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.
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.
Current methods to establish the duration of toxoplasma infection in pregnant women and for the diagnosis of toxoplasmosis in the neonate or HIV infected patient have significant limitations. We assessed the precision of a commercial ELISA for the detection of toxoplasma specific IgG and adapted the assay to measure avidity using an elution agent washing step. The sensitivity and specificity of the ELISA were 100 and 75% respectively and optimal measurement of avidity was achieved using 6 M urea as the elution agent. Toxoplasma lymphadenopathy of less than 3 months duration was associated with low avidity specific IgG but some discordant findings were recorded. Serial measurement of IgG avidity assisted the distinction between actively produced antibody in infants with congenital toxoplasmosis and passively acquired antibody of maternal origin in uninfected babies. There was no significant difference between avidity levels in HIV infected patients with or without cerebral toxoplasmosis.
During the 1976 Ebola virus outbreak in Sudan, the investigations team gained the impression that fewer haemorrhagic manifestations and few fatalities occurred during the later stages of the epidemic after the virus had undergone several generations in man. This impression was also noted in guinea pigs experimentally infected with Sudanese and Zairean strains of Ebola virus. The virulence of the Sudanese isolates was less intense than isolates emanating from Zaire. Similar findings were seen in monkeys; a Zairean isolated produced fatal infections, whereas monkeys inoculated with a Sudan strain generally recovered. Two monkeys, which had recovered from Sudanese strain infections and had developed high levels of antibody detectable by immunofluorescence, were challenged with the Zairean strain. Both developed viraemias and died. The mechanisms of this "failed protection" are discussed.
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