In this mycotoxic disease of grazing livestock, the toxic liver injury commonly results in photodynamic dermatitis. In sheep, the face is the only site of the body that is readily exposed to ultraviolet light, hence the common name. The disease is most common in New Zealand but also occurs in Australia, France, South Africa, several South American countries, and probably North America. Sheep, cattle, and farmed deer of all ages can contract the disease, but it is most severe in young animals.
Etiology and Pathogenesis
Sporidesmins are secondary metabolites of the saprophytic fungus Pithomyces chartarum, which grows on dead pasture litter. The warm ground temperatures and high humidity required for rapid growth of this fungus restrict disease occurrence to hot summer and autumn periods shortly after warm rains. By observing weather conditions and estimating toxic spore numbers on pastures, danger periods can be predicted and farmers alerted.
The sporidesmins are excreted via the biliary system, in which they produce severe cholangitis and pericholangitis as a result of tissue necrosis. Biliary obstruction may be seen, which restricts excretion of bile pigments and results in jaundice. Similarly, failure to excrete phylloerythrin in bile leads to photosensitization.
Previous ingestion of toxic spores causes potentiation, thus a succession of small intakes of the spores can lead to subsequent severe outbreaks.
Clinical Findings, Lesions, and Diagnosis
Few signs are apparent until photosensitization and jaundice appear ∼10–14 days after intake of the toxins. Animals frantically seek shade. Even short exposure to the sun rapidly produces the typical erythema and edema of photodermatitis in unpigmented skin. The animals suffer considerably, and deaths occur from one to several weeks after photodermatitis appears.
Characteristic liver and bile duct lesions are seen in all affected animals whether photosensitized or not. In acute cases showing photodermatitis, livers are initially enlarged, icteric, and have a marked lobular pattern. Later, there is atrophy and marked fibrosis. The shape is distorted, and large nodules of regenerated tissue appear on the surface. In subclinical cases, livers often develop extensive areas in which the tissue is depressed and shrunken below the normal contour, which distorts and roughens the capsule. Generally, these areas are associated with fibrosis and thickening of corresponding bile ducts. The bladder mucosa commonly shows hemorrhagic or bile-pigment-stained ulcerative erosions with circumscribed edema.
The clinical signs together with characteristic liver lesions are pathognomonic. In live animals, high levels of hepatic enzymes may reflect the extensive injury to the liver.
To minimize intake of pasture litter and toxic spores, short grazing should be avoided. Other feedstuffs should be fed during danger periods; encouraging clover dominance in pastures helps to provide a milieu unsuited to growth and sporulation of P chartarum on litter.
The application of benzimidazole fungicides to pastures considerably restricts the buildup of P chartarum spores and reduces pasture toxicity. A pasture area calculated at 1 acre (0.45 hectare)/15 cows or 100 sheep should be sprayed in midsummer with a suspension of thiabendazole. When danger periods of fungal activity are predicted, animals should be allowed only on the sprayed areas. The fungicide is effective within 4 days after spraying, provided that no more than 1 in. (2.5 cm) of rain falls within 24 hr during the 4-day period. After this time, heavy rainfall does little to reduce the effectiveness of spraying because the thiabendazole becomes incorporated within the plants. Pastures will then remain safe for ∼6 wk, after which spraying should be repeated to ensure protection over the entire dangerous season.
Sheep and cattle can be protected from the effects of sporidesmin if given adequate amounts of zinc. Zinc may be administered by drenching with zinc oxide slurry, by spraying pastures with zinc oxide, or by adding zinc sulfate to drinking water.
Sheep may be selectively bred for natural resistance to the toxic effects of sporidesmin. The heritable trait for resistance is high. Ram sires are now being selected in stud and commercial flocks for resistance either by natural field challenge or by low-level, controlled dosage of ram lambs with sporidesmin.
Last full review/revision March 2012 by Gary D. Osweiler, DVM, MS, PhD