August 1989
Volume 30, Issue 8
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Articles  |   August 1989
Experimental ocular herpesvirus infection in the cat. Sites of virus replication, clinical features and effects of corticosteroid administration.
Author Affiliations
  • M P Nasisse
    College of Veterinary Medicine, North Carolina State University, Raleigh 27606.
  • J S Guy
    College of Veterinary Medicine, North Carolina State University, Raleigh 27606.
  • M G Davidson
    College of Veterinary Medicine, North Carolina State University, Raleigh 27606.
  • W A Sussman
    College of Veterinary Medicine, North Carolina State University, Raleigh 27606.
  • N M Fairley
    College of Veterinary Medicine, North Carolina State University, Raleigh 27606.
Investigative Ophthalmology & Visual Science August 1989, Vol.30, 1758-1768. doi:
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      M P Nasisse, J S Guy, M G Davidson, W A Sussman, N M Fairley; Experimental ocular herpesvirus infection in the cat. Sites of virus replication, clinical features and effects of corticosteroid administration.. Invest. Ophthalmol. Vis. Sci. 1989;30(8):1758-1768.

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Abstract

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.

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