Ophthalmic Pathology Outline

This is a beginner's lesson in ophthalmic pathology, aimed at general pathologists or ophthalmology residents who are just starting their residency.

It is intended to give the essentials on general principles of pathology of the eye.


General reactions

Specific reactions


Limited in its reaction to insults -- usually produces degeneration of lens fibers (cataract); artifacts of preparation are prominent.

Cellular events which represent cataract formation

Pathogenesis of sugar cataract (from Kinoshita)

Lens-induced uveitis or endophthalmitis

Congenital rupture of lens capsule

Sarcoma of globe in cats

Cats who have had ocular trauma resulting in phthisis bulbi appear to be at risk for developing intraocular sarcoma. Besides a history of trauma, a common feature in these cases is rupture of the lens. It may be that the lens epithelial cells undergo malignant transformation, or the neoplastic process may be from activated retinal epithelial cells.

These neoplasms can be aggressive and spread locally and grow into the brain along the optic nerve. Therefore, phthisical eyes in cats should be enucleated even if there appear to be no problems for the individual. This should be done as soon as possible after phthisis bulbi is recognized, and as much of the optic nerve as possible should be removed with the globe.

The syndrome of ocular sarcoma following trauma appears to be a problem primarily of cats. It has not been reported in dogs and other nonhuman animals.

Ocular neovascularization



Cyclitic membrane

Choroidal neovascularization

Retinal neovascularization

Uveal tract

Conveniently described as anterior (iris and ciliary body) or posterior (choroid) uvea.


Sequelae to uveitis

Equine recurrent uveitis

Most common cause of blindness in horses, ponies and mules. Characterized by variable degree of uveitis in one or both eyes; the inflammation is recurrent at variable intervals; the anterior uvea is more commonly affected. During the clinically quiescent phase, there is continuous 'smoldering' inflammation detectable histologically.

There most likely is a multiplicity of conditions which could produce this syndrome. This chronic, relapsing form of inflammation is a nonspecific characteristic of the uveal tract most likely due to delayed hypersensitivity to damaged uveal tissue.



This is the most common primary intraocular neoplasm.


Neoplasms such as medulloepitheliomas, ciliary body adenomas and adenocarcinomas occasionally are seen.


This is an increase in intraocular pressure which causes characteristic pathological changes in the eye. May be primary (no antecedent problem), but usually is secondary in our patients.

Some factors associated with or leading to glaucoma

Pathologic changes as a result of the increased intraocular pressure

The changes of major importance are in the optic nerve and retina.



Development of the retina continues postnatally in cats, dogs, rodents. In the dog, photoreceptor inner segments begin forming on postnatal day 1; by postnatal day 16, the inner segments are 10 µm long, and outer segments are less than 3 µm; by 45-50 days, both inner and outer segments have reached their adult length of about 16 µm each. These figures hold for the posterior region of the retina: development proceeds from posterior to anterior (peripheral) so that at any stage, the posterior region is more developed than the peripheral region. This holds for developmental diseases as well, in which the posterior region of the retina shows more extensive changes than the peripheral region at early to intermediate stages of disease.


Similar to other tissues, but usually occurs as a complication of choroiditis in non-traumatic lesions. Scarring or gliosis of the retina is a sequela to inflammation and is associated with degeneration of the neural tissue and loss of vision for the area concerned (i.e., a focal lesion would be 'blind,' but surrounding normal areas would allow the individual continued vision).


Rarely seen clinically in nonhuman animals partly because it is unassociated with clinical signs until late in its course. It uncommonly is seen histologically as an incidental finding in various congenital and acquired anomalies, but usually is associated with severe intraocular inflammation.

In people, neovascularization of the retina is a frequent and disastrous complication in diabetes mellitus, retrolental fibroplasia and retinal vein occlusion. The exact stimulus for neovascularization is unknown. The iris also is involved, which implies that there may be a diffusable 'angiogenic' factor.

Heritable degenerations

Known collectively as progressive retinal degeneration (PRD). This group of diseases also is known as progressive retinal atrophy (PRA).

This is a common problem in dogs in which it has been studied more extensively than in other domestic animals. Final appearance of the retina in the heritable retinal degenerations is similar. The sensory retina may be reduced to a thin, glial membrane with little recognizable components; the retinal epithelium may be completely gone although islands of hypertrophied or hyperplastic cells may remain, or there may be migration of these cells into the sensory retina.

Although the final outcome is the same in most cases, the early pathologic changes are often different and provide a useful classification scheme.

