Antimicrobial Drug Resistance

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SummaryThree mechanisms for plasmid-mediated quinolone resistance (PMQR) have been discovered since 1998. Plasmid genes qnrA, qnrB, qnrC, qnrD, qnrS, and qnrVC code for proteins of the pentapeptide repeat family that protects DNA gyrase and topoisomerase IV from quinolone inhibition. The qnr genes appear to have been acquired from chromosomal genes in aquatic bacteria, are usually associated with mobilizing or transposable elements on plasmids, and are often incorporated into sul1-type integrons. The second plasmid-mediated mechanism involves acetylation of quinolones with an appropriate amino nitrogen target by a variant of the common aminoglycoside acetyltransferase AAC(6′)-Ib. The third mechanism is enhanced efflux produced by plasmid genes for pumps QepAB and OqxAB. PMQR has been found in clinical and environmental isolates around the world and appears to be spreading. The plasmid-mediated mechanisms provide only low-level resistance that by itself does not exceed the clinical breakpoint for susceptibility but nonetheless facilitates selection of higher-level resistance and makes infection by pathogens containing PMQR harder to treat.

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In Vitro Effect of qnrA1 , qnrB1 , and qnrS1 Genes on Fluoroquinolone Activity against Isogenic Escherichia coli Isolates with Mutations in gyrA and parC

Cited by 61 publications

References 19 publications

Contribution of QnrA, a Plasmid-Mediated Quinolone Resistance Peptide, to Survival of <i>Escherichia coli</i> Exposed to a Lethal Ciprofloxacin Concentration

Contribution of QnrA, a Plasmid-Mediated Quinolone Resistance Peptide, to Survival of <i>Escherichia coli</i> Exposed to a Lethal Ciprofloxacin Concentration

Characteristics of ciprofloxacin-resistant Enterobacteriaceae isolates recovered from wastewater of an Algerian hospital

Plasmid-Mediated Quinolone Resistance

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