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 Ricci, V.
Right arrow Articles by Piddock, L. J. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ricci, V.
Right arrow Articles by Piddock, L. J. V.

 Previous Article  |  Next Article 

Antimicrobial Agents and Chemotherapy, April 2004, p. 1344-1346, Vol. 48, No. 4
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.4.1344-1346.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Role of Topoisomerase Mutations and Efflux in Fluoroquinolone Resistance of Bacteroides fragilis Clinical Isolates and Laboratory Mutants

Vito Ricci,1 Marnie L. Peterson,1,2 John C. Rotschafer,2 Hannah Wexler,3 and Laura J. V. Piddock1*

Antimicrobial Agents Research Group, Division of Immunity and Infection, University of Birmingham, Birmingham B15 2TT, United Kingdom,1 University of Minnesota, Minneapolis, Minnesota 55455,2 Department of Medicine, University of California at Los Angeles School of Medicine, Los Angeles, California 900243

Received 21 May 2003/ Returned for modification 22 November 2003/ Accepted 19 December 2003

Twelve laboratory mutants and 32 ciprofloxacin-resistant isolates of Bacteroides fragilis were examined for the mechanism(s) of fluoroquinolone resistance. Five mutants had mutations in gyrA. One mutant and two clinical isolates contained a mutation in gyrB. Eight mutants and five clinical isolates accumulated significantly less ciprofloxacin than did wild-type isolates; the mutants and clinical isolates were restored to wild-type characteristics when carbonyl cyanide m-chlorophenylhydrazone was used.


* Corresponding author. Mailing address: University of Birmingham, Div. of Immunity and Infection, Birmingham B15 2TT, United Kingdom. Phone: 44-121-414-6969. Fax: 44-121-414-3599. E-mail: l.j.v.piddock{at}bham.ac.uk.


Antimicrobial Agents and Chemotherapy, April 2004, p. 1344-1346, Vol. 48, No. 4
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.4.1344-1346.2004
Copyright © 2004, 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 © 2004 by the American Society for Microbiology. All rights reserved.