Rod-cone dysplasia

Seen in the Irish setter and collie. Rods and cones fail to develop normally; this is histologically evident as early as 20 days postnatally in appropriately prepared tissue.

Although rod nuclei and perikarya are present (outer nuclear layer), only a small number of inner segments and very little outer segment material forms; the rod outer segment material is disoriented and disorganized. Eventually, the outer nuclear layer thins due to pyknosis and loss of tissue. By 18 weeks or later, most outer and inner segment material has degenerated completely.

Cones do not develop normally in a functional sense, but a few appear to reach morphologic maturity. Most remain diminutive as with the rods. As the rod population decreases, the cone inner segments become broad and club-shaped probably due to loss of lateral support. With time, the cones degenerate completely.

Rod dysplasia

Seen in the Norwegian elkhound and possibly in the miniature schnauzer. Rods fail to develop normally and cones degenerate secondarily.

The changes in rods are similar in extent and time-course to those in the Irish setter.

At about 47 weeks, a few cones begin to show disorganization of outer segment lamellae. This progresses slowly so that many years pass before there is complete degeneration of the cones.

Rod-cone degeneration

Seen in miniature and toy poodles and various other breeds of dogs. Rods and cones appear to develop normally, but soon after morphologic and functional maturity, they begin to degenerate slowly. Degeneration of the photoreceptors may not be complete until the animal is 3-5 years or older.

Retinal separation

This also is termed retinal detachment clinically. The site of interruption, however, is almost always at the photoreceptor outer segment-retinal epithelial junction. Because the retinal epithelium is part of the retina, the term separation may be more appropriate.

Usually caused by inflammation of the choroid which results in a breakdown of the blood-retinal barrier (retinal epithelial cells are disrupted). Any process which results in a breakdown of the blood-retinal barrier at this location can result in retinal separation. Some of the processes include systemic hypertension, renal disease and emboli or thrombi in the choriocapillaris.

There are many nonspecific degenerative changes which occur in the retinal epithelium and sensory retina due to the separation itself

Light-induced retinal degeneration

Occurs in virtually every species studied: mice, rats, hamsters, rabbits, pigs, pigeons, primates and dogs.

In albino rats and mice, as little as 24 hrs of 'normal' room illumination can cause photoreceptor damage (this is reversible even after a few days of exposure as long as the inner segment remains intact); several days of continuous light can lead to permanent degenerative changes.

In melanotic rodents, degeneration can occur, but the light must be of higher intensity or the pupils must be artificially dilated to reduce the protective effect of the melanotic iris.

In primates, dogs and pigs, only relatively high intensity light sources have been studied and have included diagnostic instruments such as the indirect ophthalmoscope, strobe flash and slit lamp. All have produced marked, focal photoreceptor damage after exposures for as little as 15 min. at intensities commonly used in clinical settings.

The major pathological effects of visible light center around the photoreceptors and retinal epithelium. The inner retinal layers usually remain normal. This is in striking contrast to the full-thickness coagulation and necrosis seen with extremely high energy sources such as laser and xenon arc where the damage is caused by marked local rises in temperature. With common visible light, a rise in local retinal temperature is insufficient to explain the degeneration seen. There most likely is a combination of photochemical and thermal factors, the former playing a major role. It is known that light in the blue end of the visible spectrum is more damaging than other wavelengths; and rhodopsin, the major visual pigment residing in the photoreceptors, has peak absorbency in this range, supporting the photochemical theory.

Peripheral microcystoid degeneration

This is an age-related process seen in most species after middle-age. Histologically, there is a variable degree of degeneration of the retina near and including the ora serrata (ora ciliaris retina); tiny-to-large cysts may occur in the retinal layers; migration of retinal epithelial cells into the sensory retina is common. This condition is considered 'normal' in that it is universal; it rarely progresses further posteriorly than a couple millimeters from the ora serrata.

The intraretinal cysts contain acid mucopolysaccharide which is sensitive to hyaluronidase. The significance of this is unclear.

Some References for Ocular Pathology


  1. Hogan, Michael J. and Zimmerman, Lorenz E. Ophthalmic Pathology: An Atlas and Textbook, Second Edition. Philadelphia, PA:W.B. Saunders Company, 1962;797.

  2. Saunders, L.Z. and Rubin, L.F. Ophthalmic Pathology of Animals: An Atlas and Reference Book. Basel:S. Karger, 1975;258.

