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Equine recurrent uveitis (ERU) is one of the most common ocular diseases in horses, classically characterized by episodes of active inflammation followed by varying periods of quiescence. During the so-called quiescent periods, low-grade, subclinical inflammation may continue in some horses. Regardless of the specific course, the inflammatory events eventually lead to secondary changes. These adverse secondary complications make this syndrome the most common cause of blindness in horses worldwide.
Etiology and Pathogenesis
ERU is an immune-mediated disease that follows an initial episode of acute uveitis. Not all horses that have an occurrence of acute uveitis will develop ERU. However, all horses with a history of a uveitic event remain at risk of developing ERU for at least 2 yr after the acute episode. Specific conditions or agents associated with the development of acute uveitis in horses include blunt or penetrating ocular trauma, leptospirosis, brucellosis, strangles (Streptococcus equi infection), onchocerciasis, equine influenza, tooth root abscess, and hoof abscess. There is no age or breed predisposition for developing acute uveitis. Among horses with ERU, Appaloosas, warmbloods, and draft breed horses are overrepresented. While horses can have an initial occurrence of ERU at any age, diagnosis at 4–8 yr old is typical. The most widely investigated infectious agents associated with ERU are the Leptospira spp, in particular L interrogans serovar pomona, although other serogroups have been implicated. A number of studies have demonstrated the persistence of leptospira in chronic ERU; however, the exact relationship between leptospirosis and ERU remains obscure.
Although the immunologic basis for the recurrent nature of uveitis has been extensively studied, detailed understanding of the factors involved remains elusive. Recent research suggests the presence of a genetic, autoimmune relationship with ERU. Taken together with the association of leptospirosis, it seems possible that the underlying pathogenesis of ERU may involve both infectious and heritable components.
Clinical Findings and Lesions
The clinical signs associated with equine recurrent uveitis include both acute signs of active inflammation and chronic secondary adverse effects. Damage to the uveal tract leads to the release of inflammatory mediators such as leukotrienes, prostaglandins, and histamines, which in turn causes increased permeability of anterior uveal vessels, breakdown of the blood-aqueous barrier, iris sphincter spasm, and ciliary body muscle spasm. The compromise of the blood-aqueous barrier allows for leakage of protein, fibrin, and cells into the aqueous. These responses account for the classic signs of acute uveitis: blepharospasm, epiphora, episcleral injection, corneal edema, aqueous flare, fibrin clots in the anterior chamber, and miosis. Often, the anterior segment signs restrict the visibility of the posterior segment. If visible, posterior segment signs of an acute episode may include an inflammatory cell infiltrate involving the retina and/or choroid, focal or diffuse retinal separation, retinal hemorrhage, and a hazy appearance to the vitreous secondary to infiltration by inflammatory cells or RBC. One or both eyes may be affected. When bilateral, it is not unusual for one eye to be more severely inflamed.
Corneal scarring, iridal fibrosis, blunting of the corpora nigra, posterior synechia, glaucoma, cataracts, and pigment clumping of the nontapetal fundus (retinal degeneration) are all signs consistent with chronic ERU. The importance of careful fundoscopy as a part of prepurchase or soundness examinations cannot be overstated. Horses with chronic uveitis may have few or no anterior segment signs but may manifest ERU by retinal degeneration. Such horses usually have normal or near-normal pupillary light responses and may not exhibit overt signs of visual compromise until late in the disease course. However, any horse with significant retinal degeneration must be suspected of having ERU and therefore also regarded as a likely candidate for future vision compromise.
Diagnosis
While the diagnosis is based on the presence of characteristic clinical signs, an attempt should be made to identify the underlying cause. Because an acute episode of uveitis can be the first sign of systemic disease, a thorough physical examination should always be performed in addition to the ophthalmic examination. A CBC and serum chemistry panel are often included as part of the minimum database. Specific tests may aid in finding an underlying cause of the initial episode of uveitis. Serologic testing for Leptospira spp is frequently advocated, although there is no evidence of a correlation between serology for Leptospira spp and leptospiral antibodies or organisms in the aqueous humor of horses with ERU. Paracentesis of either the anterior chamber or the vitreous cavity offers the possibility of identifying a causative agent; however, the procedure may cause severe intraocular damage and is discouraged.
