Equine recurrent uveitis (ERU) is a complex autoimmune disease influenced by genetic and environmental factors. During active bouts of inflammation, affected horses demonstrate epiphora, blepharospasm, corneal edema, episcleral congestion, aqueous flare, and fibrin in the anterior chamber. With chronicity, posterior synechiae, cataract, retinal detachment or degeneration, lens luxation, and glaucoma can occur. Leptospira spp have been associated with ERU, and serum, aqueous humor, and vitreous can be tested for this organism. There is currently no cure for ERU, but horses are typically managed with topical corticosteroids and atropine, systemic NSAIDs, suprachoroidal cyclosporine implants, or vitrectomy.
Equine recurrent uveitis (ERU) is an important ophthalmic condition, with a reported prevalence of 2%–25% worldwide. The classic form of ERU is characterized by episodes of active intraocular inflammation followed by variable quiescent periods. However, some horses experience insidious ERU, in which subclinical ocular inflammation persists without obvious discomfort. With chronicity, the inflammatory bouts cause secondary ocular changes such as cataracts, lens luxation, glaucoma, phthisis bulbi, and retinal degeneration. As a result, ERU is the most common cause of blindness in horses.
Etiology and Pathogenesis of Equine Recurrent Uveitis
Equine recurrent uveitis is an autoimmune syndrome that ensues after an initial episode of acute uveitis. Although not every horse with a single bout of uveitis will develop ERU, horses that have experienced acute uveitis are at risk of developing ERU for several years after the primary episode. Numerous bacterial, viral, protozoan, parasitic, and noninfectious causes, including ocular trauma, have been linked to the initiation of ERU; however, the pathophysiology of ERU is complex and multifactorial.
Of the infectious causes investigated, Leptospira spp, especially Leptospira interrogans serovar Pomona, have been most studied with regard to their role in the initiation of ERU. The precise mechanisms by which Leptospira spp initiate ERU remain unknown; however, it is likely that loss of ocular immune tolerance, cross reaction between Leptospira organisms and self-antigen, and intra- and intermolecular epitope spreading all play critical roles.
There is no sex or age predisposition for ERU. The LP gene, responsible for white spotting, can be tested for and used to evaluate ERU risk in Appaloosas.
Genes of the major histocompatibility complex (MHC) have also been investigated and likely play a role in susceptibility to ERU and to leptospirosis as an inciting trigger for ERU. The prevalence of ERU varies with geographic region, with higher rates reported in tropical and temperate climates than in arid, dry climates, an observation that may be partially attributable to differences in persistence of pathogenic Leptospira spp within the environment. Thus, the underlying cause of the primary uveitis, genetic composition of the horse, and environmental factors are all integral to the development of ERU.
Clinical Findings and Lesions in Equine Recurrent Uveitis
Clinical findings associated with equine recurrent uveitis include acute clinical signs of active inflammation as well as chronic secondary complications.
Changes in ocular immunity allow leukocytes to invade the uvea and release proinflammatory cytokines such as prostaglandins and leukotrienes. These inflammatory mediators cause increased vascular permeability within the uvea, breakdown of the blood-ocular barrier, iris sphincter muscle spasm, decreased aqueous humor production, and ciliary body muscle spasm.
These changes are responsible for the classic clinical signs of acute uveitis:
epiphora
blepharospasm
corneal edema
episcleral congestion
aqueous flare
fibrin in the anterior chamber
These clinical signs in the anterior segment often obscure the posterior segment. Active posterior segment inflammation can result in vitreous haze secondary to cellular infiltrate, fibrinous traction bands, focal or diffuse retinal detachment, or chorioretinitis (see active uveitis, equine recurrent uveitis, and optic nerve atrophy images).
Courtesy of UC Davis Veterinary Ophthalmology Service.
Courtesy of UC Davis Veterinary Ophthalmology Service.
Chronic sequelae of ERU include the following:
corneal scarring
iridial fibrosis
corpora nigra atrophy
posterior synechia
cataract
lens dislocation
glaucoma
phthisis bulbi
chorioretinal scarring
Courtesy of UC Davis Veterinary Ophthalmology Service.
ERU can be unilateral or bilateral and can affect the eyes asymmetrically.