  3. Streilein, J. Wayne. Anterior chamber associated immune deviation: The privilege of immunity in the eye. Survey of Ophthalmology 1990 (July-August);35 (1):67-73.

  4. Yanoff, Myron and Fine, Ben S. Ophthalmic Pathology: A Text and Atlas. New York, NY:Harper & Row, Publishers, 1975;747.


  1. Gilger, Brian C.; McLaughlin, Susan A.; Whitley, R. David and Wright, James C. Orbital neoplasms in cats: 21 cases (1974-1990). Journal of the American Veterinary Medical Association 1992 (1 October);201 (7):1083-1086.


  1. Bedford, P.G.C. and Longstaffe, J.A. Corneal pannus (chronic superficial keratitis) in the German shepherd dog. Journal of Small Animal Practice 1979;20:41-56.

  2. Bistner, Stephen I.; Aguirre, Gustavo and Shively, James N. Hereditary corneal dystrophy in the Manx cat: a preliminary report. Investigative Ophthalmology 1976 (January);15 (1):15-26.

  3. Buck, R.C. Cell migration in repair of mouse corneal epithelium. Investigative Ophthalmology 1979;18:767-784.

  4. Chan-Ling, Tailoi; Vannas, Antti; Holden, Brien A. and O'Leary, Daniel J. Incision depth affects the recovery of corneal sensitivity and neural regeneration in the cat. Investigative Ophthalmology and Visual Science 1990 (August);31 (8):1533-1541.

  5. Glickstein, M.; Cameron, J.D. and Yanoff, M. In vitro studies of corneal wound healing in dogs. Ophthalmic Research 1975;7:401-408.

  6. Klintworth, G.K. The cornea - structure and macromolecules in health and disease. American Journal of Pathology 1977;89:719-808.

  7. Koch, Seth A.; Langloss, John M. and Schmidt, Gretchen. Corneal epithelial inclusion cysts in four dogs. Journal of the American Veterinary Medical Association 1974 (15 June);164 (12):1190-1191.

  8. Kruse, Friedrich E.; Chen, James J.Y.; Tsai, Ray J.F. and Tseng, Scheffer C.G. Conjunctival transdifferentiation is due to the incomplete removal of limbal basal epithelium. Investigative Ophthalmology and Visual Science 1990 (September);31 (9):1903-1913.

  9. MacMillan, A.D.; Waring, G.O.; Spangler, W.L. and Roth, A.M. Crystalline corneal opacities in the Siberian husky. Journal of the American Veterinary Medical Association 1979 (15 October);175 (8):829-832.

  10. McCracken, J.S. and Klintworth, G.K. Ultrastructural observations on experimentally produced melanin pigmentation of the corneal epithelium. American Journal of Pathology 1976;85:167-176.

  11. Van Horn, D.L. and Hyndiuk, R.A. Endothelial wound repair in primate cornea. Experimental Eye Research 1975;21:113-124.

  12. Waring, George O.; Muggli, Francis M. and MacMillan, Alan. Oval corneal opacities in beagles. Journal of the American Animal Hospital Association 1977 (March/April);13:204-208.

  13. Waring G.O., Rodriques M.M., Laibson P.R. Corneal dystrophies. I. Dystrophies of the epithelium, Bowman's layer and stroma. Survey of Ophthalmology 1978;23:71-122.

  14. Waring, G.O.; Rodrigues, M.M. and Laibson, P.R. Corneal dystrophies. II. Endothelial dystrophies. Survey of Ophthalmology 1978;23:147-168.


  1. Burns, R.P.; Anderson, R.S. and Feeney-Burns, L. Cataract-webbed trait in Peromyscus. II. Biomicroscopy and histology of eyes. Investigative Ophthalmology and Visual Science 1980;19:31-42.

  2. Coulombre, A.J. Cataractogenesis: Developmental inputs and constraints. Ophthalmology 1979;86:1559-1570.

  3. Curtis, Roger. Lens luxation in the dog and cat. Veterinary Clinics of North America. Small Animal Practice 1990 (May);20 (3):755-773.

  4. Dubielzig, R.R.; Everitt, J.; Shadduck, J.A. and Albert, D.M. Clinical and morphologic features of post-traumatic ocular sarcomas in cats. Veterinary Pathology 1990 (January);27 (1):62-65.

  5. Friedlaender, R.P. et al. Ocular pathology induced by the suckling mouse cataract agent. Investigative Ophthalmology 1976;15:640-647.