Treatment, Prevention, and Control
Therapy is initiated as soon as possible once signs of the acute phase are recognized. If a specific underlying cause can be identified, it should be addressed as part of the initial treatment protocol. In addition to dealing with the causative agent, or in instances where no specific cause is found, aggressive therapy with both topical and systemic anti-inflammatory medications is started to minimize the damage associated with intraocular inflammation. Both steroidal and nonsteroidal topical medications are commonly used. Prednisolone acetate (steroid, 1% suspension), dexamethasone (steroid, 0.1% suspension or ointment), flurbiprofen (nonsteroidal, 0.03% solution), and diclofenac (nonsteroidal, 0.1% solution) have all been successfully used. When selecting a topically applied steroid, either prednisolone or dexamethasone are preferred to hydrocortisone, which penetrates the cornea poorly and is not sufficiently potent to be an effective medication for anterior uveitis. Additionally, the formulation of the topical steroid impacts penetration of the cornea and delivery of the medication to the anterior uvea. Because of this, acetate and suspension preparations are preferred over sodium phosphate formulations. Frequency of application depends on severity of the inflammation, but administration 4–6 times a day is common. As the signs resolve, the frequency can be slowly reduced. It is recommended that therapy be continued for 1 mo after the signs of acute inflammation have resolved. Topical atropine (1% solution or ointment) benefits horses with acute anterior uveitis by paralyzing the iris sphincter and ciliary body musculature. These effects reduce the likelihood of posterior synechia formation and markedly decrease the pain associated with ciliary body muscle spasm. Atropine is applied topically bid-tid until the pupil is widely dilated. The frequency can then be reduced to sid or once every other day as needed to maintain mydriasis. Although such a dosage schedule is well tolerated in most horses, gut motility should be monitored, because topically applied atropine can potentially lead to ileus.
Flunixin meglumine administered systemically, and particularly when given IV, may be the single most effective treatment of acute anterior uveitis in horses. The usual initial IV dose is 1.1 mg/kg, administered at the time of diagnosis. This is followed by a 5- to 7-day course at a dosage of 0.25–1.1 mg/kg, PO, bid. Because of the potential for GI and renal problems with the longterm use of flunixin meglumine, it is common to switch to oral phenylbutazone (2–4 mg/kg, sid-bid) after the initial treatment period. Alternatively, some horses respond better to aspirin (25 mg/kg, PO, sid-bid) after flunixin meglumine. Systemic steroids, specifically prednisolone (100–300 mg/day) and dexamethasone (5–10 mg/day) have also been successfully used to treat acute uveitis episodes, but their longterm use has been associated with laminitis. As the severity of the clinical signs lessens, the dosage and frequency of oral anti-inflammatory medications can be tapered over the 2- to 3-mo treatment period. If frequent topical medication is not feasible, subconjunctival injections of triamcinolone (10–40 mg), methylprednisolone acetate (10–40 mg), or betamethasone (5–15 mg) can supply therapeutic intraocular anti-inflammatory levels. However, these should be used with caution because they cannot be easily removed once injected and can have devastating consequences should an infectious component be present or a corneal ulcer develop. Except in instances when bacterial infection is present, systemic antibiotics are not indicated.
Historically, horses with frequent recurrences or chronic, low-grade uveitis were managed medically with daily (or every other day) doses of oral phenylbutazone or aspirin. Although most horses tolerate this regimen well, these medications can have adverse GI and hematologic adverse effects and the need for daily administration can lead to adherence problems. In addition, these regimens frequently do not eliminate recurrence.
In an attempt to address the problems of medical management alone, 2 surgical procedures have been developed. 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 saline or balanced salt solution. The theorized benefit of this procedure is that T lymphocytes and/or organisms in the vitreous significantly contribute to the chronic inflammation of ERU. By removing these elements, the frequency and severity of the inflammatory events can be minimized. Another surgical procedure for control of ERU is suprachoroidal cyclosporine implant. In this procedure, a cyclosporine A disk (~5 mm in diameter) is implanted under a scleral flap created ~8 mm posterior to the dorsolateral aspect of the limbus.
Good husbandry practices such as effective fly control, frequent bedding changes, routine worming and vaccinations, minimizing contact with cattle or wildlife, draining stagnant ponds or restricting access to swampy pastures, and maximizing nutrition have all been advocated as means to reduce the effects of ERU. While such measures benefit individual horses, the extent to which they impact the clinical course of ERU is debatable.
Last full review/revision July 2011 by Steven R. Hollingsworth, DVM, DACVO
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