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Eye Diseases
All of the information on this page comes from Dennis E. Brooks,
DVM, PhD. Dr. Brooks is a veterinary ophthalmologist who is one
of the country’s leading experts on equine eye diseases. He
is a Diplomate of the American College of Veterinary Ophthalmologists
and Professor of Ophthalmology at the University of Florida’s
College of Veterinary Medicine. Dr. Brooks is also Chief of the
Ophthalmology Service at the College of Veterinary Medicine.
He is the author of Ophthalmology for the Equine Practitioner,
available from Amazon.com here.
Dr. Brooks kindly gave us permission to post this comprehensive
overview on eye diseases. Thank you, Dr. Brooks!
The information here is not a substitute for a thorough veterinary
exam if you suspect your horse has an eye condition. Prompt medical
care can often make the difference between a horse keeping its sight
… or going blind. If your horse has any eye problems, please
consult a vet immediately.
(Click on the thumbnail images for bigger versions of the photos.)
INTRODUCTION
This web page is devoted to diseases of the horse eye. Most of the
common eye diseases of horses are described (Table
1).
VISION IN THE HORSE. WHAT DOES THE HORSE "SEE"?
The horse has a total visual field of nearly 360 degrees, meaning
a horse can just about see its tail with its head pointed forward.
A small frontal binocular field of 65E develops postnatally. The
horse retina is adapted for detection of movement. The horse utilizes
both eyes until an object approaches within 3-4 feet when it is
forced to turn or lower its head to continue to observe with one
eye. Cones are present in the horse retina suggesting that they
have the capacity for color vision. They see blues and reds. Rods
in the retina are the major type of cell and are used to see in
the dark. Horses have very good night vision.
OCULAR PROBLEMS IN THE FOAL
A newborn foal may exhibit droopy eyelids, low tear secretion, a
round pupil, reduced corneal sensitivity, lack of a menace reflex
for up to 2 weeks, and prominent lens sutures.
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(Figure 1)
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(Figure 2)
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(Figure 3)
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Entropion is an inward rolling of the eyelid margin (Figure
1). This causes the eyelid hairs to rub on the cornea.
It can be a primary problem in foals, or secondary to dehydration
or emaciation as in "downer foals." It may be repaired
to prevent corneal ulceration in the neonate by placing sutures
at the lid margin to roll out the offending eyelid margin.
Congenital cataracts in foals are common congenital eye defects
(Figure 2).
Surgery is recommended (Figure 3).
Microphthalmos or a small eye is a common ophthalmic congenital
defect in the foal. A range of lesions may be present. The microphthalmic
eye may be visual or associated with other eye problems that cause
blindness.
DISEASES AND SURGERY OF THE EYELIDS
Traumatic eyelid lacerations
Lid trauma needs to be corrected as soon and as accurately as possible
to prevent undesirable scarring and secondary corneal desiccation
and ulceration.
Eyelids are highly vascular and have a great capacity to heal and
resist infection. They can also swell quite dramatically. Minimal
debridement is needed due to their extensive blood supply, and an
eyelid "tag" or pedicle flap should never be excised as
exposure keratitis and corneal ulceration can result.
Upper eyelid damage is more significant in horses because the upper
lid moves over more of the equine cornea than does the lower lid.
Preservation of the eyelid margin is critical if at all possible
in order to preserve eyelid function (Figure 4).
The repaired lesion must be protected from "self-trauma"
with masks or hard cups.
Neoplasia of the lids
Eyelid melanomas are found in grey horses, with Arabians and Percherons
also at increased risk. Melanomas may be single or multiple. Treatment
is surgical excision and cryotherapy.
Sarcoids are solitary or multiple tumors of the eyelids and periocular
region of the horse (Figure 5). Retroviruses and
papilloma viruses may be involved in the etiology. It is suspected
that flies may be able to transfer sarcoid cells from one horse
to traumatic skin lesions in other horses. There are geographic
differences in the aggressiveness of the sarcoid in horses. Mules
appear to suffer from an aggressive form of sarcoid.