  6. Iwata, S. Process of lens opacification and membrane function: A review. Ophthalmic Research 1974;6:138-154.

  7. Jose, J.G. The role of DNA damage, its repair and its misrepair in the etiology of cataract: a review. Ophthalmic Research 1978;10:52-62.

  8. Kinoshita, Jin H. Mechanisms initiating cataract formation: Proctor Lecture. Investigative Ophthalmology 1974 (October);13 (10):713-724.

  9. Marak, G.E.; Font, R.L.; Czawlytko, L.N. and Alepa, F.P. Experimental lens-induced granulomatous endophthalmitis: Preliminary histopathologic observations. Experimental Eye Research 1974;19:311-316.

  10. Marak, G.E.; Rao, N.A.; Antonakou, G. and Sliwinski, A. Experimental lens-induced granulomatous endophthalmitis in common laboratory animals. Ophthalmic Research 1982;14:292-297.

  11. Rafferty, N.S. and Goossens, W. Ultrastructural studies of traumatic cataractogenesis: Observations of a repair process in mouse lens. American Journal of Anatomy 1975;142:177-200.


  1. Davidson, Michael G.; Nasisse, Mark P.; English, Robert V.; Wilcock, Brian P. and Jamieson, Vivian E. Feline anterior uveitis: A study of 53 cases. Journal of the American Animal Hospital Association 1991 (January/February);27 (1):77-83.

  2. Duncan, D.E. and Peiffer, R.L. Morphology and prognostic indicators of anterior uveal melanomas in cats. Progress in Veterinary and Comparative Ophthalmology 1991 (Spring);1 (1):25-32.

  3. Friedlaender, M.H.; Howes, E.L.; Hall, J.M.; Krasnobrod, H. and Wormstead, M.A. Histopathology of delayed hypersensitivity reactions in the guinea pig uveal tract. Investigative Ophthalmology and Visual Science 1978;17:327-335.

  4. Friedman, D.S.; Miller, L. and Dubielzig, R.R. Malignant canine anterior uveal melanoma. Veterinary Pathology 1989;26:523-525.

  5. Marak, G.E.; Shichi, H.; Rao, N.A. and Wacker, W.B. Patterns of experimental allergic uveitis induced by rhodopsin and retinal rod outer segments. Ophthalmic Research 1980;12:165-176.

  6. Morgan, Rhea V. Vogt-Koyanagi-Harada syndrome in humans and dogs. Compendium on Continuing Education for the Practicing Veterinarian 1989 (October);11 (10):1211-1218.

  7. Williams, R.D.; Morter, R.L.; Freeman, M.J. and Lavignette, A.M. Experimental chronic uveitis: Ophthalmic signs following equine leptospirosis. Investigative Ophthalmology 1971 (December);10 (12):948-954.

Ocular neovascularization

  1. Bicknell, Roy and Harris, Adrian L. Novel growth regulatory factors and tumour angiogenesis. European Journal of Cancer 1991 (June);27 (6):781-785.

  2. Eisenstein, Reuben; Goren, Seymour B.; Shumacher, Barbara and Choromokos, Earl The inhibition of corneal vascularization with aortic extracts in rabbits. American Journal of Ophthalmology 1979 (December);88 (6):1005-1012.

  3. Fromer, Carl H. and Klintworth, Gordon K. An evaluation of the role of leukocytes in the pathogenesis of experimentally induced corneal vascularization. I. Comparison of experimental models of corneal vascularization. American Journal of Pathology 1975 (June);79 (3):537-554.

  4. Gartner, Samuel and Henkind, Paul Neovascularization of the iris (rubeosis iridis). Survey of Ophthalmology 1978 (March-April);22 (5):291-312.

  5. Hayreh, Sohan S. Ocular neovascularization. Archives of Ophthalmology 1980 (March);98:574.

  6. Henkind, Paul Ocular neovascularization: The Krill Memorial Lecture. American Journal of Ophthalmology 1978 (March);85 (3):287-301.

  7. Odedra, R. and Weiss, J.B. Low molecular weight angiogenesis factors. Pharmacology and Therapeutics 1991;49 (1/2):111-124.

  8. Patz, Arnall I. Studies on retinal neovascularization: Friedenwald Lecture. Investigative Ophthalmology and Visual Science 1980 (September);19 (10):1133-1138.

