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Veterinary Ocular Pathology

Williams, L.W., Gelatt, K.N., Gwin, R.M., 1981. Ophthalmic neoplasms in the cat. J. Am. Anim. Hosp. Assoc. 17, 999–1008.

Gwin, R.M., Gelatt, K.N., Williams, L.W., 1982. Ophthalmic neoplasms in the dog. J. Am. Anim. Hosp. Assoc. 18, 853–866.

Dubielzig, R.R., 1990. Ocular neoplasia in small animals. Vet. Clin. North Am. Small Anim. Pract. 20, 837–848.

Uveal melanocytic neoplasia

Mould, J.R.B., Petersen-Jones, S.M., Peruccio, C., et al., 2002. Uveal melanocytic tumors. In: Peiffer Jr., R.L., Simons, K.B. (Eds), Ocular tumors in humans and animals, 1st edn. Iowa State Press, Ames, Iowa, pp. 225–288.

Dithmar, S., Albert, D.M., Grossniklaus, H.E., 2000. Animal models of uveal melanoma. Melanoma. Res. 10, 195–211.

Diters, R.W., Dubielzig, R.R., Aguirre, G.D., et al., 1983. Primary ocular melanoma in dogs. Vet. Pathol. 20, 379–395.

Bussanich, N.M., Dolman, P.J., Rootman, J.,

et al., 1987. Canine uveal melanomas: series and literature review. J. Am. Anim. Hosp. Assoc. 23, 415–422.

Ryan, A.M., Diters, R.W., 1984. Clinical and pathologic features of canine ocular melanomas. J. Am. Vet. Med. Assoc. 184, 60–67.

Trucksa, R.C., 1983. Canine ocular melanocytic neoplasms. In: Peiffer Jr., R.L. (Ed.), Comparative ophthalmic pathology. Charles C. Thomas, Springfield, pp. 170–182.

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Miwa, Y., Matsunaga, S., Kato, K., et al., 2005. Choroidal melanoma in a dog. J. Vet. Med. Sci. 67, 821–823.

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Comp. Ophthalmol. 7, 263–266.

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canine survival with primary intraocular melanocytic neoplasia. Vet. Ophthalmol. 2, 185–190.

Cook, C.S., Wilkie, D.A., 1999. Treatment of presumed iris melanoma in dogs by diode laser photocoagulation: 23 cases. Vet. Ophthalmol. 2, 217–225.

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Feline diffuse iris melanoma

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Bjerkas, E., Arnesen, K., Peiffer Jr., R.L., 1997. Diffuse amelanotic iris melanoma in a cat. Vet. Comp. Ophthalmol. 7, 190–191.

Kalishman, J.B., Chappell, R., Lisa Flood, L.A., et al., 1998. Matched observational study of survival in cats with enucleation due to diffuse iris melanoma. Vet. Ophthalmol. 1, 25–29.

Harris, B.P., Dubielzig, R.R., 1999. Atypical primary ocular melanoma in cats. Vet. Ophthalmol. 2, 121–124.

Stiles, J., Bienzle, D., Render, J.A., et al., 1999. Use of nested polymerase chain reaction (PCR) for detection of retroviruses from formalin-fixed, paraffin-embedded uveal melanomas in cats. Vet. Ophthalmol. 2, 113–116.

Equine uveal melanocytic neoplasms

Equine melanoma

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Latimer, C.A., Wyman, M., 1983. Sector iridectomy in the management of iris melanoma in a horse. Equine Vet. J. Suppl. 2, 101–104.

Matthews, A.G., Barry, D.R., 1987. Bilateral melanoma of the iris in a horse. Equine Vet. J. 19, 358–360.

Barnett, K.C., Platt, H., 1990. Intraocular melanomata in the horse. Equine Vet. J. (Suppl. 10), 76–82.

Davidson, H.J., Blanchard, G.L., Wheeler, C.A., et al., 1991. Anterior uveal melanoma, with secondary keratitis, cataract, and glaucoma,

in a horse. J. Am. Vet. Med. Assoc. 199, 1049–1050.

Scotty, N.C., Barrie, K.B., Brooks, D.E., et al., 2008. Surgical management of a progressive iris melanocytoma in a Mustang. Vet. Ophthalmol. 11, 75–80.

Iris and ciliary body epithelial neoplasms

Peiffer Jr., R.L., 1983. Ciliary body epithelial tumours in the dog and cat; a report of thirteen cases. J. Small Anim. Pract. 24, 347–370.

