Photosensitization and Photophobic Response in Horses

Most horses enjoy some time lazy time in the sun, but must also be able to access to a shady or covered area. The majority of horses are just fine when exposed to the sun, but just like humans some horses have reactions when exposed to the sun. In the cases of these horses their skin will often be sensitive and their eyes can be photosensitive, too. Head shaking may be present in a horse that has photosensitivity, as well.

Horses who have pink skin, that is, skin that does not have dark pigment are often photosensitive. The reason for this is because pink skin often lacks the protection that dark skin has to the UV rays of the sun. You will see horses with white muscles and pink skin around the eyes often present with actual sun burn. They will have scabs. Also, these horses are more prone to cancer. If you see a horse with runny eyes, squinting eyes, or rubbing its eyes the horse might be photosensitive. Protective masks or creams should be used to help protect your horse. I had a flee bitten grey TB who had sensitive skin around her muzzle. She would sun burn. I put on zinc oxide and mixed a bit of wormer paste in it. It seemed to work quite well for my horse. Of course, always ask your vet first.

It should also be noted that some horses are photophobic. Their eyes are sensitive to the sunlight. Often this condition will lead to uveitis which is the major cause of blindness in horses. Cataracts are more prevalent in horses who are sensitive to light. Also corneal ulcers can often be seen in horses who have light sensitivity. They rub their eyes often and can cause damage to the cornea by rubbing on foreign objects. Also, horses with parasites in the eye such as onchocerca will be more light sensitive. A viral or bacterial infection can cause a horse to be photophobic, as well. In the Nelson Survey (1994), of 68 horses with uveitis, 22 were chestnut. Scientific data seems to indicate that some chestnut colored horses may carry a gene that predisposes them to be photophobic.

The Merck Vet Manual describes photosensitization in the following way:

"Photosensitization is a clinical condition in which skin (areas exposed to light and lacking significant protective hair, wool, or pigmentation) is hyperreactive to sunlight due to the presence of photodynamic agents. Molecules of photosensitizing agents present in the skin are energized by light. When the molecules return to the less energized state, the released energy is transferred to receptor molecules that quickly initiate chemical reactions in various skin components. Tissue injury is thought to result from the production of reactive oxygen intermediates or from alterations in cell membrane permeability. Photosensitization can be difficult to differentiate clinically from actual sunburn. Photosensitization is often classified according to the source of the photodynamic pigment. These categories are primary or type I photosensitivity, aberrant endogenous pigment synthesis or type II photosensitivity, and type III or secondary (hepatogenous) photosensitivity. Sometimes a fourth category has been identified, labeled idiopathic type IV photosensitivity. (See also congenital erythropoietic porphyria, Congenital Erythropoietic Porphyria: Introduction, and protoporphyria, Cutaneous Manifestations of Multisystemic and Metabolic Defects.)

A wide range of chemicals, including some that are fungal and bacterial in origin, may act as photosensitizing agents. However, most compounds that are important causes of photosensitivity in veterinary medicine are plant-derived. Photosensitization occurs worldwide and can affect any species, but is probably most commonly seen in cattle, sheep, goats, and horses.

The clinical signs associated with photosensitivity are similar regardless of the cause. Photosensitive animals are photophobic immediately when exposed to sunlight and squirm in apparent discomfort. They scratch or rub lightly pigmented, exposed areas of skin (e.g., ears, eyelids, muzzle). Severe phylloerythrinemia and bright sunlight can induce typical skin lesions, even in black-coated animals. Erythema develops rapidly and is soon followed by edema. If exposure to light stops at this stage, the lesions soon resolve. When exposure is prolonged, serum exudation, scab formation, and skin necrosis are marked. In cattle, and especially in deer, exposure of the tongue while licking may result in glossitis, characterized by ulceration and deep necrosis.

Clinical signs are easily recognized in cases of marked photosensitivity but are similar to the primary actinic effects of sunburn in early or mild cases. Reference to the specific diseases in which photosensitization is an objective sign may assist in diagnosis of the underlying disease. Evaluation of serum liver enzymes and liver biopsies may be necessary to confirm the presence of hepatic disease. Examination of blood, feces, and urine for porphyrins can also be performed.

Treatment involves mostly palliative measures. While photosensitivity continues, animals should be shaded fully or, preferably, housed and allowed to graze only during darkness. The severe stress of photosensitization and extensive skin necrosis can be highly debilitating and increase mortality. Corticosteroids, given parenterally in the early stages, may be helpful. Secondary skin infections and suppurations should be treated with basic wound management techniques, and fly strike prevented. The skin lesions heal remarkably well, even after extensive necrosis.

The prognosis and eventual productivity of an animal is related to the site and severity of the primary lesion and/or hepatic disease, and to the degree of resolution."

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