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Looking Towards Treatments for Equine Recurent Uveitis

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Looking Towards Treatments for Equine Recurent Uveitis Vet Times The website for the veterinary profession https://www.vettimes.co.uk LOOKING TOWARDS TREATMENTS FOR EQUINE RECURENT UVEITIS Author : Claudia Hartley Categories : Vets Date : May 25, 2009 Claudia Hartley discusses a condition that, according to some estimates, can affect up to 25 per cent of horses, and reveals her opinions on care EQUINE recurrent uveitis (ERU) is an immune-mediated inflammation of one or both eyes that is relapsing and remitting in nature. Prevalence rates have been estimated to be between eight and 25 per cent in a number of studies. The first episode of uveitis typically occurs between four and eight years of age, although not exclusively. Subsequent inflammation flare-ups follow an unpredictable course, as recurrences can be seen weeks or months after quiescence from the first attack. Initially, recurrences were thought to follow the moon cycles and, therefore, the condition was originally known as moon blindness. Horses or ponies that suffer a single episode of uveitis are not considered to have ERU until a relapse is seen – in effect, until they suffer two or more episodes of uveitis. As a relapse may be seen up to two years after the first attack, the risk of developing ERU is very much less if more than two years pass without a second episode. The same is true for unilateral cases; these may become bilateral with time, but that risk is much reduced if two or more years pass without the fellow eye being affected. 1 / 22 Studies have identified a genetic susceptibility associated with equine leucocyte antigen-9 (ELA-9), similar to the association of certain human leucocyte antigen haplotypes and some autoimmune uveitides in humans. The Appaloosa breed is particularly prone to ERU, and when it occurs, it appears to be particularly aggressive in this breed. Figure 1 shows an example of some clinical signs. Note the blepharospasm of the right eye. Where this is more subtle, the angle of the eyelashes is a good indicator of ocular pain, as they are directed more vertically, rather than at 45º. Examination of the affected eye often initiates profuse lacrimation and discomfort, necessitating sedation with or without local nerve blocks. These include an auriculopalpebral block (Figure 2), which is a motor block allowing the eye to be opened, and a supraorbital block (Figure 3), which is a sensory block that is particularly useful if a lavage system is to be placed in the upper eyelid. The conjunctiva may be hyperaemic, and deeper layers – such as the episcleral vessels – are similarly affected. Corneal oedema may or may not be present, secondary to endothelial cell dysfunction caused by the intraocular inflammation. Aqueous flare, due to increased protein leakage into the aqueous humour, can be seen with a focal bright light, particularly if held at a tangent while examining the eye (seen rather like smoke across a pub room lit by a torch – although not these days), and is pathognomonic for uveitis. This is usually accompanied by miosis, which is often best appreciated by looking at both eyes from a distance using a direct ophthalmoscope to retroilluminate the pupils. Posterior uveitis may appear relatively benign externally, and is frequently missed by owners. A more insidious form of ERU may be present, with persistent low-grade intraocular inflammation that leads to vision loss in the absence of outwardly painful episodes. This insidious ERU has been reported to be more common in Appaloosas and draft breeds. Evidence of chorioretinitis (either active inflammation, seen as grey-white changes within the retina, or inactive scarring, seen as either areas of tapetal hyperreflectivity in the tapetal fundus or depigmentation in the non-tapetal fundus) may be apparent, and is often accompanied by vitreal degeneration. Clumps and strands of inflammatory material are frequently seen in the anterior vitreous, near the ciliary body. Figures 4a and 4b and show a cob pony with bilateral severe acute uveitis following foaling. Figure 5 displays a horse with ERU of the left eye that had been on treatment for two weeks, while Figure 6 shows a pony with chronic uveitis of the right eye. Calcific band keratopathy (Figure 7a) is also seen as a chronic lesion of ERU, presenting as an area of corneal lipid and/or calcium deposition in the anterior stroma of the cornea. The interpalpebral 2 / 22 portion of the cornea is most commonly affected – thus forming a band-shaped lesion. This area may ulcerate, causing ocular pain and complicating the treatment of the ERU with topical steroids. It is best treated with a superficial keratectomy (Figure 7b) to remove the affected stroma. Once healed, this will allow continued treatment of the uveitis with topical steroids. Immunohistochemistry Immunohistochemistry has demonstrated how ERU inflammation is largely CD4+ T cell driven. The ciliary body epithelium has also been shown to produce cytokines that stimulate equine lymphocytes. High interferon-( and interleukin-2 concentrations have been demonstrated