Abstract

Facial Eczema (FE) is a metabolic disease resulting from liver and bile-duct damage, caused by ingestion of the mycotoxin sporidesmin A, found in the spores of the fungus Pithomyces chartarum. Risk of FE is associated with temperature, humidity and dead leaf matter (Mitchell et al. 1959; Brook 1963; Di Menna & Bailey 1973). While FE is predominantly prevalent in the North Island of New Zealand, climatic change projections indicate that there will be an increase in the geographical spread of the fungus and associated sporidesmin, resulting in FE spreading to regions that are currently unaffected (Dennis et al. 2014). Clinical FE is characterised by photosensitisation due to liver injury; however, reduced production (Smith 2000) and reproduction (Moore et al. 1983; Mcmillan et al. 1988; Morris et al. 1991) is also observed in both clinically and sub-clinically affected animals. The heritability of liver damage at slaughter post-sporidesmin challenge was estimated to be 0.42 ± 0.09 (Campbell et al. 1981). In the live animal, serum gamma glutamyltransferase (GGT) collected 2 to 3 weeks after sporidesmin challenge can be used as a measure of liver damage (Towers & Stratton 1978). Romney FE selection lines, initially selected for resistance or susceptibility on the basis of liver damage, were established in 1975...

KM, Mcrae, NG Cullen, NC Amyes, and Johnson PL

Proceedings of the New Zealand Society of Animal Production, Volume 76, Adelaide, 43-45, 2016