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Equine Recurrent Uveitis
by Noelle La Croix, DVM, Dip. ACVO

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Equine Recurrent Uveitis
The complicated anatomy of the eye can be roughly divided into 3 layers: an outer fibrous layer (cornea and sclera), a middle vascular layer (choroid and iris), and an inner neurological layer (retina). Uveitis is defined as inflammation within the middle layer commonly called the uvea (Latin for ‘grape’). The name probably derives from early anatomists that would remove this small bluish-purple (grape-like) tissue from the human eye.

Inflammation is the body’s response to foreign invaders (bacteria, fungi, and viruses). This inflammation (Latin for ‘a setting of fire’) is mediated in verterbrates by white blood cells that release factors (cytokines) that cause swelling, redness, pain, and a sensation of heat. These immune processes are normal and they protect the body from disease. However, the delicate tissues of the eye can be easily damaged by these immune responses.

Many tissues of the eye are generally considered immunoprivileged. A special blood ocular barrier prevents small peptides (antigens), derived from foreign invaders, from freely flowing into or out of the eye. If some of these antigens do bypass the barrier, immune responses to them are then dampened by specialized T lymphocytes (white blood cells) and immunosuppressive cytokines. This ocular immune system will attempt to clear any foreign proteins from the eye, but the minimal response will supress any collateral damage to the eye. Ocular immune responses are therefore limited in nature, or wholly suppressed, so that any significant ocular inflammation is considered aberrant.

Some foreign antigens (particularly if present in great numbers) can overcome the blood ocular barrier and intensify an ocular immune response resulting in uveitis. There are three primary etiologies of uveitis: infectious, neoplastic, and autoimmune/idiopathic. The appropriate treatment for uveitis will depend upon its underlying etiology, a dampening of immune responses causing collateral damage, and the alleviation of any associated pain.

In suspected cases of equine uveitis, an initial evaluation should include a physical examination, an ocular examination, and basic serology (complete blood count with differential, and blood chemistry). Inflammation confined to the eye is not normally associated with elevations in inflammatory proteins (e.g. fibrinogen or serum amyloid A) within the bloodstream. Horses with suspected uveitis should also be tested for leptospirosis that has been associated with equine recurrent uveitis (ERU). Any other underlying causes for inflammation (e.g. an intraocular tumor) will also need to be addressed for full resolution of some cases of equine uveitis. If an underlying etiology cannot be determined, the uveitis is assumed to be autoimmune-mediated or idiopathic.

Medical therapy for equine uveitis includes pain management and the dampening of any immune response that may permanently damage the eye. Pain associated with ciliary body spasms can be alleviated with 1% atropine ointment applied maximally 4 times daily. Fecal output (as well as gut sounds) of the horse should be carefully monitored during this treatment. Systemic therapy for inflamation and pain can be tempered with oral Banamine (flunixin meglumine). Banamine is one of the most potent ocular anti-inflammatories prescribed for horses. Additional topical anti-inflammatories (either 0.1% dexamethasone or 1% prednisolone acetate) can also be applied from hourly to once daily as they are tapered. Other topical non-steroidal medications have been shown to be less effective than both dexamethasone and prednisolone in treating equine uveitis. Antiinflammatory dosages are initially maintained for 1 to 2 weeks and only tapered following the resolution of clinical signs. Fully resolved equine uveitis will typically require 6 to 8 weeks of treatment. It is advisable to continue medial therapy for an additional 1 to 2 weeks following resolution.

In cases of equine uveitis, it is important to consider if the occurrence was unique and self-limiting, or if it is part of a progressive recurring syndrome known as ERU. Appaloosa horses are especially prone to the development of ERU. A loss of ocular immune privilege may be the root cause of ERU in which the blood ocular barrier has permanently broken down allowing continuous exposure of the eye to foreign antigens, immune cells, and/or inflammatory cytokines derived from the bloodstream. In cases of ERU, white blood cells entering from the bloodstream form “follicles” within the eye creating a chronic state of inflammation. Leptospirosis may also be responsible for promoting an autoimmune response to the equine eye. Foreign peptides derived from invading Leptospira may promote and select for immune cells that cross-react with proteins of the equine eye. This “molecular mimicry” can result in a continuous immune response directed against the eye lasting well after the initial Leptospira have been eliminated.

There are three subclasses of ERU that have been described as classic, posterior, and insidious. Classic and posterior ERU present as recurrent bouts of uveitis associated with pain that are typically appreciated by horse owners (Figure 1). There is a predispostion for both classic and posterior uveitis in warmblood horses, and for classic ERU in Icelandic horses. In cases of insidious ERU owner’s do not typically appreciate their horse’s pain, but rather a color change of the horse’s eye (Figure 2). Insidious ERU presents low-grade inflammation with a gradual loss of function and/or necrosis of the eye (Figure 3). There is a predisposition for insidious ERU in the Appaloosa, Knabstrupper, and draft horse.

Recurrent equine uveitis that arises every 3 to 4 months, and that requires longer durations of treatment with each occurrence, can result in debilitating ocular complications including glaucoma and blindness. There are treatments shown to dampen these recurrent immune responses including intravitreal injections of steroids and/or gentamicin sulfate, as well as supracoroidal injections of steroids. Surgical options for ERU include suprachoroidal implantation of sustained release cyclosporine, and a dual-port pars plana vitrectomy. However, conservative medical management is the first line of therapy following an initial diagnosis of ERU. Horses diagnosed with ERU require diligent lifelong care to prevent blinding and painful complications. Care of horses with ERU is optimally facilitated by the guidance of a veterinary ophthalmologist.

Noelle La Croix, DVM, Dip. ACVO
Veterinary Medical Center of Long Island
75 Sunrise Highway
West Islip, New York 11795
(631) 587-0800; fax (631) 587-2006

Figure 1: Typical signs of classic ERU in the right eye of a warmblood horse with epiphora and blepharospasm.

Typical signs of classic ERU in the right eye of a warmblood horse with epiphora and blepharospasm.

Figure 2: Insidious ERU in the right eye of an Appaloosa horse.

Insidious ERU in the right eye of an Appaloosa horse.

Figure 3: Phthisis bulbi in the right eye of an Appaloosa horse with insidious ERU.

Phthisis bulbi in the right eye of an Appaloosa horse with insidious ERU.

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