Environmental Diseases

Stephen D. White

Frostbite

Frostbite is an uncommon injury among healthy, well-nourished animals, with all species being susceptible. It is caused by prolonged exposure to subfreezing temperatures.

Frozen tissue must be handled gently and thawed rapidly in warm water 38° to 44°C (100.2° to 111.1°F) as soon as possible after it is known that refreezing can be prevented. Tissue damage is greatly increased if thawing and subsequent refreezing occur (freeze/thaw-freeze/thaw syndrome). Tissue thawing is painful, and analgesics should be administered. Slow thawing is less painful than rapid thawing but results in much greater tissue damage. Frozen tissue should not be massaged during warming. Damaged areas are best left exposed during the healing process rather than covered with occlusive dressings, and premature debridement should be avoided because more tissue may be viable than first apparent. The animal should be given good supportive care and may have to be restrained to prevent self-mutilation. Management practices should be changed to prevent recurrence. Tissues previously damaged by freezing are more susceptible to cold injury when reexposed to subnormal temperatures.^1,2

Photosensitization

Photosensitivity is an abnormal reaction of the skin when exposed to light. For photosensitization to occur, there must be (1) a photodynamic agent, (2) white or lightly pigmented skin, and (3) ultraviolet A (UVA) range (320 to 400 nm). Melanin in the skin screens UV light, thereby limiting photosensitivity reactions to the white and light-colored areas of the body.³

There are three generally recognized categories of causes of photosensitivity:

Type I—ingestion of a photodynamic agent

Type II—congenital abnormalities in porphyrin or liver metabolism

Type III—liver disease due to a plant or toxin, which leads to accumulation of phylloerythrin and a breakdown product of chlorophyll.

Type I

Numerous plants contain various photodynamic agents^3-7:

Common Name

St. John's wort Buckwheat Perennial ryegrass Whiteheads

Roadside leafbract Cegadera

Texas snake cotton

Biserrula

Scientific Name

Hypericum perforatum

Polygonum fagopyrum

Lolium perenne

Sphenosciadium capitellatum

Malachra fasciata Heterophyllaea spp. Froelichia humboldtiana Biserrula pelecinus

Agent

Hypericin

Fagopyrin

Perloline

Unknown

Unknown

Anthraquinones

Unknown

Unknown

Additional reports describe photosensitivities apparently induced by the ingestion of gluten in horses and of cocoa shells in calves.^8,9

Type II

There are two bovine diseases and one ovine disease in this category:

Congenital erythropoetic porphyria: seen in Holstein, Shorthorn, and Jamaican breeds. Commonly called “pink tooth” because of the coloration of the dentition, which will glow under a Wood's lamp, as will the urine. The cow may also have anemia. The cause is a deficiency of uroporphyrinogen III cosynthetase, which leads to a defect in the heme synthesis and an accumulation of uroporphyrin and coproporphyrin, which are photodynamic agents.

Bovine protoporphyria: seen in Limousin and Blond d' Aquitaine and Charolais breeds. Neither tooth discoloration nor anemia is present. This disease is caused by another defect in heme synthesis, as a defect in ferrochelatase, which leads to an accumulation of protoporphyrin, another photodynamic agent.

In Corriedale sheep, a congenital defect in liver function leads to an accumulation of phylloerythrin (see below under Type III).

Type III

As mammals ingest plants containing chlorophyll, this molecule is degraded by bacteria in the intestine into the porphyrin phylloerythrin. Some phylloerythrin is normally absorbed into the portal circulation, removed by the liver, and excreted by the bile. In liver disease the hepatic excretion of phylloerythrin is decreased, leading to excessive levels in the peripheral circula­tion and eventually in the skin, causing photosensitivity in about 25% of horses with liver dysfunction.^10-12 One of the more common reasons for liver disease in horses in the United States is ingestion of the following plants containing pyrroli- zidine alkaloids:

Common Name

Common groundsel Ragwort, stinking Willie Tarweed

Rattleweed

Salvation Jane

Scientific Name

Senecio vulgaris Senecio jacobaea

Amsinckia intermedia Crotalaria spp.

Echium lycopsis

The following plants cause hepatic dysfunction (especially in ruminants), as they contain photosensitizing saponins, whose metabolites crystalize in the bile causing biliary blockage and cholangitis:

Common Name

Puncture vine

Agave

Signal grass

Sacahuista, Bunchgrass

Narthecium

Scientific Name

Tribulus terrestris Agave spp.

Brachiaria decumbens Nolina texana Narthecium ossifragum

Consumption of alsike clover (Trifolium hybridum) may induce hepatic dysfunction (with histologic lesions distinct from those caused by pyrrolizidine alkaloids), leading to photosensitization signs (alsike clover poisoning, dew poisoning). Cases seem to be correlated to years with heavy rainfall and ingestion of the plant blossoms.¹³ Finally, the saprophytic fungus Pithomyces chartarum, which grows on perennial ryegrass, contains the heptotoxin sporidesmin.

Ingested plants and feed should be noted and collected for future analysis. Environmental considerations include the type of pasture (or other material) with which the animal is in contact, the amount of time the animal is exposed to sunlight, any seasonality of the condition, and any other horses involved. A seasonal incidence would tend to negate liver disease; multihorse involvement should arouse suspicion of an ingested or contact photosensitizer. A thorough history of recent drug therapy should be obtained.

Physical examination usually reveals lesions limited to the hairless, white, or lightly pigmented areas of the skin. The involved skin is erythematous, swollen, and painful. The lesions may progress to serum exudation, thickening, fissuring, and in severe cases, necrosis and sloughing (Fig. 40.15).

Therapy is related to etiology. Chronic liver disease carries a guarded prognosis. Removal of foodstuffs containing pho­todynamic agents, or removal of the animal from a pasture with plants containing these agents, will often result in full recovery if the animal is also kept out of the sun for 1 to 2 weeks. Corticosteroids are helpful in controlling inflammation and pruritus. Oral prednisolone at 1 mg/kg daily for 1 week, then halving the daily dosage for a second week, is an effective regimen in this regard.