Immunotherapy for sarcoids includes using attenuated Mycobacterium
bovis cell wall extracts such as the immunostimulant Bacillus Calmette-Gaérin
(BCG).
Shrinking the sarcoid lesion with antipsoriasis skin ointments
and/or topical 5-fluorouracil (5-FU) for two weeks may be beneficial
before using BCG. Cryotherapy, hyperthermia, carbon dioxide laser
excision, intralesional chemotherapy, and intralesional radiotherapy
can also be effective for sarcoid. Intralesional chemotherapeutics
including 5-FU or cisplatin have been used with varying success
rates. Homeopathic ointments and caustic chemical lotions are effective
in some sarcoids.
Squamous cell carcinoma (SCC) is the most common tumor of the eye
and lids in horses (Figures 6 and 7). The cause
may be related to the ultraviolet (UV) component of solar radiation,
periocular pigmentation, and an increased susceptibility to carcinogenesis.
The UV component is the most plausible carcinogenic agent associated
with SCC.
Prevalence in horses increases with age. Belgians, Clydesdales and
other draft horses have a high prevalence of ocular SCC, followed
by Appaloosas and Paints, with the least prevalence found in Arabians,
Thoroughbreds and Quarterhorses.
White, grey-white, and palomino hair colors predispose to ocular
SCC, with less prevalence in bay, brown and black hair coats.
Cryotherapy, immunotherapy, irradiation, radio-frequency hyperthermia,
CO2 laser ablation, or intralesional chemotherapy should follow
surgical excision of equine ocular SCC.
DISEASES OF THE CORNEA
EQUINE CORNEAL ULCERATION
Equine corneal ulceration is very common in horses and is a sight
threatening disease requiring early clinical diagnosis, laboratory
confirmation, and appropriate medical and surgical therapy.
Ulcers can range from simple, superficial breaks or abrasions in
the corneal epithelium, to full-thickness corneal perforations with
iris prolapse. The prominent eye of the horse may predispose to
traumatic corneal injury. Both bacterial and fungal keratitis in
horses may present with a mild, early clinical course, but require
prompt therapy if serious ocular complications are to be avoided
(Figure 8).
Corneal ulcers in horses should be aggressively treated no matter
how small or superficial they may be. Corneal infection and uveitis
are always major concerns for even the slightest corneal ulcerations.
Iridocyclitis or uveitis is present in all types of corneal ulcers
and must be treated in order to preserve vision.
Proteinases in the tear film
Tear film proteinases normally provide a surveillance and repair
function to detect and remove damaged cells or collagen caused by
regular wear and tear of the cornea. These enzymes exist in a balance
with inhibitory factors to prevent excessive degradation of normal
tissue.
In pathologic processes such as ulcerative keratitis, excessive
levels of these proteinases can lead to rapid degeneration of collagen
and other components of the stroma, potentially inducing keratomalacia
or corneal "melting".
Corneal sensitivity in foals and adult horses
Corneal sensation is important for corneal healing. The cornea of
the adult horse is very sensitive compared to other animals.
Corneal touch threshold analysis revealed the corneas of sick or
hospitalized foals were significantly less sensitive than those
of adult horses or normal foals. This decreased sensitivity may
partially explain the lack of clinical signs often seen in sick
neonates with corneal ulcers.
Corneal Healing in the Horse
The thickness of the equine cornea is 1.0 to 1.5 mm in the center
and 0.8 mm at the periphery. Healing of large diameter, superficial,
noninfected corneal ulcers is generally rapid and linear for 5-7
days, and then slows. Healing of ulcers in the second eye may be
slower than in the first and is related to increased tear proteinase
activity. Healing time of a 7-mm diameter, noninfected corneal wound
was nearly 12 days in horses (0.6 mm/day).
The Equine Corneal Microenvironment
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(Figure 9)
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(Figure 10)
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(Figure 11)
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(Figure 12)
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The environment of the horse is such that the conjunctiva and cornea
are constantly exposed to bacteria and fungi. The corneal epithelium
of the horse is a formidable barrier to the colonization and invasion
of potentially pathogenic bacteria or fungi normally present on
the surface of the horse cornea and conjunctiva.
