Equine Uveitis Study Guide

Overview and Clinical Importance

Equine recurrent uveitis (ERU), also known as moon blindness or periodic ophthalmia, is the most common cause of blindness in horses worldwide. This immune-mediated condition affects 2-25% of horses globally, with approximately 56% of affected horses eventually becoming blind. ERU is characterized by recurrent episodes of intraocular inflammation affecting the uveal tract (iris, ciliary body, and choroid), followed by variable periods of quiescence.

The clinical and economic impact of ERU is substantial: more than 60% of affected horses cannot return to their previous level of work, and many require enucleation due to intractable pain or blindness. Understanding this condition is essential for NAVLE success, as questions frequently test knowledge of clinical signs, breed predispositions, pathophysiology, and treatment approaches.

Anatomy of the Uveal Tract

The uveal tract (also called the uvea) is the middle vascular layer of the eye and consists of three structures. The iris controls pupil size and light entry. The ciliary body produces aqueous humor and contains muscles for accommodation. The choroid provides blood supply to the outer retina. Inflammation of any part of this tract constitutes uveitis.

Classification of Equine Uveitis

Anatomical Classification

Three Clinical Forms of ERU

Classic ERU: Most common form. Characterized by acute inflammatory episodes alternating with periods of quiescence. Episodes are painful with obvious clinical signs. Most common in Warmbloods and Icelandic horses.

Insidious ERU: Low-grade, persistent inflammation without obvious painful episodes. Often goes unrecognized until significant ocular damage has occurred. Most common in Appaloosas and leopard complex spotted breeds.

Posterior ERU: Inflammation predominantly affects the posterior segment (vitreous, choroid, retina). Most common in Warmbloods, draft breeds, and horses imported from Europe.

Etiology and Pathophysiology

Leptospira spp. and ERU

Leptospira interrogans is the most strongly implicated infectious cause of ERU. Key serovars include Pomona (most common in North America), Grippotyphosa (common in Europe and North America), and Bratislava. Horses become infected through contaminated water, wet pastures, or contact with wildlife urine (especially rodents).

Pathogenesis: After systemic infection, Leptospira organisms can persist in the vitreous humor, protected from the immune system. The eye is considered an 'immune-privileged' site. Research has demonstrated that Leptospira forms biofilms within the vitreous, explaining the recurrent nature of inflammation and resistance to antibiotic therapy. Molecular mimicry occurs between leptospiral antigens (LruA, LruB, LruC outer membrane proteins) and equine ocular tissues (lens, cornea, retina), triggering autoimmune destruction.

Immune-Mediated Mechanisms

ERU is driven by CD4+ T cells with both Th1 (IFN-gamma producing) and Th17 (IL-17 producing) phenotypes. These autoreactive T cells cross the blood-retinal barrier during inflammatory flares, causing progressive destruction of uveal tissues. The release of prostaglandins, leukotrienes, and histamine causes the characteristic clinical signs of increased vascular permeability, ciliary muscle spasm, and breakdown of the blood-aqueous barrier.

Other Causes of Equine Uveitis

Breed Predispositions and Genetic Factors

Appaloosas: 8.3 times more likely to develop uveitis than other breeds. Four times more likely to become blind. The LP (TRPM1) gene responsible for leopard complex spotting is a major genetic risk factor. Homozygous LP/LP horses are at highest risk. Appaloosas typically develop insidious ERU with bilateral disease.

European Warmbloods and Draft breeds: Increased susceptibility, often develop classic or posterior ERU. MHC (major histocompatibility complex) genes on ECA1 are associated with disease risk.

Icelandic Horses: High prevalence of classic ERU with painful inflammatory episodes.

