Pathophysiology of shock and hemorrhage in a fulminating viral infection (ebola)

S. P. Fisher-Hoch*, G. S. Platt, A. Baskerville, R. T. Raymond, Graham Lloyd, G. H. Neild, T. Southee, D. I.H. Simpson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

149 Citations (Scopus)

Abstract

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 <.02 and P <.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.

Original languageEnglish
Pages (from-to)887-894
Number of pages8
JournalJournal of Infectious Diseases
Volume152
Issue number5
DOIs
Publication statusPublished - 1 Nov 1985

Bibliographical note

Funding Information:
Dr. Fisher-Hoch was supported by a WellcomeTrust Fellowship.

Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.

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