In vitro resistance to thrombin-induced platelet microbicidal protein is associated with enhanced progression and hematogenous dissemination in experimental Staphylococcus aureus infective endocarditis.
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.
Dhawan
V K
VK
Charles Drew University-Martin Luther King Medical Center, Los Angeles, California 90059, USA.
Bayer
A S
AS
Yeaman
M R
MR
D000818:Animals; D001798:Blood Proteins / Q000502:physiology*; D004697:Endocarditis, Bacterial / Q000276:immunology*; D011817:Rabbits; D013203:Staphylococcal Infections / Q000276:immunology*; D013211:Staphylococcus aureus / Q000472:pathogenicity; D013917:Thrombin / Q000494:pharmacology*
D001798:Blood Proteins; C077150:platelet microbicidal protein, Oryctolagus cuniculus; D013917:Thrombin