Molecular mechanisms of fluoroquinolone resistance in Pseudomonas aeruginosa isolates from cystic fibrosis patients.

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Molecular mechanisms of fluoroquinolone resistance in Pseudomonas aeruginosa isolates from cystic fibrosis patients. / Jalal, S; Ciofu, O; Høiby, Niels; Gotoh, N; Wretlind, B.

In: Antimicrobial Agents and Chemotherapy, Vol. 44, No. 3, 2000, p. 710-2.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Jalal, S, Ciofu, O, Høiby, N, Gotoh, N & Wretlind, B 2000, 'Molecular mechanisms of fluoroquinolone resistance in Pseudomonas aeruginosa isolates from cystic fibrosis patients.', Antimicrobial Agents and Chemotherapy, vol. 44, no. 3, pp. 710-2.

APA

Jalal, S., Ciofu, O., Høiby, N., Gotoh, N., & Wretlind, B. (2000). Molecular mechanisms of fluoroquinolone resistance in Pseudomonas aeruginosa isolates from cystic fibrosis patients. Antimicrobial Agents and Chemotherapy, 44(3), 710-2.

Vancouver

Jalal S, Ciofu O, Høiby N, Gotoh N, Wretlind B. Molecular mechanisms of fluoroquinolone resistance in Pseudomonas aeruginosa isolates from cystic fibrosis patients. Antimicrobial Agents and Chemotherapy. 2000;44(3):710-2.

Author

Jalal, S ; Ciofu, O ; Høiby, Niels ; Gotoh, N ; Wretlind, B. / Molecular mechanisms of fluoroquinolone resistance in Pseudomonas aeruginosa isolates from cystic fibrosis patients. In: Antimicrobial Agents and Chemotherapy. 2000 ; Vol. 44, No. 3. pp. 710-2.

Bibtex

@article{23c23480ba2111ddae57000ea68e967b,
title = "Molecular mechanisms of fluoroquinolone resistance in Pseudomonas aeruginosa isolates from cystic fibrosis patients.",
abstract = "Twenty P. aeruginosa isolates were collected from six cystic fibrosis (CF) patients, aged 27 to 33, in 1994 (9 isolates) and 1997 (11 isolates) at the CF Center, Copenhagen, Denmark, and were typed by pulse-field gel electrophoresis (PFGE) or ribotyping. Five of the patients had isolates with the same PFGE or ribotyping patterns in 1997 as in 1994, and ciprofloxacin had a two- to fourfold higher MIC for the isolates collected in 1997 than those from 1994. Genomic DNA was amplified for gyrA, parC, mexR, and nfxB by PCR and sequenced. Eleven isolates had mutations in gyrA, seven isolates had mutations at codon 83 (Thr to Ile), and four isolates had mutations at codon 87 (Asp to Asn or Tyr). Sixteen isolates had mutations in nfxB at codon 82 (Arg to Leu). Increased amounts of OprN were found in six isolates and OprJ in eight isolates as determined by immunoblotting. No isolates had mutations in parC or mexR. Six isolates had mutations in efflux pumps without gyrA mutations. The average number of mutations was higher in isolates from 1997 than in those from 1994. The results also suggested that efflux resistance mechanisms are more common in isolates from CF patients than in strains from urine and wounds from non-CF patients, in which mutations in gyrA and parC dominate (S. Jalal and B. Wretlind, Microb. Drug Resist. 4:257-261, 1998).",
author = "S Jalal and O Ciofu and Niels H{\o}iby and N Gotoh and B Wretlind",
note = "Keywords: Adult; Anti-Infective Agents; Bacterial Outer Membrane Proteins; Bacterial Proteins; Ciprofloxacin; Cystic Fibrosis; DNA Gyrase; DNA Topoisomerase IV; DNA Topoisomerases, Type II; DNA-Binding Proteins; Drug Resistance, Microbial; Electrophoresis, Gel, Pulsed-Field; Humans; Microbial Sensitivity Tests; Molecular Sequence Data; Norfloxacin; Pseudomonas Infections; Pseudomonas aeruginosa; Sequence Analysis, DNA; Transcription Factors",
year = "2000",
language = "English",
volume = "44",
pages = "710--2",
journal = "Antimicrobial Agents and Chemotherapy",
issn = "0066-4804",
publisher = "American Society for Microbiology",
number = "3",

}

RIS

TY - JOUR

T1 - Molecular mechanisms of fluoroquinolone resistance in Pseudomonas aeruginosa isolates from cystic fibrosis patients.

