Nasisse M P, Guy J S, Davidson M G, Sussman W A, Fairley N M
College of Veterinary Medicine, North Carolina State University, Raleigh 27606.
Invest Ophthalmol Vis Sci. 1989 Aug;30(8):1758-68.
Experimentally induced ocular feline herpesvirus 1 (FHV-1) infection was studied in 30 specific pathogen-free cats. In ten cats, the ability of five field isolates of FHV-1 to replicate in the epithelium and substantia propria of cornea and conjunctiva was demonstrated by histochemical techniques. Feline herpesvirus 1 was found to preferentially infect and induce necrosis of conjunctival epithelium. Although significant histologic lesions were not induced, all FHV-1 strains were observed to replicate in corneal epithelium; minimal viral antigen was detected in the corneal stroma. The course and clinical features of ocular FHV-1 infection were then studied over a period of 60 days in two groups of ten cats: in one group, infection was preceded by administration of subconjunctival betamethasone. In each of these groups, a distinct clinical syndrome developed. In cats not receiving corticosteroids, a course of epithelial keratitis, characterized by the formation of punctate and dendritic epithelial lesions, persisted for up to 24 days postinfection. In the corticosteroid treated group, a chronic (greater than 60 days) stromal keratitis developed, characterized by geographic epithelial ulceration, interstitial edema and deep vascularization. Other complications observed in corticosteroid-treated animals included decreased tear production, calcific-band keratopathy and a unique stromal disorder of cats termed corneal sequestration. The results of this study indicate that while epithelial keratitis may occur during primary infection, stromal keratitis does not, unless immune responsiveness to FHV-1 is concomitantly suppressed. This feature is similar to naturally occurring HSV-1 keratitis of humans, but contrasts to other animal model systems in which stromal keratitis predictably occurs during primary infection. Study of this animal model, therefore, may allow unique insights into the events preceding the establishment of stromal keratitis.
在30只无特定病原体的猫身上研究了实验性诱导的猫疱疹病毒1型(FHV-1)眼部感染。在10只猫中,通过组织化学技术证明了5株FHV-1野外分离株在角膜和结膜上皮及固有层中的复制能力。发现猫疱疹病毒1型优先感染并诱导结膜上皮坏死。虽然未诱导出明显的组织学病变,但观察到所有FHV-1毒株都在角膜上皮中复制;在角膜基质中检测到极少的病毒抗原。然后在两组各10只猫中对眼部FHV-1感染的病程和临床特征进行了为期60天的研究:一组在感染前结膜下注射倍他米松。在每组中,都出现了一种独特的临床综合征。在未接受皮质类固醇治疗的猫中,上皮性角膜炎病程以点状和树枝状上皮病变形成为特征,在感染后持续长达24天。在皮质类固醇治疗组中,出现了慢性(超过60天)基质性角膜炎,其特征为地图状上皮溃疡、间质水肿和深层血管化。在接受皮质类固醇治疗的动物中观察到的其他并发症包括泪液分泌减少、钙化性带状角膜病变以及一种称为角膜分离的猫独特的基质疾病。这项研究的结果表明,虽然原发性感染期间可能发生上皮性角膜炎,但除非同时抑制对FHV-1的免疫反应,否则不会发生基质性角膜炎。这一特征与人类自然发生的HSV-1角膜炎相似,但与其他动物模型系统不同,在其他动物模型系统中,原发性感染期间可预测地会发生基质性角膜炎。因此,对这个动物模型的研究可能会让人对基质性角膜炎形成之前的事件有独特的见解。