Parker County Today PCT June 2018 - Page 86

our expertise: VET COLUMN Corneal Ulcerations By Tom Hutchins, DVM, DABVP North Texas Veterinary Hospital 8283 FM 920 • Weatherford, Tx E 84 quine corneal ulceration is a sight-threaten- ing disease requiring early clinical diagnosis, laboratory confirmation, and appropriate medi- cal and/or surgical therapy. Both bacterial and fungal keratitis (inflammation of the cornea) may present with a mild, early clinical course, but require prompt therapy if serious eye complica- tions are to be avoided. Ulcers can range from simple, superficial breaks or abrasions in the corneal surface, to full-thickness corneal per- forations with prolapse of the iris (the colored portion of the eye). The thickness of the cornea is only 1.0–1.5 millimeters (mm). The normal equine cornea is 8-10 cell layers thick but increases to 10-15 lay- ers thick with inflammation of the basal cells fol- lowing corneal injury. The basement membrane is not completely formed 6 weeks following corneal injury in the horse, in spite of the cor- neal epithelium (surface cells) covering the ulcer site. Healing time of a 7mm-diameter ulcer that is only partial thickness can take up to 2 weeks to heal if there is no bacterial infection associ- ated with the ulcer. The environment of the horse is such that the cornea and the inside of the eyelids are constantly exposed to bacterial and fungal organisms. Some common causes of corneal ulceration aside from trauma are Staphylococ- cus, Streptococcus, Pseudomonas, Aspergillus, and Fusarium species. The corneal epithelium is a formidable barrier to the invasion of bacteria and fungi. A defect in the tear film or corneal epithelium allows bacteria or fungi to adhere to the cornea and to initiate infection. Epithelial Dr. Tom Hutchins defects need not be full-thickness, as corneas with partial-thickness defects are more suscep- tible to adherence by certain organisms than are corneas that are fully intact. There are certain cells, some bacteria and fungi within the tear film that contain highly destructive enzymes that can result in rapid cor- neal thinning and perforation in the horse. Ex- cessive enzyme activity is termed “melting” and results in a gelatinous appearance of the cornea. Total corneal ulceration ultimately requires the degradation of collagen, which forms the frame- work of the cornea. There is no proven genetic predisposition to corneal ulceration in the horse, but the unique corneal healing properties of the horse in regard to excessive corneal vascularization and fibrosis appear to be strongly species specific. All ages and breeds of horses in all types of environments are at risk. The clinical signs of early ulceration may be focal cloudiness of the cornea, redness of the sclera (white part of the eye), and pain demon- strated by constant closure of the eye. Twitch- ing of the eyelids and excessive tearing are usually present as well. With small ulcers, the upper eyelid may droop slightly and not be fully closed. Signs of anterior uveitis or inflammation