Peiffer Jr., R.L., 1983. Ciliary body epithelial tumors. In: Peiffer Jr., R.L. (Ed.), Comparative ophthalmic pathology. Charles C. Thomas, Springfield, pp. 183–212.

Lavach, J.D., 1984. Iridociliary adenoma in a dog. J. Am. Anim. Hosp. Assoc. 20, 468–470.

Clerc, B., 1996. Surgery and chemotherapy for the treatment of adenocarcinoma of the iris and ciliary body in five dogs. Vet. Comp.

Ophthalmol. 6, 265–270.

Dubielzig, R.R., Steinberg, H., Garvin, H., et al., 1998. Iridociliary epithelial tumors in 100 dogs and 17 cats: a morphological study. Vet. Ophthalmol. 1, 223–231.

Zarfoss, M.K., Dubielzig, R.R., 2007. Metastatic Iridociliary Adenocarcinoma in a Labrador Retriever. Vet. Pathol. 44, 672–676.

Klosterman, E., Colitz, C.M., Chandler, H.L., et al., 2006. Immunohistochemical properties of ocular adenomas,

adenocarcinomas and medulloepitheliomas. Vet. Ophthalmol. 9, 387–394.

Hendrix, D.V., Donnell, R.L., 2007. Lenticular Invasion by a ciliary body adenocarcinoma in a dog. Vet. Pathol. 44, 540–542.

Langloss, J.M., Zimmerman, L.E., Krehibiel, J.D., 1976. Malignant intraocular teratoid medulloepithelioma in three dogs. Vet. Pathol. 13, 343–352.

Lahav, M., Albert, D.M., Kircher, C.H., et al., 1976. Malignant teratoid medulloepithelioma in a dog. Vet. Pathol. 13, 11–16.

Wilcock, B., Williams, M.M., 1980. Malignant intraocular medulloepithelioma in a dog. J. Am. Anim. Hosp. Assoc. 16, 617–619.

Jensen, O.A., Kaarsholm, S., Prause, J.U., et al., 2003. Neuroepithelial tumor of the retina in a dog. Vet. Ophthalmol. 6, 57–60.

Aleksandersen, M., Bjerkas, E., Heiene, R., et al., 2004. Malignant teratoid medulloepithelioma with brain and kidney involvement in a dog. Vet. Ophthalmol. 7, 407–411.

Bistner, S.I., 1974. Medullo-epithelioma of the iris and ciliary body in a horse. Cornell. Vet. 64, 588–595.

Eagle Jr., R.C., Font, R.L., Swerczek, T.W., 1978. Malignant medulloepithelioma of the optic nerve in a horse. Vet. Pathol. 15, 488–494.

Szymanski, C.M., 1987. Malignant teratoid medulloepithelioma in a horse. J. Am. Vet. Med. Assoc. 190, 301–302.

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Chapter

 

 

9

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Riis, R.C., Scherlie, P.H., Rebhun WC, 1990. Intraocular medulloepithelioma in a horse. Equine Vet. J. Suppl. 10, 66–68.

Knottenbelt, D.C., Hetzel, U., Roberts, V., 2007. Primary intraocular primitive neuroectodermal tumor (retinoblastoma) causing unilateral blindness in a gelding. Vet. Ophthalmol. 10, 348–356.

Hendrix, D.V., Bochsler, P.N., Saladino, B., et al., 2000. Malignant teratoid

medulloepithelioma in a llama. Vet. Pathol. 37, 680–683.

Schmidt, R.E., Becker, L.L., McElroy, J.M., 1986. Malignant intraocular medulloepithelioma in two cockatiels. J. Am. Vet. Med. Assoc. 189, 1105–1106.

Bras, I.D., Gemensky-Metzler, A.J., Kusewitt, D.F., et al., 2005. Immunohistochemical characterization of a malignant intraocular teratoid medulloepithelioma in a cockatiel. Vet. Ophthalmol. 8, 59–65.

Shields, J.A., Eagle Jr., R.C., Shields, C.L., et al., 1996. Acquired neoplasms of the nonpigmented ciliary epithelium (adenoma and adenocarcinoma). Ophthalmology 103, 2007–2016.

