Simian Hemorrhagic Fever

II. Studies in Pathology

Anton M. AllenNational 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. PalmerNational 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. TaurasoNational 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 ShelokovNational 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.

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