H M Tabery1. 1. Lund University, Department of Ophthalmology, Malmö University Hospital, Sweden.
Abstract
PURPOSE: To examine early corneal epithelial changes in recurrent herpes simplex virus (HSV) type 1 keratitis. MATERIAL AND METHODS: Three patients presenting early (< or =18, < or =24 and < or =29 hours) after the onset of symptoms were examined by means of non-contact in vivo photomicrography. RESULTS: Case 1 (< or =18 hours) showed about 60 rounded or irregularly shaped and partly confluent intraepithelial lesions. In case 2 (< or =24 hours) similar lesions and a dendritic figure with a broken pattern were present. Case 3 (< or =29 hours) showed four separate lesions and a large dendrite. Some lesions appeared as dark protrusions in the fluorescein stained tear film, others stained green; of these, some additionally showed fluorescein diffusion into the surroundings. The smallest discernible entities were abnormal cells of about 10 microm in diameter, present both within the lesions and scattered elsewhere, and clearly swollen cells of about 15 microm of diameter. CONCLUSIONS: The distribution of the precursors shows the multifocal origin of HSV dendritic figures. The dark protruding lesions with abnormal cells covered by intact overlying cell layer(s) seem to be the earliest HSV epithelial changes so far captured in the living human cornea. The protrusions are probably the result of cell swelling representing the incipient stage of HSV cytopathic effect, and the subsurface location of the abnormal cells suggests that the initial virus target are the deeper epithelial layers. The morphological features of the remaining lesions are consistent with successive stages of cell degeneration, i.e. cell swelling leading to surface disruptions, burst of the cells, and cell desquamation resulting in surface ulcerations. The contemporaneous presence of all these stages is typical of recurrent HSV type 1 infections.
PURPOSE: To examine early corneal epithelial changes in recurrent herpes simplex virus (HSV) type 1 keratitis. MATERIAL AND METHODS: Three patients presenting early (< or =18, < or =24 and < or =29 hours) after the onset of symptoms were examined by means of non-contact in vivo photomicrography. RESULTS: Case 1 (< or =18 hours) showed about 60 rounded or irregularly shaped and partly confluent intraepithelial lesions. In case 2 (< or =24 hours) similar lesions and a dendritic figure with a broken pattern were present. Case 3 (< or =29 hours) showed four separate lesions and a large dendrite. Some lesions appeared as dark protrusions in the fluorescein stained tear film, others stained green; of these, some additionally showed fluorescein diffusion into the surroundings. The smallest discernible entities were abnormal cells of about 10 microm in diameter, present both within the lesions and scattered elsewhere, and clearly swollen cells of about 15 microm of diameter. CONCLUSIONS: The distribution of the precursors shows the multifocal origin of HSV dendritic figures. The dark protruding lesions with abnormal cells covered by intact overlying cell layer(s) seem to be the earliest HSV epithelial changes so far captured in the living human cornea. The protrusions are probably the result of cell swelling representing the incipient stage of HSV cytopathic effect, and the subsurface location of the abnormal cells suggests that the initial virus target are the deeper epithelial layers. The morphological features of the remaining lesions are consistent with successive stages of cell degeneration, i.e. cell swelling leading to surface disruptions, burst of the cells, and cell desquamation resulting in surface ulcerations. The contemporaneous presence of all these stages is typical of recurrent HSV type 1 infections.