Corneal Disease

Corneal Disease

Photo: iStock

Editor's Note: This article was revised by the author to reflect new and updated information in November 2017.

Corneal diseases can range from minor annoyances to serious problems resulting in blindness

Corneal diseases are collectively termed keratopathies. Keratopathies can be ulcerated or non-ulcerated, and infected or non-infected. Keratopathies can be rather benign diseases, or can be so severe that they result in corneal scarring and blindness if not properly diagnosed and treated.

Corneal Lacerations/Perforations

Ocular eye trauma can vary widely. Trauma from whips, nails, buckets, light fixtures, plants, and tree branches can result in corneal/scleral lacerations.

Corneal lacerations in the horse are always accompanied by varying degrees of iridocyclitis (inflammation of the iris and ciliary body, also called anterior uveitis). The eye might be cloudy, red, and painful, and squinting and tearing are present with focal (localized) or generalized corneal edema (swelling). Slight droopiness of the eyelashes of the upper eyelid could be a subtle sign of corneal ulceration.

Full-thickness corneal/scleral perforations are usually associated with iris prolapse, a shallow anterior chamber, and hyphema (hemorrhage within the anterior chamber of the eye). If the corneal lesion extends to the limbus, the sclera should be carefully checked for perforation because the scleral wound can be obscured by conjunctival swelling and hemorrhage. Failure to detect a scleral tear will result in chronic, low intraocular pressure and shrinking of the eyeball (phthisis bulbi).

Fluorescein dye staining of the cornea will reveal the laceration, and might enter the anterior chamber. Leakage of clear aqueous humor from the anterior chamber into the fluorescein-stained tear film will be seen as a clearing of the fluorescein, and that positively identifies the location of the leak.

Small corneal lacerations can heal quickly if surgical and medical therapy is instituted quickly. Larger lesions are associated with more uveitis (inflammation of the uvea) and can heal more slowly. Medical therapy is similar to that used for ulcers and should be sufficient for cases of superficial, non-perforating (not making a full-thickness hole) lacerations. Topically applied antibiotics, atropine, serum, and systemic non-steroidal anti-inflammatory drugs (NSAIDs) are recommended. Systemic NSAIDs and broad-spectrum parenteral antibiotics are also indicated for full-thickness lesions.

Deep or irregular corneal lacerations require surgical support of the cornea and more aggressive therapy for anterior uveitis and infection. Direct corneal suturing and conjunctival flaps can be done to more rapidly restore corneal integrity. Both small and large full-thickness corneal perforations should be surgically repaired. Complications include infection, iris prolapse, anterior synechia (a disease of the eye in which the iris adheres to the cornea or the capsule of the crystalline lens), cataract formation, and persistent anterior uveitis. Both small and large corneal or scleral full-thickness defects can result in phthisis bulbi (eye atrophy) if left untreated.

A horse eye with a traumatic corneal perforation such that the eye contents have extensively prolapsed, severe hemorrhage within the eye, or evidence of bacterial infection should have the affected eye removed. Septic intrusion (infection) into the eye results in painful endophthalmitis (inflammation of the eye's internal structures); such infection can spread to surrounding soft tissues and requires removal of the eye.

Corneal Foreign Bodies

A small red, raised lesion turns out to contain a foreign body. The removal of the foreign body resulted in quick healing of the lesion.

Photo: Dennis Brooks, DVM, PhD, Dipl.ACVO

Foreign bodies, such as pieces of wood, metal, insects, or dirt, in the cornea cause varying degrees of keratitis and uveitis, and are common in horses. Superficial foreign bodies can be removed under topical anesthesia and the subsequent ulcer treated medically. Deep corneal and penetrating foreign bodies can cause severe uveitis/endophthalmitis and require more aggressive care.

Burdock Pappus Bristle Keratopathy

In the northeastern United States, a bristle from the burdock pappus plant can become lodged in the horse's cornea and cause ulceration. Surgical removal of the bristle foreign body and surrounding tissue is necessary.