AU - Jalal, S

AU - Ciofu, O

AU - Høiby, Niels

AU - Gotoh, N

AU - Wretlind, B

N1 - Keywords: Adult; Anti-Infective Agents; Bacterial Outer Membrane Proteins; Bacterial Proteins; Ciprofloxacin; Cystic Fibrosis; DNA Gyrase; DNA Topoisomerase IV; DNA Topoisomerases, Type II; DNA-Binding Proteins; Drug Resistance, Microbial; Electrophoresis, Gel, Pulsed-Field; Humans; Microbial Sensitivity Tests; Molecular Sequence Data; Norfloxacin; Pseudomonas Infections; Pseudomonas aeruginosa; Sequence Analysis, DNA; Transcription Factors

PY - 2000

Y1 - 2000

N2 - Twenty P. aeruginosa isolates were collected from six cystic fibrosis (CF) patients, aged 27 to 33, in 1994 (9 isolates) and 1997 (11 isolates) at the CF Center, Copenhagen, Denmark, and were typed by pulse-field gel electrophoresis (PFGE) or ribotyping. Five of the patients had isolates with the same PFGE or ribotyping patterns in 1997 as in 1994, and ciprofloxacin had a two- to fourfold higher MIC for the isolates collected in 1997 than those from 1994. Genomic DNA was amplified for gyrA, parC, mexR, and nfxB by PCR and sequenced. Eleven isolates had mutations in gyrA, seven isolates had mutations at codon 83 (Thr to Ile), and four isolates had mutations at codon 87 (Asp to Asn or Tyr). Sixteen isolates had mutations in nfxB at codon 82 (Arg to Leu). Increased amounts of OprN were found in six isolates and OprJ in eight isolates as determined by immunoblotting. No isolates had mutations in parC or mexR. Six isolates had mutations in efflux pumps without gyrA mutations. The average number of mutations was higher in isolates from 1997 than in those from 1994. The results also suggested that efflux resistance mechanisms are more common in isolates from CF patients than in strains from urine and wounds from non-CF patients, in which mutations in gyrA and parC dominate (S. Jalal and B. Wretlind, Microb. Drug Resist. 4:257-261, 1998).

AB - Twenty P. aeruginosa isolates were collected from six cystic fibrosis (CF) patients, aged 27 to 33, in 1994 (9 isolates) and 1997 (11 isolates) at the CF Center, Copenhagen, Denmark, and were typed by pulse-field gel electrophoresis (PFGE) or ribotyping. Five of the patients had isolates with the same PFGE or ribotyping patterns in 1997 as in 1994, and ciprofloxacin had a two- to fourfold higher MIC for the isolates collected in 1997 than those from 1994. Genomic DNA was amplified for gyrA, parC, mexR, and nfxB by PCR and sequenced. Eleven isolates had mutations in gyrA, seven isolates had mutations at codon 83 (Thr to Ile), and four isolates had mutations at codon 87 (Asp to Asn or Tyr). Sixteen isolates had mutations in nfxB at codon 82 (Arg to Leu). Increased amounts of OprN were found in six isolates and OprJ in eight isolates as determined by immunoblotting. No isolates had mutations in parC or mexR. Six isolates had mutations in efflux pumps without gyrA mutations. The average number of mutations was higher in isolates from 1997 than in those from 1994. The results also suggested that efflux resistance mechanisms are more common in isolates from CF patients than in strains from urine and wounds from non-CF patients, in which mutations in gyrA and parC dominate (S. Jalal and B. Wretlind, Microb. Drug Resist. 4:257-261, 1998).

M3 - Journal article

C2 - 10681343

VL - 44

SP - 710

EP - 712

JO - Antimicrobial Agents and Chemotherapy

JF - Antimicrobial Agents and Chemotherapy

SN - 0066-4804

IS - 3

ER -

ID: 8744952