Equine Ophthalmology - IVIS · Equine Ophthalmology Dennis E. Brooks, DVM, PhD Author’s address: American College of Veterinary Ophthalmologists, University of Florida, PO Box

Equine Ophthalmology

Dennis E. Brooks, DVM, PhD

Author’s address: American College of Veterinary Ophthalmologists, University of Florida, PO Box100126, Gainesville, FL 32610. © 2002 AAEP.

1. Vision in the Horse: What Does the Horse “See”?

The horse has a total visual field of nearly 360°, mean-ing a horse can just about see its tail with its headpointed forward.1 A small frontal binocular field of 65°is present. The horse retina is adapted for detectionof movement because it contains significant numbersof large-diameter ganglion cells.2 The nasal extensionof the retina, the laterality of the eyes, and the hori-zontal pupil facilitate tremendous peripheral vision forthe horse standing with its head up.

The horse has weak accommodative ability of thelens and therefore has limited near focus capability.The horse uses both eyes until an object approacheswithin 3–4 ft, when it is forced to turn or lower itshead to continue to observe with one eye. Horsesneed to accommodate �2 D to maintain a focusedimage on the retina. Mean refractive error ofhorses is �1.0 D. This seems to be similar to 20/33vision on the Snellen chart. Horses have poor acu-ity in the peripheral retina.3

Rods significantly outnumber cones, indicatingthe high capacity for night vision in horses, butcones are present in the horse retina with the capac-ity for color vision. Horses see blues and yellowsbut may have more trouble with longer wavelengthcolors such as red. 1

2. The Foal Eye

A newborn foal may exhibit lagophthalmos, low tearsecretion, slow pupillary light reflexes until 5 days of

age, an oval-shaped pupil, reduced corneal sensitiv-ity, lack of a menace reflex for up to 2 wk, hyaloidartery remnants containing blood for several hoursafter birth, prominent lens Y sutures, and a round,pale pink to deep red optic disc with smoothmargins.1

Tapetal color is initially green to yellow-green infoals. Color-dilute foals have a red fundic reflectionfrom a lack of a tapetum and consequential exposureof choroidal vessels.1

3. Ocular Problems in the Foal

Dermoids (choristomas) are neoplastic aggregatesof skin tissue aberrantly located in the conjunctiva,cornea, or eyelid. Hair follicle development in adermoid may cause ocular irritation or corneal ul-ceration. Treatment would be a keratectomy forcorneal dermoids and blepharoplasty for eyelidlesions.

Entropion is an inward rolling of the eyelid mar-gin (Fig. 1). This causes the eyelid hairs to rub onthe cornea. It can be a primary problem or it can besecondary to dehydration or emaciation in “downerfoals.” Entropion should be repaired in foals byplacing vertical mattress sutures to evert the offend-ing eyelid margin, preventing corneal ulceration.1,4

Hotz-Celsus type entropion surgery should be re-served for older horses.

Lacrimal puncta agenesis or duct atresiamay be unilateral or bilateral. Clinical signs are a

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IN DEPTH: OPHTHALMOLOGY

NOTES

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Proceedings of the Annual Convention of the AAEP 2002

chronic mucoid and eventually copious mucopuru-lent discharge in a young horse (Fig. 2). Presumptivediagnosis of duct or punctal agenesis with dacryo-cystitis may be made by noting the lack of a distalpuncta opening of the nasolacrimal duct at the mu-cocutaneous junction within the nares. Dacryocys-torhinography will identify the specific location ofthe obstruction. Surgical repair of the congenitaldefect and medical treatment of the associateddacryocystitis are required.4

Microphthalmos is a common ophthalmic con-genital defect in the foal (Fig. 3).1 The entire globe issmall. The microphthalmic eye may be visual or isassociated with other eye problems that cause blind-ness. Strabismus is deviation of the globe from itsnormal orientation and may be noted alone or withother congenital ocular deformities. AnteriorSegment Dysgenesis of the Rocky MountainHorse consists of increased corneal curvature, irishypoplasia, congenital miosis, uveal cysts, cataracts,and retinal dysplasia.5

Persistent pupillary membranes (PPMs) areembryonic remnants of the iris seen as linear tissueconnections between the iris and iris, iris and lens,

and/or iris and cornea. PPMs seldom cause anyvisual impairment, although focal lens or cornealopacities may be present. There is generally noneed for surgical transection of PPMs.1,4

Congenital cataracts or lens opacities in foalsare common congenital eye defects in the horse (Fig.4).1,4 Blindness can occur if cataracts are mature.Phacoemulsification cataract surgery has a highsuccess rate in foals with blinding cataracts.6 Con-genital lens luxation from zonular weakness is asevere eye problem that also requires surgery forresolution.1,4

Persistent superficial corneal ulcers in theneonatal foal may be associated with decreased cor-neal sensation. These superficial ulcers requireearly detection and treatment to prevent ulcerprogression.1,4

Iridocyclitis in the foal is generally secondary tosepticemia and may be unilateral or bilateral. Fi-brin, hyphema, and/or hypopyon may be present.Infectious and toxic etiologies are reported in foals.Severe unilateral, blinding, fibrinous uveitis second-ary to plant toxins has been noted primarily in Thor-oughbred foals and yearlings in the southern UnitedStates.

Fig. 1. Entropion in a foal.

Fig. 2. Dacryocystitis found with nasolacrimal duct atresia.

Fig. 3. Microphthalmic eye in a foal.

Fig. 4. Nearly mature cataract in a foal.

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Congenital glaucoma and congenital retinal de-tachment are found periodically in foals and repre-sent severe blinding eye problems with no therapyavailable.1,4

4. Diseases and Surgery of the Eyelids

Traumatic Eyelid LacerationsLid trauma needs to be corrected as soon and asaccurately as possible to prevent undesirable lidscarring and secondary corneal desiccation and ul-ceration. Eyelids are highly vascular and have agreat capacity to heal and resist infection. Theycan also swell quite dramatically. Minimal de-bridement is needed because of their extensive bloodsupply, and an eyelid “tag” or pedicle flap shouldnever be excised because exposure keratitis and cor-neal ulceration can result (Fig. 5).

Upper eyelid damage is more significant in horsesbecause the upper lid moves over more of the equinecornea than does the lower lid. Medial canthal lidtrauma can involve the nasolacrimal system. It isimportant to thoroughly examine the globe both ex-ternally and through ophthalmoscopy. The naso-lacrimal system should also be evaluated for damagewhen medial canthal injuries are present. Preser-vation of the eyelid margin is critical if at all possibleto preserve eyelid function. The repaired lesionmust be protected from “self-trauma” with masks orhard cups.1,4

Neoplasia of the LidsEyelid melanomas are found in grey horses; Ara-bians and Percherons also have an increased risk.Melanomas may be single or multiple. Treatmentis surgical excision and cryotherapy.

