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Antimicrobial Agents and Chemotherapy, March 2000, p. 710-712, Vol. 44, No. 3
0066-4804/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Molecular Mechanisms of Fluoroquinolone Resistance in Pseudomonas aeruginosa Isolates from Cystic Fibrosis Patients

Shah Jalal,1,* Oana Ciofu,2 Niels Høiby,3 Naomasa Gotoh,4 and Bengt Wretlind1

Division of Clinical Bacteriology, Huddinge University Hospital, S-14186 Huddinge, Sweden1; Institute of Medical Microbiology and Immunology, University of Copenhagen,2 and Department of Clinical Bacteriology, Rigshospitalet,3 Copenhagen, Denmark; and Department of Microbiology, Kyoto Pharmaceutical University, Yamashina, Kyoto, Japan4

Received 28 June 1999/Returned for modification 17 September 1999/Accepted 9 December 1999

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).

* Corresponding author. Mailing address: Division of Clinical Bacteriology, Huddinge University Hospital F82, S-14186 Huddinge, Sweden. Phone: 46-8-5858 1162. Fax: 46-8-711 3918. E-mail: shah.jalal{at}impi.ki.se.

Antimicrobial Agents and Chemotherapy, March 2000, p. 710-712, Vol. 44, No. 3
0066-4804/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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