Equine recurrent uveitis (ERU) is the leading cause of blindness in horses. The disease has been recorded worldwide and affects all breeds of horse although some (Appaloosa, European Warmbloods) seem to be more predisposed to the disease. ERU is not a disease that we can completely cure in most cases and the goal of treatment is to control the signs of the disease and reduce vision loss and discomfort. The disease can occur at any age but often appears at between 4-8 years of age and can affect one or both (in about 20% of horses) eyes.
What is ERU?
ERU is recurring
inflammation of the vascular layers of the eye - the iris, ciliary body and choroid. The uvea is responsible for production of the aqueous humor of the eye which provides nutrition to other ocular structures - the cornea, lens and retina. Inflammation of the uvea affects aqueous production which in turn affects the metabolism and function of these other structures. Uveal inflammation can also cause scarring inside the eye which will further affect vision. At each recurrent flare up of the inflammation more damage occurs in the eye, leads to to increased scarring and reducing vision. In between periods when the inflammation is active the eye may go through periods when the inflammation is much reduced (quiescent). Some horses seem to have continuous persistent inflammation which merely varies in severity over time.
Long term consequences of chronic uveitis are cataract formation, lens dislocation due to zonule damage, glaucoma and retinal detachment. (top of page)
What causes ERU in horses?
We still do not definitively know the cause of ERU. Over many years of study a consensus has emerged that ERU is mediated by the immune system - attacking either organisms infecting the eye or ocular tissues in the eye itself that may to the immune system resemble organisms. The most common worldwide association with an infectious disease has been Leptospirosis. However other possible bacterial, viral, parasitic and immunological causes have been cited over the years. It is likely that many factors (including the horses own genetic makeup) could be involved in causing or affecting the progress of ERU.
Recent research suggests that some insult to the eye (infection with bacteria or virus or an ocular injury) initiates the first bout of inflammation. Inflammatory cells (lymphocytes) enter the eye and contribute to the inflammation. The inflammation gradually subsides but lymphocytes remain in the eye. Over time these cells become re-activated against various antigens in the eye resulting in recurring bouts of inflammation.
There is also the likelihood that ERU is not simply one disease but rather a group of diseases which vary in the breeds most affected and in their cause in different parts of the world. The diagnosis of ERU is based on the clinical signs and the history of recurrence - periods of active inflammation interspersed with quiescent periods. In many cases the inflammation never entirely subsides but persists with mere variations in the severity over time. (top of page)
Can horses develop eye inflammation that is not ERU?
Horses often develop uveitis that is not ERU - this may be associated with injures to the eye, corneal ulceration, other intraocular diseases such as cataract and tumors of the uvea. It is important to differentiate these from ERU since some will readily respond to treatment and not recur whereas others (tumors) need to be treated in a very different way to the manner in which we treat ERU. To be considered ERU the inflammation becomes clinically apparent on at least 2 occasions.
What are the signs that a horse has ERU?
Horses with ERU often have increased blinking and squinting (blepharospasm), increased tearing (lacrimation) and are often photophobic (keep eye closed in bright light). The first sign often noticed by owners in the squinting and tearing down the face below the eye. Some horses with inflammation in the posterior parts of the eye (retina, choroid and optic nerve) may not show these signs but rather have visual deficits on the affected side). I have seen horses blind in one eye from ERU where owners were not aware there was a significant problem.
The white part of the eye may be red (conjunctival hyperemia) and the cornea (clear window at front of the eye) may appear cloudy due to fluid accumulation (edema). The cloudy appearance may be increased by protein (aqueous flare) and inflammatory cells in the anterior chamber between the cornea and iris and lens. Other signs that may be detected during an ophthalmic examination are clot material (fibrin) in the anterior chamber and inflammation cells layered at the bottom of the anterior chamber (hypopyon).
The pupil is often small in the affected eye and the iris may adhere to the lens capsule (synechia) and cataracts may be found. Vision may be limited the inflammatory changes in the front part of the eye or by inflammation in the back of the eye affecting the retina, choroid or optic nerve.
