ENCEPHALOPATHY IN CATTLE EXPERIMENTALLY INFECTED WITH THE SCRAPIE AGENT

Ten 8- to 10-month-old cattle were each inoculated intramuscularly, su bcutaneously, intracerebrally, and orally with the scrapie agent to de termine whether cattle are susceptible to it. Two inocula, both 10% ho mogenates of cerebrum, were used. One inoculum was from a sheep used f or the second experimental ovine passage of the agent from 4 naturally affected Suffolk sheep. The other inoculum was from a goat used for t he first experimental caprine passage of the agent from 2 naturally af fected dairy goats living with the Suffolk sheep, the source of their infection. Between 27 and 48 months after inoculation, neurologic dise ase was observed in 1 of 5 cattle given the sheep brain homogenate and in 2 of 5 given the goat brain homogenate. In all 3 affected cattle, the disease was expressed clinically as increasing difficulty in risin g from recumbency, stilted gait of the pelvic limbs, disorientation, a nd terminal recumbency during a 6- to 10-week course. Neurohistologic changes, though consistent with those of scrapie, were slight and subt le: moderate astrocytosis with sparse rod cells, some neuronal degener ation, a few vacuolated neurons, and scant spongiform change. Clinical ly and neurohistologically, the experimentally induced disease differe d from bovine spongiform encephalopathy. The differences emphasize tha t such infections in cattle induce diverse responses, presumably depen ding largely on the strain of the agent. Pathologists should keep this variability in mind when looking for microscopic evidence of a scrapi e-like encephalopathy in cattle.