A defect in the corneal epithelium allows bacteria or fungi to adhere
to the cornea and to initiate infection. Infection should be considered
likely in every corneal ulcer in the horse. Fungal involvement should
be suspected if there is a history of corneal injury with vegetative
material, or if a corneal ulcer has received prolonged antibiotic
and/or corticosteroid therapy with slight or no improvement.
Excessive proteinase activity is termed "melting", and
results in a liquefied, grayish-gelatinous appearance to the stroma
near the margin of the ulcer.
Horse corneas demonstrate a pronounced fibrovascular healing response.
The unique corneal healing properties of the horse in regards to
excessive corneal vascularization and fibrosis appear to be strongly
species specific.
Horses with painful eyes need to have their corneas stained with
both fluorescein dye and rose bengal dye as fungal ulcers in the
earliest stage will be negative to the fluorescein but positive
for the rose bengal (Figures 9, 10,11,12).
Corneal cultures should be obtained first and then followed by corneal
scrapings for cytology. Mixed bacterial and fungal infections can
be present.
Medical therapy
Once a corneal ulcer is diagnosed, the therapy must be carefully
considered to ensure comprehensive treatment. Medical therapy almost
always comprises the initial major thrust in ulcer control, albeit
tempered by judicious use of adjunctive surgical procedures. This
intensive pharmacological attack should be modified according to
its efficacy.
Antibiotics
Topically applied antibiotics, such as chloramphenicol, bacitracin-neomycin-polymyxin
B, gentamicin, ciprofloxacin, or tobramycin ophthalmic solutions
may be utilized to treat bacterial ulcers. Frequency of medication
varies from q2h to q8h.
Cefazolin (55mg/ml), chloramphenicol, bacitracin, and carbenicillin
are effective against beta hemolytic Streptococcus.
Ciloxan (ciprofloxacin), amikacin (10 mg/ml), and polymyxin B (0.25%
IV solution) may be used topically for gentamicin resistant Pseudomonas.
Collagenolysis prevention
Severe corneal inflammation secondary to bacterial (especially,
Pseudomonas and beta hemolytic Streptococcus) or, much less commonly,
fungal infection may result in sudden, rapid corneal liquefaction
and perforation. Activation and/or production of proteolytic enzymes
by corneal epithelial cells, leucocytes and microbial organisms
are responsible for stromal collagenolysis or "melting".
Serum is biologically nontoxic and contains an alpha-2 macroglobulin
with antiproteinase activity. Serum administered topically can reduce
tear film and corneal protease activity in corneal ulcers in horses.
The serum can be administered topically as often as possible, and
should be replaced by new serum every 8 days.
Treat Uveitis
Atropine sulfate is a common therapeutic agent for equine eye problems.
Topically applied atropine (1%) is effective in stabilizing the
blood-aqueous barrier, reducing vascular protein leakage, minimizing
pain from ciliary muscle spasm, and reducing the chance of synechia
formation by causing pupillary dilatation.
Atropine may be utilized topically q4h to q6h with the frequency
of administration reduced as soon as the pupil dilates.
Topical atropine has been shown to prolong intestinal transit time,
reduce and abolish intestinal sounds, and diminish the normal myoelectric
patterns in the small intestine and large colon of horses. Some
horses appear more sensitive than others to these atropine effects,
and may "respond" by displaying signs of colic and/or
prolonged intestinal transit time.
Systemically administered NSAIDs such as phenylbutazone (1 gm BID
PO) or flunixin meglumine (1 mg/kg BID, IV, IM or PO) can be used
orally or parenterally, and are effective in reducing uveal exudation
and relieving ocular discomfort from the anterior uveitis in horses
with ulcers.
Topical nonsteroidal antiinflammatory drugs (NSAIDs) such as profenol,
flurbiprofen and diclofenamic acid (BID to TID) can also reduce
the degree of uveitis.
Horses with corneal ulcers and secondary uveitis should be stall-rested
till the condition is healed. Intraocular hemorrhage and increased
severity of uveitis are sequelae to overexertion.
