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