Endothelial Detachment Following Blunt Trauma

Profound, persistent corneal edema might be present following blunt trauma to the eye. Detachment of the endothelium is a proposed mechanism of this syndrome, and the prognosis for a return to normal eye function is poor. Hypertonic solutions (5% sodium chloride) administered topically might be beneficial in the early stages to reduce the amount of edema. Thermatokeratoplasty (a surgical technique where focal burns of the corneal epithelium allow the fluid trapped in the cornea to escape) might be necessary to reduce the edema in severe cases. Endothelial cell reattachment and cellular hypertrophy (overgrowth) might occur to resolve the condition in some horses.

Eosinophilic Keratitis

The eosinophil is a type of white blood cell that responds to allergic and parasitic stimuli. When eosinophils invade the equine cornea, a disease called eosinophilic keratitis results. This disease is associated with eyelid squinting, conjunctival swelling and redness, a mucoid (resembling mucus) tear discharge, and corneal ulcers covered by raised, white superficial plaques of dead tissue.

Signs of eosinophilic keratitis are squinting, conjunctival swelling/redness, mucoid tear discharge, and corneal ulcers covered with white, dead tissue.

Photo: Dennis Brooks, DVM, PhD, Dipl.ACVO

Diagnosis is based on clinical signs and corneal scrapings that contain numerous eosinophils and a few mast cells, lymphocytes, and plasma cells. Fungal, bacterial, allergic, parasitic, and neoplastic (new or abnormal growth of tissues) causes for this keratopathy must be considered in the diagnosis. It is possible that eosinophilic keratitis in the horse is an allergic, immune-mediated, or inflammatory result of parasitic microfilaria such as Onchocerca, but the specific cause of this disorder is not known.

Treatment can last several months. Topical corticosteroids are beneficial in the early stages, but medical therapy used in conjunction with surgery to remove the plaques significantly speeds healing. Topical antibiotics, corticosteroids, atropine, and phospholine iodide, in combination with systemic NSAIDs, can be beneficial.

Viral Keratitis

Corneal opacities, whether multiple, superficial, white, focal, or linear, with or without fluorescein dye retention, can be associated with viral keratopathy (corneal disease) in the horse. Varying amounts of eye pain, conjunctivitis, and anterior uveitis are present. Some of these lesions will retain rose bengal stain when your veterinarian is diagnosing the problem. Equine herpesvirus-2 and -5 have been cultured from some lesions. Treatment with cidofovir has been successful, but recurrence is common. Multiple horses in a herd can be affected.

Band Keratopathy

Band opacities are thin areas of Descemet's membrane and might be associated with increased intraocular pressure.

Photo: Dennis Brooks, DVM, PhD, Dipl.ACVO

Linear white "bands" can be seen in the corneas of normal horses, in horses at risk of developing glaucoma, and in horses with glaucoma. They can occur after a blunt trauma, and can be single or multiple. The bands can be any thickness, and can be connecting or solitary. They appear to be thin areas of Descemet's membrane rather than breaks in this basement membrane. Glaucoma is diagnosed when the intraocular pressure is elevated and causes multiple branching bands. 

Calcific Band Keratopathy

This is a complication of anterior uveitis. These corneal lesions appear as dense, white bands in the central cornea. When your veterinarian uses fluorescein dye for diagnosis, there might be scattered areas of dye retention.

Calcium deposition might cause pain and occur following chronic equine recurrent uveitis.

Photo: Dennis Brooks, DVM, PhD, Dipl.ACVO

In horses with calcific band keratopathy, calcium deposited in the corneal epithelial basement membrane accumulates and disrupts the epithelium to result in painful ulcers. Superficial keratectomy (removal of the outer part of the cornea) is generally necessary to remove the calcium deposits and eliminate the pain caused by the ulcers, but topically administered calcium chelating drugs that bind the calcium and help remove it from the eye can also be beneficial. Diamond burring surgery is best for this problem.