Lymphoma and histiocytic neoplasia

Carlton, W.C., Hutchinson, A.K., Grossniklaus, H.E., 2002. Ocular lymphoid proliferations. In: Peiffer Jr., R.L., Simons, K.B. (Eds.), Ocular tumors in animals and humans,

1st edn. Iowa State Press, Ames, Iowa, pp. 379–413.

Corcoran, K.A., Peiffer Jr., R.L., Koch SA, 1995. Histopathologic features of feline ocular lymphosarcoma: 49 cases (1978–1992). Vet. Comp. Ophthalmol. 5, 35–41.

Nell, B., Suchy, A., 1998. ‘D-shaped’ and ‘reverse-D-shaped’ pupil in a cat with lymphosarcoma. Vet. Ophthalmol. 1, 53–56.

Dubielzig, R., Steinberg, H., Fischer, B., et al., 2000. Feline primary ocular lymphosarcoma: immunophenotyping of leukocytes, FeLV status and relationship to idiopathic lymphoplasmacytic uveitis. In: Proceedings of the 31st Annual Meeting of the American College of Veterinary Ophthalmology, Montreal, Canada, p. 46.

Couto, G.C., 2001. What is new on feline lymphoma? J. Feline Med. Surg. 3, 171–176.

Grahn, B.H., Peiffer, R.L., Cullen, C.L., et al., 2006. Classification of feline intraocular neoplasms based on morphology, histochemical staining, and immunohistochemical labeling. Vet. Ophthalmol. 9, 395–403.

Brightman, A.H. 2nd, Ogilvie, G.K., Tompkins, M., 1991. Ocular disease in FeLV-positive cats: 11 cases (1981–1986). J. Am. Vet. Med. Assoc. 198, 1049–1051.

Cello, R.M., Hutcherson, B., 1962. Ocular changes in malignant lymphoma of dogs. Cornell. Vet. 52, 492–523.

Krohne, S.G., Henderson, N.M., Richardson, R.C., et al., 1994. Prevalence of ocular involvement in dogs with multicentric lymphoma: prospective evaluation of 94

cases. Vet. Comp. Ophthalmol. 4, 127– 135.

Kilrain, C.G., Saik, J.E., Jeglum, K.A., 1994. Malignant angioendotheliomatosis with retinal detachments in a dog. J. Am. Vet. Med. Assoc. 204, 918–921.

Cullen, C.L., Caswell, J.L., Grahn, B.H., 2000. Intravascular lymphoma presenting as bilateral panophthalmitis and retinal detachment in a dog. J. Am. Anim. Hosp. Assoc. 36, 337–342.

Bush, W.W., Throop, J.L., McManus, P.M., et al., 2003. Intravascular lymphoma involving the central and peripheral nervous systems in a dog. J. Am. Anim. Hosp. Assoc. 39, 90–96.

McDonough, S.P., Van Winkle, T.J., Valentine, B.A., et al., 2002. Clinicopathological and immunophenotypical features of canine intravascular lymphoma (malignant angioendotheliomatosis). J. Comp. Pathol. 126, 277–288.

Affolter, V.K., Moore, P.F., 2002. Localized and disseminated histiocytic sarcoma of

dendritic cell origin in dogs. Vet. Pathol. 39, 74–83.

Naranjo, C., Dubielzig, R.R., Friedrichs, K.R., 2007. Canine ocular histiocytic sarcoma. Vet. Ophthalmol. 10, 179–185.

Moore, P.F., 1984. Systemic histiocytosis of Bernese mountain dogs. Vet. Pathol. 21, 554–563.

Moore, P.F., Rosin, A., 1986. Malignant histiocytosis of Bernese mountain dogs. Vet. Pathol. 23, 1–10.

Rosin, A., Moore, P., Dubielzig, R., 1986. Malignant histiocytosis in Bernese Mountain dogs. J. Am. Vet. Med. Assoc. 188, 1041–1045.

Brearley, M.J., Dunn, K.A., Smith, K.C., et al., 1994. Systemic histiocytosis in a Bernese mountain dog. J. Small Anim. Pract. 35, 271–274.

Paterson, S., Boydell, P., Pike, R., 1995. Systemic histiocytosis in the Bernese mountain dog. J. Small Anim. Pract. 36, 233–236.

Other ocular neoplasms

Sato, T., Yamamoto, A., Shibuya, H., et al., 2005. Intraocular peripheral nerve sheath tumor in a dog. Vet. Ophthalmol. 8, 283–286.

