The size of the nearly round to oval cornea (vertical/horizontal) varies by animal species: dog (8.5 × 9.5 mm), cat (8.4 × 8.9 mm), horse (16.6 × 17.9 mm), and cow (15.2 × 16.4 mm). The animal cornea consists of the superficial epithelium and basement membrane, large and relatively acellular stroma, deeper Descemet membrane, and deep single layer endothelium. The cornea maintains a strong and durable barrier between the eye and environment, as well as a transparent medium to permit passage of light and images into the posterior segment. Corneal diseases are common in most animal species and fortunately can be treated successfully by medical, surgical, or a combination of these methods. The accessibility of the cornea permits several detailed and noninvasive diagnostic techniques.
Superficial keratitis is common in all species and is characterized by corneal vascularization and opacification, which may be due to edema, cellular infiltrates, pigmentation, or fibroplasia. If ulceration is present, pain—manifest by epiphora and blepharospasm—is an outstanding sign. Unilateral keratitis frequently is traumatic in origin. Mechanical factors, such as lid conformational defects and foreign bodies, should always be eliminated as possible causes, because improvement will not occur until they are resolved. Ulcerative keratitis may be complicated by secondary invasion by bacteria and, in horses, by saprophytic fungi. Bilateral superficial keratitis may be immune-mediated or associated with a lack of tears, eyelid conformational defects, or infectious agents.
Pannus, or Uberreiter disease, is a specific, bilateral, progressive, proliferative, chronic, superficial keratitis that begins laterally and/or medially at the limbus and eventually extends from all quadrants to cover the cornea. Inflammatory cells (lymphocytes and plasma cells) infiltrate the cornea from the limbus, accompanied by superficial blood vessels. This immune-mediated keratitis is common in German Shepherds, Belgian Tervurens, Border Collies, Greyhounds, Siberian Huskies, and Australian Shepherds. Specific therapy consists of topical antibiotics, antiviral or antimycotic agents when appropriate, removal of any mechanical irritants, tear replacement when deficient, and corticosteroids or cyclosporin A (or both) when immune-mediated. The latter may need to be continued indefinitely and the frequency varied depending on the response. Chronic superficial keratitis when immune-mediated is a lifelong disease, requiring lifelong topical anti-inflammatory therapy. The disease appears more aggressive in young dogs and in dogs that live outside in higher altitudes. Generally, topical 1% prednisolone, 0.1% dexamethasone, or 0.2%–1% cyclosporine instilled in both eyes bid-qid is sufficient to control the disease and prolong vision. The intensity of the inflammatory response in both eyes is quite variable and may change by age, season, amount of time the dog spends outside, and other factors. To minimize costs and adverse effects, but control the disease, topical therapy is adjusted to the individual animal (topical therapy ranges from one drop in the affected eye every other day to as frequent as one drop in the affected eyes qid).
Interstitial keratitis is a deep involvement of the corneal stroma that represents one of the clinical signs associated with all chronic and many acute cases of anterior uveitis. The corneal vascularization is less branching, finer, and deeper than in superficial keratitis; if the endothelium has been disrupted, corneal edema is often marked. Systemic diseases, such as infectious canine hepatitis, bovine malignant catarrhal fever, systemic mycoses in many species, and neonatal septicemias that localize in the eye, can cause bilateral or unilateral interstitial keratitis. Therapy is directed at the anterior uveitis, the systemic infection, or both. A specific, nonulcerative, peripheral, stromal keratitis and persistent anterior uveitis (keratouveitis) occurs in horses; prognosis and response to treatment are poor.
Ulcerative keratitis may be divided based on onset, depth, and position within the cornea. Ulcerative keratitis (based on depth) may be superficial, deep, deep with descemetocele, or perforating. Progression of the corneal ulcer is based on the microbes involved and on the release of microbe and tissue enzymes that digest the corneal stroma. Pain, corneal irregularity, edema, and eventually vascularization are signs of ulceration. A dense, white infiltrate at the ulcer margin indicates strong leukotaxis and bacterial involvement. To detect small ulcers, topical fluorescein may be required. In dogs and horses, most ulcers are mechanical in origin; in cattle, sheep, goats, cats, and reindeer, infectious agents and mechanical causes are important; in cats and horses, herpesvirus infection is a frequent cause. All ulcers have the potential for secondary bacterial contamination as well as endogenous proteinase “melting” of the stroma. Therapy for superficial ulcers is usually medical and consists of topical broad-spectrum antibiotic(s) administered 3–6 times daily, correction of any mechanical factors, and limited 1% topical atropine to maintain iridocycloplegia and reduction of ocular pain. Adverse effects of atropine-induced reduced tear production in all species and colic in horses must be considered. Antiproteinase therapy for melting stromal ulcers includes topical serum and other drugs, and for acute ulcerations they may be instilled 4–6 times daily for the first several days. Corneal healing is monitored by frequent clinical examinations and gradual reduction in the size of the fluorescein retention by the nonepithelialized ulcer.