  9. Schultz, G.S. and Grant, M.B. Neovascular growth factors. Eye 1991;5 (2):170-180.


  1. Brooks, Dennis E. Glaucoma in the dog and cat. Veterinary Clinics of North America. Small Animal Practice 1990 (May);20 (3):775-797.

  2. Martin, Charles L. and Wyman, Milton Primary glaucoma in the dog. Veterinary Clinics of North America. Small Animal Practice 1978 (May);8 (2):257-286.

Retina and optic nerve

  1. Acland, G.M. and Aguirre, G.D. Retinal degenerations in the dog: IV. Early retinal degeneration (erd) in Norwegian elkhounds. Experimental Eye Research 1987;44:491-521.

  2. Aguirre, Gustavo Retinal degenerations in the dog. I. Rod dysplasia. Experimental Eye Research 1978;26:233-253.

  3. Aguirre, G.D. and Rubin, L.F. Rod-cone dysplasia (progressive retinal atrophy) in Irish setters. Journal of the American Veterinary Medical Association 1975 (15 January);166 (2):157-164.

  4. Aguirre, G.; Farber, D.; Lolley, R.; Fletcher, R.T. and Chader, G.J. Rod-cone dysplasia in Irish setters: A defect in cyclic GMP metabolism in visual cells. Science 1978 (22 September);201:1133-1134.

  5. Aguirre, Gustavo; Alligood, James; O'Brien, Paul and Buyukmihci, Ned Pathogenesis of progressive rod-cone degeneration in miniature poodles. Investigative Ophthalmology and Visual Science 1982 (November);23 (5):610-630.

  6. Buyukmihci, N.; Aguirre, G. and Marshall, J. Retinal degenerations in the dog. II. Development of the retina in rod-cone dysplasia. Experimental Eye Research 1980;30:575-591.

  7. Buyukmihci, Ned Photic retinopathy in the dog. Experimental Eye Research 1981;33:95-109.

  8. Buyukmihci, Ned; Goehring-Harmon, Faye and Marsh, Richard F. Photoreceptor degeneration preceding clinical scrapie encephalopathy in hamsters. Journal of Comparative Neurology 1982;205:49-54.

  9. Buyukmihci, Ned; Goehring-Harmon, Faye and Marsh, Richard F. Retinal degeneration during clinical scrapie encephalopathy in hamsters. Journal of Comparative Neurology 1982;205:153-160.

  10. Chader, Gerald J. Animal mutants of hereditary retinal degeneration: General considerations and studies on defects in cyclic nucleotide metabolism. Progress in Veterinary and Comparative Ophthalmology 1991 (Summer);1 (2):109-126.

  11. Feeney, L. Lipofuscin and melanin of human retinal pigment epithelium. Fluorescence, enzyme cytochemical and ultrastructural studies. Investigative Ophthalmology and Visual Science 1978;17:583-600.

  12. Fischer, M.W. and Slatter, D.H. Preparation and orientation of canine retinal vasculature. A modified trypsin digestion technique. Australian Journal of Ophthalmology 1978;67:46-50.

  13. Hayreh, S.S. Fluids in the anterior part of the optic nerve in health and disease. Survey of Ophthalmology 1978;23:1-25.

  14. Lanum, Jackie The damaging effects of light on the retina. Empirical findings, theoretical and practical implications. Survey of Ophthalmology 1978 (January-February);22 (4):221-249.

  15. Machemer, Robert and Laqua, Horst Pigment epithelium proliferation in retinal detachment (massive periretinal proliferation). American Journal of Ophthalmology 1975 (July);80 (1):1-23.

  16. Narfström, Kristina and Nilsson, Sven Erik Morphological findings during retinal development and maturation in hereditary rod-cone degeneration in Abyssinian cats. Experimental Eye Research 1989;49:611-628.

  17. Noell, Werner K.; Walker, Virgil S.; Kang, Bok Soon and Berman, Steven Retinal damage by light in rats. Investigative Ophthalmology 1966 (October);5 (5):450-473.

  18. Parshall, Charles J.; Wyman, Milton; Nitroy, Susan; Acland, Gregory and Aguirre, Gustavo Photoreceptor dysplasia: An inherited progressive retinal atrophy of miniature schnauzer dogs. Progress in Veterinary and Comparative Ophthalmology 1991 (Fall);1 (3):187-203.

  19. Stone, Jonathan The Wholemount Handbook: A Guide to the Preparation and Analysis of Retinal Whole Mounts. Sydney:Maitland Publications Pty. Ltd., 1981;128.

