Further Observations on the Production of Scrapie in Sheep by Oral Dosing with Foetal Membranes from Scrapie-Affected Sheep

Pattison, I.H.; Hoare, Margaret N.; Jebbett, Jean N.; Watson, W.A.

doi:10.1016/s0007-1935(17)35851-7

Cited by 74 publications

(31 citation statements)

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“…The placental trophoblast cells may acquire nonspecifically pathogens at the interface during the physiological process of uptake nutrients during gestation. The present study and studies by others showed that scrapie infectivity (7)(8)(9)43), PrP-Sc (9), and PrP-C (44) are present in the ovine uterus and placenta; therefore, PrP-Sc in the cotyledonary chorioallantois may be derived from direct phagocytosis of or conversion by the maternal PrP-Sc in the caruncular endometrium of infected ewes. As the embryo develops, the amnion is formed and filled with amniotic fluid in which the embryo is suspended.…”

Section: Pk Susceptibility Of Prp-c and Prp-sc In The Reproductive Fsupporting

confidence: 59%

PrP-C and PrP-Sc at the Fetal-Maternal Interface

Tuo

Zhuang

Knowles

et al. 2001

Journal of Biological Chemistry

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Scrapie is a naturally occurring prion (PrP) disease causing a fatal neurodegenerative disorder in sheep and goats. Previous studies suggest that scrapie is transmitted naturally through exposure to the scrapie agent in wasted placentas of infected ewes. This study determined the distribution and biochemical properties of PrP cellular (PrP-C) and the distribution of PrP scrapie (PrP-Sc) in reproductive, placental, and selected fetal tissues and fetal fluids in sheep. Glycosylated, N-terminally truncated, proteinase K-sensitive PrP-C with apparent molecular masses of 23-37 kDa was present in reproductive, placental, and fetal tissues and fetal fluids. PrP-C was low or undetectable in intercotyledonary chorioallantois, amnion, urachus, amniotic fluid, and fetal urine. In pregnant ewes, cotyledonary chorioallantois, allantoic fluid, and caruncular endometrium contained higher levels of PrP-C than did intercaruncular endometrium, myometrium, oviduct, ovary, fetal bladder, or fetal kidney. Caruncular endometrial PrP-C was up-regulated during pregnancy. Despite the wide distribution of PrP-C in reproductive, placental, and selected fetal tissues and fetal fluid, PrP-Sc was detected only in caruncular endometrium and cotyledonary chorioallantois of pregnant scrapie-infected ewes. The embryo/fetus may not be exposed to scrapie in utero because it is separated physically from PrP-positive allantois and chorioallantois by PrP-negative amnion.

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Section: Pk Susceptibility Of Prp-c and Prp-sc In The Reproductive Fsupporting

confidence: 59%

PrP-C and PrP-Sc at the Fetal-Maternal Interface

Tuo

Zhuang

Knowles

et al. 2001

Journal of Biological Chemistry

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“…Attempts to define the physical mechanism of spread have yielded conflicting results (Pattison et al 1972(Pattison et al , 1974Hadlow et al 1982;Hourrigan et al 1979). Similarly, whereas PIP alleles encoding Val-136 may be a risk factor in some breeds (Laplanche et al 1993b) and in experimental scrapie (Goldmann et al 1991a), they are nota prerequi-Cold Spring Harbor Laboratory Press on May 9, 2018 -Published by genesdev.cshlp.org Downloaded from site; such alleles are absent from three autochthonous {indigenous) French breeds endemically affected with natural scrapie (Laplanche et al 1993a}.…”

Section: Scorresponding Authormentioning

confidence: 99%

Homozygosity for prion protein alleles encoding glutamine-171 renders sheep susceptible to natural scrapie.

Westaway

Zuliani²,

Cooper³

et al. 1994

Genes Dev.

238

166

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Natural scrapie has been viewed both as a recessive trait and as a contagious disease modulated by a host locus. To address this conundrum, we determined the structure of the sheep prion protein (PrP) gene, which contains three exons and extends over 20 kb of DNA. In the United States 86.4% of scrapie cases occur in Suffolk sheep, and within this breed 49__.6% (+_s.D., n=69) of healthy animals carry one or more PrP alleles encoding Arg (R)-171. Four scrapie-affected sheep were homozygous for wild-type PrP open reading frames encoding the alternative Gin (Q)-171 allele. Analysis of additional cases revealed that all were Q/Q-171 homozygotes (n= 31), yielding a probability of 0.000004 that PrP genotype is unrelated to susceptibility. These data imply that homozygosity for Q-171 codons is necessary but not sufficient for the development of natural scrapie, echo reports of recessive manifestation, and parallel over-representation of PRNP codon 129 homozygotes in Crentzfeldt-Jakob disease of humans. Whereas progress has been substantial regarding experimental scrapie in rodents, the occurrence and spread of disease in flocks of sheep has remained enigmatic. Appreciation of the relationship between codon 171 genotype and susceptibility may help define the molecular basis of natural scrapie.

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“…Scrapie is perpetuated principally by maternal transmission, possibly as a result of perinatal contact with the infected placenta, but it has been noted that 'the role of the placenta in either vertical or lateral transmission of scrapie in sheep is a matter for speculation' (Dickinson & Fraser, 1979). Specific routes whereby perinatal infection is initiated have not been established but experiments have shown that administering infectivity to sheep through the conjunctiva (Haralambiev et al, 1973) or by oral dosing (Pattison & Millson, Author for correspondence: D. M. 1961; Gordon, 1966a, b;Pattison et al, 1974) can produce disease. Further possible routes of entry might be through the unhealed umbilical stump, or skin which became damaged around the time of birth.…”

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confidence: 99%