A history of facial eczema (pithomycotoxicosis) research.


Facial eczema, also referred to as pithomycotoxicosis in some countries, and now referred to in South Africa as sporidesmin induced liver disease (SILD), is a photosensitization of ruminants grazing pasture, particularly perennial ryegrass in South Africa. Facial eczema is a poor description as the photosensitization affects the skin also, in fact mostly, in cows over the back and backsides; therefore the change in terminology. Even pithomycotoxicosis may not be appropriate, as the fungus Pithomyces chartarum which produces the toxin sporidesmin is now called Pseudopithomyces chartarum. Thus, we would prefer use of SILD as the preferred term, as it is a correct description of the disease.

SILD has been known for a long time, particularly in New Zealand, where the major research as cited has been done. The fungus grows on the litter at the base of the pasture and spores profusely under warm moist conditions from early summer to early autumn. P. chartarum when sporing produces the toxin sporidesmin which, when ingested by grazing livestock, causes liver injury with inflammation and blockage of bile ducts. Phylloerythrin, a photodynamic breakdown product of chlorophyll, is then 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 in early research delayed discovery of the causative agent, first thought to be 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 SILD 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 SILD in the field was first by avoiding toxic pasture, detected by P. chartarum spore counts on herbage, then also by reducing the fungus population by spraying thiabendazole-like fungicides, and later by protecting animals with oral doses of zinc at close to toxic levels. ZnSO4 was initially used in the drench but later abandoned because of the narrow margin between therapeutic and toxic doses. More recently ZnO has been used, because of a better safety margin, and this has since been the general practice but primarily as a supplement in the feed. The effective level of Zn which is close to toxicity and needs to be supplemented over an extended period, remains of concern as pancreatic damage has been shown and productivity will most probably be reduced, with animal health and financial consequences.

A long term solution for particular species could be selection as sheep have shown to vary considerably in their sensitivity to sporidesmin, either under field conditions in SILD outbreaks or when dosed orally with sporidesmin. This, however will not apply to dairy cows, at least in South Africa, as they are mostly bred out of imported seed from bulls not exposed to sporidesmin.

Whilst SILD outbreaks have been most severe in New Zealand, the disease has been reported from an increasing number of countries or regions 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 such as South Africa do not. Therefore, it is important to characterise the isolates which do and those which do not.