Sarcoids are solitary or multiple tumors of theeyelids and periocular region of the horse. Retro-viruses and papilloma viruses may be involved inthe etiology. It is suspected that flies may be ableto transfer sarcoid cells from one horse to traumaticskin lesions in other horses. There are geographic

differences in the aggressiveness of the sarcoid inhorses.7

The sarcoid lesion induces a fibrovascular inflam-matory response that may mask the actual size ofthe sarcoid. Shrinking the sarcoid lesion with an-tipsoriasis skin ointments and/or topical 5-fluoro-uracil (5-FU) for 2 wk may be beneficial before usingBacillus Calmette-Gaerin (BCG).7 Surgical resec-tion of necrotic tissue is controversial, with someexperts suggesting it will exacerbate the sarcoid.

Immunotherapy for sarcoids includes autogenousvaccines and immunomodulators of mycobacterialproducts. Immunomodulation using attenuatedMycobacterium bovis cell wall extracts such as theimmunostimulant BCG, however, has produced rea-sonable remission rates.7

Cryotherapy, hyperthermia, carbon dioxide laserexcision, intralesional chemotherapy, and intrale-sional radiotherapy can also be effective for sarcoid.Intralesional chemotherapeutics including 5-FU orcisplatin have been used with varying success rates.Interferon has been used systemically for very large,aggressive equine sarcoids. Homeopathic oint-ments and caustic chemical lotions are effective insome sarcoids.7

Squamous cell carcinoma (SCC) is the mostcommon tumor of the eye and adnexa in horses (Fig.6). The etiopathogenesis may be related to the ultra-violet (UV) component of solar radiation, periocularpigmentation, and an increased susceptibility to car-cinogenesis. The UV component is the most plau-sible carcinogenic agent associated with SCC,because it targets the tumor suppressor gene p53,which is altered in equine SCC.8,9

Prevalence of SCC in horses increases with age.Draft horses have a high prevalence of ocular SCC,followed by Appaloosas and Paints, with the leastprevalence found in Arabians, Thoroughbreds, andQuarter Horses. White and palomino hair colorspredispose to ocular SCC, with less prevalence inbay, brown, and black hair coats.

Fig. 5. (a) Severe lower lid laceration. (b) Healed laceration 3 wk after surgery.





Cryotherapy, immunotherapy, irradiation, radio-frequency hyperthermia, CO2 laser ablation, or in-tralesional chemotherapy should follow surgicalexcision of equine ocular SCC. Additionally, recon-structive eyelid surgery may be required when eye-lid margins are lost after tumor excision, andconjunctival grafts are indicated after keratectomyfor corneal SCC.

Immunotherapy with BCG cell wall extract hasbeen used successfully for large periocular SCC inhorses. Chemotherapy of invasive eyelid SCC withintralesional, slow release cisplatin has been usedwith and without surgical debulking. Topical 51%5-FU (q8h) can be effective for epithelial dysplasiaand corneal SCC in situ and may be beneficial forextensive periocular SCC.1,4

Tumors may be removed by surgical excisionalone if adequate margins can be obtained. How-ever, adjunctive therapy is often recommended toimprove the chance for a complete cure, especiallywith large or invasive tumors. Small, superficialtumors may be treated with radiofrequency hyper-thermia or cryosurgery. Malignant cells are killedwith local temperatures of 41–50°C, after surgicalexcision. Cryosurgery with liquid nitrogen or ni-trous oxide induces cryonecrosis of malignant cellswhen temperatures of �20°C to �40°C are achievedusing a double freeze-thaw technique.1,4

Excision of corneal limbal SCC followed by CO2laser ablation has also been advocated. Radio-therapy with beta irradiation (strontium 90) is verybeneficial in superficial SCC of the cornea and lim-bus after superficial keratectomy. Brachytherapyusing iridium 192 may be employed after surgicaldebulking of invasive eyelid tumors. Interstitialradiation therapy has the advantage of providingcontinuous exposure of the tumor to high levels ofradiation over a period of time.

5. Diseases of the Cornea

Corneal Healing in the HorseThe thickness of the equine cornea is 1.0–1.5 mm inthe center and 0.8 mm at the periphery.

The normal equine corneal epithelium is 8–10 celllayers thick and increases after corneal injury.The stroma is primarily collagen. Descemet’smembrane is the 21-�m-thick basement membraneof the inner endothelial cell layer.10,11

Healing of large diameter, superficial, noninfectedcorneal ulcers is generally rapid and linear for 5–7days, and then slows or lags till healing is com-plete.11 Healing of ulcers in the second eye may beslower than in the first and is related to increasedtear proteinase activity. Healing time of a 7-mmdiameter, midstromal depth, noninfected cornealtrephine wound was nearly 12 days in horses (0.6mm/day).10 The epithelial basement membrane isnot completely formed 6 wk after corneal injury inthe horse, despite the fact that the epithelium com-pletely covered the ulcer site.10

Corneal Sensitivity in Foals and Adult Horses

Corneal sensation is important for corneal healing.The cornea of the adult horse is very sensitive com-pared with other animals. Corneal touch thresholdanalysis revealed the corneas of sick or hospitalizedfoals were significantly less sensitive than those ofadult horses or normal foals. The incidence of cor-neal disease is also much higher in sick neonatesthan in healthy foals of similar age.8

Ulcerative keratitis in the equine neonate oftendiffers from adult horses in clinical signs and dis-ease course. Foals may not show characteristic epi-phora, blepharospasm, or conjunctivitis, and theulcers may be missed without daily fluoresceinstaining. This decreased sensitivity may partiallyexplain the lack of clinical signs often seen in sickneonates with corneal ulcers.

Proteinases in the Tear Film

Tear film proteinases normally provide a surveil-lance and repair function to detect and remove dam-aged cells or collagen caused by regular wear andtear of the cornea. These enzymes exist in a bal-ance with inhibitory factors to prevent excessivedegradation of normal tissue. Two major familiesof proteinases that may affect the cornea include thematrix metalloproteinases (MMP) and the serineproteinases (neutrophil elastase [NE]). MMP-9and NE predominate in the horse.12

Bacterial and fungal pathogens induce corneal ep-ithelial cells, corneal stromal fibroblasts, and leuko-cytes (PMN) in the tear film to up-regulate tumornecrosis factor (TNF)-�. TNF-� induces formationof cytokines interleukin (IL-1, IL-6, and IL-8) thatinduce MMP-2, MMP-9, and neutrophil elastaseproduction to elicit inflammatory processes. Pro-teinases that may contribute to corneal ulceration inthe early stages of infection could be of bacterial orcorneal cell origin.12 In the later stages, as PMNsaccumulate, PMN-derived proteinases predominateas the main factor in corneal tissue destruction.Tear film neutrophils and some bacteria and fungiare associated with highly destructive collagenase

Fig. 6. Large squamous cell carcinoma at medial canthus.





enzymes that can result in rapid corneal stromalthinning, descemetocele formation, and perforation.Excessive proteinase activity is termed “melting”and results in a liquefied, grayish-gelatinous ap-pearance to the stroma near the margin of theulcer.12

Equine Corneal MicroenvironmentThe environment of the horse is such that the con-junctiva and cornea are constantly exposed to bac-teria and fungi.1 The corneal epithelium of the horseis a formidable barrier to the colonization and inva-sion of potentially pathogenic bacteria or fungi nor-mally present on the surface of the horse cornea andconjunctiva. A defect in the corneal epithelium al-lows bacteria or fungi to adhere to the cornea and toinitiate infection. Staphylococcus, Streptococcus,Pseudomonas, Aspergillus, and Fusarium sp. arecommon causes of corneal ulceration in the horse.1,13

6. Equine Corneal Ulceration

Equine corneal ulceration is very common in horsesand is a sight-threatening disease requiring earlyclinical diagnosis, laboratory confirmation, and ap-propriate medical and surgical therapy.

