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Antimicrobial Agents and Chemotherapy, July 2000, p. 1842-1845, Vol. 44, No. 7
Service de
Bactériologie-Virologie-Hygiène, Hôpital Henri
Mondor, Créteil,1 and
Faculté de Pharmacie, Lille,2
France
Received 1 February 2000/Returned for modification 30 March
2000/Accepted 21 April 2000
We determined whether gyrA mutations were present in
fluoroquinolone-resistant laboratory mutants derived from the
Bacteroides fragilis reference strain ATCC 25285 and in
clinical isolates of B. fragilis. The two first-step
mutants selected on ciprofloxacin (CIP) were devoid of gyrA
mutations, whereas two of the three CIP-selected second-step mutants
studied presented the same gyrA mutation leading to a
Ser82Phe change. Unusual GyrA alterations, Asp81Asn or Ala118Val, were
detected in two of the three first-step mutants selected on
trovafloxacin (TRO), Mt3 and Mt1, respectively. The Ala118Val change
had no effect on the susceptibility of Mt1 to CIP. No second-step
mutant could be obtained with TRO as a selector. For the 12 clinical
isolates studied, a Ser82Phe change in GyrA was found only in the 3 strains which showed the highest levels of TRO resistance (MIC, 4 µg/ml). Thus, the resistance phenotypes and genotypes observed in
fluoroquinolone-resistant clinical isolates of B. fragilis
were similar to those found in CIP-selected laboratory mutants, whereas
peculiar mutational events could be selected in vitro with TRO.
0066-4804/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Roles of gyrA Mutations in Resistance of
Clinical Isolates and In Vitro Mutants of Bacteroides
fragilis to the New Fluoroquinolone Trovafloxacin
*
Corresponding author. Mailing address: Service de
Bactériologie-Virologie-Hygiène, Hôpital Henri
Mondor, 51 Avenue du Maréchal de Lattre de Tassigny, 94 010 Créteil, France. Phone: 33-1-49812828. Fax: 33-1-49812839. E-mail: jacques.tankovic{at}hmn.ap-hop-paris.fr.
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