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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.


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