Superficial Corneal Erosions

Chronic superficial corneal ulcers (erosions) with a shiny grayish color and surprisingly faint retention of fluorescein dye are associated with a thin coating of broken-down protein on the surface of the ulcer site. These erosions are surrounded by a loose lip of epithelium, corneal blood vessels, and crystalline stromal deposits and are very slow to heal. The epithelium at the edge of the erosion is not attached to the deeper cornea. This failure to attach results in delayed healing. Blood vessels and other compounds (the "deposits") indicate slow healing. Superficial keratectomy, diamond burring, and conjunctival graft placement are the treatments of choice, as epithelial migration to cover this erosion can take months.

The etiology of these superficial erosions is unknown. I have seen them develop secondary to acute corneal ulceration from rubbing of the silicone tubing of subpalpebral lavage medication systems. These ulcers are notoriously slow to heal.

Squamous Cell Carcinoma

Squamous cell carcinoma (SCC) is the most common tumor of the eye and surrounding tissues in horses. The way the tumor grows and spreads might be related to the ultraviolet (UV) component of solar radiation, periocular (around the eye) pigmentation, and an increased genetic susceptibility to tumor formation. The UV component is the most plausible carcinogenic agent associated with SCC, as it targets the tumor suppressor gene p53 that is altered in equine SCC.

The prevalence of SCC increases with age. Draft horses have a higher prevalence, followed by Haflingers, Appaloosas and Paints, with the least prevalence found in Arabians, Thoroughbreds, and Quarter Horses. White, gray-white, and palomino hair colors predispose horses to ocular SCC.

Squamous cell carcinoma of the cornea is fairly common in older horses.

Photo: Dennis Brooks, DVM, PhD, Dipl.ACVO

The cornea, conjunctiva, and limbus are commonly affected. These tumors are generally pink, fleshy masses that are raised or flat. Diagnosis is by biopsy, and treatment selection depends on tumor location, tumor size, extent of tumor invasion, presence of vision or blindness, treatments available, and the owner's financial constraints. Untreated SCC in horses can invade local soft tissues, the bony orbit, sinuses, brain, and metastasize to regional lymph nodes, salivary glands, and the thorax.

Surgical excision of equine ocular SCC should be followed by either radiation, cryotherapy (cold therapy), hyperthermia (heat therapy), or intralesional chemotherapy to kill tumor cells not removed by surgery. Beta radiation is most beneficial in superficial SCC of the cornea and limbus following keratectomy. A CO2laser can also be used effectively on the cornea after keratectomy. Topical 5-fluorouracil (1% 5-FU three times per day) might be effective for superficial SCC. Cisplatin or carboplatin can be used for chemotherapy of SCC.

Iris Prolapse

Corneal perforation with iris prolapse (when some portion of the iris seeps out through a hole in the cornea) might follow traumatic insult to the globe or orbit, as well as infectious and non-infectious diseases of the cornea. Iris prolapse in the horse most frequently follows acute ocular trauma, particularly sharp, perforating corneal injuries or blunt injuries causing rupture of the cornea, limbus, and/or sclera. Corneal perforation can occur secondary to rapid enzymatic breakdown of stromal collagen due to infectious or non-infectious ulcerative keratitis (inflammation of the cornea).

Perforating corneal lacerations with iris prolapse that are confined to the cornea and measure 0.6 inches (15 mm) or less in length tend to have a favorable visual outcome after surgical repair. Conversely, iris prolapse with corneal lesions longer than 0.6 inches (15 mm) and extending beyond the limbus generally have a poor visual outcome and often require removal of the eye. Chances of retaining vision can also be substantially reduced if full-thickness corneal wounds are accompanied by anterior hemorrhage. Removal of the eye should be more seriously considered in cases with these clinical and surgical findings.

