We therefore urge FDA to act immediately and take the most prudent course and to ban feeding of mammal protein, including swine, to all food animals. Furthermore, we urge FDA not to exclude gelatin and blood from coverage under the proposed rule. However, the favored theory at present maintains that the agent responsible for TSEs, of which BSE in the United Kingdom is one example, is an abnormal form of a naturally occurring protein, called a prion. Its normal function is unknown. TSEs are characterized by long latency periods, the fact that they are invariably fatal and the fact that the infectious agent is incredibly resistant to deactivation.
Animals can contract the disease by eating infected animals or parts of infected animals.
Cooking the protein, or even rendering it at high temperatures, does not completely eliminate infectivity. Some of these are inherited diseases, and appear to be related to a mutation in the human prion gene. Since the cause of human and animal TSEs is similar, and since all mammals have prion genes, it is not unreasonable to expect that there is a spontaneous mutation rate that will lead to TSEs in all mammals that contain prion genes. If this is true, then we could expect that cattle, pigs, sheep, etc. will all spontaneously develop a TSE at some low rate. This possibility raises grave concerns for our food supply, given our current and comparatively recent practice of feeding animal protein back to food animals on a massive scale.