Zarfoss, M.K., Klauss, G., Newkirk, K., et al., 2007. Uveal Spindle Cell Tumor of Blue-Eyed Dogs: An Immunohistochemical Study. Vet. Pathol. 44, 276–284.

Feline post-traumatic ocular sarcoma

Woog, J., Albert, D.M., Gonder, J.R., et al., 1983. Osteosarcoma in a phthisical feline eye. Vet. Pathol. 20, 209–214.

Dubielzig, R.R., 1984. Ocular sarcoma following trauma in three cats. J. Am. Vet. Med. Assoc. 184, 578–581.

Dubielzig, R.R., Everitt, J., Shadduck, J.A., et al., 1990. Clinical and morphologic features of post-traumatic ocular sarcomas in cats. Vet.

Pathol. 27, 62–65.

Dubielzig, R.R., Hawkins, K.L., Toy, K.A., et al., 1994. Morphologic features of feline ocular sarcomas in 10 cats: light microscopy, ultrastructure, and immunohistochemistry. Vet. Comp. Ophthalmol. 4, 7–12.

Cullen, C.L., Haines, D.M., Jackson, M.L., et al., 1998. The use of immunohistochemistry and the polymerase chain reaction for detection of feline leukemia virus and feline sarcoma virus in six cases of feline ocular sarcoma. Vet. Ophthalmol. 1, 189–193.

Grossniklaus, H.E., Zimmerman, L.E., Kachmer, M.L., 1990. Pleomorphic adenocarcinoma of the ciliary body. Immunohistochemical

and electron microscopic features. Ophthalmology 97, 763–768.

Zeiss, C.J., Johnson, E.M., Dubielzig, R.R., 2003. Feline intraocular tumors may arise from transformation of lens epithelium. Vet. Pathol. 40, 355–362.

Carter, R.T., Giudice, C., Dubielzig, R.R., et al., 2005. Telomerase activity with concurrent loss of cell cycle regulation in feline post-traumatic ocular sarcomas. J. Comp. Pathol. 133, 235–245.

Neoplasia metastatic to the eye

Dubielzig, R.R., Grendahl, R.L., Orcutt, J.C., et al., 2002. Metastases. In: Peiffer Jr., R.L., Simons, K.B. (Eds), Ocular tumors in animals and humans. Iowa State Press, Ames, Iowa, pp. 337–378.

Ladds, P.W., Gelatt, K.N., Strafuss, A.C., et al., 1970. Canine ocular adenocarcinoma of mammary origin. J. Am. Vet. Med. Assoc. 156, 63–69.

Szymanski, C.M., 1972. Bilateral metastatic intraocular hemangiosarcoma in a dog. J. Am. Vet. Med. Assoc. 161, 803–805.

Bellhorn, R.W., 1972. Secondary ocular adenocarcinoma in three dogs and a cat. J. Am. Vet. Med. Assoc. 160, 302–307.

Carlton, W.W., 1983. Intraocular tumors. In: Peiffer Jr., R.L. (Ed.), Comparative

ophthalmic pathology. Charles C. Thomas, Springfield, pp. 289–298.

Render, J.A., Carlton, W.W., Vestre, W.A., et al., 1982. Osteosarcoma metastatic to the globes in a dog. Vet. Pathol. 19, 323–326.

Schmidt, R.E., 1981. Transitional cell carcinoma metastatic to the eye of a dog. Vet. Pathol. 18, 832–834.

Szymanski, C., Boyce, R., Wyman, M., 1984. Transitional cell carcinoma of the urethra metastatic to the eyes in a dog. J. Am. Vet. Med. Assoc. 185, 1003–1004.

Lavach, J.D., 1984. Disseminated neoplasia presenting with ocular signs: a report of two cases. J. Am. Anim. Hosp. Assoc. 20, 459–462.

HogenEsch, H., Whiteley, H.E., Vicini, D.S., et al., 1987. Seminoma with metastases in

the eyes and the brain in a dog. Vet. Pathol. 24, 278–280.

Nyska, A., Hermalin, A., Jacobson, B., et al., 1992. Intraocular vascular embolization of a malignant canine pheochromocytoma. Prog. Vet. Comp. Ophthalmol. 2, 129–132.

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Habin, D.J., Else, R.W., 1995. Parotid salivary gland adenocarcinoma with bilateral ocular and osseous metastases in a dog. J. Small Anim. Pract. 36, 445–449.

