Sunburn, Photosensitivity, or Contact Dermatitis in Horses?

In mid summer, when horses are in the middle of their show season, owners are often disturbed by the loss of hair from the white-skinned areas of the horse’s body. This is particularly noticeable on the legs and face of the horse. The difficulty is determining whether the hair loss is due to sunburn, contact dermatitis or photosensitization. The diagnosis of sunburn, (overexposure to ultraviolet light) as a primary diagnosis without other confounding factors is probably a diagnosis of exclusion in most cases. The quest for a diagnosis is often only for academic interest since the treatment is commonly the same – removal from exposure to ultraviolet (UV) light and the feeding of dry hay. However, the common conditions that lead to crusty, dry, peeling skin include:

1. Contact dermatitis from irritants such as fly spray and buttercups

2. Primary Photosensitization

3. Secondary Photosensitization (Hepatogenous photosensitization)

4. Photosensitivity of uncertain etiology

5. Infectious skin conditions, e.g., mud fever

1. Contact dermatitis is a result of a chemical or mechanical reaction causing injury to the skin. It commonly occurs from a reaction induced by a chemical(s) in fly sprays or plants, such as buttercups. Some horses are more sensitive to these chemicals than others. The reaction to fly sprays is acerbated by applying these products prior to saddling and tacking; this compresses the offending chemical between equipment and hot sweaty skin.

Buttercup in a fresh state can also cause a local irritation on the muzzle of horses that is difficult to differentiate from photosensitization. The volatile chemical dissipates within a few days of the plant being cut in hay or being frozen. Horses are often seen eating the buttercups in the pasture a few days after a hard frost without any adverse reaction.

2. Primary Photosensitization - Photosensitivity is commonly seen as a result of ingesting photodynamic agents from a number of plant and chemical toxins. When an animal consumes a plant or chemical containing these pigments (e.g., polyphenolic), the pigments circulate to the skin where they are exposed to UV light, fluoresce and cause oxidative injury to the cells of the skin (1). Buckwheat and St. John’s wort cause primary photosensitization (1). Phosphorus fertilizer, coal tar pitch, wood preservatives, pentachloro-phenols, aflatoxin B in moldy feed, as well as a number of veterinary medicines, such as tetracycline and phenothiazine tranquilizers, can all act as photodynamic agents, absorbing the ultraviolet light and passing the energy to adjacent cells resulting in cell damage (1, 2).

3. Secondary Photosensitization occurs when a toxin damages the liver and results in the inability to excrete phylloerythrin. Phylloerythrin is a porphyrin compound formed by microbial degradation of chlorophyll in the gut. It is normally removed by the liver and excreted in the bile (1). If the liver is severely diseased, phylloerythrin accumulates in the blood. As it circulates through to the skin, it is exposed to UV light, fluoresces and causes oxidative injury to the blood vessels and tissues of the skin (1). Pyrrolizidine alkaloid is the most important causative agent in this group. Tansy ragwort, groundsel, fiddleneck, common heliotrope, vipers bugloss, and rattlebox contain pyrrolizidine alkaloid and cause hepatogenous photosensitivity (1).

4. Photosensitivity of uncertain etiology includes many forage-related photosensitivities. It has been reported in cattle, sheep and horses grazing lush pasture (3). Alfalfa has been incriminated in cases of secondary photosensitization in cattle, where compromised hepatic function is not necessarily the prerequisite for the photosensitization (3).

Alsike clover is well recognized for causing photosensitization as well as oral ulcers and hepatitis. It is unclear whether the photosensitization is primarily a photodynamic agent problem or a secondary phototoxic reaction due to liver damage or whether alsike clover and its metabolites are truly the culprit (4). The photosensitization reaction could also be associated with mycotoxins produced on the plant. A similar syndrome has also been observed with horses consuming lush white clover in the fall (5).

5. Infectious skin conditions, e.g., mud fever and dermatophilus, can also cause skin irritation and hair loss but they will not be discussed in this information sheet.

Prevention and Treatment

Horses that are at the greatest risk of plant-induced photosensivity are those that are grazing poor pastures that contain a lot of weeds, especially in the fence-line area. Normally, horses affected by primary photosensitization recover completely when contact with the offending chemical is discontinued. Since it is not always possible to identify the plant responsible for the problem, owners are advised to remove the horse from pasture and discontinue any application of fly sprays or chemicals. The horse should be fed dry hay in the stable and not directly exposed to UV light.

Horses that have been exposed to plants containing pyrrolizidine alkaloid have a poor prognosis due to the underlying liver damage that has occurred. They should be removed from the offending plants and given a low-protein, easily digestible diet.

In the case of acute alsike clover poisoning, a complete recovery is normally seen in a matter of a week. Chronic cases of alsike clover have a poor prognosis and may die of liver failure, much like horses exposed to pyrrolizidine alkaloid.

Prevention is the key. Pastures should be checked regularly and pyrrolizidine alkaloid-containing plants removed. If white clover is over abundant in pastures and causing a problem, the application of a herbicide may be required to reduce the white clover concentration.

Further information and details on how to differentiate between the different clovers are available in the information sheet Alsike Clover Poisoning, Photosensitization or Photodermatitis in Horses


1. Knight AP, Walter RG. A Guide to Plant Poisoning of Animals in North America. Jackson, Wyoming: Teton New Media,

2001: 142-150.

2. Smith BP. Large Animal Internal Medicine, 2nd ed. Mosby, 1996: 1443.

3. Radostits OM, Gay CC, Blood DC, Hinchcliff KW. Veterinary Medicine, 9th ed. WB Saunders, 2000: 587-589.

4. Blood DC, Radostits OM. Veterinary Medicine, 7th ed. WB Saunders, 1989: 1338.

5. Wright RG, Ireland MJ. Case report: alsike clover poisoning, an old but should not be forgotten problem. Proceedings

of the Equine Nutrition and Physiology Society 2003: 236-237.