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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.

Six rhesus and two vervet monkeys were infected intraperitoneally with Ebola virus. They developed an acute haemorrhagic fever with skin rash 4 days later and died 6--12 days after infection. Histopathological lesions of acute necrosis were present in the liver, spleen, lymph nodes, lungs and testes. The presence of fibrin thrombi in several organs was suggestive of the occurrence of disseminated intravascular coagulation during the infection.

Experimental infection of rhesus and vervet monkeys with Ebola virus produced a uniformly fatal illness. The course of the disease resembled that found in man with weight loss, anorexia, fever, haemorrhages and skin rash being frequently seen. Viraemia was obvious within two days of infection and persisted until death which occurred between days five and eight. Virus was found in high concentrations in several organs but particularly in the liver, spleen, and lungs.

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