Horses with primary ocular disease, especially corneal disease, experience many clinical signs typical of ERU, especially epiphora, blepharospasm, miosis, and corneal edema. It is critical to differentiate primary corneal disease from ERU, considering the marked differences in treatment. A thorough ophthalmic examination and fluorescein stain are essential. A thorough ophthalmic examination, including fundoscopy, is also critical during prepurchase or soundness examinations. Horses with chronic ERU may exhibit subtle or no anterior segment clinical signs but have appreciable retinal degeneration and thus potential for vision compromise.
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Diagnosis of Equine Recurrent Uveitis
Thorough examination of both eyes
Tonometry
Fluorescein stain
Diagnosis of equine recurrent uveitis is based on characteristic clinical signs combined with a history of recurrent or persistent episodes of uveitis.
A thorough ophthalmic examination of the anterior and posterior segment is critical to observing clinical signs consistent with ERU and to excluding other primary ocular diseases. Tonometry should be performed in all cases to exclude glaucoma and document hypotony that is common with ERU. Application of fluorescein stain is important to assess corneal epithelial integrity and exclude reflex uveitis from ulcerative keratitis.
In cases of acute uveitis, a physical examination is performed to exclude systemic disease.
A CBC and serum biochemistry panel are often warranted as part of the minimum database. Specific tests may assist in determining the underlying cause of a primary bout of uveitis. Serological testing for Leptospira spp may confirm exposure to this common risk factor but is not helpful in determining treatment.
Anterior chamber or vitreous cavity paracentesis may help identify a causative organism; however, this procedure may cause severe intraocular damage and is not recommended.
Treatment, Prevention, and Control of Equine Recurrent Uveitis
Topical steroids and systemic NSAIDs to decrease inflammation
Topical atropine to decrease intraocular pain and cause mydriasis
Suprachoroidal implant or vitrectomy to decrease the uveitic episodes
Enucleation for blind, painful eyes
The primary goals of treatment for equine recurrent uveitis are to decrease inflammation, relieve discomfort, and prevent vision loss. If possible, the specific underlying cause should be diagnosed and addressed as part of the initial treatment regimen. Except in cases in which bacterial infection is present, systemic antimicrobials are not indicated.
Regardless of whether the underlying cause is identified, aggressive treatment with systemic and topical anti-inflammatory medications is initiated immediately to minimize damage from intraocular inflammation. Flunixin meglumine administered systemically (especially IV) is critical to the initial management of acute uveitis in horses. The typical initial IV dosage is 1.1 mg/kg, administered at the time of diagnosis, followed by 0.5–1.1 mg/kg, PO, every 12 hours for 5–7 days. As inflammation resolves, the dosage can be decreased to 0.25–0.5 mg/kg, every 24–48 hours for 1–3 months.
Because of the potential for renal toxicity, serum creatinine concentration is monitored weekly if flunixin meglumine is used for > 1 week. Horses treated with flunixin meglumine should also be observed for clinical signs of GI ulceration, and concurrent prophylactic administration of omeprazole (2 mg/kg, PO, every 24 hours) may be indicated.
If flunixin meglumine is not tolerated, phenylbutazone (2–4 mg/kg, PO, every 12–24 hours) or aspirin (10–25 mg/kg, PO, every 12–24 hours) can be used; however, neither is as potent or effective. Historically, horses with frequent recurrences of chronic, low-grade uveitis were managed medically with oral phenylbutazone or aspirin every 24–48 hours. Although most horses tolerate this regimen well, these medications can have adverse GI, hematologic, or renal effects, and these regimens frequently do not eliminate recurrence.
Systemic steroids, particularly prednisolone (100–300mg/500 kg horse (0.2–0.6 mg/kg), PO, every 24 hours), have been used to treat acute uveitis episodes; however, their longterm use has been associated with laminitis.
Topical steroidal medications, including dexamethasone (0.1% suspension or ointment) and prednisolone acetate (1% suspension), are very effective at decreasing inflammation and may initially be applied every 4–6 hours, depending on severity of the condition. The frequency of dosing should be decreased with improvement. Topical acetate and suspension preparations of steroids are designed to penetrate the cornea and achieve adequate uveal concentrations and are thus preferred to sodium phosphate formulations. The patient should be monitored for the development of corneal ulcers while undergoing treatment because healing may be complicated by topical steroids. Topical hydrocortisone should be avoided, because it lacks adequate corneal penetration and is not sufficiently potent to treat anterior uveitis.
