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Simian Hemorrhagic Fever
II. Studies in Pathology
Anton M. Allen
Anton M. Allen
National Institutes of Health, Division of Research Services, Laboratory Aids Branch, Comparative Pathology Section, Animal Conditioning Section, Primate Quarantine Unit, and Division of Biologics Standards, Laboratory of Virology and Rickettsiology, Bethesda, Maryland 20014
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Amos E. Palmer
Amos E. Palmer
National Institutes of Health, Division of Research Services, Laboratory Aids Branch, Comparative Pathology Section, Animal Conditioning Section, Primate Quarantine Unit, and Division of Biologics Standards, Laboratory of Virology and Rickettsiology, Bethesda, Maryland 20014
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Nicola M. Tauraso
Nicola M. Tauraso
National Institutes of Health, Division of Research Services, Laboratory Aids Branch, Comparative Pathology Section, Animal Conditioning Section, Primate Quarantine Unit, and Division of Biologics Standards, Laboratory of Virology and Rickettsiology, Bethesda, Maryland 20014
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Alexis Shelokov
Alexis Shelokov
National Institutes of Health, Division of Research Services, Laboratory Aids Branch, Comparative Pathology Section, Animal Conditioning Section, Primate Quarantine Unit, and Division of Biologics Standards, Laboratory of Virology and Rickettsiology, Bethesda, Maryland 20014
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Summary
The lesions of simian hemorrhagic fever included capillary-venous hemorrhages in the intestine, lung, nasal mucosa, dermis, spleen, perirenal and lumbar subperitoneum, adrenal gland, liver, and periocular connective tissue. Evidence of vasodilation, stasis, and venous thrombosis often was found in association with the hemorrhages. Shock was therefore suspected as an underlying causative factor. Vascular fragility, blood-clotting defects, and trauma appeared to be associated factors, particularly in connection with certain of the skin petechiae, the hemorrhages under the renal capsule, and those occurring around lung-mite lesions. The direct effects of virus invasion of tissues were not determined. Degenerative changes in the liver, kidney, brain, lymphatic tissue, and bone marrow were believed to be due to blood stasis and hypoxia. The peculiar splenomegaly in simian hemorrhagic fever evidently was caused by follicular hemorrhage and engorgement of the cords with plasma and fibrin.
Author Notes
Present address: Division of Biologics Standards, Laboratory of Pathology.
| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 360 | 129 | 3 |
| Full Text Views | 19 | 6 | 1 |
| PDF Downloads | 19 | 7 | 1 |