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:
- Contact dermatitis from irritants such as fly spray and buttercups
- Primary Photosensitization
- Secondary Photosensitization (Hepatogenous photosensitization)
- Photosensitivity of uncertain etiology
- Infectious skin conditions, e.g., mud fever
- 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.
- 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).
- 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).
- 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
- 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,
available on the OMAF web site.
- Knight AP, Walter RG. A Guide to Plant Poisoning of Animals
in North America. Jackson, Wyoming: Teton NewMedia, 2001: 142-150.
- Smith BP. Large Animal Internal Medicine, 2nd ed. Mosby, 1996:
- Radostits OM, Gay CC, Blood DC, Hinchcliff KW. Veterinary Medicine,
9th ed. WB Saunders, 2000: 587-589.
- Blood DC, Radostits OM. Veterinary Medicine, 7th ed. WB Saunders,
- 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.
For more information:
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