Syndromes of very slow-healing and recurrent superficial ulcers occur in dogs, cats, and horses; in dogs, they may be due to basement membrane disease causing faulty attachment of the corneal epithelium, whereas in cats and horses, and recently in dogs, herpesvirus should be suspected. Initial therapy is ulcer debridement followed by topical antibiotics and atropine. For refractory cases in dogs, multiple punctures or cross-hatching (punctate and grid keratotomies) of affected corneas with a 22-gauge needle stimulates most indolent ulcers to heal within 7–10 days. Early reports suggest these keratotomies in cats may predispose to corneal sequestration and should be used with great care. Nictitating membrane flaps (or soft contact lenses or collagen shields) act as a pressure bandage and often are therapeutic for shallow ulcers. Medical treatment of deep ulcers is similar to that of superficial ulcers, but many deep ulcers also require conjunctival grafts to strengthen and maintain the integrity of the cornea.
Corneal sequestration and keratitis appear to be unique to the cat. It occurs in all breeds of cats but may be more frequent in the Siamese, Persian, and Himalayan breeds. Initially, a very small dark area develops within the anterior stroma and under intact corneal epithelium (that stains with rose Bengel and occasionally very faintly with topical fluorescein). Eventually, the stromal spot becomes larger and either dark brown or black, and is not covered by epithelium. There is variable pain and a central to paracentral, brown to black opacity composed of necrotic stroma, vascularization, and surrounding inflammation. Spontaneous extrusion may occur, especially with superficial sequestra. Treatment consists of superficial keratectomy of the entire sequestrum, that, with deeper lesions, is covered with conjunctival grafts.
Corneal stromal abscesses in horses may be sequelae of healing corneal ulcers or defects and the trapping of bacteria or fungal organisms (or both) within the stroma after reepithelialization. Recently, fungi (both Candida and Aspergillus) have been demonstrated in horses' subepithelial cornea devoid of iridocyclitis, suggesting another mode of entry. A variable, white to yellow, stromal infiltrate is surrounded by an intense stromal keratitis and vascularization and a variable but sometimes intense anterior uveitis. At least seven to nine different species of fungi have been isolated in corneal ulcers and stromal abscesses in horses, but Aspergillus and Fusarium spp are the most frequent isolates. Treatment consists of intensive topical and occasional systemic antibiotics (and if indicated, antifungals), iridocycloplegics, NSAIDs, and often surgical removal of the abscess with conjunctival and tectonic corneal grafts.
Corneal dystrophies and degenerations occur frequently in dogs, infrequently in cats, and rarely in horses. Corneal dystrophies are bilateral and often thought inherited in dogs. The appearance of these two diseases may be divided into the following categories: 1) part of cornea affected (epithelium, stroma [anterior, middle, and deep], and endothelium), 2) area of the involved cornea (central, paracentral, and limbal), and 3) possible cause (primary/inherited or secondary). Corneal dystrophies may affect the epithelium and endothelium but appear clinically to involve the stroma most frequently. The corneal degenerations are secondary to other ocular disease or systemic conditions.
Corneal dystrophies affecting the epithelium are associated with recurrent corneal erosions in dogs. The defective corneal epithelium fails to normally adhere to its defective basement membrane and results in recurrent superficial erosions (more frequent in the Boxer breed) and prolonged healing.
The stromal dystrophies appear as white, irregular deposits within the different depths of the stroma and are sometimes labeled corneal lipidosis. Corneal dystrophies are most frequent in dogs, appear inherited in ~20 breeds, affect mostly the corneal stroma, and are usually bilateral. Of the breeds affected, the Siberian Husky corneal stromal dystrophy has been investigated in the greatest detail. Most often, the corneal opacities consist of triglycerides and both intracellular and extracellular cholesterol. Treatment is not usually necessary unless vision is impaired or the deposits become irritating. For these lipid deposits to be viewed histologically, the corneas must be processed as frozen sections and alcohol dehydration processing avoided.
The corneal endothelial dystrophies occur in dogs and rarely in cats (Manx breed). In dogs, it primarily affects older Boston Terriers, Chihuahuas, and Dachshunds.
Female Boston Terriers are affected more frequently than males (with a mean age of ~7.5 yr), and this breed's disease has both clinical and histopathology similarities to those of Fuch corneal endothelial dystrophy in people. With the dystrophic and degenerating endothelium, progressive but painless bilateral corneal edema develops starting centrally. With extensive and full-thickness corneal edema, corneal epithelial bullae may develop and are quite painful. Treatment of early cases before complete corneal involvement consists of topical hyperosmotics (2%–5% sodium chloride or 40% glucose) applied frequently and, for advanced cases, thermokeratoplasty (Salaras procedure) or full-thickness (penetrating) keratoplasty.
Corneal degenerations are often unilateral and usually secondary to ocular or systemic diseases. Deposits of triglycerides, cholesterol, and also calcium are present in corneal degenerations. Corneal degeneration may be associated with other ocular diseases, such as corneal ulcerations, phthisis bulbus, lagophthalmos, and prolonged NSAID therapy. If associated with hyperlipoproteinemias or hypercholesterolemia and high-fat diets, corneal degenerations can affect both eyes, and these deposits are usually associated with corneal vascularization. They also can be altered by significant changes in diet. Baby rabbits or puppies fed whole cow milk may develop extensive lipid deposits in the corneal stroma sufficient to impair vision. Treatment for most corneal degenerations is not usually necessary, unless related to dietary or systemic diseases.