The incidence of natural scrapie in sheep is associated with polymorphisms of the PrP gene, particularly those at codons 136, 154 and 171. In many breeds, the PrP allele encoding valine at codon 136 confers an extremely high risk of scrapie, but in Suffolk sheep this allele is vanishingly rare. In this study of a single closed flock of Suffolk sheep in Scotland, scrapie occurred primarily in animals which were homozygous for glutamine at codon 171, a genotype which was significantly less frequent in healthy flockmates. However, the apparent linkage between glutamine at codon 171 and scrapie was not completely recessive because two of 64 scrapie cases were heterozygous glutamine/arginine. These results suggest that breeding for increased resistance to scrapie in Suffolks by the selection of animals according to their PrP genotype is a feasible option.

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SUMMARYIn animals exposed to foot-and-mouth disease virus by indirect contact, virus was recovered from the blood, milk, pharynx, vagina and rectum for variable periods of time before clinical disease was apparent. Virus instilled into the mammary gland multiplied rapidly and virus concentrations greater than 107 p.f.u./ml. were recorded within 8-32 hr., depending on the virus strain and dose inoculated. Virus multiplication was accompanied by clinical signs of mastitis but the classical signs of foot-and-mouth disease did not appear for 52-117 hr. Dissemination of virus from the mammary gland occurred within 4-24 hr. and in some animals samples taken from the pharynx, mouth, nose and vagina contained virus for periods up to 97 hr. before the appearance of vesicular lesions. Virus production in the udder declined with the appearance of virus neutralizing activity in the blood and the milk but persisted in some animals for periods of 3-7 weeks. The ability of foot-and-mouth disease virus to persist in mammary tissue was confirmed by the demonstration of virus multiplication in the udders of immune animals.

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SUMMARYDaily observations were made on the excretion of African swine fever (ASF) virus by pigs infected intranasally or by contact. Two strains of virus having mean death times of approximately 3 and 6 days were used, the latter being recently isolated from a warthog.First excretion usually occurred by the nasopharyngeal route, as early as 1 or 2 days before the onset of fever in many cases. The titres of pharyngeal and nasal swabs rose rapidly to reach mean levels of about 104-105 HAD 50 at 48-72 hr. following the onset of pyrexia. Virus in the secretions of the conjunctiva or lower urogenital tract appeared later and did not attain such high levels. Faecal and urinary excretion was of relatively little significanoe, except in slower infections caused by the recent warthog virus.These results are discussed in relation to the known failure of infected pigs to transmit the disease to stallmates during the first 12-24 hr. of pyrexia and also in relation to recent work on the pathogenesis of ASF in domestic swine.