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Infection and Immunity, September 2000, p. 5443-5446, Vol. 68, No. 9
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.
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
*
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.
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