Clinical Signs

Acute/Active Uveitis Signs

Pain indicators: Blepharospasm (squinting), epiphora (tearing), photophobia, enophthalmos

Anterior segment: Corneal edema (cloudiness), episcleral/conjunctival injection (ciliary flush), aqueous flare, miosis (constricted pupil), fibrin in anterior chamber, hypopyon (settling of WBCs ventrally), hypotony (decreased IOP, typically less than 15 mmHg)

Posterior segment: Vitreous haze, vitreal cellular infiltrate, chorioretinitis, retinal detachment

Chronic/Quiescent Stage Signs

Iris changes: Posterior synechiae (iris-lens adhesions), iris hyperpigmentation, corpora nigra atrophy/degeneration, iris depigmentation at pupil margin, dull or 'muddy' iris appearance, rubeosis irides (iris neovascularization)

Lens changes: Pigment deposits on anterior lens capsule ('tombstone lesions' or 'footprints of synechiae'), cataract formation (focal or diffuse), lens subluxation or luxation

Posterior segment: Peripapillary chorioretinal scars ('butterfly lesions' - wing-shaped depigmentation), 'target lesions' (circular focal depigmentation), vitreal liquefaction with floaters, fibrinous traction bands, retinal degeneration/detachment

End-stage changes: Phthisis bulbi (globe shrinkage), secondary glaucoma, complete blindness

Diagnosis

Diagnostic Criteria for ERU

ERU is diagnosed when a horse has two or more separate episodes of uveitis in the same eye, OR evidence of chronic/insidious inflammation. A single episode of uveitis does not confirm ERU - horses remain at risk for years following an initial bout.

Complete Ophthalmic Examination

Laboratory Diagnostics

Serum Leptospira MAT: Low specificity due to high seroprevalence in normal horses (up to 75%). A titer greater than or equal to 1:100 is considered positive, but does not confirm ERU.

Aqueous/Vitreous Humor Analysis: More specific than serum testing. PCR for Leptospira DNA is 70% sensitive in ERU horses. MAT on ocular fluids is 90% positive in ERU vitreous samples. Calculate C-value (aqueous titer divided by serum titer) - a value greater than 1 indicates local antibody production.

Minimum Database: CBC and serum biochemistry to rule out systemic disease, especially in acute uveitis.

Differential Diagnosis

Treatment

Treatment goals: Decrease inflammation, relieve pain, prevent posterior synechiae, and minimize progression to blindness. Early aggressive treatment is associated with better outcomes.

Medical Management of Acute Episodes

Surgical Options

Suprachoroidal Cyclosporine Implant: A 5-6 mm sustained-release device implanted under a scleral flap approximately 8 mm posterior to the limbus. Provides therapeutic cyclosporine A concentrations for 3-4 years. Suppresses T-lymphocyte activity. Long-term studies show 78% retention of vision. Best candidates are horses with ERU controllable by medical therapy but with frequent recurrences. Not effective if already blind or have advanced cataracts.

Pars Plana Vitrectomy: Surgical removal of the vitreous through an incision posterior to the limbus, replaced with saline. Removes Leptospira organisms, inflammatory debris, and biofilm. Greater than 95% success rate in preventing further ERU episodes when Leptospira-associated. Requires general anesthesia, clear ocular media, and maximal pupil dilation. Contraindicated in eyes with glaucoma, phthisis bulbi, or retinal detachment.

Intravitreal Gentamicin Injection: Low-dose (4-6 mg) gentamicin injected intravitreally for Leptospira-associated ERU. Positive outcomes in 88-94% of eyes. Still considered investigational.

Enucleation: Recommended for eyes that are blind and painful, or those with intractable disease. Improves quality of life and eliminates ongoing pain.

Prognosis

Long-term prognosis for ERU is guarded to poor. Current treatments can slow progression but are not curative. Key prognostic factors include breed (Appaloosas have worse outcomes), time to diagnosis (early intervention improves prognosis), development of complications (cataracts and glaucoma worsen prognosis), and response to initial treatment.

Statistics: Approximately 56% of ERU-affected horses eventually become blind. More than 60% cannot return to previous levels of work. Horses with glaucoma or cataracts secondary to ERU are more likely to become blind and require enucleation.

Prevention and Environmental Management

While ERU cannot be completely prevented, the following husbandry practices may reduce risk and severity: minimize contact with wildlife and cattle (Leptospira reservoirs), drain stagnant water sources and restrict access to swampy pastures, provide clean drinking water, implement effective fly control, perform routine worming and vaccinations, ensure proper dental care, include regular eye examinations in routine health checks, and consider LP gene testing in Appaloosas before purchase.