Ulcers can range from simple, superficial breaksor abrasions in the corneal epithelium to full-thick-ness corneal perforations with iris prolapse. Theprominent eye of the horse may predispose to trau-matic corneal injury.1,4

Both bacterial and fungal keratitis in horses maypresent with a mild, early clinical course, but re-quire prompt therapy if serious ocular complicationsare to be avoided. Corneal ulcers in horses shouldbe aggressively treated no matter how small or su-perficial they may be. Infection should be consid-ered likely in every corneal ulcer, no matter howsmall, in the horse.1,4 Fungal involvement should besuspected if there is a history of corneal injury with

vegetative material, or if a corneal ulcer has re-ceived prolonged antibiotic and/or corticosteroidtherapy without improvement. Iridocyclitis ispresent in all types of equine corneal ulcers andmust also be treated to preserve vision. Globe rup-ture, phthisis bulbi, and blindness are possible se-quelae to corneal ulceration in horses.

Horse corneas demonstrate a pronounced fibro-vascular healing response.1,4 The unique cornealhealing properties of the horse in regards to exces-sive corneal vascularization and fibrosis seem to bestrongly species specific. Many early cases ofequine ulcerative keratitis present, initially, as mi-nor corneal epithelial ulcers or infiltrates, withslight pain, blepharospasm, epiphora, and photo-phobia. At first, anterior uveitis and corneal vas-cularization may not be clinically pronounced.Slight droopiness of the eyelashes of the uppereyelid may be an early, yet subtle sign of cornealulceration (Fig. 7).

A vicious cycle may be initiated after the firstinjury to the cornea, with “second injury to the cor-nea” occurring because of the action of inflammatorycytokines.14 Ulcers, uveitis, blepharitis, conjunctivi-tis, glaucoma, and dacryocystitis must be consideredin the differential for the horse with a painful eye.Corneal edema may surround the ulcer or involvethe entire cornea. Signs of anterior uveitis arefound with every corneal ulcer in the horse andinclude miosis, fibrin, hyphema, or hypopyon. Per-sistent superficial ulcers may become indolent be-cause of hyaline membrane formation on the ulcerbed.

Fluorescein and Rose Bengal Dyes and Other DiagnosticsAll corneal injuries should be fluorescein stained todetect corneal ulcers (Fig. 8). Horses with painfuleyes need to have their corneas stained with bothfluorescein dye and rose bengal dye because fungal

Fig. 7. (a) Upper eyelashes perpendicular to the cornea in a normal eye. (b) Upper eyelashes pointed down in a painful eye.





ulcers in the earliest stage will be negative to thefluorescein but positive for the rose bengal. Fluo-rescein dye retention is diagnostic of a full-thicknessepithelial defect or corneal ulcer. Faint fluoresceinretention may indicate a microerosion or partial ep-ithelial cell layer defect caused by infiltration offluorescein dye between inflamed epithelial celljunctions (Fig. 9).1,4,9

Rose bengal retention indicates a defect in themucin layer of the tear film. Fungi may inducechanges in the tear film mucin layer before attach-ment to the cornea. Early fungal lesions that re-tain rose bengal are multifocal in appearance andmay be mistaken for viral keratitis.1,4

Microbiologic culture and sensitivity for bacteriaand fungi are recommended for horses with rapidlyprogressive and deep corneal ulcers. Corneal cul-tures should be obtained first and then followed bycorneal scrapings for cytology. Mixed bacterial andfungal infections can be present.

Vigorous corneal scraping at the edge and base ofa corneal ulcer is used to detect bacteria and fungalhyphae. Samples can be obtained with the handleend of a sterile scalpel blade and topical anesthesia.Superficial scraping with a cotton swab cannot beexpected to yield organisms in a high percentage ofcases.1,4

Medical TherapyOnce a corneal ulcer is diagnosed, the therapy mustbe carefully considered to ensure comprehensivetreatment. Medical therapy almost always com-prises the initial major thrust in ulcer control, albeittempered by judicious use of adjunctive surgical pro-cedures. This intensive pharmacological attackshould be modified according to its efficacy. Sub-palpebral or nasolacrimal lavage treatment systemsare employed to treat a fractious horse or one with apainful eye that needs frequent therapy.

The clarity of the cornea, the depth and size of theulcer, the degree of corneal vascularization, theamount of tearing, the pupil size, and intensity ofthe anterior uveitis should be monitored. Serialfluorescein staining of the ulcer is indicated to as-sess healing. As the cornea heals the stimulus forthe uveitis will diminish, and the pupil will dilatewith minimal atropine therapy. Self-traumashould be reduced with hard or soft cup hoods.

A “crater-like” defect that retains fluorescein dyeat its periphery but is clear in the center is a de-scemetocele and indicates the globe is at high risk ofrupture. Descemet’s membrane does not retain flu-orescein dye, whereas deep ulcers that continue tohave stroma anterior to Descemet’s membrane willretain fluorescein. Deep penetration of the stromato Descemet’s membrane with perforation of the cor-nea is a possible sequelae to all corneal ulcers inhorses. An iris prolapse will occur if Descemet’smembrane ruptures from a progressive ulcer or cor-neal laceration. Iris prolapse surgical repair is bestfor traumatic lacerations, small corneal lesions, andrecent rupture (Fig. 10).1,4

AntibioticsBacterial and fungal growth must be halted and themicrobes rendered non-viable. Broad- spectrumtopical antibiotics are usually administered withculture and sensitivity tests aiding selection. Topi-cal antibiotic solutions interfere with corneal epithe-lial healing less than ointments. Gentamicin

Fig. 8. Fluorescein and rose bengal dyes are extremely impor-tant to the examination of the horse eye.

Fig. 9. (a) Ulcer retaining fluorescein dye. (b) Early fungal ulcers with rose bengal retention.





should be used in ulcers with evidence of stromalmelting only.1,4

Topically applied antibiotics, such as chloram-phenicol, gramicidin-neomycin-polymyxin B, genta-micin, ciprofloxacin, or tobramycin ophthalmicsolutions may be used to treat bacterial ulcers.Frequency of medication varies from q2h to q8h.

