AAC
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bébéar, C. M.
Right arrow Articles by Renaudin, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bébéar, C. M.
Right arrow Articles by Renaudin, J.

 Previous Article  |  Next Article 

Antimicrobial Agents and Chemotherapy, September 1998, p. 2304-2311, Vol. 42, No. 9
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Alterations in Topoisomerase IV and DNA Gyrase in Quinolone-Resistant Mutants of Mycoplasma hominis Obtained In Vitro

Cécile M. Bébéar,1,2,* Hélène Renaudin,1 Alain Charron,1 Joseph M. Bové,2 Christiane Bébéar,1 and Joel Renaudin2

Laboratoire de Bactériologie, Université Bordeaux 2, 33076 Bordeaux cedex,1 and Laboratoire de Biologie Cellulaire et Moléculaire, Institut National de la Recherche Agronomique, 33883 Villenave d'Ornon cedex,2 France

Received 3 November 1997/Returned for modification 23 January 1998/Accepted 24 March 1998

Mycoplasma hominis mutants were selected stepwise for resistance to ofloxacin and sparfloxacin, and their gyrA, gyrB, parC, and parE quinolone resistance-determining regions were characterized. For ofloxacin, four rounds of selection yielded six first-, six second-, five third-, and two fourth-step mutants. The first-step mutants harbored a single Asp426right-arrowAsn substitution in ParE. GyrA changes (Ser83right-arrowLeu or Trp) were found only from the third round of selection. With sparfloxacin, three rounds of selection generated 4 first-, 7 second-, and 10 third-step mutants. In contrast to ofloxacin resistance, GyrA mutations (Ser83right-arrowLeu or Ser84right-arrowTrp) were detected in the first-step mutants prior to ParC changes (Glu84right-arrowLys), which appeared only after the second round of selection. Further analysis of eight multistep-selected mutants of M. hominis that were previously described (2) revealed that they carried mutations in ParE (Asp426right-arrowAsn), GyrA (Ser83right-arrowLeu) and ParE (Asp426right-arrowAsn), GyrA (Ser83right-arrowLeu) and ParC (Ser80right-arrowIle), or ParC (Ser80right-arrowIle) alone, depending on the fluoroquinolone used for selection, i.e., ciprofloxacin, norfloxacin, ofloxacin, or pefloxacin, respectively. These data indicate that in M. hominis DNA gyrase is the primary target of sparfloxacin whereas topoisomerase IV is the primary target of pefloxacin, ofloxacin, and ciprofloxacin.


* Corresponding author. Mailing address: Laboratoire de Bactériologie, Université Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux cedex, France. Phone: (33) 5.57.57.16.25. Fax: (33) 5.56.79.56.11. E-mail: cecile.bebear{at}labbebear.u-bordeaux2.fr.


Antimicrobial Agents and Chemotherapy, September 1998, p. 2304-2311, Vol. 42, No. 9
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Clin. Vaccine Immunol. Clin. Microbiol. Rev.
J. Clin. Microbiol. ALL ASM JOURNALS

Copyright © 1998 by the American Society for Microbiology. All rights reserved.