The Journal of Pathology · 1985 · 134 citations · 10 references
MedicineInfectious DiseasesPathologyRenal PathologyRenal PathophysiologyVirologyInfectious Disease PathophysiologyInfectious PathologyNecrosisRenal IschemiaViral InfectionsViral PathologyGlomerular AnatomyGlomerular HistopathologyHemorrhagic Viral DiseaseInfection-induced Tissue DamageNecrosis In Viral InfectionSeminiferous Epithelium InjuryUltrastructural AlterationsUltrastructural Pathology
Monkeys infected with Ebola were examined by light and electron microscopy during the acute stage of the disease. Ebola infection caused focal coagulative necrosis and widespread mild vascular damage in liver, spleen, kidney, lung, and testis, intense brain congestion without inflammation, extensive microvascular injury with endothelial necrosis, tight‑junction separation, and basement‑membrane detachment leading to oedema and haemorrhage, and renal damage from direct viral invasion and ischemic thrombosis, while virus also replicated in lymphocytes, monocytes, and testis interstitial cells, with spermatogenic degeneration likely secondary to ischemia.
The organs of monkeys infected with Ebola haemorrhagic fever were examined by light and electron microscopy during the acute stage of the disease. The virus caused focal coagulative necrosis in the liver, spleen, kidney, lung and testis and widespread mild vascular damage. In the brain there was intense congestion, with erythrocyte 'sludging', but no inflammatory reaction. There was significant injury to the microvasculature in all organs. Virus replicated in endothelial cytoplasm causing focal necrosis, separation of tight junctions and detachment from basement membranes. These changes were associated with oedema and haemorrhage, but though contributing to the hypovolaemic shock were not sufficiently extensive to account for the severity of vascular collapse. Renal involvement was also clinically important. Some renal cellular injury was caused by direct virus invasion of glomerular endothelium and tubular epithelium, but much tubular damage was probably due to ischaemia resulting from thrombosis in the peritubular capillaries. The virus also replicated in lymphocytes and monocytes and in interstitial cells of the testis. Since particles were not found in seminiferous epithelium, the degeneration of spermatogonia and spermatocytes was probably secondary to ischaemia.
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VIRAL HÆMORRHAGIC FEVER IN SOUTHERN SUDAN AND NORTHERN ZAIRE
E. T. W. Bowen, G. Lloyd, William J. Harris et al. · The Lancet · 1977 · 266 citations
The pathology of experimental Ebola virus infection in monkeys
A. Baskerville, E. T. W. Bowen, G.S. Platt et al. · The Journal of Pathology · 1978 · 115 citations