Cefazolin (55 mg/ml), chloramphenicol, bacitracin,and carbenicillin are effective against beta-hemolyticStreptococcus. Ciprofloxacin, amikacin (10 mg/ml),and polymyxin B (0.25% IV solution) may be usedtopically for gentamicin resistant Pseudomonas.

Collagenolysis PreventionSevere corneal inflammation secondary to bacterial(especially, Pseudomonas and beta-hemolytic Strep-tococcus), or much less commonly, fungal infection,may result in sudden, rapid corneal liquefaction andperforation (Figs. 11 and 12). Activation and/or pro-duction of proteolytic enzymes by corneal epithelialcells, leucocytes, and microbial organisms are re-sponsible for stromal collagenolysis or “melting.”1,4

Serum is biologically nontoxic and contains analpha-2 macroglobulin with antiproteinase activity.Growth factors are present in serum, but not foundin plasma. Autogenous serum administered topi-cally can reduce tear film and corneal protease ac-tivity in corneal ulcers in horses. The serum can be

administered topically as often as possible andshould be replaced by new serum every 5 days.Acetylcysteine (5–10%) and/or 0.17% sodium ethyl-enediamine tetra-acetic acid (EDTA) can be instilledhourly, in addition to the other indicated drugs, forantimelting effect until stromal liquefaction ceases.It may be necessary to use serum, EDTA, and ace-tylcysteine simultaneously in severe cases.1,4

Treat UveitisAtropine sulfate is a common therapeutic agent forequine eye problems. Topically applied atropine(1%) is effective in stabilizing the blood-aqueous bar-rier, reducing vascular protein leakage, minimizingpain from ciliary muscle spasm, and reducing thechance of synechia formation by causing pupillarydilatation. Atropine may be used topically q4h toq6h with the frequency of administration reduced assoon as the pupil dilates.1,4

Topical atropine has been shown to prolong intes-tinal transit time and reduce and abolish intestinalsounds in the small intestine and large colon of

Fig. 10. (a) Iris prolapse in a horse. (b) Conjunctival flapcovers the defect to save sight and the eye 3 wk after surgery.

Fig. 11. Severe melting from a Pseudomonas-infected ulcer.

Fig. 12. Fungal ulcer with melting.





horses. Some horses seem more sensitive than oth-ers to these atropine effects and may “respond” bydisplaying signs of colic. Cecal impaction may oc-cur secondary to topical atropine administration.1,4

Systemically administered nonsteroidal anti-in-flammatory drugs (NSAIDs) such as phenylbuta-zone (1 g, q12h, PO) or flunixin meglumine (1 mg/kg,q12h, IV, IM, or PO) can be used orally or parenter-ally and are effective in reducing uveal exudationand relieving ocular discomfort from the anterioruveitis in horses with ulcers.

Topical NSAIDs such as diclofenamic acid (q12hto q8h) can also reduce the degree of uveitis.

Adjunctive Surgical Therapy

Bandage Soft Contact Lens

Bandage soft contact lens (SCLs) help to maintainapposition of the healing epithelium to the stroma,reduce pain, and protect the new epithelium. Dis-advantages include an occasional poor fit in horses,thereby resulting in limited retention times.1,4

Debridement, Keratectomy, and Keratotomy

Removing necrotic tissue and microbial debris bykeratectomy speeds healing, minimizes scarring,and decreases the stimulus for iridocyclitis. De-bridement to remove abnormal epithelium of refrac-tory superficial erosions can be accomplished withtopical anesthesia and a cotton-tipped applicator.Superficial punctate or grid keratotomy of superfi-cial ulcers with a 20-gauge needle can increase theability of the epithelial cells to migrate and adhereto the ulcer surface in superficial ulcers.1,4

Conjunctival Flaps

Conjunctival grafts or flaps are used frequently inequine ophthalmology for the clinical managementof deep, melting, and large corneal ulcers, desce-metoceles, and perforated corneal ulcers with andwithout iris prolapse. To augment lost cornealthickness and strength, deep corneal ulcers threat-ening perforation may require conjunctival flapplacement. Conjunctival flaps are associated withsome scarring of the ulcer site. Coverage with a360°, hood, island, pedicle, or bridge flap shouldbe maintained for 4–12 wk. Reoccurrence of theinflammation may occur after premature flapremoval.1,4

Amniotic Membrane Flaps

Amniotic membrane transplantation may providedecreased fibrosis, reduced vascularization of cor-neal ulcers, and faster reepithelialization in horseswith superficial and/or deep corneal ulcers. Theymay be used alone or with conjunctival flaps. Theycontain antiproteinases that inhibit the proteinasesfound in the tears of horse eyes with cornealulcers.15

Third-Eyelid FlapsNictitating membrane flaps are used for superficialcorneal diseases including corneal erosions, neuro-paralytic and neurotropic keratitis, temporary expo-sure keratitis, superficial corneal ulcers, superficialstromal abscesses, and to reinforce a bulbar conjunc-tival graft.

Temporary TarsorrhaphyHorizontal mattress sutures enter the eyelid 2–3mm from the eyelid margin with the cutting needleemerging from at the central aspect (Meibomiangland line) of the eyelid margin and then reenteringthe apposing lid margin to exit in the skin; 4–0 silkor nylon is commonly used for this procedure.

EnucleationPanophthalmitis after perforation of an infected cor-neal stromal ulcer has a poor prognosis. Phthisisbulbi is likely to result after a chronically painfulcourse. Affected horses can be febrile and manifestsigns of septicemia. To spare the unfortunate ani-mal this severe pain, enucleation is the humanealternative.

Inappropriate Therapy and UlcersTopical corticosteroids may encourage growth ofbacterial and fungal opportunists by interferingwith non-specific inflammatory reactions and cellu-lar immunity. Corticosteroid therapy by all routesis contraindicated in the management of cornealinfections. Even topical corticosteroid instillation,to reduce the size of a corneal scar, may be disas-trous if organisms remain indolent in the cornealstroma.

