Detection and Control of Prion Diseases in Food Animals

Table 1

Comparative analysis of prion diseases of food animals.

TSE	Age of onset (yr)	Disease variants	Mode of transmission	Genetic predisposition	Clinical signs	Cross-species infectivity
Scrapie	2–4 [33]	Classical atypical/Nor98	Amniotic fluid and placenta [34]	Susceptibility; 136V, 154R, 171Q [15]; Reduced susceptibility; 136A, 154R, 171R [16]	Weight loss; Ataxia; Abnormal behavior; Sensory changes; Incoordination; Head tremors; Recumbency [35]	Cattle, goat, mouse, hamster, rat, bank vole, deer, and elk [36–38]
BSE	4-5 [39]	Classical; H-type; L-type	Contaminated feed [39]	Susceptibility [40, 41]; 23 bp PRNP promoter insertion/deletion; 12 bp PRNP intron insertion/deletion E211K	Weight loss; Ataxia; Abnormal behavior; Sensory changes; Incoordination; Bradycardia; Reduced rumination; Decreased milk yield [42]	Bison, sheep, goat, deer, pig, mink, marmoset, cat, mouse, human, nonhuman primates [43]
CWD	2–4 [24]	Possible varied conformer population [44, 45]	Animal contact and environmental contamination [20]	Susceptibility [20]; Elk-132MM; Mule Deer-132SS–225SS; Cervid rigid Loop-S170N [46] -N174T [47]; Reduced susceptibility [48]; White tail Deer-Q95H-G96S	Weight loss; Abnormal behavior; Listlessness; Incoordination; Polydipsia; Polyuria; Hypersalivation; Lowering of the head and ears; Anorexia [21]	Moose, cattle, sheep, goat, mouse, hamster, ferret, mink, and squirrel monkey [20]