Facial eczema (pithomycotoxicosis), a photosensitisation of ruminants grazing pasture, has been known in New Zealand for over 100 years, but its cause, a toxin produced by a largely saprophytic fungus, Pithomyces chartarum, growing on litter at the base of pasture and sporing profusely under warm moist conditions in late summer and autumn, was found only 50 years ago. As the fungus spores it produces the toxin sporidesmin which, when eaten by sheep, cattle, goats or deer, causes liver injury with inflammation and blockage of bile ducts. Phylloerythrin, a photodynamic breakdown product of chlorophyll, is no longer excreted but circulates in the blood, causing lesions of unpigmented skin when the affected animal is exposed to sunlight. Lesions do not appear until at least a week after sporidesmin has been ingested, and this lag period delayed discovery of the causative agent, first thought to have been an abnormal metabolite of rapidly growing ryegrass. However, before the role of P. chartarum was discovered, the pathology of the disease had been described, toxic extracts had been made from herbage mown from pastures associated with facial eczema outbreaks, and the weather conditions preceding outbreaks had been defined. When the causative agent was identified, cultures of P. chartarum on artificial media produced sporidesmin for chemical characterisation and animal dosing trials. Control of facial eczema in the field was first by avoiding toxic pasture, detected by P. chartarum spore counts on herbage, later by reducing P. chartarum pasture populations by spray application of substituted thiabendazole fungicides, and later still by protecting animals with oral doses of zinc at close to toxic levels. Sheep vary widely in their sensitivity to sporidesmin, either under field conditions in facial eczema outbreaks or when dosed orally with sporidesmin, and breeding resistant animals by selection after sporidesmin challenge is the best long-term control method at present. Whilst facial eczema outbreaks have been most severe in New Zealand, the disease has been reported from an increasing number of countries with warm temperate climates in which ruminants are intensively grazed on pasture. The great majority of New Zealand isolates of P. chartarum produce sporidesmin, but varying proportions of those in other countries do not.