Perforating corneal ulcers and iris prolapse due to ulcerative keratitis that has lasted for more than two weeks, and/or iris prolapse due to melting ulcers and/or ulcers with accompanying fungal and bacterial infections, tend to have a poor visual outcome or result in eye removal in a majority of such cases.

Non-Ulcerative Keratouveitis

Non-ulcerative keratouveitis appears as a pink, non ulcerated lesion of the limbus and is suspected to be an immune-mediated disease of horses in the southeastern United States.

Photo: Dennis Brooks, DVM, PhD, Dipl.ACVO

This is an unusual corneal disease only seen in the southern United States. It is characterized by a non-ulcerated, pink-colored infiltrate involving the corneal stroma near the limbus. These pink lesions are in the peripheral cornea only. The eyes are very painful, but no ulcer is present. Signs of anterior uveitis, including severe eye pain and squinting, are very prominent. This might be an immune-mediated disease, as no organisms have been cultured from the lesion sites or noted in biopsy specimens. This is likely to be an immune-mediated keratitis.

Treatment initially consists of topically administered corticosteroids and cyclosporine A. Radiation therapy and systemic NSAIDs such as flunixin meglumine (Banamine) or phenylbutazone (Bute) might be necessary. The pain in some cases can be so severe that the eye must be surgically removed.

Immune mediated keratitis

Four forms of immune mediated keratitis have been recently described. The epithelial form is generally very faint in appearance and occurs in the central cornea. The superficial stromal form occurs under the upper eyelid. A deeper stromal form has orangish green discoloration of the stroma. These three more superficial forms of immune mediated keratitions are generally in one eye, slightly painful, and respond to topical steroid, topical nonsteroidal drugs, and topical cyclosporine. Subconjunctival cyclosporine implants can be very helpful for horses with the superficial forms of immune mediated keratitis.

The deeper endothelial form of immune mediated keratitis appears as corneal edema in one or both eyes in the early stage of the disease. The edema progresses and the eye becomes painful. Glaucoma can develop. This is a serious problem. Oral steroids are helpful but this endothelial disease is vision threatening.

Epithelial IMMK
Faint fluorescein staining of corneal abrasions in epithelial immune mediated keratitis of the central cornea are present.

Superficial IMMK
Haziness of the cornea beneath the upper lid is present in superficial immune mediated keratitis.

Deep Stromal IMMK
Corneal edema and greenish discoloration of the stroma are present in the deep stromal form of immune mediated keratitis.

Vertical corneal edema is found with endotheliitis immune mediated keratitis.

Editor's note: This is the seventh in a series of eye articles by Dr. Brooks. See the first, "Eye Anatomy and Physiology,"  at for more information on eye anatomy.


  • Brooks, D.E., Matthews A.G.: Chapter 25, Equine Ophthalmology.  In Gelatt, K.N. (ed.), Veterinary Ophthalmology, 4th ed., Blackwell Pub, Ames, IA,, pp 1165-1274, 2007.
  • Brooks DE: “Equine Ophthalmology-Made Easy- edition,  2. TetonNewMedia, Jackson Hole, WY, 2008.
  • Brooks DE: Section Editor-Ophthalmology. Blackwell’s Five-Minute Veterinary Consult: Equine. Lavoie J-P, Hinchcliff KW (eds). Wiley-Blackwell, Ames, IA, 2008
  • Gilger BC: Equine Ophthalmology, 3rd Edition. Wiley-Blackwell, Hoboken, NJ 2016.

About the Author

Dennis E. Brooks, DVM, PhD, Dipl. ACVO

Dennis E. Brooks, DVM, PhD, Dipl. ACVO, is a professor of ophthalmology at the University of Florida. He has lectured extensively, nationally and internationally, in comparative ophthalmology and glaucoma, and has more than 140 refereed publications. He is a recognized authority on canine glaucoma, and infectious keratitis, corneal transplantation, and glaucoma of horses.

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