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Collie eye anomaly is a congenital, recessively inherited, ocular defect with variable expression in rough- and smooth-coated Collies. It also occurs in Shetland Sheepdogs, Border Collies, Australian Shepherds, and Lancashire Heelers. The basic lesion is an area of choroidal or chorioretinal hypoplasia that on ophthalmoscopy appears as a focal, variable-sized, pale area lateral to the optic disk. More severely affected dogs (10-20%) can have additional colobomatous
lesions of the optic papilla or peripapillary region, and occasional retinal detachments. Intraocular hemorrhage may occur. Vision is not appreciably affected unless retinal detachment is present. |
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Retinal dysplasia is a congenital, focal, geographic, or generalized maldevelopment of the retina that may arise from trauma, genetic defect, or intrauterine damage, such as viral infections. Most forms of retinal dysplasia in dogs are inherited. Maternal viral infections, especially during early fetal development, can result in multiple ocular anomalies with retinal dysplasia in kittens (panleukopenia), lambs (bluetongue disease), puppies (herpesvirus), and calves
(bovine viral diarrhea). Breeds of dogs with focal, geographic, and generalized retinal dysplasia thought to be inherited as an autosomal recessive trait include American Cocker Spaniels, Beagles, Labrador Retrievers, Rottweilers, and Yorkshire Terriers. Focal areas of retinal maldevelopment may be asymptomatic or interfere with central vision. Generalized retinal dysplasia with retinal detachment, visual impairment, or blindness is inherited in English Springer Spaniels, Bedlington
Terriers, Sealyham Terriers, Labrador Retrievers, Doberman Pinschers, and Australian Shepherds. Other ocular anomalies, including microphthalmia and congenital cataracts, often accompany the generalized forms. In Labrador Retrievers and Samoyeds, retinal dysplasia may be associated with skeletal dysplasia (shortening) of the forelegs. |
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Progressive retinal atrophy (PRA) is a group of degenerative retinopathies consisting of inherited photoreceptor dysplasia and degenerations that have a similar clinical appearance. The photoreceptor dysplasias inherited as autosomal recessive traits in which clinical signs develop in the first year occur in Irish Setters, Collies, Norwegian Elkhounds, Miniature Schnauzers, and Belgian Sheepdogs. The photoreceptor degenerations inherited as autosomal recessive traits in
which clinical signs develop at 3-5 yr occur in Miniature and Toy Poodles, English and American Cocker Spaniels, Labrador Retrievers, Tibetan Terriers, Miniature Longhaired Dachshunds, Akitas, and Samoyeds. In Siberian Huskies, PRA is inherited as an X-linked trait, while in Bull Mastiffs, PRA is inherited as an autosomal dominant. Many other breeds of dogs are also suspected of having inherited PRA. In Abyssinian cats, PRA occurs as both photoreceptor dysplasia and degeneration.
Night blindness is noted early and progresses to total blindness over months to years. Ophthalmoscopic lesions are a bilateral symmetric increase in reflectivity of the tapetal fundus, decreased pigmentation of the nontapetal fundus, attenuation and a decrease in the number of retinal vessels, and eventual atrophy of the optic papilla. Electroretinography is often used to investigate and diagnose the condition. Cortical cataracts are common late in the course of PRA in many breeds
and may mask the underlying retinopathy. No effective therapy is available. Blood and buccal mucosa-based DNA marker and specific gene tests have been developed to detect carrier and affected dogs before clinical signs develop in many breeds. |
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Retinal pigment epithelial dystrophy (central progressive retinal atrophy) occurs in Labrador Retrievers, smooth and rough Collies, Border Collies, Shetland Sheepdogs, and Briards. The condition is inherited in Labrador Retrievers as a dominant trait with variable penetrance. Early ophthalmoscopic findings (often before clinical signs are apparent) are small foci of irregular pigmentation in the tapetal fundus, which eventually coalesce and fade as reflectivity of the
tapetal fundus increases. The pigmented nontapetal fundus becomes mottled, the retinal vasculature gradually decreases, and the optic disk atrophies. Progressive visual impairment occurs gradually over several years. Cataract formation occurs late in the disease. There is no treatment. Recent studies suggest vitamin E disorders may also be important in the pathogenesis of this disease complex. |
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