In chronic cases, in addition to the signs above, there may be total development of cataract, elevation of intraocular pressure (glaucoma), dislocation of the lens and retinal detachment fro the back of the eye.
A thorough examination of BOTH eyes by a veterinary ophthalmologist is recommended to identify all of the lesions present and to differentiate ERU from other masquerading diseases.
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What other diagnostic tests may be needed?
Although the diagnosis of ERU is based on the recurring (or persistent) appearance of the signs mentioned above, there are some tests that may be performed to aid in making the diagnosis or identifying the extent of the lesions. In horses with cataracts, ultrasonography may be needed to examine the back of the eye.
Serology on blood samples to look for antibodies to Leptospirosis (leptospiral microagglutination test) may indicate previous exposure to this organism. In some cases a more valuable approach is to look for antibodies against Leptospirosis in the ocular fluids and compare the results to the blood values.
A complete blood cell count and serum biochemistries may be taken and in some cases tests for other infectious diseases such as equine viral arteritis and lyme's disease may be indicated. Since some cases of ERU have been associated with parasites and fecal sample may be requested to look for evidence of parasites in the intestinal tract.
ERU has been associated with a major histocompatibility antigen of the leukocytes (MHC class I haplotype ELA-A9) this may be tested for to determine whether the ocular inflammation present is likely to be ERU or some other form of uveitis.
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What is the treatment for ERU?
In many cases there is no cure for this disease. Treatment aims to slow the progression and limit damage in the eye with each recurrent flare up of inflammation. Some lifelong treatment may be needed.
Medical therapy involves the use of corticosteroids (like prednisolone) and non-steroidal anti-inflammatory drugs (NSAIDs - like flurbiprofen) applied topically to the eye or given systemically by injection or oral medication. Discomfort and dilation of the pupil (to reduce iris scarring to the lens surface) is achieved with drugs like atropine when started early in the disease. Some cases receive systemic antibiotics.
ERU treatment can be complicated if corneal ulcers develop in a painful eye - use of corticosteroids s can prolong ulcer haling and may predispose to corneal fungal infections. in some parts of the USA it is quite common t see horses teated for ERU (especially given injections of steroids beneath the conjunctiva) develop fungal infection in the cornea.
In most cases we recommend initial hospitalization so that the condition can be treated vigorously when first diagnosed. We place a sub-palpebral lavage in the eyelid to facilitate frequent administration of medication during the initial 2 week period after which the medication frequency is tapered over a further 2-6 weeks - this can be done at home with ointments applied to the eye.
It is vitally important when treating ERU that flare ups are treated aggressively and that the use of medications is tapered off very slowly.
Are there any surgical treatments for ERU?
We have used suprachoroidal cyclosporine slow release implants to prolong the quiescent periods in ERU. This therapy is only indicated in cases in which the inflammation can be reduced by medications and the eye still has vision present. In the future other drugs such as tacrolimus may be used in similar implants to control ERU. Equine Eye Vets are participating in research on the use of cyclosporine implants with Dr. Brian Gilger, University of North Carolina.
Surgical removal of the vitreous gel from the back of the eye has been used in Europe to treat ERU. The rationale is that the vitreous gel of the eye may act as a reservoir of organisms or inflammatory cells. Vitrectomy is primarily recommended in cases which primarily involve the posterior part of the eye resulting in opacification of the vitreous gel.There is some evidence that this may be less effective in some of the cases seen in the USA. This may reflect breed related or geographic variations in the form of uveitis or a lack of experience with the surgical procedures in the USA. Further research is needed to evaluate this treatment. Horses which undergo vitrectomy may develop cataracts which may require further surgery to restore vision. Retinal detachment is another potential complication of this surgery.
In the near future new drugs may be available which will be injected into the eye to suppress the inflammatory cells involved in the disease. Although this is commonly used presently in people with recurrent uveitis some of the commonly used drugs may predispose horses to other problems such as fungal infections. We have to be careful not to merely extrapolate results from other species but devise treatment strategies which are specific for the horse to avoid such complications.
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