  20. Tso, Mark O.M. Experiments on visual cells by nature and man: In search of treatment for photoreceptor degeneration. Friedenwald Lecture. Investigative Ophthalmology and Visual Science 1989 (December);30 (12):2430-2454.

  21. West-Hyde, Leigh and Buyukmihci, Ned Photoreceptor degeneration in a family of cats. Journal of the American Veterinary Medical Association 1982 (1 August);181 (3):243-247.

  22. Wirtschafter, Jonathan D.; Rizzo, Frank J. and Smiley, B. Carroll Optic nerve axoplasm and papilledema. Survey of Ophthalmology 1975 (November-December);20 (3):157-189.

  23. Zinn, Keith M. and Marmor, Marmor F. (eds) The Retinal Pigment Epithelium. Cambridge, MA:Harvard University Press, 1979;521.

Ocular manifestation of systemic disease

  1. Aguirre, Gustavo; Carmichael, Leland and Bistner, Stephen Corneal endothelium in viral induced anterior uveitis: Ultrastructural changes following canine adenovirus type 1 infection. Archives of Ophthalmology 1975 (March);93:219-224.

  2. Aguirre, Gustavo; Stramm, Lawrence and Haskins, Mark Feline mucopolysaccharidosis VI: General ocular and pigment epithelial pathology. Investigative Ophthalmology and Visual Science 1983 (August);24 (8):991-1007.

  3. Anderson, Wayne I.; Rebhun, William C.; de Lahunta, Alexander; Kallfelz, Francis A. and Klossner, Michael C. The ophthalmic and neuro-ophthalmic effects of a vitamin A deficiency in young steers. Veterinary Medicine 1991 (November);86 (11):1143-1148.

  4. Angell, Jann A.; Merideth, Reuben E.; Shively, James N. and Sigler, Ron L. Ocular lesions associated with coccidioidomycosis in dogs: 35 cases (1980-1985). Journal of the American Veterinary Medical Association 1987 (15 May);190 (10):1319-1322.

  5. Buyukmihci, N.C. and Moore, P.F. Microscopic lesions of spontaneous ocular blastomycosis in dogs. Journal of Comparative Pathology 1987;97:321-328.

  6. Carastro, Susan M.; Dugan, Steven J. and Paul, Allan J. Intraocular dirofilariasis in dogs. Compendium on Continuing Education for the Practicing Veterinarian 1992 (February);14 (2):209-217.

  7. da Costa, P.D. and Hoskins, J.D. The role of taurine in cats: Current concepts. Compendium on Continuing Education for the Practicing Veterinarian 1990;12:1235-1240.

  8. Davidson, Michael G.; Breitschwerdt, Edward B.; Nasisse, Mark P. and Roberts, Steven M. Ocular manifestations of Rocky Mountain spotted fever in dogs. Journal of the American Veterinary Medical Association 1989 (15 March);194 (6):777-781.

  9. English, Robert V.; Davidson, Michael G.; Nasisse, Mark P.; Jamieson, Vivian E. and Lappin, Mike R. Intraocular disease associated with feline immunodeficiency virus infection in cats. Journal of the American Veterinary Medical Association 1990 (1 April);196 (7):1116-1119.

  10. Jolly, R.D.; Gibson, A.J.; Healy, P.J.; Slack, P.M. and Birtles, M.J. Bovine ceroid-lipofuscinosis: Pathology of blindness. New Zealand Veterinary Journal 1992 (September);40 (3):107-111.

  11. Lane, India F.; Roberts, Steven M. and Lappin, Michael R. Ocular manifestations of vascular disease: Hypertension, hyperviscosity, and hyperlipemia. Journal of the American Animal Hospital Association 1993 (January/February);29 (1):28-36.

  12. Lavach, J.D. Ocular manifestations of systemic diseases. Veterinary Clinics of North America. Equine Practice 1992 (December);8 (3):627-636.

  13. Nasisse, Mark P. Feline herpesvirus ocular disease. Veterinary Clinics of North America. Small Animal Practice 1990 (May);20 (3):667-680.

  14. Olson, M.E.; Gard, S.; Brown, M.; Hampton, R. and Morck, D.W. Flavobacterium indologenes infection in leopard frogs. Journal of the American Veterinary Medical Association 1992 (1 December);201 (11):1766-1770.

  15. Swanson, James F. Ocular manifestations of systemic disease in the dog and cat: Recent developments. Veterinary Clinics of North America. Small Animal Practice 1990 (May);20 (3):849-867.