The ocular fundus consists of the upper tapetal fundus, ventral and surrounding nontapetal fundus, retinal vasculature, and optic disk (optic nerve head or optic papilla). Histologically, the posterior segment consists, from superficial to deep, of the following structures: 1) posterior sclera; 2) choroid, which contains pigmented cells, blood vessels to support the high metabolic needs of the outer retina, and the tapetum lucidum to enhance vision in dim light (tapetum cellulosum in carnivores and tapetum fibrosum in herbivores); 3) retina, which consists of the 9 layers of neurosensory retina and the outer retinal pigment epithelium; and 4) the optic disk, where the retinal ganglion axons leave the eye through a weak and fenestrated scleral lamina cribrosa to synapse in the lateral geniculate body (vision) or middle brain (pupillary light reflex [Edinger-Westphal nucleus] or dazzle reflex [midbrain and rostral colliculi]).
Diseases of the ocular fundus may be primary or may be manifestations of systemic diseases. Inherited abnormalities may be congenital or appear later, and are important in the pathogenesis of retinopathies in dogs and cats. Trauma, metabolic disturbances, systemic infections, neoplasms, blood dyscrasias, hypertension, and nutritional deficiencies are possible underlying causes for retinopathies in all species.
Collie eye anomaly is a congenital, recessively inherited, ocular defect with variable expression in rough- and smooth-coated Collies. It also is seen in Shetland Sheepdogs, Border Collies, Australian Shepherds, Lancashire Heelers, and Nova Scotia Duck Tolling Retrievers. 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 (2–5%). Intraocular hemorrhage may occur. Vision is not appreciably affected unless retinal detachment develops.
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.
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, Tibetan Spaniels, Papillons, English Springer Spaniels, Miniature Longhaired Dachshunds, Akitas, and Samoyeds. In Siberian Huskies, PRA is inherited as an X-linked trait, while in Old English Mastiffs and 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. The list of breeds affected with inherited retinal degenerations and causative genes continues to increase; for current information consult the recent literature.
Retinal pigment epithelial dystrophy (central progressive retinal atrophy) is seen 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. A similar condition in horses, equine motor neuron disease (p 1141), has focal yellow-brown areas scattered throughout the tapetal fundus and has also been associated with vitamin E deficiency.
Chorioretinitis frequently is a manifestation of systemic infectious disease; it is important as both a convenient diagnostic clue and a prognosticator of visual function. Unless the lesions are generalized or involve the optic nerve, they often are “silent.” Scars may be differentiated from active lesions by the haze and ill-defined borders of the latter. Routine ophthalmoscopic examinations of all animals with systemic diseases often permit rapid diagnosis of many specific diseases. Chorioretinitis may be present with canine distemper, systemic mycoses in dogs and cats, protothecosis, feline toxoplasmosis, tuberculosis, bacterial septicemias in young animals, feline infectious peritonitis, thromboembolic meningoencephalitis in cattle, bovine malignant catarrhal fever, classical swine fever, and leptospirosis and onchocerciasis in horses. Therapy is directed at the systemic disease.
Retinal detachments occur in most species. In dogs, retinal detachment or separation of the neurosensory retina from the retinal pigment epithelium is associated with congenital retinal disorders (retinal dysplasia and Collie eye anomaly), chorioretinitis, trauma, intraocular surgery, and posterior segment neoplasia. In cats, retinal detachments occur with chorioretinitis associated with feline infectious peritonitis, feline viral leukemia, and systemic hypertension. In horses, the most frequent causes are trauma, intraocular surgery, and recurrent uveitis.
Retinal detachments are divided clinically into nonrhegmatogenous (serous, exudative, hemorrhagic, secondary to vitreal syneresis) and rhegmatogenous (with retinal breaks [hole or tear]). Clinical signs include mydriasis, anisocoria, vision impairment, and intraocular hemorrhage. Diagnosis is by ophthalmoscopy and, in eyes with an opaque cornea or lens, ocular ultrasonography.
Nonrhegmatogenous retinal detachments are usually treated medically with therapy directed at the primary disease. Retinal reattachment occurs with resolution of the subretinal exudates and hemorrhage. Variable retinal degeneration may follow in the detached areas. Rhegmatogenous retinal detachments with retinal breaks generally require surgical correction.
Last full review/revision July 2011 by Kirk N. Gelatt, VMD, DACVO