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Infect Immun, July 1998, p. 3476-3479, Vol. 66, No. 7
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

In Vitro Resistance to Thrombin-Induced Platelet Microbicidal Protein Is Associated with Enhanced Progression and Hematogenous Dissemination in Experimental Staphylococcus aureus Infective Endocarditis

Vinod K. Dhawan,1,2 Arnold S. Bayer,2,3,* and Michael R. Yeaman2,3

Charles Drew University-Martin Luther King Medical Center, Los Angeles, California 900591; UCLA School of Medicine, Los Angeles, California 900242; and St. John's Cardiovascular Research Center, Harbor-UCLA Medical Center, Torrance, California 905023

Received 29 January 1998/Returned for modification 6 March 1998/Accepted 10 April 1998

We examined the influence of thrombin-induced platelet microbicidal protein 1 (tPMP-1) on the progression and hematogenous dissemination of experimental endocarditis caused by isogenic Staphylococcus aureus strains differing in tPMP susceptibility (tPMPs) or resistance (tPMPr) in vitro. Following simultaneous challenge of animals with both strains, significantly higher tPMPr bacterial densities were present in vegetations (P < 0.0001), kidneys (P < 0.0001), and spleens (P < 0.0001) compared with those for the tPMPs strain. These data indicate that tPMP-1 limits the intravegetation proliferation and hematogenous dissemination of a tPMPs strain in experimental endocarditis, while the tPMPr phenotype confers a selective advantage associated with the enhanced progression of this infection.

* Corresponding author. Mailing address: Harbor-UCLA Medical Center, Division of Infectious Diseases, St. John's Cardiovascular Research Center, Room 225, 1000 West Carson St., Torrance, CA 90509. Phone: (310) 222-6422. Fax: (310) 782-2016. E-mail: bayer{at}humc.edu.

Infect Immun, July 1998, p. 3476-3479, Vol. 66, No. 7
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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