Effect of thrombocytopenia on the early course of streptococcal endocarditis
Publisher DOI
PubMed ID
8376837
Abstract
Although platelets are a major factor in the pathogenesis of endocarditis, it is unclear if these cells promote or limit disease progression. To address this issue, the effects of thrombocytopenia on the early course of endovascular infection were examined. Aortic valve endocarditis was produced in rabbits by using Streptococcus sanguis M99. Thrombocytopenia was induced by intravenous administration of antiplatelet serum. Compared with controls (infected rabbits given nonimmune serum), thrombocytopenic rabbits had higher densities of streptococci within vegetations (mean log10 cfu/g, 9.78 vs. 8.11, P < .002) and a higher total number of bacteria per valve (mean log10 total cfu/valve, 8.96 vs. 7.43, P < .004). When tested for its interactions with platelets in vitro, strain M99 bound, activated, and aggregated rabbit platelets extensively and was rapidly killed by platelet microbicidal protein. These results indicate that platelets can limit disease progression in endocarditis. The host defense properties of platelets may in part be mediated by platelet microbicidal protein.
Date Issued
1993
Publication Type
Article
Language(s)
en
Author(s)
Sullam, PM | |
Frank, U | |
Yeaman, MR | |
Bayer, AS | |
Chambers, HF |
Additional Credits
Journal
Journal of infectious diseases
Publisher
Oxford University Press
ISSN
0022-1899
ISBN
8376837
Access(Rights)
metadata.only