Conjunctival Flaps
Conjunctival grafts or flaps are used frequently in equine ophthalmology
for the clinical management of deep, melting, and large corneal
ulcers, descemetoceles, and for perforated corneal ulcers with and
without iris prolapse.
Inappropriate therapy and ulcers
Topical corticosteroids may encourage growth of bacterial and fungal
opportunists by interfering with non-specific inflammatory reactions
and cellular immunity.
Corticosteroid therapy by all routes is contraindicated in the
management of corneal infections. Even topical corticosteroid instillation,
to reduce the size of a corneal scar, may be disastrous if organisms
remain indolent in the corneal stroma.
**IMPORTANT POINTS**
• CORNEAL ULCERS ARE FREQUENTLY NOT CLEARLY VISIBLE.
• ALL RED OR PAINFUL EYES MUST BE STAINED WITH FLUORESCEIN
AND ROSE BENGAL DYES.
• A SLOWLY PROGRESSIVE COURSE OFTEN BELIES THE SERIOUSNESS
OF THE ULCER.
• CORNEAL ULCERS IN HORSES MAY RAPIDLY PROGRESS TO EYE
RUPTURE.
• TOPICAL CORTICOSTEROIDS ARE BAD WHEN THE CORNEA RETAINS
FLUORESCEIN STAIN.
• UVEITIS CAUSED BY A CORNEAL ULCER OR STROMAL ABSCESS
MAY BE VERY DIFFICULT TO CONTROL.
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FUNGAL ULCERS IN HORSES
Fungi resemble mushrooms and are normal inhabitants of the equine
environment and conjunctival microflora, but can become pathogenic
following corneal injury. Aspergillus, Fusarium, Cylindrocarpon,
Curvularia, Penicillium, Cystodendron, yeasts, and molds are known
causes of fungal ulceration in horses.
Saddlebreds appear to be prone to severe keratomycosis, while standardbreds
are resistant.
Therapy is quite prolonged and scarring of the cornea may be prominent.
The fungi are overall more susceptible to antifungal drugs in this
order: natamycin = miconazole > itraconazole > ketoconazole
> fluconazole.
CORNEAL STROMAL ABSCESSES
Focal trauma to the cornea can inject microbes and debris into
the corneal stroma through small epithelial ulcerative micropunctures.
A corneal abscess may develop after epithelial cells adjacent to
the epithelial micropuncture divide and migrate over the small traumatic
ulcer to encapsulate infectious agents or foreign bodies in the
stroma. Epithelial cells are more likely to cover a fungal than
a bacterial infection.
Medical therapy consists of aggressive use of topical and systemic
antibiotics, topical atropine, and topical and systemic NSAIDs.
Deep lamellar and penetrating keratoplasties (PK) are utilized
in abscesses near Descemet's membrane, and eyes with rupture of
the abscess into the anterior chamber. PK eliminates sequestered
microbial antigens, and removes necrotic debris, cyotokines and
toxins from degenerating leukocytes in the abscess (Figures
13 and 14).
CATARACTS IN THE HORSE
Cataracts are opacities of the lens and are the most frequent congenital
ocular defect in foals. Horses manifest varying degrees of blindness
as cataracts mature. Very small incipient lens opacities are common
and not associated with blindness. As cataracts mature and become
more opaque, the degree of blindness increases.
Equine Cataract Surgery
Most veterinary ophthalmologists recommend surgical removal of cataracts
in foals less than 6 months of age if the foal is healthy, no uveitis
or other ocular problems are present, and the foal's personality
will tolerate aggressive topical medical therapy.
Phacoemulsification cataract surgery is the most useful technique
for the horse. This extracapsular procedure through a 3.2mm corneal
incision utilizes a piezoelectric handpiece with an ultrasonic titanium
needle in a silicone sleeve to fragment and emulsify the lens nucleus
and cortex following removal of the anterior capsule. The emulsified
lens is then aspirated from the eye while intraocular pressure is
maintained. The thin posterior capsule is left intact. There is
little inflammation postoperatively in most horses following phacoemulsification
cataract surgery and a quicker return to normal activity with phacoemulsification
than other surgical techniques.
