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
Right arrow Citation Map
Services
Right arrow E-mail this article to a friend
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
Google Scholar
Right arrow Articles by Moubareck, C.
Right arrow Articles by Périchon, B.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Moubareck, C.
Right arrow Articles by Périchon, B.

 Previous Article  |  Next Article 

Antimicrobial Agents and Chemotherapy, September 2009, p. 3657-3663, Vol. 53, No. 9
0066-4804/09/$08.00+0     doi:10.1128/AAC.00338-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

VanA-Type Staphylococcus aureus Strain VRSA-7 Is Partially Dependent on Vancomycin for Growth {triangledown}

Carole Moubareck, Djalal Meziane-Cherif, Patrice Courvalin,* and Bruno Périchon

Institut Pasteur, Unité des Agents Antibactériens, Centre National de Référence de la Résistance aux Antibiotiques, Paris Cedex 15 75724, France

Received 12 March 2009/ Returned for modification 4 April 2009/ Accepted 30 May 2009

VanA-type Staphylococcus aureus strain VRSA-7 was partially dependent on glycopeptides for growth. The vanA gene cluster, together with the erm(A) and the ant(9)-Ia resistance genes, was carried by the ca. 35- to 40-kb conjugative plasmid pIP848 present at five copies per cell. The chromosomal ddl gene had a mutation that led to a N308K substitution in the D-Ala:D-Ala ligase that resulted in a 1,000-fold decrease in activity relative to that of strain VRSA-6. Strain VRSA-7 grown in the absence or in the presence of vancomycin mainly synthesized precursors ending in D-Ala-D-Lac, indicating that the strain relied on the vancomycin resistance pathway for peptidoglycan synthesis. Greatly enhanced growth in the presence of glycopeptides and the absence of mutations in the genes for VanR and VanS indicated the inducible expression of resistance. Thus, a combination of loose regulation of the vanA operon by the two-component system and a gene dosage effect accounts for the partial glycopeptide dependence of VRSA-7. Since peptidoglycan precursors ending in D-Ala-D-Lac are not processed by PBP 2', the strain was fully susceptible to oxacillin, despite the production of a wild-type PBP 2'.

* Corresponding author. Mailing address: Institut Pasteur, Unité des Agents Antibactériens, 25, Rue du Docteur Roux, Paris Cedex 15 75724, France. Phone: (33) (1) 45 68 83 20. Fax: (33) (1) 45 68 83 19. E-mail: patrice.courvalin{at}pasteur.fr

{triangledown} Published ahead of print on 15 June 2009.

Antimicrobial Agents and Chemotherapy, September 2009, p. 3657-3663, Vol. 53, No. 9
0066-4804/09/$08.00+0     doi:10.1128/AAC.00338-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2010 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»