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SUMMARY

Ten 8- to 10-month-old cattle were each inoculated intramuscularly, subcutaneously, intracerebrally, and orally with the scrapie agent to determine whether cattle are susceptible to it. Two inocula, both 10% homogenates of cerebrum, were used. One inoculum was from a sheep used for the second experimental ovine passage of the agent from 4 naturally affected Suffolk sheep. The other inoculum was from a goat used for the first experimental caprine passage of the agent from 2 naturally affected dairy goats living with the Suffolk sheep, the source of their infection. Between 27 and 48 months after inoculation, neurologic disease 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 rising from recumbency, stilted gait of the pelvic limbs, disorientation, and terminal recumbency during a 6- to 10-week course. Neurohistologic changes, though consistent with those of scrapie, were slight and subtle: moderate astrocytosis with sparse rod cells, some neuronal degeneration, a few vacuolated neurons, and scant spongiform change. Clinically and neurohistologically, the experimentally induced disease differed from bovine spongiform encephalopathy. The differences emphasize that such infections in cattle induce diverse responses, presumably depending largely on the strain of the agent. Pathologists should keep this variability in mind when looking for microscopic evidence of a scrapie-like encephalopathy in cattle.

Free access
in American Journal of Veterinary Research

Summary

Reciprocal embryo transfers were made between scrapie-inoculated and scrapie-free sheep (Cheviot and Suffolk breeds) to measure scrapie transmission via the embryo (using offspring from embryos of scrapie-inoculated donors and scrapie-free recipients) and via the uterus (using offspring from embryos of scrapie-free donors and scrapie-inoculated recipients taken by cesarean section). Two control groups of offspring, 1 from scrapie-free parents (negative) and 1 from scrapie-inoculated parents (positive), also were included. All sheep were observed for clinical signs of scrapie until death or for a minimum of 60 months. Final diagnosis was made on the basis of histopathologic findings or results of mouse inoculation and/or proteinase-K-resistant protein analysis. Thirty to 61% of the scrapie-inoculated donor/recipient sheep within groups developed scrapie within 8 to 44 months after inoculation. None of the scrapie-free donor/recipients, including those gestating embryos from scrapie-inoculated donors, developed scrapie. Also, none of the offspring observed to ≥ 24 months of age from reciprocal cross, via embryo (0/67), or via the uterus (0/25), or from the negative-control group (0/33) developed scrapie. Fifty-six of the offspring via embryo, 19 of these via the uterus, and 31 negative controls survived to ≥ 60 months of age. Of the 21 sheep in the positive-control group, 2 (9.5%) developed scrapie, 1 at 31 months of age and 1 at 42 months of age. In the Cheviot offspring, the percentage of sheep carrying the short incubation allele ranged from 24 to 44% and the percentage in the Suffolk offspring ranged from 61 to 83%. These proportions indicate high degree of susceptibility to the disease. Results indicate that under the conditions of these experiments, scrapie was not transmitted to the offspring via the embryo or the uterus.

Free access
in American Journal of Veterinary Research