Please Remember the Following

● Corneal ulcers are frequently not clearly visi-ble even with proper examination lighting

● All red or painful eyes must be stained withfluorescein and rose bengal dyes

● A slowly progressive, indolent course often be-lies the seriousness of the ulcer

● Corneal ulcers in horses may rapidly progressto descemetoceles

● Topical corticosteroids are contraindicatedwhen the cornea retains fluorescein stain

● Anterior uveitis caused by a corneal ulcer orstromal abscess may be very difficult to control

● Local anesthetics should not be used in treat-ment of corneal ulcers as they retard epithelialhealing

7. Fungal Ulcers in Horses

Fungi are normal inhabitants of the equine environ-ment and conjunctival microflora but can becomepathogenic after corneal injury. Aspergillus, Fusar-ium, Cylindrocarpon, Curvularia, Penicillium, Cys-todendron, yeasts, and molds are known causes offungal ulceration in horses.1,4





Ulcerative keratomycosis is a serious, sight-threatening disease in the horse.16 Blindness canoccur. The most often proposed pathogenesis of ul-cerative fungal keratitis in horses begins with slightto severe corneal trauma resulting in an epithelialdefect, colonization of the defect by fungi normallypresent on the cornea, and subsequent stromal in-vasion. Seeding of fungi from a foreign body ofplant origin is also possible. Some fungi may, how-ever, also have the ability to invade the cornealepithelium after disruption of the tear film.9

Stromal destruction results from the release ofproteinases and other enzymes from the fungi,tear film leukocytes, and keratocytes (Fig. 12).Fungi may produce antiangiogenic compoundsthat inhibit vascularization. Fungi seem to havean affinity for Descemet’s membrane with hyphaefrequently found deep in the equine cornea.Deeper corneal invasion can lead to sterile or in-fectious endophthalmitis. Saddlebreds seem tobe prone to severe keratomycosis, while Standard-breds are resistant.1,4

Diagnostic tests should include fluorescein androse bengal staining, corneal cytology, corneal cul-ture with attempted growth on both fungal and aer-obic plates, and biopsy if surgery is performed.Prompt diagnosis and aggressive medical therapywith topically administered antifungals, antibioticsand atropine, and systemically administeredNSAIDs will positively influence visual outcome andmay negate the need for surgical treatment.

Treatment must be directed against the fungi aswell as against the iridocyclitis that occurs afterfungal replication and fungal death. Therapy isquite prolonged and scarring of the cornea may beprominent. The fungi are overall more susceptibleto antifungal drugs in this order: natamycin � mi-conazole � itraconazole � ketoconazole � flucon-azole. Natamycin, 1% miconazole, 1% itraconazole/30% dimethyl sulphoxide, (DMSO) 0.2% fluconazole,0.15% amphotericin B, 2% Betadine solution, andsilver sulfadiazine can be used topically.1,4

Uveitis may be worse the day after initiation ofantifungal therapy caused by fungal death. Lufenu-ron (5 mg/kg, q6h, PO) is a chitin synthase inhibitorused orally to attack the fungal cell wall in horseswith keratomycosis. Systemically administereditraconazole (3 mg/kg, q12h, PO) or fluconazole (1mg/kg, q6h, PO) may be useful in recalcitrantcases.1,4

Conjunctival flap and penetrating keratoplastyare used in treating aggressive keratomycosis inhorses.

Viral Keratitis is seen as a superficial punctatekeratitis but is uncommon. Slight fluoresceinand/or rose bengal dye retention may be seen super-ficial to stromal neovascular capillary tufts. Clini-cal signs can intermittently wax and wane. Equineherpesvirus-2 has been identified. There is a vari-able response to topical antivirals, but topical

NSAIDs can be helpful. This can be seen as a herdproblem!1,4

8. Corneal Stromal Abscesses

Focal trauma to the cornea can inject microbes anddebris into the corneal stroma through small epithe-lial ulcerative micropunctures.1,4 A corneal abscessmay develop after epithelial cells adjacent to theepithelial micropuncture divide and migrate overthe small traumatic ulcer to encapsulate infectiousagents or foreign bodies in the stroma. Epithelialcells are more likely to cover a fungal than a bacte-rial infection. Reepithelialization forms a barrierthat protects the bacteria or fungi from topicallyadministered antimicrobial medications. Reepi-thelialization of stromal abscesses interferes withboth routine diagnostics and treatment (Fig. 13).1,4

Corneal stromal abscesses can be a vision-threat-ening sequelae to apparently minor corneal ulcer-ation in the horse. A painful, blinding chroniciridocyclitis may result. Most stromal abscesses in-volving Descemet’s membrane are fungal infections.The fungi seem “attracted” to Descemet’s membrane.

Medical therapy consists of aggressive use of top-ical and systemic antibiotics, topical atropine, andtopical and systemic NSAIDs. Both superficial anddeep stromal abscesses do not heal until they be-

Fig. 13. (a) Stromal abscess partially covered by blood vessels.(b) Stromal abscess deep in the cornea.





come vascularized. The patterns of corneal vascu-larization are often unique suggesting thatvasoactive factors are being released from the ab-scess that influences the vascular response.

Superficial stromal abscesses may initially re-spond positively to medical therapy. If reduced in-flammation of the cornea and uvea are not foundafter 2–3 days of medical treatment, surgical re-moval of the abscess should be considered. Dailyremoval of superficial epithelium may speed drugpenetration to the abscess site.

Penetrating Keratoplasty for Deep Corneal StromalAbscessesDeep lamellar and penetrating keratoplasties (PK)are used in abscesses near Descemet’s membrane,and eyes with rupture of the abscess into the ante-rior chamber. PK eliminates sequestered microbialantigens and removes necrotic debris, cytokines,and toxins from degenerating leukocytes in theabscess.1,4

Corneal transplantation is performed to restorevision, to control medically refractory corneal dis-ease, and to re-establish the structural integrity ofthe eye. Penetrating keratoplasty is consideredhigh-risk for rejection in infected, vascularized cor-neal tissue. Nearly all PKs in horses are in high-risk corneas. Fresh corneal grafts are preferred inhorse PK, but frozen tissue can be used. Fewequine PK grafts remain clear after theirvascularization.1,4

9. Cataracts in the Horse

Cataracts are opacities of the lens and are the mostfrequent congenital ocular defect in foals.1,4,6,17,18

Horses manifest varying degrees of blindness as cat-aracts mature. Very small incipient lens opacitiesare common and not associated with blindness.As cataracts mature and become more opaque, thedegree of blindness increases. The tapetal reflec-tion is seen with incipient and immature cataractsbut is not seen in mature cataracts.

Examination of the fundus may be difficult be-cause of the cataract. The rate of cataract progres-sion and development of blindness cannot bepredicted in most instances. Heritable, traumatic,nutritional, and post-inflammatory etiologies havebeen proposed for equine cataracts. Cataracts sec-ondary to equine recurrent uveitis (ERU) or traumaare frequently seen in adults. True senile cataractsthat interfere with vision are found in horses olderthan 20 yr. Increased cloudiness of the lens nor-mally occurs with age and is called nuclear sclerosis.It is common in older horses, but vision is clinicallynormal, because nuclear sclerosis does not causevision loss.

Equine Cataract Surgery

Most veterinary ophthalmologists recommendsurgical removal of cataracts in foals less than 6mo of age if the foal is healthy, no uveitis, or other

ocular problems are present, and the foal’s person-ality will tolerate aggressive topical medical therapy.Horses considered for lens extraction should bein good physical condition. General anesthesiawith its attendant risks is required for cataractsurgery.1,4,6,18

Slow or absent pupillary light reflexes (PLRs) mayindicate active iridocyclitis with or without posteriorsynechiation, retinal disease, optic nerve disease, oriris sphincter muscle atrophy. Afferent pupillarydefects in a cataractous eye cannot be attributed tothe cataract alone, as well as the fact that normalPLRs do not exclude some degree of retinal or opticnerve disease.

