IAI FigSearch
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 Entenza, J. M.
Right arrow Articles by Moreillon, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Entenza, J. M.
Right arrow Articles by Moreillon, P.

 Previous Article  |  Next Article 

Infection and Immunity, September 2000, p. 5443-5446, Vol. 68, No. 9
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Contribution of Clumping Factor B to Pathogenesis of Experimental Endocarditis due to Staphylococcus aureus

J. M. Entenza,1 T. J. Foster,2 D. Ni Eidhin,2 P. Vaudaux,3 P. Francioli,1 and P. Moreillon1,*

Division of Infectious Diseases, Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne,1 and Division of Infectious Diseases, Hôpital Universitaire de Genève, 1211 Geneva,3 Switzerland, and Department of Microbiology, Moyne Institut of Preventive Medicine, University of Dublin, Trinity College, Dublin 2, Ireland2

Received 2 March 2000/Returned for modification 29 March 2000/Accepted 1 June 2000

Staphylococcus aureus Newman with an insertion mutation in clfB, the gene encoding clumping factor B, only marginally decreased infection rate (P > 0.05) in rats with experimental endocarditis. In contrast, clfB complementation on a multicopy plasmid significantly increased infectivity (P < 0.05) over the deleted mutants. Although clfB could affect endovascular infection, its importance in experimental endocarditis was limited.


* Corresponding author. Mailing address: Division of Infectious Diseases, Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland. Phone: 41-21-314.10.26. Fax: 41-21-314.10.36. E-mail: pmoreill{at}chuv.hospvd.ch.


Infection and Immunity, September 2000, p. 5443-5446, Vol. 68, No. 9
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2000 by the American Society for Microbiology. All rights reserved.