Ординатура / Офтальмология / Английские материалы / Small Animal Ophthalmology Secrets_Riis_2002

BIBLIOGRAPHY

I. AcIand G. Aguirre GD, Chader GJ, et al: Canine early onset hereditary retina] degenerations: Genetic and biochemical distinction of 3 diseases. Proc Am Coli Vet Ophthalrnol ] l i l , ]980.

2.American College of Veterinary Ophthalmologists Genetics Committee: Ocular Disorders Presumed to be Inherited in Dogs, 2nd ed. AVCO, ] 999. Available from Canine Eye Registration Foundation, West Indianapolis, IN.

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Genetic transmission and influence on offspring vitality. J Small Anim Pract 41 :254-258, 2000.

10.Wallin-Hakanson B, Wallin-Hakanson N, Hedhammar A: Influence of selective breeding on the prevalence of chorioretinal dysplasia and coloboma in the rough collie in Sweden. J Small Anim Pract 41:56-59,2000.

11.Yakely WL: Collie eye anomaly: Decreased prevalence through selective breeding. J Am Vet Med Assoc 161:1103, 1972.

Figure 5. Advanced PRA showing avascularity in the tapetal-nontapetal periphery.

Figure 6. Advanced PRA in the nontapetal fundus of a standard poodle.

Figure 7. Advanced PRA in the non tapetal fundus of a toy poodle.

significantly within the degenerated zones and especially the periphery. Hyperrefiectivity is dependent on the incidence of light so it is variable from being dull to bright with an indirect ophthalmoscopic evaluation. A slight decrease in pigmentation may be noted in the nontapetum. Changes in the optic disc are slight and may be hard to document unless a normal eye is close by to compare (Figs. 8 and 9).

Figure 8. Moderately affected PRA fundus with hyperreflectivity and vascular attenuation

Figure 9. PRA in a miniature poodle. Moderately attenuated peripheral vasculature.

Early PRA is sometimes difficult to diagnose. Slight peripheral tapetal color changes can be misleading, especially if the dog is darkly pigmented where diffusion of pigment into the peripheral tapetum appears gray. If it is PRA, the vasculature will show attenuation of the vessel diameters especially in the periphery and circumciliary vessels. Vessels in the mid periphery may have variable wall diameters (called "boxcarring" or "beading"). Usually, the nontapetal area and optic disc look pretty good (Figs. 10-13).

6.How can the diagnosis of PRA be confirmed?

The electroretinogram (ERG) and the DNA blood test are both diagnostic (see Chapters 1

and 41).

7.What if the owner doesn't give consent for those tests?

A simple visual ability test can be performed through a maze in different lighting. Keep in

mind that most dogs can see normally far better than we can in the darkness. Schedule future ophthalmoscopic examinations, which may show the progressive character of the degeneration as well as the visual impairment.

8.What should the owners of PRA dogs be advised concerning breeding?

Becauase most PRA is passed as an autosomal recessive trait, definitely advise against breeding.

9.If PRA is in the early-to-midstage of development, should the dog be dietarily supplemented?

Studies have been done in both humans and animals with vitamin A, E, and long-chain fatty acids to bolster the diet with these supplements since it is known that these are vital to the health of the retina. Unfortunately, the course of the degeneration is not altered, and blindness is not curtained. In fact, vitamin A supplements seem to hasten the degeneration (i.e., supplements are not recommended).

10.What other ocular abnormalities occur in PRA?

The pupillary reflex becomes more sluggish as PRA progresses. In advanced PRA, the rest-

ing pupil is often wider than in normal-aged matched dogs. In some dogs, the major complaint from the owner may be "large pupils" and "clumsiness." Cataracts are frequently secondary to PRA in some breeds.

11.Why do cataracts develop in some PRA breeds?

The exact etiology has not been proven, but several theories make sense. The preferred the-

ory is that the lens environment is no longer conducive to lens health. The degenerating retina contaminates the fluids of the eye, affecting the lens fibers. The analogy is similar to fish in a pond; polluted water eventually destroys the fish (Fig. 14).

Figure 14. Cataracts secondary to PRA in an

American cocker spaniel.

12.Are central progressive retinal atrophy (CPRA) cases different than PRA?

Yes, the degenerated retinas look different. The CPRA retinas have multifocal discolorations

throughout the tapetum with hyperreflective areas in between. The vasculature attenuates similar to PRA, and the optic disc undergoes changes similar to PRA in the advanced stages. Histopathologically, the lesions differ predominantly by the accumulation of lipopigment material within the retinal pigment epithelium; hence, the preferred term is now retinal pigment epithelial dystrophy (RPED). The lipopigment is responsible for the multifocal discoloration (Figs. 15 and 16).

Figure 15. Central fundus of RPED. Note the multifocal dark areas in the tapetum.

Figure 16. Peripheral tapetal fundus of RPED. Note the vascular absence and the multifocal accumulations throughout.

13.Are there dissimilarities within PRA?

Yes, PRA seems to fall into 2 broad categories: developmental or abiotrophy and degenera-

tive diseases of the photoreceptors. Within these categories, more unique differences have and will be discovered at the cellular and molecular levels, ultimately identifying each with gene symbols.

14. How can I keep these categories straight in my mind?

The degenerative categories are those retinas that were normal at some earlier point in time and progressed to photoreceptor cell death. The abiotrophy or developmental categories encompass retinas that are structurally or biochemically abnormal before the retinas become mature. Eventually both categories end up in blindness, but the developmental category is usually much sooner.

15. Is there any other way to think about these categories?

Yes, the developmental category has also been given the description of photoreceptor dys- plasias, because the condition becomes clinically obvious before the first 1-1 1/2 years of life.

248 Retinal Degenerations

Photoreceptor Dysplasias

16. What are some examples of PRA photoreceptor degeneration?

17.What does prcd stand for?

Progressive rod-cone degeneration indicates a PRA that affects the rods primarily and then

the cones. It is always bilateral histopathologically. It may vary slightly electrophysiologically and ophthalmoscopically in the early and moderate stages.

18. List the purebred dogs that have been diagnosed with retinal degeneration.

19.Does retinal degeneration develop in the cat?

Yes, with a similar classification as found in dogs. Known classifications are abiotrophies,

degenerations or atrophies, infections, metabolic, nutritional, and toxic (Figs. 17 and 18).

20.What is known about the retinal abiotrophies in cats?

The most significant reports are in Persian cats that have a photoreceptor dysplasia that is au-

tosomal recessive. Abyssinian cats have been reported to have a rod-cone dysplasia that is auto-

Figure 17. Cat retinal degeneration. Note the vascular attenuation. The hyperreflective character was so intense that a green filter was used to prevent overexposure.