Ferreira, A.J., Jaggy, A., Varejao, A.P.,

et al., 2000. Brain and ocular metastases from a transmissible venereal tumour in a dog. J. Small Anim. Pract. 41, 165– 168.

Pereira, J.S., Silva, A.B., Martins, A.L., et al., 2000. Immunohistochemical characterization of intraocular metastasis of a canine transmissible venereal tumor. Vet. Ophthalmol. 3, 43–47.

Esson, D., Fahrer, C.S., Zarfoss, M.K., et al., 2007. Suspected uveal metastasis of a nail

322

bed melanoma in a dog. Vet. Ophthalmol. 10, 262–266.

Extraskeletal osteosarcoma and chondrosarcoma

Patnaik, A.K., 1990. Canine extraskeletal osteosarcoma and chondrosarcoma: a clinicopathologic study of 14 cases. Vet. Pathol. 27, 46–55.

Hayden, D.W., 1976. Squamous cell carcinoma in a cat with intraocular and orbital metastases. Vet. Pathol. 13, 332–336.

Murphy, C.J., Canton, D.C., Bellhorn, R.W.,

et al., 1989. Disseminated adenocarcinoma with ocular involvement in a cat. J. Am. Vet. Med. Assoc. 195, 488–491.

Hamilton, H.B., Severin, G.A., Nold, J., 1984. Pulmonary squamous cell carcinoma with intraocular metastasis in a cat. J. Am. Vet. Med. Assoc. 185, 307–309.

Cook, C.S., Peiffer Jr., R.L., Stine, P.E., 1984. Metastatic ocular squamous cell carcinoma in a cat. J. Am. Vet. Med. Assoc. 185, 1547–1549.

Gionfriddo, J.R., Fix, A.S., Niyo, Y., et al., 1990. Ocular manifestations of a metastatic pulmonary adenocarcinoma in a cat. J. Am. Vet. Med. Assoc. 197, 372–374.

Cassotis, N.J., Dubielzig, R.R., Gilger, B.C., et al., 1999. Angioinvasive pulmonary

carcinoma with posterior segment metastasis in four cats. Vet. Ophthalmol. 2, 125–131.

10

Chapter 10

Diseases of the Lens

CHAPTER CONTENTS

 

Normal anatomy

323

Congenital or hereditary conditions

323

Posterior lenticonus/lentiglobus

323

Aphakia, microphakia, lens coloboma

324

Congenital cataract

324

Cataract

327

Cataract categorized by the extent of disease

327

Cortical cataract, the opacification of the lens

 

fiber

328

Subcapsular cataract, opacification and metaplasia

 

of the lens epithelial cell

328

Inherited cataract in dogs

328

Age-related cataract

328

Secondary cataract

329

Lens protein breakdown or lens capsule rupture

 

and its significance in inflammatory eye disease

330

Morphologic features suggesting pathologic lens

 

capsule rupture

330

Phacolytic uveitis (lens-induced uveitis)

330

Phacoclastic uveitis

330

Septic implantation syndrome

335

Phacoclastic uveitis in rabbits associated with the

 

microsporidium, Encephalitozoon cuniculi

335

The lens epithelium and its role in disease after lens

 

capsule rupture

337

Lens luxation

339

Subluxation

339

Anterior luxation

339

Posterior luxation

339

Detecting pre-existing lens luxation in the

 

enucleated globe

339

Vision-threatening consequences of lens luxation

339

Causes of secondary lens luxation include

341

Breed-related zonular ligament dysplasia as a risk

 

factor for canine primary lens luxation

341

NORMAL ANATOMY (Fig. 10.1)

The lens has only one cell type, the lens epithelial cell

At all stages of lens development, except embryonic, normal lens epithelial cells are only present anteriorly, where they form a monolayer of cuboidal epithelium (Chapter 3 provides a more detailed discussion of lens development)

At the lens equator, the lens epithelial cell elongates, rotates and is pushed inward. The cell then continues to elongate until the anterior and posterior tips of each lens fiber reach opposite poles of the lens. The fully differentiated lens fiber cells lose their nuclei and become compacted towards the center of the lens, as new fibers continue to form throughout life

The lens is surrounded by a thick capsule which represents the basement membrane of the lens epithelium. Throughout life, the anterior lens capsule continues to thicken while the posterior capsule remains thin, since there are no lens epithelial cells at the posterior pole

In mammals, the lens is held in place on the anterior vitreous face by a combination of the gentle pressure exerted from behind by the vitreous body, and the tension of zonular ligaments that suspend the lens circumferentially. These zonules are secreted by the ciliary epithelium and insert in a crossover pattern onto the equatorial lens capsule.

