Diseases of the canine cornea

Ulcerative keratitis/corneal ulcer is commonly used as the diagnosis of any disruptment of the corneal epithelium, which leads to a staining with fluorescein. A corneal ulcer may be differentiated from corneal abrasion, which is disruption of epithelial cells , but not denuding the corneal hydrophillic stroma. The depth of a corneal ulceration may be determined by slit-lamp biomicroscopy and divided into three categories (Schmidt 1977):

· erosion : only corneal epithelium is involved

· superficial ulcer : involving epithelium and no more than 3/4 of the stroma

· deep ulcer : involving more than 3/4 of the stroma including descemetoceles, staphylomas and corneal lacerations.

The location of the ulcer may help in the prediction of the underlying cause of the ulcer, as a central oval ulcer frequently is caused by lagophthalmos, and lesions in the periphery of the cornea are caused by entropion, ectropion or distichiasis (Schmidt 1977). Infected ulcers usually show marked conjunctival hyperaemia and the ulcer bed is cloudy gray or yellow (Kirschner 1990).

Bacterial keratitis in the canine is usually secondary to a primary disease, as most bacteria cannot invade an intact, healthy cornea with a normal tear production. A defect in the corneal epithelium causes hydration of the corneal stroma, resulting in a slight corneal edema. The corneal edema in corneal ulcers has decreased long before the thickness of the stroma has been regained (Bolliger et al 1997). In the normal healthy canine cornea there are no blood vessels (Spreull 1966). Neovascularization of the cornea can occur in diseases of the cornea. Shortly after ulceration of the cornea, leukocytes invade the ulcer; these cells mainly invade via the tear film as the cornea is non-vascular. Experiments in neovascularization of the cornea have proven that a leukocyt-infiltration as well as Prostaglandin E1 are important angiogenic factors (Klintworth and Burger 1983), which may be inhibited by anti-inflammatory agents. Dendritic vessels typically accompany superficial disease, and straight parallel vessels indicate deep corneal vascularization. Vessels invade the cornea no faster than 1mm/day (Nasisse 1985). In the healing process of the corneal stroma, secreted collagen remodels, but will never regain the original fibrillar organization (Kern 1990), thus a scarrification will be present. If the stromal ulcer was deep the healing may result in a permanent depression, a facet (Spreull 1966) Epithelial wounds extending beyond the limbus will be re-epitheliazed by the conjunctival epithelium (Kern 1990). After re-epithelialization topically administered corticosteroids may decrease scarrification of the cornea (Nassise 1985). Atropine has often been added to the therapy of any corneal ulcer. It is important to recognize that atropin is utilized to counteract iris spasms (resulting in anterior uveitis) and has no analgesic action. Atropine decreases tear flow, which is not desirable in healing of the cornea, so atropin should only be used where there is evidence of corneal penetration (eg. thorn) or anterior uveitis ( flare and/or cells) (Vierheller 1981). Hypopyon is produced by the action of toxins and is due the the presence of toxins in the anterior chamber; hypopyon is thus usually bacteriologically sterile (Holt 1966).

Corneal Dystrophies

Epithelial dystrophy

Several breeds (most often Boxers) may have superficial erosions of the corneal epithelium, caused by epithelial basement disease (Cooley and Dice 1990). Treatment is currently grid- keratotomy, multiple-punctate keratotomy or a superficial keratectomy (Stanley et al 1998). In the Shetland Sheepdog superficial grey or white irregular rings have been observed on the cornea (Cooley and Dice 1990), in these dogs STT-values of 10-12mm/min were observed together with decreased BUT (Tear break-up time). .

