Equine Recurrent Uveitis (ERU) is the most common cause of equine blindness and it has an estimated yearly cost to the equine
community of 100 to 250 million dollars. The prevalence of equine uveitis has been estimated to be anywhere from 8 to 25%
in the general equine population. Overt costs accrue from medications for treatment and veterinary care. Indirect losses result
from poor performance, disruption of training, missed competitions and loss of use. Euthanasia for practical and economic
reasons is not uncommon. A clear understanding of the disease and client education is of paramount importance to support the
well being of the patient.
Uveitis can also be divided into two separate syndromes Classic ERU and Insidious ERU, which is the form most commonly found
in Appaloosas. Cases of classic ERU are characterized by intense bouts of intraocular inflammation followed by periods of
clinical quiescence. Research has shown however, that even in the absence of overt inflammation intraocular damage is ongoing.
The insidious form of uveitis does not show overt painful episodes of inflammation. Subtle signs of low grade chronic intraocular
inflammation often go unnoticed until the disease is far progressed. Uveitis in the horse is considered recurrent if more
than two episodes have been observed to occur. After a single episode of inflammation the risk of recurrent episodes is decreased
after two or more years of a disease free state.
Anatomy of ERU:
The anterior uvea consists of the iris and the ciliary body, while the posterior uvea is made up of the choroid. The choroid
is the major blood supply to the retina in the horse and this structure lies between the sclera and the retina. In total,
the uveal tract contains the majority of the blood supply to the eye and maintenance of ocular health depends upon maintenance
of a barrier between the vascular system and the internal ocular environment via the blood ocular barrier. The blood ocular
barrier prevents the migration of large molecules into the intraocular environment and maintains the eye's immune-privileged
status.
Ocular Pathology & ERU:
All cases of uveitis result from damage to the uveal tract causing the release of inflammatory mediators, prostaglandins,
leukotrienes and histamines. Inflammation of the uveal tissues manifests as vascular congestion. Dilation of scleral and
conjunctival blood vessels appears as a "ciliary flush" that gives an inflamed eye its red appearance. Inflammatory mediators
cause the ciliary and iris sphincter muscles to spasm and cause discomfort. Additionally, inflammatory mediators cause increased
vascular permeability and breakdown of the blood aqueous barrier which leads to the leakage of protein, fibrin and cells into
the aqueous humor. These inflammatory responses cause the common clinical signs of uveitis, including blepharospasm, increased
lacrimation, aqueous flare, hypopyon, fibrin accumulation and miosis.
Uveitis also frequently causes inflammation of the eyelids, conjunctiva, cornea, lens, retina, and optic nerve can be observed.
Blepharospasm, increased serous to mucopurulent discharge, chemosis and conjunctival hyperemia are typical in cases of ERU.
Corneal cloudiness or edema is commonly seen. Edema results from inflammatory damage to the corneal endothelial cells in contact
with the aqueous humor. Normally, the metabolic pump mechanism within the endothelial cells draws water out of the corneal
stroma and replaces it into the aqueous humor; this function is diminished in the inflamed eye. In addition to edema, 360
degrees of neovascularization of the corneal stromal tissue occurs after several days of inflammation.
Aqueous flare, the cloudy appearance of floating particles with in the anterior chamber, is a hallmark of ERU. The accumulation
of non-cellular exudate causes the disfunction of the ciliary body resulting in a reduction in aqueous humor production giving
the hypotonia that is found in uveitic eyes. Hypopyon, can be observed with the settling of inflammatory cells into the ventral
aspect of the anterior chamber and intraocular bleeding occur in severe cases.
The iris spincter and ciliary body muscles are affected by the inflammatory mediators in uveitis, causing ciliary body and
spincter muscles to spasm resulting in marked miosis. The iris can also take on a dull appearance with mottled pigmentation
and hyperemia. Chronic cases of ERU can exhibit atrophy of the granular irides (corpra nigra) and hyperpigmentation of the
iris tissue.
Early lens opacities in uveitis consist of inflammatory exudate adhering to the lens capsule. Areas of pigment can develop
on the lens surface from pigment migration from the iris or from posterior synechia of the iris to the lens. With changes
in aqueous humor composition, the metabolism of the lens is compromised, and lens transparency is reduced resulting in cataract
development. In chronic cases of ERU the inflammation can cause the premature degeneration or detachment of lens zonules resulting
in anterior or posterior lens luxation.