Comparative Comments

The lens is a simple structure histologically and in the human generally conforms to the description given for the lens in other species

The remarkable complexity of the lens is hidden at the molecular and functional levels.

CONGENITAL OR HEREDITARY CONDITIONS

(see Ch. 3)

Posterior lenticonus/lentiglobus (Fig. 10.2)

Posterior lenticonus or lentiglobus is characterized by the localized axial elongation and increased curvature of the

323

Veterinary Ocular Pathology

 

 

 

Figure 10.1  The normal lens. (A) Gross

 

 

 

photograph of normal canine lens in

 

 

 

place in situ. (B) Photomicrograph of the

 

 

 

anterior pole of a Davidson’s-fixed canine

 

 

 

lens showing crisp outlines of individual

 

 

 

lens fibers. (C) Photomicrograph of

 

 

 

canine lens showing the equatorial lens

 

 

 

nuclear bow. Cuboidal lens epithelial

 

 

 

cells from the anterior pole first elongate,

A

B

 

rotate and then become incorporated

 

into the lens cortex (arrow). (D)

 

 

 

 

 

 

Photomicrograph showing the posterior

 

 

 

pole and posterior suture (*) of a canine

 

 

 

lens in a Davidson’s-fixed specimen. (E)

 

 

 

Gross photograph of a canine globe

 

 

 

sectioned across the equator and

 

 

 

postfixed in acetic acid to make the

 

 

 

zonular ligaments more opaque. The

 

 

 

photograph shows the distribution of

 

 

*

zonular fibers. (F) Photomicrograph of

 

 

the lens equator showing remnants of

 

 

 

 

 

 

zonular ligament fibers (arrow).

C

D

 

 

E F

posterior lens, leading to a conical or spherical protrusion of the posterior pole of the lens

Stretching, thinning or discontinuity of the posterior capsule are frequent findings in posterior lenticonus/lentiglobus.

Aphakia, microphakia, lens coloboma (Fig. 10.3)

Congenital absence of the lens, an abnormally small lens, or an irregular lens shape may result from developmental abnormalities affecting the orientation, induction and separation of the lens vesicle. Microphakia and irregularities of lens shape can be seen alone or, more often, as a part of a syndrome of developmental abnormalities involving the anterior segment of the globe

Diffuse or focal lack of zonular tension at the lens equator may result in spherophakia or so-called lens coloboma respectively. These abnormalities in lens shape probably do not represent primary abnormalities in lens development, rather they are associated with anterior segment developmental abnormalities that affect the ciliary processes and zonular integrity.

324

Congenital cataract (Figs 10.4, 10.5)

Morphologic features which typify congenital cataract include:

Cataractous changes in the lens nucleus characterized by an abnormal position of the nucleus or lysis of the nucleus

Abnormal relationship between the epithelium and lens capsule such as duplication, wrinkling, or segmental changes

Posterior migration of lens epithelial cells

Vascular or pigmented structures adherent to the lens capsule might indicate a cataract associated with

abnormal development of the fetal vasculature (persistent pupillary membranes, persistent hyperplastic primary vitreous, or persistent hyperplastic tunica vasculosa lentis)

Congenital cataract and associated ocular abnormalities, that may include microphthalmia syndromes and abnormalities in the fetal hyaloid vasculature, are described in detail in Chapter 3.

Diseases of the Lens Chapter 10

Figure 10.2  Lenticonus. (A) Siberian Husky, 18 months old: the arrows delineate the area of posterior lenticonus. (B) Newfoundland, 1 year old: the dark irregular circle represents the area of lenticonus. Radiating cortical opacities and water vacuoles (arrow) are also present at the lens equator. (C) Low magnification photomicrograph of an equine eye showing posterior lenticonus. (D,E) Photomicrographs of the posterior

pole from the same eye as (C) showing a complex relationship between the lens capsule and the proliferating lens epithelium. In (E), the lens epithelium has undergone spindle cell metaplasia (arrow) and collagen deposition (*).

A B

C

*

D E

325

Veterinary Ocular Pathology

 

 

Figure 10.3  Developmental problems of

 

 

the lens. (A) Dachshund, 4 months old:

 

 

in addition to being small, the lens was

 

 

also rounder than normal (spherophakic).