B-scan ultrasound and electroretinography arebeneficial in assessing the anatomical and func-tional status of the retina if a cataract ispresent.1,4

Phacoemulsification cataract surgery is themost useful technique for the horse. This extracap-sular procedure through a 3.2-mm corneal incisionuses a piezoelectric handpiece with an ultrasonictitanium needle in a silicone sleeve to fragment andemulsify the lens nucleus and cortex after removalof the anterior capsule. The emulsified lens is thenaspirated from the eye while intraocular pressure ismaintained. The thin posterior capsule is left in-tact. There is little inflammation postoperativelyin most horses following successful phacoemulsifica-tion cataract surgery and a quicker return to normalactivity with phacoemulsification.1,4

Postoperative Cataract Surgery Therapy and Results

Topically applied antibiotics, such as chloram-phenicol, gentamicin, ciprofloxacin, or tobramycinophthalmic solutions may be used pre- and postop-eratively. Topically applied 1% atropine is effec-tive in stabilizing the blood-aqueous barrier,minimizing pain from ciliary muscle spasm, andcauses pupillary dilatation. Topically applied cor-ticosteroids are essential to suppress postoperativeinflammation. Systemically administered NSAIDscan be used orally or parenterally, and are effectivein reducing anterior uveitis in horses with cataracts.Topically administered NSAIDs such as diclofenac,flurbiprofen, and suprofen must also be used to sup-press signs of anterior uveitis.

The results of cataract surgery in foals by experi-enced veterinary ophthalmologists are generallyvery good, with success near 80%. The cataractsurgical results in adult horses with cataractscaused by ERU are often poor.6,18

Aphakic Vision in Horses

Most reliable reports of vision in successful cataractsurgery in horses indicate vision is functionally nor-mal postoperatively. From an optical standpoint,the aphakic eye should be quite far-sighted or hy-peropic postoperatively. Images close to the eyewould be blurry and appear magnified.19





10. Diseases of the Uveal Tract

Equine Recurrent Uveitis (Periodic Ophthalmia, MoonBlindness, Iridocyclitis)

Equine recurrent uveitis (ERU) is a common causeof blindness in horses.1,4,20,21 It is an autoimmunedisease with multiple causes. Recurrence of ante-rior uveitis is the hallmark of ERU. The disease isbilateral in approximately 20%. Hypersensitivityto infectious agents such as Leptospira interrogansserovars is commonly implicated as a possible cause.ERU may represent a case of molecular mimicrywhere ocular antigens found in the horse eye areidentical to antigens found in Leptospiral and othermicrobial organisms. The presence of living Lepto-spira organisms is not necessary for disease produc-tion but is found in many cases.1,4 Autoimmuneactivity against retinal proteins and antigens is alsoan etiologic component of this disease.

Toxoplasmosis, brucellosis, salmonellosis, strepto-coccus, Escherichia coli, Rhodococcus equi, borrelio-sis, intestinal strongyles, onchocerciasis, parasitessuch as Halicephalobus deletrix, and viral infections(e.g., equine influenza virus, herpes virus 1 and 4,arteritis virus, and infectious anemia virus) havealso been implicated as causes of ERU with no con-sistency in isolation of these organisms from af-fected horses.1,4

Serology for Leptospira pomona can be used forprognostic evaluation of the likelihood of blindnessoccurring in one or both eyes. Seropositive (�1:400) Appaloosas (100%) � seronegative Appaloosas(72%) � seropositive non-Appaloosas (51%) � sero-negative non-Appaloosas (34%) at having blindnessoccur in at least one eye within 11 yr of the firstattack.21

Horses with ERU display increased lacrimationand blepharospasm. Subtle corneal edema, con-junctival hyperemia, and ciliary injection will bepresent initially and can become prominent as thecondition progresses. Aqueous flare, hyphema, in-traocular fibrin, and hypopyon may be observed.Miosis is usually a prominent sign and can result ina misshapen pupil and posterior synechiae. In-traocular pressure (IOP) is generally low, but ERUmay be associated with intermittent and acute ele-vations in IOP. Cataract formation may occur ifthe inflammation does not subside quickly. Cho-roiditis may result in focal or diffuse retinitis andexudative retinal detachments. The vitreous maydevelop haziness because of leakage of proteins andcells from retinal vessels.1,4

In acute stages of ERU, lymphocytic infiltrationwith some neutrophils can be found in the uvealtract, resulting in edema and plasmoid vitreous.Lymphocytes and plasma cells can surround theblood vessels of the iris, ciliary body, choroid, andretina. In chronic cases, corneal vascularization,permanent corneal edema, synechiation, cataractformation, and iris depigmentation or hyperpigmen-tation can result. Retinal degeneration indicated

by focal to generalized peripapillary regions of de-pigmentation in the nontapetum can result. Theoptic nerve head will appear pale if atrophic. Sec-ondary glaucoma and phthisis bulbi occur. Irre-versible blindness is a common sequelae to ERU.1,4

ERU Therapy

The major goals of treatment of ERU are to preservevision, decrease pain, and prevent or minimize therecurrence of attacks of uveitis. Specific preventionand therapy is often difficult, because the etiology isnot identified in each case. Treatment should beaggressive and prompt to maintain the transpar-ency of the ocular structures. Medications shouldbe slowly reduced in frequency once clinical signsabate. Therapy can last for weeks or months andshould not be stopped abruptly or recurrence mayoccur. Overall, the prognosis for ERU is usuallypoor for a cure to preserve vision, but the disease canbe controlled. The Appaloosa breed seems to sufferfrom the most severe cases.1,4

Some horses require life-long therapy!It is imperative to immediately differentiate a

painful eye in a horse as a result of ulcerative ker-atitis or stromal abscessation from the pain associ-ated with ERU by employing a fluorescein dye test.While corticosteroids are the treatment of choice forERU, they can lead to the rapid demise of an eyewith a corneal ulcer or abscess.

Anti-inflammatory medications, specifically corti-costeroids and nonsteroidal drugs, are used to con-trol the generally intense intraocular inflammationthat can lead to blindness. Medication can beadministered topically as solutions or ointments,subconjunctivally, orally, intramuscularly, and/orintravenously. Prednisolone acetate or dexameth-asone should be applied topically initially. Sys-temic corticosteroids may be beneficial in severe,refractory cases of ERU, but pose some risk of in-ducing laminitis.

The NSAIDs can provide additive anti-inflamma-tory effects to the corticosteroids and are effective atreducing the intraocular inflammation when acorneal ulcer is present. Flunixin meglumine, phe-nylbutazone, or aspirin are frequently used system-ically to control intraocular inflammation. Somehorses become refractory to the beneficial effects ofthese medications, and it may be necessary to switchto one of the other NSAID to ameliorate the clinicalsigns of ERU. Cyclosporine A, an immunosuppres-sive drug, can be effective topically for ERU.

