Progressive Retinal Atrophy (PRA) is an inherited disease of the retina (the “film in the camera”) in dogs, in which the rod cells in the retina are programmed to die. PRA occurs in both eyes simultaneously and is nonpainful. There are many different types of inherited retinal degenerative diseases in purebred dogs, and discussing these are beyond the scope of this article. PRA occurs in most breeds of dogs and also occurs in mixed breeds. It is recessively inherited in all breeds studied, with the following exceptions: PRA is dominantly inherited in Old English Mastiffs and Bullmastiffs, and is sex-linked and found primarily in male dogs in Siberian Husky and Samoyed breeds.
Because PRA makes rods die, and rods are responsible for vision in dim light (“night vision”), the first clinical signs that the owner often notices are night-blindness (poor vision in dim light) and that the pupils are dilated; owners often notice a “glow” and increased “eye shine” from the eyes. Clinical signs in dogs with PRA vary from the dog first becoming night blind in the early stage of PRA, to the entire visual field in all light levels becoming affected in advanced PRA. In the final stage of PRA, the dog is completely blind. The natural course of the disease, if specific daily antioxidant supplementation is not given, is that all dogs with PRA will become blind within one year of diagnosis. Sadly, some affected dogs are already completely blind by the time a veterinary ophthalmologist first examines them.
PRA reduces vision in most affected dogs and cannot be cured, but in the opinion of many veterinary ophthalmologists, including Dr. McCalla, PRA is no longer a hopeless disease that always leads to complete blindness. New insight into the mechanisms of retinal damage from oxidative stress has resulted in much more hope for prolonging vision of affected dogs. Typical PRA is a disease caused by a mutation in the rod photoreceptors (rods are responsible for night vision/ vision in dim light) leading to their death. Cones are responsible for daytime vision/ vision in bright light, and also for color vision (dogs do see color, but not as well as humans do). The human retina has about 120 million photoreceptors (rods and cones); of these, only about 6 million are cones (5%). The dog retina has more photoreceptors than humans, but only 1.2 million cones. Thus, PRA kills 95% of the photoreceptors!
When the rods die, there is a lot of “left-over”, excessive oxygen delivered to the retina that the dead rods can’t use anymore. Cone death subsequently occurs due to excessive oxygen exposure in the face of rod death from damaging oxidative stress mechanisms. After the rods die, the excessive “left-over” oxygen is toxic, causing oxidative damage and ultimate death of cones. Specific antioxidant support with a canine vision supplement helps protect cones in the face of oxidative damage . The earlier that affected dogs can be provided antioxidant support, the better.
While there is no cure and no medical treatment for PRA, specific antioxidant supplementation helps support the retinal health of affected dogs. Affected dogs diagnosed with PRA before complete vision loss occurs may be helped by antioxidant support, to save some day vision (cone function). The clinical experience of veterinary ophthalmologists is very encouraging in patients given daily specific antioxidant vision support, especially BEFORE toxic cataracts have formed or progressed. Some PRA-affected dogs have been supplemented for over seven years, and these patients have not lost all of their vision by the end of their lifetimes. In contrast, unsupplemented dogs will become blind within 1 year of diagnosis of PRA – either the remaining cones die, the toxic cataracts progress to become mature cataracts, or both.