EFFECT OF THROMBOCYTOPENIA ON THE EARLY COURSE OF STREPTOCOCCAL ENDOCARDITIS

Although platelets are a major factor in the pathogenesis of endocardi tis, 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 endocardi tis was produced in rabbits by using Streptococcus sanguis M99. Thromb ocytopenia was induced by intravenous administration of antiplatelet s erum. 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 t otal 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 ex tensively and was rapidly killed by platelet microbicidal protein. The se results indicate that platelets can limit disease progression in en docarditis. The host defense properties of platelets may in part be me diated by platelet microbicidal protein.