The results of cataract surgery in foals by experienced veterinary
ophthalmologists are generally very good, but the cataract surgical
results in adult horses with cataracts caused by ERU are often poor.
The problem is that new blood vessels form on the iris and anterior
lens capsule in the eyes with ERU and they can bleed during the
surgeries. The surgeon often cannot stop the hemorrhage and severe
hyphema results.
DISEASES OF THE UVEAL TRACT
Equine recurrent uveitis (Periodic ophthalmia, moon blindness, iridocyclitis)
Equine recurrent uveitis (ERU) is a common cause of blindness in
horses. It is a group of immune-mediated diseases of multiple origins
cause inflammation of the iris, ciliary body, choroid, and retina
(Figure 15).
Recurrence of anterior uveitis is the hallmark of ERU. The disease
is bilateral in approximately 20%.
While the pathogenesis is clearly immune-mediated, the specific
causes of ERU are unknown. Hypersensitivity to infectious agents
such as Leptospira interrogans is commonly implicated as a possible
cause.
Leptospiral titers for L. pomona, L. bratislava and L. autumnalis
should be requested in the United States. Positive titers for serovars
of 1:400 or greater are of importance.
Serology for Leptospira pomona can be used for prognostic evaluation
of the likelihood of blindness occurring in one or both eyes. Seropositive
Appaloosas (100%) > seronegative Appaloosas (72%) > seropositive
non-Appaloosas (51%) > seropositive non-Appaloosas (34%) at having
blindness occur in at least one eye within 11 years of the first
attack.
A complete ophthalmic examination should be performed to determine
if the uveitis is associated with a corneal ulcer. The presence
of a corneal ulcer precludes the use of topical corticosteroids,
but not topical nonsteroidal drugs.
Inflammation of the brain is found in ERU.
Irreversible blindness is a common sequelae to ERU, and is due to
retinal detachment, cataract formation or severe chorioretinitis.
ERU Therapy
- The major goals of treatment of ERU are to preserve vision,
decrease pain, and prevent or minimize the recurrence of attacks
of uveitis. Specific prevention and therapy is often difficult,
as the etiology is not identified in each case.
- Treatment should be aggressive and prompt in order to maintain
the transparency of the ocular structures.
- Medications should be slowly reduced in frequency once clinical
signs abate.
- Therapy can last for weeks or months and should not be stopped
abruptly or recurrence may occur.
Some horses with ERU require life-long therapy!
Overall, the prognosis for ERU is usually poor for a cure to preserve
vision, but the disease can be controlled. The Appaloosa breed seems
to suffer from the most severe cases.
Anti-inflammatory medications, specifically corticosteroids and
nonsteroidal drugs, are used to control the generally intense intraocular
inflammation that can lead to blindness. Medication can be administered
topically as solutions or ointments, subconjunctivally, orally,
intramuscularly, and/or intravenously.
Prednisolone acetate or dexamethasone should be applied initially.
When the frequent application of topical steroids is not practical,
the use of subconjunctival corticosteroids may be used. Systemic
corticosteroids may be beneficial in severe, refractory cases of
ERU, but pose some risk of inducing laminitis and should be used
with caution.
The nonsteroidal anti-inflammatory drugs (NSAID) can provide additive
anti-inflammatory effects to the corticosteroids, and are effective
at reducing the intraocular inflammation when a corneal ulcer is
present. Cyclosporine A can be effective topically for ERU.
Flunixin meglumine, phenylbutazone, or aspirin are frequently used
systemically to control intraocular inflammation. Some horses become
refractory to the beneficial effects of these medications, and it
may be necessary to switch to one of the other NSAID to ameliorate
the clinical signs of ERU.
Topical atropine minimizes synechiae formation by inducing mydriasis,
and alleviates some of the pain of ERU by relieving spasm of ciliary
body muscles.
