Toxicoses in the field affect ruminants grazing on improved pastures. Sporidesmins are the natural toxins and are rapidly absorbed from the gut and quickly concentrated in the liver and biliary tract, causing reduced bile flow and hepatitis with hepatogenous photosensitization, particularly photosensitization of the face. In live animals, serum hepatic enzymes are markedly elevated, and gross lesions include an enlarged, icteric liver in acute cases and in subacute cases an atrophied liver with marked fibrosis and distorted shape with thickening of bile ducts.
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 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 of Facial Eczema in Animals
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 rapidly absorbed from the GI tract, concentrated in the liver and bile, and excreted via the biliary system, in which they produce severe cholangitis and pericholangitis as a result of tissue necrosis. Biliary obstruction may occur, 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 of Facial Eczema in Animals
Few signs are apparent until photosensitization and jaundice appear about 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 nonpigmented skin (particularly ears, eyelids, face, and lips). The animals suffer considerably, and deaths occur from one to several weeks after photodermatitis appears.
Histopathologic findings in the liver include degenerative changes in bile duct epithelium with both intrahepatic and extrahepatic bile ducts involved, biliary occlusion by inspissated bile and necrotic cells, hepatocellular vacuolation, particularly centrilobular hepatocytes. In a recovering liver, lesions can include proliferation of bile ducts and periportal fibroplasia, with areas of atrophy and regeneration occurring in the liver. Characteristic liver and bile duct lesions are evident 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 hepatic enzyme activity may reflect the extensive injury to the liver. Liver damage can be detected with serum chemistry changes of increased bilirubin concentration, cholesterol concentration, triacylglycerols concentration, bile acids concentration, gamma-glutamyl transaminase (GGT) activity, aspartate aminotransferase (AST) activity, and glutamate dehydrogenase activity; a decrease in serum albumin concentration and increased prothrombin time can also be observed in affected animals. The diagnosis is usually based on clinical signs and the season, and a pasture spore count of Pithomyces chartarum can confirm whether the pasture is dangerous. A spore count of 100,000 or more per gram of grass is considered dangerous.
Treatment, Control, and Prevention of Facial Eczema in Animals
Benzimidazole fungicides on pastures
Treatment of the affected animals is supportive. Animals with photosensitization should be housed, provided with deep shade and put out to graze only at night. Secondary bacterial infections should be treated as necessary. Many animals showing no obvious signs of photosensitization may have liver injury and may need shade and additional treatment. Because of the delay of 10–14 days before appearance of clinical signs in animals, the use of zinc salts may be of little benefit to affected animal, but zinc salts may prevent further toxicosis in animals to be placed on high spore count pastures. 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) per 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 hours 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 weeks, 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 sheep with zinc oxide slurry, by spraying pastures with zinc oxide, or by adding zinc sulfate to drinking water. Zinc salts are not effective if administered after sporidesmin exposure in animals.
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.
Facial eczema is also known as sporidesmin toxicosis and pithomycotoxicosis, is caused by the fungus Pithomyces chartarum growing on dead plant material, and is frequently associated with perennial ryegrass pasture in New Zealand.
The sporidesmin toxins cause liver and bile duct lesions, jaundice, and photosensitization about 10 to 14 days after animals are placed on a toxic pasture.
Zinc salts administered by drenching to animals can prevent toxicosis in livestock before placement on toxic pastures.
Control of the disease in ruminants, particularly sheep, involves avoiding use of pastures with dead litter, particularly ryegrass pastures, and those pastures with high P charatrum spore counts per gram of grass. Avoid overgrazing of pasture by animals.
Pasture treatment with benzimidazole fungicides can reduce buildup of P chartarum spores and reduce pasture toxicity.
For More Information
DiMenna ME, Smith BL, Miles CO. A history of facial eczema (pithomycotoxicosis) research. N Z J Agric Res 2009;52:345-376.
Dalefield R. Sporidesmin. In: Plumlee KH, ed. Clinical Veterinary Toxicology. St. Louis: Mosby, 2004;264-268.