Baskerville A, Fisher-Hoch S P, Neild G H, Dowsett A B
J Pathol. 1985 Nov;147(3):199-209. doi: 10.1002/path.1711470308.
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.
在感染埃博拉出血热的猴子处于疾病急性期时，对其器官进行了光镜和电镜检查。该病毒在肝脏、脾脏、肾脏、肺和睾丸中引起局灶性凝固性坏死，并造成广泛的轻度血管损伤。在大脑中，有严重充血，伴有红细胞“淤滞”，但无炎症反应。所有器官的微血管均有明显损伤。病毒在内皮细胞质中复制，导致局灶性坏死、紧密连接分离以及与基底膜脱离。这些变化与水肿和出血有关，尽管它们导致了低血容量性休克，但程度尚不足以解释血管塌陷的严重程度。肾脏受累在临床上也很重要。一些肾细胞损伤是由病毒直接侵入肾小球内皮和肾小管上皮引起的，但许多肾小管损伤可能是由于肾小管周围毛细血管血栓形成导致的缺血所致。该病毒还在淋巴细胞、单核细胞以及睾丸间质细胞中复制。由于在生精上皮中未发现病毒颗粒，精原细胞和精母细胞的退化可能继发于缺血。