 

 

The ciliary processes with zonular fibers

 

 

can be seen at both arrows. (B) German

 

 

Shepherd Dog, 6 months old: the small

 

 

round lens luxated totally into the

 

 

anterior chamber, resulting in corneal

 

 

edema. (C) Gross photograph of a canine

 

 

globe with microphakia. (D)

 

 

Photomicrograph of an equine globe

 

 

with microphakia. (E) Bouin’s-fixed ferret

 

 

globe with lens coloboma. (F) Gross

 

 

photograph of canine globe with

A

B

microphakia and posterior capsular

rupture. Opaque lens proteins exude into

 

 

the vitreous (*).

C D

*

E F

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Diseases of the Lens

Chapter

 

 

10

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure 10.4  Congenital and early onset

 

 

 

cataract, clinical. (A) Labrador Retriever,

 

 

 

10 weeks old: posterior capsular and

 

 

 

cortical opacity resulted from the

 

 

 

 

 

 

persistent hyaloid artery and its

 

 

 

 

 

 

branching vessels, persistent hyperplastic

 

 

 

tunica vascularis lentis (arrow). (B) Great

 

 

 

Dane, 8 weeks old: multiple persistent

 

 

 

pupillary membranes attached to the

 

 

 

axial anterior lens creating an anterior

 

 

 

capsular opacity. (C) Boston Terrier, 3.5

 

 

 

months old: the diffuse nuclear opacity

 

 

 

with clear cortex was present in both

 

 

 

eyes. (D) Bassett Hound, 3 years old: the

 

 

 

lens nucleus is totally opaque with

 

 

 

 

 

 

diffuse cortical opacities. The lens has an

 

 

 

irregular shape (coloboma). Fine zonular

 

A

B

fibers are present only segmentally

 

 

 

 

 

 

(arrow).

 

 

 

 

C D

Comparative Comments

In man, as in animals, in addition to the congenital and hereditary abnormalities, primary aphakia with complete failure of lens formation has been reported in rare instances. More commonly, a small or incompletely formed lens, giving the clinical impression of aphakia, has been observed

Other congenital abnormalities that are also seen the human lens include conditions of imperfect or delayed lens-corneal separation, anterior lenticonus, and spherophakia. In the latter condition, the lens is relatively more rounded than normal and usually smaller (microphakic)

An important congenital condition in humans is rubella cataract, which occurs in the fetus if the mother is exposed to rubella virus during the first or second trimester of pregnancy. Rubella virus may be cultured from surgically removed lenses

Although tumors of the lens do not occur in humans, the lens anlage has been reported to develop aberrantly in the lower lid, in a condition known as phakomatous choristoma.

CATARACT

Cataract is the pathological opacification of the lens including its capsule

Cataract may be categorized according to extent of lens involvement, location within the lens, or etiopathogenesis.

Cataract categorized by the extent of disease (Figs 10.6–10.10)

Incipient cataracts involve less than 15% of the lens

Immature cataracts affect more than 15% of the lens but lens involvement is incomplete and they do not completely obscure the fundus reflection

Mature cataracts affect the lens cortex circumferentially and completely obstruct visualization of the fundus reflection

Hypermature cataracts show evidence of lens shrinkage, such as lens capsule wrinkling, associated with leakage and resorption of altered cortical lens proteins.

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Veterinary Ocular Pathology

 

 

Figure 10.5  Congenital cataract,

 

 

pathology. (A) Low magnification

 

 

photomicrograph of a dog lens with

 

 

congenital cataract. The cataractous

 

 

changes are predominantly nuclear. The

 

 

posterior pole and the equatorial cortex

 

 

remain near normal (arrow). (B) Low

 

 

magnification photomicrograph showing

 

 

a focal dysplastic and wrinkled lens

 

 

capsule (arrow). (C) The same focus as

 

 

(B) with higher magnification showing

 

 

the relationship between the duplicated

A

B

lens capsule and the lens epithelium.

(D,E) Two photomicrographs of the

 

 

anterior poles of two lenses showing

 

 

duplications in the lens capsule and lens

 

 

epithelium in canine congenital cataracts.