Surgical considerations for ERU
Vitrectomy appears more beneficial in European warmbloods with ERU
than in Appaloosas with ERU in the USA. The reasons for this are
not known. Cataracts occur in a high percentage of cases post-vitrectomy
in both regions. Retinal detachment can also occur postoperatively.
Sustained release suprachoroidal cyclosporine A implants may also
be beneficial to treating ERU.
GLAUCOMA
An elevation in the pressure inside the eye is termed glaucoma
(Figure 16). This intraocular pressure (IOP) averages 23
mmHg in the horse eye. Glaucoma is associated with ERU. It is most
common in Appaloosas. Therapy for the uveitis and laser therapy
for the glaucoma is recommended.
RETINAL DISEASE
Congenital stationary night blindness
Congenital Stationary Night Blindness (CSNB) is found mainly in
the Appaloosa, and is inherited as a sex-linked recessive trait.
Cases are also noted in Thoroughbreds, Paso Finos, and Standardbreds.
Clinical signs include visual impairment in dim light with generally
normal vision in daylight, and behavioral uneasiness and unpredictability
occurring at night. CSNB does not generally progress, hence its
name, but cases of progression to vision difficulties in the daytime
are noted.
Ophthalmoscopic examination is normal (Figure 17).
Diagnosis is by clinical signs, breed, and ERG with decreased scotopic
b-wave amplitude and a large negative, monotonic a-wave.
CSNB appears to be caused by functional abnormality of neurotransmission
in the middle retina. There is no therapy for this condition but
affected animals should not be bred.
SUDDEN BLINDNESS
Acute blindness may be associated with head or ocular trauma, ERU,
glaucoma, cataracts, intraocular hemorrhage, exudative optic neuritis,
retinal detachment, or CNS disease. Acutely blind horses are extremely
agitated, anxious and dangerous.
Horses can adapt amazingly well to blindness, whether unilateral
or bilateral, if allowed to adjust to their new condition. Several
internet websites are devoted to the care of blind horses and other
blind animals.
Table 1. EYE DISEASES ASSOCIATED WITH SPECIFIC
HORSE BREEDS
| APPALOOSA |
1. Congenital stationary night blindness (CSNB)
2. Congenital cataracts
3. Glaucoma
4. ERU
5. Optic disc colobomas
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| ARABIAN |
1. Congenital cataracts |
| BELGIAN DRAFT HORSES |
1. Aniridia and secondary cataracts
2. Cataracts |
| MORGAN |
1. Cataracts - nuclear, bilateral, symmetrical, and non-progressive |
| QUARTER-HORSE |
1. Congenital cataracts
2. Entropion |
ROCKY MOUNTAIN HORSE
(chocolate coat color most often affected).
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Collectively the cornea, iris and ciliary body lesions are
termed anterior segment dysgenesis.
1. Congenital miosis, and corpora nigra and iris hypoplasia
2. Macrocornea
3. Ciliary Cysts
4. Cataract, Lens Luxation
5. Retinal Dysplasia, Retinal Detachment |
| THOROUGHBRED |
1. Congenital cataracts
2. Microphthalmia associated with multiple ocular defects
3. Retinal dysplasia associated with retinal detachments in
some cases
4. Entropion
5. Progressive retinal atrophy |
| COLOR DILUTE BREEDS |
1. Iridal hypoplasia - photophobia |
| STANDARDBREDS |
1. Retinal detachments
2. Congenital Stationary Night Blindness |
| PASO FINO |
1. Congenital Stationary Night Blindness
2. Glaucoma |
| AMERICAN SADDLEBRED |
1. Cataracts
2. Aggressive keratomycosis |
| WARM BLOODS |
1. Glaucoma
2. ERU |
| MINIATURE HORSES |
1. Cataracts |
| MULES |
1. Aggressive sarcoids |
REFERENCES
• Brooks DE: Equine Ophthalmology. Made Easy. Teton NewMedia,
Jackson, WY, 2002.
• Gelatt KN: Veterinary Ophthalmology, 3rd edition. Lippincott
Williams and Wilkins. Philadelphia, 1999.
• Veterinary Ophthalmology 3(2/3): Equine Special Issue, 2000.
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