In 1982, Stanley Prusiner discovered prions and showed that they cause scrapie. Polymorphisms at sites 136, 154, and 171 are associated with varying susceptibility to ovine scrapie. Codon 171 has been determined to be the major genetic factor in scrapie susceptibility. The sheep brain disease scrapie appeared to be infectious but did not involve a microorganism. An infectious, persistent, and spontaneous disease, animals infected with scrapie must be quarantined and destroyed. The pathogenesis of scrapie involves the lymphatic system. The lymphatic system has been identified in the pathogenesis of scrapie. However, PrP-ARR polymorphisms are susceptible to atypical scrapie, so this may prove unfruitful. Breeds such as Cheviot and Suffolk are more susceptible to scrapie than other breeds. They dubbed the gene sinc for scrapie incubator. Between 1978 and 2004, scrapie recurred on 33 farms. They take advantage of the fact that Tasmania is free of BSE and scrapie. "Post mortem" examination is important for the diagnosis of scrapie. Historically, scrapie had been considered to be an animal health issue. Scrapie usually affects sheep around three to five years of age.