Pathophysiology of shock and hemorrhage in a fulminating viral infection (Ebola).
Eleven rhesus monkeys were monitored intensively during experimental infection with Ebola virus. Prominent neutrophilia with left shift and lymphopenia were the earliest abnormalities and were statistically significant by day 4 (P less than .02 and P less than .01, respectively). By day 4 falls in platelet counts were not statistically significant, whereas in vitro platelet aggregation was markedly depressed, progressing rapidly to complete failure by the time of maximum illness. Intraplatelet protein studies suggested this event was the result of in vivo activation and degranulation. Coagulation cascade defects were mainly in the intrinsic system and were surprisingly mild, with no evidence of selective consumption or production deficit of factor VII or VIII. When the possibility of indirectly mediated damage to endothelium possibly by a nonspecific immune response was examined, weight loss was less severe in drug-treated monkeys, and all had detectable plasma prostacyclin metabolites, but there was no improvement in survival.
D000818:Animals; D001777:Blood Coagulation; D029043:Ebolavirus / Q000254:growth & development; D005260:Female; D006482:Hemorrhagic Fevers, Viral / Q000097:blood / Q000382:microbiology / Q000503:physiopathology*; D006996:Hypocalcemia; D007008:Hypokalemia; D007010:Hyponatremia; D007958:Leukocyte Count; D008253:Macaca mulatta; D008297:Male; D009504:Neutrophils; D010974:Platelet Aggregation; D010976:Platelet Count; D012769:Shock / Q000209:etiology*; D014810:Vitamin E / Q000627:therapeutic use
D014810:Vitamin E