Facial eczema is a severe photosensitisation disease of sheep and cattle caused by ingestion of sporidesmin, a mycotoxin produced by the fungus Pithomyces chartarum. It is a major welfare concern in New Zealand and parts of Australia, causing significant suffering and economic loss.
Sporidesmin damages bile duct cells in the liver, causing cholangitis and bile duct obstruction. As bile accumulates in the blood, phylloerythrin (a breakdown product of chlorophyll) builds up in the skin. When exposed to sunlight, phylloerythrin generates free radicals that cause severe cell damage. The result is photosensitisation — inflammation, necrosis, and ulceration of the non-pigmented, sun-exposed areas of the face and ears.
Affected animals show intense skin irritation, rubbing their faces against fences and objects. The white areas of the face, around the eyes, and the ears become red, swollen, and weeping. Skin peels away in severe cases, leaving raw, painful lesions. Animals seek shade and may stop eating due to pain. The welfare impact is severe — affected sheep experience chronic pain, persistent pruritus, and significant distress. Even animals that survive visible facial eczema often have permanent liver damage that impairs long-term health and productivity.
Facial eczema risk is highest when P. chartarum spore counts on pasture exceed threshold levels, which typically occurs in warm, moist conditions (>10°C night temperatures, >25mm rainfall) after a dry period. Spore counts above 70,000–100,000 per gram of dry matter are considered dangerous. The disease mainly affects ewes and lambs on lush pasture in late summer and autumn in New Zealand and spring in Australia.
Zinc supplementation: Zinc reduces sporidesmin absorption and is the primary prevention method. Zinc can be provided as: in-feed zinc oxide (at recommended rates), zinc boluses, drenching with zinc sulphate, or zinc-containing lick blocks. Dosing must be precise — inadequate zinc is ineffective, while excess causes copper antagonism and zinc toxicity.
Pasture management: Reducing pasture contamination through fungicide application (thiabendazole) before dangerous spore count periods can reduce risk but is expensive and not always practical.
Genetic selection: Facial eczema tolerance has heritable components. Breeding programmes that use plasma GGT measurements after controlled sporidesmin dosing have identified more-tolerant lines in New Zealand Merino and Corriedale breeds.
Spore count monitoring: Regular laboratory monitoring of pasture spore counts during risk periods provides advance warning, allowing protective supplementation before dangerous exposure levels are reached.
Once clinical disease is established, treatment focuses on reducing further damage and supporting recovery. Moving animals off contaminated pasture and providing shade reduces ongoing exposure. Non-pigmented skin should be protected from sunlight. Anti-inflammatories reduce pain in severe cases. Severely affected animals may require humane euthanasia. Liver recovery takes weeks to months; some animals with severe cholangiohepatitis never fully recover.
Regular clinical inspection during risk periods allows early identification of affected animals. Serum GGT (gamma-glutamyl transferase) elevation is a sensitive indicator of subclinical liver damage, often detectable before clinical signs appear. Batch blood testing provides flock-level welfare monitoring that identifies liver damage even when visible facial lesions are absent.
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