D

C E

Cortical cataract, the opacification of the lens fiber (Fig. 10.11)

There is not a perfect correlation between the clinical observation of lens opacity and a histologically observable morphologic change in the lens cortex

Many changes in the lens protein can represent either genuine pathology or artifact of processing. Therefore, it may be impossible to determine the significance of observed morphologic changes

Reliable morphologic indicators of cortical cataract include:

Bladder cells: swollen, rounded lens fibers that still contain a nucleus

Morgagnian globules: swollen, rounded lens fibers with no nucleus

Lens mineralization may occur in long-standing cataracts.

Subcapsular cataract, opacification and metaplasia of the lens epithelial cell (Fig. 10.12)

Normal lens epithelial cells are positioned immediately adjacent to the lens capsule and their tropism for the lens capsule is seldom altered in disease states

In subcapsular cataract the opacity is directly related to abnormalities of the lens epithelial cells

Morphologic features of subcapsular cataract include:

Proliferation of lens epithelial cells to form a localized aggregate

Metaplasia, involving a change in the cells from an epithelial phenotype to a mesenchymal phenotype more characteristic of a myofibroblast

328

Secretion of collagen around the metaplastic lens epithelial cells

Loss of the lens epithelial cells leaving behind cell-free collagen matrix

Mineralization.

Inherited cataract in dogs

Inherited cataract is very common in the purebred canine population. An inherited basis for cataract development is proven or suspected in over 100 canine breeds, of which many appear to demonstrate complex patterns of inheritance. In some canine breeds, a genetic basis for cataract development has been clearly established, e.g. mutations in the HSF4 gene are associated with early-onset cataract in several breeds, including the Staffordshire bull terrier and Boston Terrier

Clinical phenotype is highly variable between and within affected breeds. This variability may result from the influence of multiple genes and other metabolic and environmental factors.

Age-related cataract

Cataracts are a common feature of senescence in most species

Senile cataracts should be distinguished, both clinically and histomorphologically, from the normal process of nuclear sclerosis which is not associated with true lens opacity

In nuclear sclerosis, the density of the lens nucleus increases with age as older lens fibers are progressively tightly packed centrally and take on a more homogeneous in appearance, as new cortical fibers are formed more peripherally.

Diseases of the Lens Chapter 10

Figure 10.6  Incipient cataracts, clinical.

(A) Siberian Husky, 10 months old: feathering along the posterior cortical suture lines (arrow) was present in both lenses. (B) Cavalier King Charles Spaniel, 8 weeks old: the equatorial cortex was overhydrated (arrow) in this immature cataract. This overhydration cleared in the adult. (C) Golden Retriever, 3 years old: the posterior cortical suture is opaque as was the axial subcapsular cortex surrounding the suture line. (D) Italian Greyhound, 5 years old: equatorial cortical water vacuoles are present (arrow). The opacity at 10 o’clock represents vitreous degeneration.

A B

C D

Secondary cataract

Cataract may occur secondary to other intraocular disease; such as uveitis, glaucoma, neoplasia or advanced retinal degeneration; or as a result of trauma, electrocution, nutritional imbalance, exposure to toxins or metabolic disease, such as diabetes mellitus.

Metabolic cataract is recognized in almost all diabetic dogs (Fig. 10.10)

Diabetic dogs are far more likely to develop cortical cataract because of the conversion of glucose to sorbitol within the lens cells and the resulting influx of water

Diabetic cataracts often develop rapidly and can lead to serious inflammatory changes if the lens capsule ruptures (see below) or to secondary glaucoma caused by lens swelling (intumescent cataract)

The diabetic state can also contribute to complications following cataract surgery

In general, however, substantial differences in postoperative outcomes are not apparent compared to non-diabetic dogs

Although diabetic cataracts are usually cortical cataracts, there are no specific morphologic features which allow a diabetic

cataract to be distinguished from any other cortical cataract morphologically

Although diabetes mellitus is fairly common in cats and humans, diabetic cataract is not common in these species

The lower incidence of diabetic cataract in cats may relate to lower levels of activity of the enzyme aldose reductase in the lens of older cats, compared to dogs.

Comparative Comments

The types of cataracts occurring in humans and other species appear to be extremely similar, although they have been further subdivided into a greater number of types in humans

An extremely interesting entity is the exfoliation syndrome, also known as pseudoexfoliation, in which a fibrillary protein-like material is deposited on the anterior lens capsule

The major systemic disorders associated with cataract development in humans are diabetes mellitus, galactosemia, hypercupremia, Fabry disease and Down syndrome

Numerous drugs give rise to cataracts in humans, the most common being corticosteroids.

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