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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Corneal diseases in the Cat and the Dog are of great variety and present similitudes with human corneal disorders, as demonstrated by the present report which discusses dystrophies, degenerations and inflammations of the cornea successively. Deep endothelial dystrophies are rare, poorly understood, and related to certain breeds; lipid dystrophies are frequent and either primary, occurring in some breeds only, or secondary to hyperlipemia; calcareous dystrophies are breed-related affections. Primary corneal degeneration has been described in the cat only and is a very rare affection. Keratitis is by far the commonest corneal lesion reported, and may be of herpes virus origin in the Cat and due to adenovirus in the Dog. Dry keratitis as in humans has also been observed. Two types of keratitis of allergic origin are described which are closely related to two breeds of dog: Alsatians and the long-haired dachshund. Recurrent corneal erosions, poorly recognized in veterinary medicine, are now described; their etiology and histological appearances are comparable with those reported in humans. These findings emphasize the interest of using animal models for human pathology investigations.
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PMID:[Corneal pathology in the cat and dog]. 661 Jun 98

A subset of victims of ocular sulfur mustard (SM) exposure develops an irreversible, idiotypic keratitis with associated secondary pathologies, collectively referred to as mustard gas keratopathy (MGK). MGK involves a progressive corneal degeneration resulting in chronic ocular discomfort and impaired vision for which clinical interventions have typically had poor outcomes. Using a rabbit corneal vapor exposure model, we previously demonstrated a clinical progression with acute and chronic sequelae similar to that observed in human casualties. However, a better understanding of the temporal changes that occur during the biphasic SM injury is crucial to mechanistic understanding and therapeutic development. Here we evaluate the histopathologic, biochemical and ultrastructural expressions of pathogenesis of the chronic SM injury over eight weeks. We confirm that MGK onset exhibits a biphasic trajectory involving corneal surface regeneration over the first two weeks, followed by the rapid development and progressive degeneration of corneal structure. Preclinical markers of corneal dysfunction were identified, including destabilization of the basal corneal epithelium, basement membrane zone abnormalities and stromal deformation. Clinical sequelae of MGK appeared abruptly three weeks after exposure, and included profound anterior edema, recurring corneal erosions, basement membrane disorganization, basal cell necrosis and stromal degeneration. Unlike resolved corneas, MGK corneas exhibited frustrated corneal wound repair, with significantly elevated histopathology scores. Increased lacrimation, disruption of the basement membrane and accumulation of pro-inflammatory mediators in the aqueous humor provide several mechanisms for corneal degeneration. These data suggest that the chronic injury is fundamentally distinct from the acute lesion, involving injury mechanisms that operate on different time scales and in different corneal tissues. Corneal edema appears to be the principal pathology of MGK, in part resulting from persistent necrosis of the basal corneal epithelium and deterioration of the basement membrane. The findings also provide a potential explanation as to why administration of anti-inflammatories transiently delays, but does not prevent, the development of MGK sequelae.
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PMID:Architectural and biochemical expressions of mustard gas keratopathy: preclinical indicators and pathogenic mechanisms. 2290 56