Topical atropine minimizes synechiae formationby inducing mydriasis and relieving spasm of ciliarybody muscles. It also reduces capillary leakage.Although topically administered atropine can lastseveral days in the normal equine eye, its effect maybe only a few hours in duration in the inflamed ERUeye. The ease with which mydriasis can beachieved with intermittent use of atropine is animportant indication as to the stimulus intensity ofthe ERU. Gut motility can be markedly reduced by





atropine in some horses. Should gut motility de-crease during treatment with topically administeredatropine, one can either discontinue the drug orchange to the shorter acting tropicamide.

The use of systemically and topically adminis-tered antibiotics is often recommended for ERU.Antibiotics should be broad spectrum and appropri-ate for the geographic location of the patient. Topi-cal antibiotics are indicated in cases of uveitiscaused by penetrating ocular trauma or ulcerativekeratitis. Antibiotic treatment for horses with pos-itive titers for Leptospira remains speculative butstreptomycin (11 mg/kg, q12h, IM) may be a goodchoice for horses at acute and chronic stages of thedisease. Penicillin G sodium (10,000 U/kg, q6h, IVor IM) and tetracycline (6.6–11 mg/kg, q12h, IV) athigh dosages may be beneficial during acute lepto-spiral infections.

Tissue plasminogen activator (TPA) has been usedto accelerate fibrinolysis and clear hypopyon in theanterior chamber of horses with severe iridocyclitis.An intracameral injection of 50–150 �g/eye can bemade at the limbus with a 27-gauge needle undergeneral anesthesia. TPA should be avoided if re-cent hemorrhage (�48 h) is present.

Alternative Therapy for ERU

Homeopathic remedies (e.g., poultices of chamomileand oral methylsulfonylmethane) for ERU havebeen used. Acupuncture has been used to treatERU.8,9

Surgical Considerations for ERU

In addition to medical treatment, pars plana vitrec-tomy in horses with ERU has been used successfullyto remove fibrin, inflammatory cells, and debristrapped in the vitreous to improve vision and delaythe progression of the clinical signs. Vitrectomyseems more beneficial in European Warmbloodswith ERU than in Appaloosas with ERU in theUnited States. The reasons for this are not known.Cataract formation and acceleration occur in up to50% of eyes post-vitrectomy in both regions. Reti-nal detachment can also occur postoperatively aftervitrectomy.22

Sustained release intravitreal cyclosporine A im-plants may also be beneficial to treating ERU.Cyclosporine A inhibits T-lymphocytes to suppressthe immune response of the leukocytes present inthe horse uveal tract. This is a physiologicallysound approach to ERU therapy. Implants maylast 5 yr. Cataract acceleration is also a problemwith this technique.

11. Equine Glaucoma

The glaucomas are a group of diseases resultingfrom alterations of aqueous humor dynamics thatcause an intraocular pressure (IOP) increase abovethat which is compatible with normal function of theretinal ganglion cells and optic nerve.1,4

Horses with previous or concurrent uveitis, agedhorses, and Appaloosas are at increased risk for thedevelopment of glaucoma.1,4 Iris and ciliary bodyneoplasms can cause secondary glaucoma. Con-genital glaucoma is associated with developmentalanomalies of the iridocorneal angle in foals.

The infrequency of diagnosis in the horse may becaused, in part, by the limited availability of tonom-eters in equine practice, but also to the fact thatlarge fluctuations in IOP, even in chronic cases, maymake documentation of elevated IOP difficult (Fig.14). Dilated pupils, corneal band opacities, de-creased vision, lens luxations, mild iridocyclitis, andoptic nerve atrophy/cupping may also be found ineyes of horses with glaucoma.

The topically administered carbonic anhydrase in-hibitor dorzolamide (q12h), and the beta-blockertimolol maleate (0.5% q12h) have been used to lowerIOP in horses with varying degrees of success.The newer prostaglandin derivatives cause lowgrade uveitis and may exacerbate the IOP in horseswith glaucoma. Topical atropine therapy was oncethought to reduce the incidence of glaucoma inhorses with uveitis, but should be used cautiously inhorses with glaucoma as it may cause IOP spikes.

Laser destruction of the ciliary body (cyclophoto-coagulation) works the best at controlling IOP andpreserving vision in horses.

Contraindications/Possible Interactions

Conventional glaucoma treatment with miotics mayprovide varying amounts of IOP reduction in horses.Miotics and prostaglandins can potentiate the clin-ical signs of uveitis and should be used cautiously inhorses with anterior uveitis. The horse eye seemsto tolerate elevations in IOP for many months toyears that would blind a dog; however, blindness isthe end result. Buphthalmia can be associatedwith exposure keratitis.

Fig. 14. Tonopen used to check for glaucoma.





12. Retinopathies

Chorioretinitis

Chorioretinitis is inflammation of the choroid andretina. Inactive lesions are more often reportedthan active lesions. The tapetal region is rarelyaffected. It is manifested in equine eyes as focal“bullet-hole” retinal lesions, diffuse chorioretinal le-sions, horizontal band lesions of the nontapetal ret-ina, and chorioretinal degeneration near the opticnerve head. Active chorioretinitis appears as focalwhite spots with indistinct edges and as large dif-fuse gelatinous grey regions of retinal edema. In-active chorioretinitis can appear as circulardepigmented regions with hyperpigmented centers,or large areas of depigmentation that appear insome cases as the wings of a butterfly. Chorioreti-nitis may be found with or without the signs ofanterior uveitis found with ERU.

Lesions can be caused by infectious agents (e.g.,leptospirosis, EHV-1, Onchocerca cervicalis), im-mune-mediated uveitis of unknown origin, trauma,or vascular disease.1,4

Systemic NSAID medication is administered forchorioretinitis. Flunixin meglumine, phenylbuta-zone, or aspirin are indicated. Topical medicationdoes not reach the retina and is only indicated ifsigns of anterior uveitis are also present.

Congenital Stationary Night Blindness

Congenital stationary night blindness (CSNB) isfound mainly in the Appaloosa and is inherited as asex-linked recessive trait. Cases are also noted inThoroughbreds, Paso Finos, and Standardbreds.CSNB seems to be caused by a functional abnormal-ity of neurotransmission in the middle retina.1,4

Clinical signs include visual impairment in dimlight with generally normal vision in daylight andbehavioral uneasiness and unpredictability occur-ring at night. CSNB does not generally progress,hence its name, but cases of progression to visiondifficulties in the daytime are noted. Ophthalmo-scopic examination is normal.

Diagnosis is by clinical signs, breed, and electro-retinogram (ERG) with decreased scotopic b-waveamplitude and a large negative, monotonic a-wave.There is no therapy for this condition but affectedanimals should not be bred.

