Zheng X, Wu J, Wang H
Department of Ophthalmology, Ist Affiliated Hospital, China Medical University, Shenyang.
Zhonghua Yan Ke Za Zhi. 1997 Jan;33(1):49-52.
In order to investigate the histological and ultrastructural changes at different post infection days in herpes simplex keratitis (HSK).
The corneas of New Zealand white rabbit eyes experimentally infected with primary HSK were studied by light microscopy and electron microscopy. The histological and ultrastructural changes in the rabbit corneas at 3, 7, 14, 21, 60 post infection days were investigated by light microscopy with HE, Mallory dyes and electron microscopy.
Infiltration of corneas with inflammatory cells was found in rabbit eyes infected with HSK, polymorphonuclear leukocytes being predominant. Contact of inflammatory cells with fibroblast cells and corneal edema were seen in the stroma on acute post infection days 3 and 7. In severe cases inflammatory cells incarcerated in the endothelium. Only did two cases of the specimens present with herpes simplex virus type I granules in the acute stage under electron microscopy.
The direct HSK-1 destruction together with immunopathogenetic injury caused by the body immune system may serve as the pathologic base of HSK. Decompensation of corneal endothelial function due to infiltration with inflammatory cells may be responsible for corneal edema.
探讨单纯疱疹病毒性角膜炎（HSK）感染后不同时间的组织学及超微结构变化。
用原发性HSK实验感染新西兰白兔眼，应用光镜和电镜进行研究。用苏木精-伊红（HE）染色、马洛里染色法及电镜观察感染后3、7、14、21、60天兔角膜的组织学及超微结构变化。
HSK感染兔眼中可见角膜有炎性细胞浸润，以多形核白细胞为主。感染后急性阶段的第3天和第7天，在角膜基质中可见炎性细胞与成纤维细胞接触及角膜水肿。严重病例中炎性细胞嵌顿于内皮。电镜下仅2例标本在急性期出现Ⅰ型单纯疱疹病毒颗粒。
HSK-1的直接破坏以及机体免疫系统引起的免疫病理损伤可能是HSK的病理基础。炎性细胞浸润导致角膜内皮功能失代偿可能是角膜水肿的原因。
