Quinolone resistance by mutations in chromosomal gyrase genes. Just the tip of the iceberg?

Martínez, José-Luis; Alonso, Ana; Gómez-Gómez, José María; Baquero, Fernando

doi:10.1093/jac/42.6.683

Cited by 60 publications

(42 citation statements)

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“…The presence of horizontallyacquired genes accounted in part for elevated nalidixic acid MICs in strains that harboured these genes, but not completely. It is therefore possible that other resistance mechanisms, such as ParE polymorphisms, other horizontally acquired resistance genes, over-active efflux, or even novel mechanisms are present in some of the isolates (Martínez et al, 1998).…”

Section: Amentioning

confidence: 99%

Antibacterial resistance pattern among Escherichia coli strains isolated from Mansoura hospitals in Egypt with a special reference to quinolones

El‐Sokkary¹,

Abdelmegeed²

2015

Afr. J. Microbiol. Res.

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Extensive use of fluoroquinolone antibacterial in clinical practice has been associated with increasing frequency of quinolone-resistant Escherichia coli strains. In the current study, a total of 80 E. coli clinical isolates from Mansoura hospitals patients in Egypt were studied for antibacterial susceptibility pattern against 15 different antibacterials. These strains were tested for quinolones resistance by minimum inhibitory concentration (MIC) determination using broth micro-dilution method. The resistance rate of ciprofloxacin and levofloxacin for E. coli isolates was found to be 60%. PCR was performed for detection of plasmid-mediated quinolone resistance genes including qnrA, qnrB and qnrS. 30 and 61.3% of E. coli isolates were positive for qnrA and qnrB, respectively, whereas qnrS was identified in only 15% of isolates. Quinolone resistance-determining region (QRDR) of gyrA and ParC genes was characterized for 17 ciprofloxacin and levofloxacin resistant E. coli isolates (MIC 12.5-200 µg mL -1 ). Two mutation sites in gyrA were detected in 17 tested E. coli isolates. However, two mutation sites in parC were detected in four E. coli isolates. The amino acid change at Ser-83 and aspartic-87 in GyrA were the most common mutation sites identified in the isolates. These results indicated that multiple mechanisms of quinolone-resistance are commonly found in E. coli isolated from Mansoura hospitals.

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Section: Amentioning

confidence: 99%

Antibacterial resistance pattern among Escherichia coli strains isolated from Mansoura hospitals in Egypt with a special reference to quinolones

El‐Sokkary¹,

Abdelmegeed²

2015

Afr. J. Microbiol. Res.

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“…So far, five qnr genes were recognized (qnr A, B, S, C and D) which encode Qnr proteins that inhibit quinolones binding to their bacterial targets (Kulková et al, 2014, Azadpour et al, 2014, Alheib et al, 2015. These qnr genes best owa low resistance level to quinolones, however, it supportsthe selection of chromosomal mutations resulting in resistance development in the host strain (Martinez et al, 1998).…”

Section: Introductionmentioning

confidence: 96%

Plasmid Mediated Quinolone Resistance Determinants among Nosocomial Clinical Pseudomonas aeruginosa Isolates

Saleh¹,

Balboula²

2017

Int.J.Curr.Microbiol.App.Sci

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“…High-level fluoroquinolone resistance does not develop by a single-step gyrA mutation, in contrast to nalidixic acid resistance (29,34). parC, which encodes topoisomerase IV, is also targeted by quinolone antibiotics, presumably because the QRDR of parC is highly homologous to that of gyrA.…”

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confidence: 99%

Single-Nucleotide Polymorphism Mutation Spectra and Resistance to Quinolones in Salmonella enterica Serovar Enteritidis with a Mutator Phenotype

Levy

Sharma

Cebula

2004

Antimicrob Agents Chemother

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Resistance to quinolone antibiotics has been associated with single-nucleotide polymorphisms (SNPs) in the quinolone resistance-determining region (QRDR) of gyrA. Mutations in the gyrA gene were compared by using mutant populations derived from wild-type Salmonella enterica serovar Enteritidis and its isogenic mutS::Tn10 mutator counterpart. Spontaneous mutants arising during nonselective growth were isolated by selection with either nalidixic acid, enrofloxacin, or ciprofloxacin. QRDR SNPs were identified in approximately 70% (512 of 695) of the isolates via colony hybridization with radiolabeled oligonucleotide probes. Notably, transition base substitution SNPs in the QRDR were dramatically increased in mutants derived from the mutS strain. Some, but not all, antibiotic-resistant mutants lacking QRDR SNPs were resistant to tetracycline and chloramphenicol, consistent with alterations in nonspecific efflux pumps or other membrane transport mechanisms. Changing the selection conditions shifted the mutation spectrum. Selection with ciprofloxacin was least likely to yield a mutant harboring either a QRDR SNP or chloramphenicol resistance. Selection with enrofloxacin was more likely to yield mutants containing Ser833Phe mutations, whereas selection with ciprofloxacin or nalidixic acid favored recovery of Asp873Gly mutants. Fluoroquinolone-resistant Salmonella strains isolated from veterinary or clinical settings frequently display a mutational spectrum with a preponderance of transition SNPs in the QRDR, the pattern found in vitro among mutS mutator mutants reported here. Both the preponderance of transition mutations and the varied mutation spectra reported for veterinary and clinical isolates suggest that bacterial mutators defective in methyl-directed mismatch repair may play a role in the emergence of quinolone and fluoroquinolone resistance in feral settings.

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Quinolone resistance by mutations in chromosomal gyrase genes. Just the tip of the iceberg?

Cited by 60 publications

References 0 publications

Antibacterial resistance pattern among Escherichia coli strains isolated from Mansoura hospitals in Egypt with a special reference to quinolones

Antibacterial resistance pattern among Escherichia coli strains isolated from Mansoura hospitals in Egypt with a special reference to quinolones

Plasmid Mediated Quinolone Resistance Determinants among Nosocomial Clinical Pseudomonas aeruginosa Isolates

Single-Nucleotide Polymorphism Mutation Spectra and Resistance to Quinolones in Salmonella enterica Serovar Enteritidis with a Mutator Phenotype

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