Corneal dystrophy (Stromal) The lesion which is grey-white or silver, almost metallic, is often bilateral and symmetric (Crispin and Barnett 1983). The shape is typically oval, with the lesion being sub-epithelial with intact epithelium overlying the lesion (Crispin and Barnett 1983); no vascularization, inflammation or pigmentation is present. Histopathology showed predominance of extracellular crystals and lipid droplets (Crispin and Barnett 1983). Corneal dystrophies may have a high degree of inheritance in the canine as a study in Crystalline Corneal Dystrophy in the Siberian Husky (Waring and MacMillan 1986) proved. In this study all puppies were affected as the result of breeding affected x affected adults, concluding that the corneal dystrophy was recessively inherited. Corneal Endothelial Dystrophy This disease is a chronic degeneration of the corneal endothelium resulting in a progressive corneal edema, for which to date only corneal transplantation has been a successive therapy (Gwin et al 1982). An endothelial dystrophy has been reported in Boston Terriers, Chihuahua, wire-haired terrier, Dachshound, poodle and boxer (Gwin et al 1982). A type of posterior polymorphous dystrophy has been observed in the American Cocker Spaniel (Cooley and Dice 1990).

Chronic Superficial Keratitis (CSK, Pannus) Chronic Superficial Keratitis (CSK) is most often seen in the German Shepherd Dog, thus having the synonym, German Shepherd Pannus. CSK is easily diagnosed, having patognomonic symptoms. CSK is a chronic inflammation of the cornea, with cellular infiltration and vascularization progressing into granulation tissue replacement, and an end stage of heavily pigmented cornea with loss of vision (Slatter et al 1977, Clerc 1996). Often the owner will notice a deficiency in the dog's inferior fields if the lower two-thirds of the cornea is affected. The temporal (lateral) quadrants of the cornea are mostly affected in the early stages (Slatter et al 1977). The aetiology of CSK has still not been revealed, although factors of importance to the pathogenesis have been established. Slatter et al (1977) found 463 cases of Überreiter's Syndrome in dogs in the Rocky Mountain area and found 95,3% of the dogs living in altitudes over 4500ft (1372m). This indicated a higher altitude with a higher amount of UV-exposure to be a factor. Slatter et al (1977) found the breeds German Shapherd, Siberian Husky, Scotch Collie, Greyhound and Border Collie to be predisposed to CSK. Clerc (1996) found Belgian Shepherd dogs to be predisposed as well. The disease in German Shepherds occurs most frequently during the 4th year of life and gradually decreases thereafter (Slatter et al 1977). The prognosis was best for dogs older than 5 years old with slowly progressing lesions (Slatter et al 1977). Campbell et al (1975) found CSK-affected dogs to have significant increases in hypersensitivity cellular responses against corneal and iris antigens. Campbell and Synder (1973) didn't succeed in isolating and diagnosing Chlamydia as an infective agent involved in CSK in four German Shepherd dogs with CSK. Überreiter et al (1971) didn't find Chlamydia to be involved in CSK, also finding that no infectious agent is involved in the syndrom after injecting diseased corneal material (from CSK-corneas) into the conjunctiva and cornea of two healthy dogs. Petrick and Van Rensburg (1989) found that German Shepherds have thinner layers of corneal epithelium than other breeds and a looser structure of the substantia propria, indicating breed predisposing factors to CSK. Immunohistological examination of corneas from CSK-affected dogs showed increased amounts of Ig but no antibodies against epithelial cell structures, indicating that CSK is not an auto-immune disease of the pemphigus group, but may well be an immune-mediated disease (Eichenbaum et al 1986). The evidence of CSK responding well to steroid (Clerc 1996, Überreiter et al1971) and cyclosporine (Bigelbach 1993, Jackson et al 1991) treatment further supports the aetiology being immune-mediated; with a strong breed predisposition and exaberated by UV-exposure. Although other types of treatment including superficial keratectomies, beta irradiation and sub-conjunctival injections of corticosteroids (Slatter et al 1977) have been used in the past, topical steroids and/or cyclosporine is usually the choice of treatment, leaving superficial keratectomies as the last choice of treatment. CSK occurs frequently in association (approximately one in five cases) with lymphoplasmacytic infiltration of the third eyelid (Clerc 1996).

This page was authored by T. F. Evans October 2000.