in the aqueous and vitreous humour of ERU cases. Identifying triggering factors for relapses is a major area of research. A huge amount of speculation surrounds the cause of ERU. Leptospirosis has been implicated as a cause of ERU, with some evidence supporting this hypothesis. Experimental infection of ponies with Leptospira interrogans s erovar pomona resulted in uveitis in all cases nearly a year following exposure, with some ponies developing repeated episodes of ocular inflammation. Leptospiral DNA has been identified in the aqueous humour and vitreous humour in ERU cases. In Germany, this has been documented more substantially than similar studies in the USA. So far, similar studies in the UK have not been published. A serological survey of ERU cases in the UK was reported, but did not show a significant association between serum titres and uveitis. Subsequent studies have, however, shown that serological titres are poorly correlated with disease and that the presence of leptospiral organisms, DNA or antibodies can be demonstrated in the absence of serological conversion. Studies from the USA and Germany suggest that leptospiral molecular mimicry of ocular antigens exists, and may be responsible for the development of repeated episodes of uveitis. Elegant research, again in Germany and the USA, has demonstrated that a number of selfantigens are implicated in recurrent inflammation, most notably retinal S-antigen and interphotoreceptor- binding protein. Medical therapy Vision preservation and pain relief are the goals of therapy for ERU. Control of ocular inflammation is, therefore, the mainstay of treatment. Where high titres or, better still, rising titres are demonstrated to L interrogans serovars, antibacterial therapy should be considered. Vaccination against Leptospira using bovine vaccines 3 / 22 in horses has not been demonstrated to be beneficial. Treatment to control ocular inflammation should be aggressive. Apparent failures of treatment are often due to treatment inadequacies. Topical corticosteroids are the most commonly employed anti- inflammatory drugs. Prednisolone acetate or dexamethasone hydrochloride (also available in combination with neomycin and polymixin B) have good ocular penetration. The minimum treatment should be a six-times-daily application, and as this is frequently difficult for horse owners, a subpalpebral lavage system should be considered to facilitate treatment. Infusion pumps can be connected to this system, allowing hourly medication and the avoidance of a head- shy horse. The subpalpebral lavage system can be placed in the upper or lower eyelid, and opinions vary as to the most suitable location. It is important that the footplate of the lavage system is placed well into the conjunctival fornix, so that it cannot impinge on the cornea and cause an ulcer. Such complications are difficult to deal with, given that topical corticosteroids must be discontinued and, therefore, one arm of inflammatory control would be lost. Atropine application will help to dilate the pupil and relieve ciliary spasm, thereby alleviating a great deal of ocular pain. Atropine is also reported to assist in stabilising the blood aqueous barrier. It should only be applied in a manner sufficient to keep the pupil maximally dilated; some atropine will be absorbed systemically and can cause ileus. Monitoring for signs of colic is important in horses receiving atropine, and all owners should be made aware of the risks. If a pupil fails to dilate with two applications of atropine, it is unlikely to do so with atropine alone. Aggressive control of ocular inflammation may enhance the mydriatic effect of atropine by removing the miotic stimulus. The addition of phenylephrine to the topical medications may assist in mydriasis. However, topical 10 per cent phenylephrine has been associated with hypertension in humans and, therefore, should be used with caution in animals with cardiovascular disease. Systemic NSAIDs are an important facet of treatment. The most severe cases usually require flunixin, often in excess of the licensed five-day course. Again, owners must be made aware of this, as well as the risks of gastric and renal side effects. Once inflammation is better controlled, weaning on to phenylbutazone may be appropriate, although risks of gastric and renal side effects do remain. The use of corticosteroids systemically can be considered, but the attendant laminitis risks should be thoroughly discussed with the owner. In addition, the dose should be tapered, not abruptly ceased. 4 / 22 Identifying triggering factors for relapses is a major area of research. Treating inflammatory episodes fails to tackle the underlying disease, with each episode causing increasing permanent damage and a closer step toward blindness. This has led to the development of surgical treatments for ERU that aim to reduce the frequency and severity of future attacks. Surgical treatments • Pars plana vitrectomy Vitrectomy (Figure 8) is a highly specialised procedure, where the vitreous gel’s core is removed and replaced with saline. The idea is to remove inflammatory cells and cytokines that are sequestered in the vitreous humour.
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