A fluorescein stain is warranted before initiation of topical steroids because these medications are contraindicated with corneal ulceration or infection. Topical nonsteroidal medications include flurbiprofen (0.03% solution) and diclofenac (0.1% solution); they are less potent than topical steroids but offer a wider safety margin in cases of concurrent corneal disease. Frequency of administration depends on inflammation severity; initially, administration may be every 4–6 hours. With improvement in clinical signs, frequency of administration of topical steroidal or nonsteroidal medications can be gradually decreased. However, treatment should continue for 1 month after complete resolution of active inflammation.
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Topical atropine (1% solution or ointment) causes mydriasis (which decreases the likelihood of posterior synechia formation) and cycloplegia (which decreases pain associated with ciliary body muscle spasm) and stabilizes the blood-aqueous barrier. Atropine is applied topically every 8–12 hours until the pupil is widely dilated; the frequency can then be adjusted to maintain mydriasis. Because atropine decreases GI motility, horses treated with topical atropine should be monitored for clinical signs of ileus.
Topical cyclosporine does not adequately penetrate the cornea and reach therapeutic concentrations in the aqueous humor, so it is not an appropriate treatment for ERU.
If frequent topical medication is not possible, subconjunctival injections of triamcinolone acetamide (1–2 mg) provide adequate intraocular anti-inflammatory concentrations for 7–10 days. Triamcinolone acetamide is less likely to cause abscess or granuloma formation than other steroids, including methylprednisolone acetate (10–40 mg). However, all subconjunctival steroids should be used with caution, because they cannot be easily removed once injected and can have devastating consequences if an infectious component is present or a corneal ulcer develops. Doses of subconjunctival anti-inflammatories should not be administered more frequently than once every 1–3 weeks.
Two surgical procedures are commonly used in longterm management. A suprachoroidal cyclosporine implant is a sustained-release medication device that provides therapeutic concentrations of cyclosporine A, an immunosuppressive T-cell inhibitor, for approximately 3 years after implantation. During this procedure, a cyclosporine A disk (approximately 5 mm in diameter) is implanted under a scleral flap created approximately 8 mm posterior to the dorsolateral aspect of the limbus. Horses with implants have markedly fewer uveitic episodes than they did before surgery, and this device results in effective longterm control of ERU (see suprachoroidal cyclosporine implant image).
Courtesy of UC Davis Veterinary Ophthalmology Service.
Core vitrectomy removes virtually all of the vitreous through an incision posterior to the dorsolateral aspect of the limbus. The vitreous is then replaced with either balanced salt solution or saline (0.9% NaCl) solution. The theorized benefit of this procedure is that organisms, especially Leptospira spp, or inflammatory cells in the vitreous substantially contribute to the chronic inflammation of ERU. By removing these factors, the frequency and severity of uveitic episodes are minimized.
Enucleation should be recommended for eyes that are blind or painful from ERU.
Good husbandry practices to manage ERU can ensure proper health maintenance, prevent ocular trauma, and decrease environmental triggers. Specific management recommendations include the following:
routine deworming and vaccinations
proper nutrition and dental care
quality fly masks
minimizing contact with cattle or wildlife
draining stagnant ponds or restricting access to swampy pastures
effective fly control
frequent bedding changes
Although such measures appear anecdotally to benefit individual horses, the extent to which they impact the clinical course of ERU has not been specifically evaluated.
Key Points
Equine recurrent uveitis is a common condition that can result in blindness and ocular pain.
Prompt diagnosis combined with medical, and sometimes surgical, management is typically necessary to maintain vision and ocular comfort.
For More Information
Kingsley NB, Sandmeyer L, Bellone RR. A review of investigated risk factors for developing equine recurrent uveitis. Vet Ophthalmol. 2022;26(2):86-100. doi:10.1111/vop.13002
McMullen RJ, Fischer BM. Medical and surgical management of equine recurrent uveitis. Vet Clin North Am Equine Pract. 2017;33(3):465-481. doi:10.1016/j.cveq.2017.07.003
Also see pet health content regarding equine recurrent uveitis.