13. Retinal Detachments

Retinal detachment is a separation of the nine lay-ers of the sensory retina from the retinal pigmentepithelium (RPE). It is associated with slowly pro-gressive or acute blindness in horses. It can becongenital in newborn foals or acquired later in lifein adults. Retinal detachments can occur bilater-ally or unilaterally, and be partial or complete.Retinal detachments are a complication of ERU andare also associated with microphthalmos, headtrauma, perforating globe wounds, cataract surgery,and may be secondary to intraocular tumors.1,4

Complete retinal detachments are seen clinicallyas free-floating, undulating, opaque veils in the vit-reous overlying the optic disc. The tapetum is hy-perreflective. If the media of the eye are so opaque(e.g., corneal edema, cataract) that the fundus can-not be visualized, b-scan ultrasound can be used todiagnose the classic “seagull sign” of retinaldetachment.

Laser surgery and pneumatic retinopexy to reat-tach the retina are well described for the dog, buthave not yet been reported for the horse.

14. Sudden Blindness

Acute blindness may be associated with head orocular trauma, ERU, glaucoma, cataracts, intraocu-lar hemorrhage, exudative optic neuritis, retinal de-tachment, or CNS disease.1,4 Acutely blind horsesare extremely agitated, anxious, and dangerous.Horses recovering from anesthesia after enucleationof sighted eyes for SCC can be very confused andagitated in the postoperative period. Extreme careshould be used and the animals approached cau-tiously on the blind surgical side until the horseadapts to its condition.

Horses can adapt amazingly well to blindness,whether unilateral or bilateral, if allowed to adjustto their new condition. Several internet websitesare devoted to the care of blind horses and otherblind animals.

15. Eye Diseases Associated with Specific HorseBreeds

Appaloosa

1. CSNB2. Congenital cataracts3. Glaucoma4. ERU5. Optic disc colobomas

Arabian

1. Congenital cataracts

Belgian Draft Horses

1. Aniridia and secondary cataracts2. Cataracts

Morgan

1. Cataracts—nuclear, bilateral, symmetrical,and non-progressive

Quarter Horse

1. Congenital cataracts2. Entropion

Rocky Mountain HorseThe chocolate coat color is most often affected. Col-lectively the cornea, iris, and ciliary body lesions aretermed anterior segment dysgenesis.





1. Congenital miosis and corpora nigra and irishypoplasia

2. Macrocornea3. Ciliary cysts4. Cataract, lens luxation5. Retinal dysplasia, retinal detachment

Thoroughbred

1. Congenital cataracts2. Microphthalmia associated with multiple oc-

ular defects3. Retinal dysplasia associated with retinal de-

tachments in some cases4. Entropion5. Progressive retinal atrophy

Color Dilute Breeds

1. Iridal hypoplasia—photophobia

Standardbreds

1. Retinal detachments2. CSNB

Paso Fino

1. CSNB2. Glaucoma

American Saddlebred

1. Cataracts2. Aggressive keratomycosis

Warmbloods

1. Glaucoma2. ERU

Miniature Horses

1. Cataracts

Mules

1. Aggressive sarcoids

References1. Brooks DE. Equine ophthalmology. In: Gelatt KN, ed. Vet-

erinary ophthalmology, 3rd ed. Philadelphia, PA: LippincottWilliams & Wilkins, 1999;1053–1116.

2. Brooks DE, Blocker TL, et al. Histomorphometry of theoptic nerves of normal horses and horses with glaucoma. VetComp Ophthalmol 1995;5:193–210.

3. Roberts SM. Equine vision and optics. Vet Clin North Am[Equine Pract] 1992;8:451–457.

4. Brooks, DE. Equine ophthalmology—made easy. JacksonHole, WY: Teton NewMedia, 2002.

5. Ramsey DT, Ewart SL, Render JA, et al. Congenital ocularabnormalities of Rocky Mountain Horses. Vet Ophthalmol1999;2:47–59.

6. Cutler TJ, Brooks DE, Andrew SE, et al. Visual outcome inyoung horses undergoing phacoemulsification. Sarasota,FL: American College of Veterinary Ophthalmologists, 2001;31.

7. Knottenbelt DC, Kelly DF. The diagnosis and treatment ofperiorbital sarcoid in the horse: 445 cases from 1974 to1999. Vet Ophthalmol 2000;3:169–192.

8. Brooks DE, Clark CK, Lester GD. Cochet-bonnet aesthesi-ometer determined corneal sensitivity in neonatal foals andadult horses. Vet Ophthalmol 2000;3:133–138.

9. Brooks DE, Andrew SE, Denis HM, et al. Rose bengal pos-itive epithelial microerosions as a manifestation of equinekeratomycosis. Vet Ophthalmol 2000;3:83–86.

10. Neaderland MH, Riis RC, Rebhun WC, et al. Healing ofexperimentally induced corneal ulcers in horses. Am J VetRes 1987;48:427–430.

11. Burling K, Seguin MA, Marsh P, et al. Effect of topicaladministration of epidermal growth factor on healing of cor-neal epithelial defects in horses. Am J Vet Res 2000;61:1150–1155.

12. Strubbe DT, Brooks DE, Schultz GS, et al. Evaluation oftear film proteinases in horses with ulcerative keratitis. VetOphthalmol 3:111–120, 2000.

13. Samuelson DA, Andresen TL, Gwin RM. Conjunctival fun-gal flora in horses, cattle, dogs, and cats. J Am Vet MedAssoc 1984;184:1240–1242.

14. Sotozono C. Second injury in the cornea. The role of in-flammatory cytokines in corneal damage and repair. Cornea2000;19(suppl 3):S155–S159.

15. Lee SH, Tseng SC. Amniotic membrane transplantation forpersistent epithelial defects with ulceration. Am J Ophthal-mol 1997;123:303–312.

16. Andrew SE, Brooks DE, Smith PJ, et al. Equine ulcerativekeratomycosis: visual outcome and ocular survival in 39cases (1987–1996). Equine Vet J 1998;30:109–116.

17. Millichamp NJ, Dziezyc J. Cataract surgery in horses.Invest Ophthalmol Vis Sci 1996;37:S763.

18. Dziezyc J, Millichamp NJ, Keller CB. Use of phacofragmen-tation for cataract removal in horses: 12 cases (1985–1989).J Am Vet Med Assoc 1991;198:1774–1778.

19. Farrall H, Handscombe C. Follow-up report of a case ofsurgical aphakia with an analysis of equine visual function.Equine Vet J Suppl 1990;10:91–93.

20. Matthews AG, Handscombe MC. Uveitis in the horse:a review of the aetiological and immunopathological aspectsof the disease. Equine Vet J Suppl 1983;2:61–64.

21. Dwyer AE, Crockett RS, Kalsow CM. Association of lepto-spiral seroreactivity and breed with uveitis and blindness inhorses: 372 cases (1986–1993). J Am Vet Med Assoc 1995;207:1327–1331.

22. Werry H, Gerhards H. The surgical therapy of equine re-current uveitis. Tierarztl Prax 1992;20:178–186.





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Equine Ophthalmology - IVIS · Equine Ophthalmology Dennis E. Brooks, DVM, PhD Author’s address: American College of Veterinary Ophthalmologists, University of Florida, PO Box