Spread of scrapie by contact to goats and sheep

Brotherston, J G.; Renwick, C.C.; Stamp, J.T.; Zlotnik, I.; Pattison, I.H.

doi:10.1016/0021-9975(68)90107-2

Cited by 95 publications

(41 citation statements)

References 13 publications

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“…Natural scrapie also appears to be transmissible between sheep and goats from infected to uninfected animals, if they are reared in close proximity (Greig, 1950 ;Brotherston et al, 1968). Evidence for the transmission of BSE from an infected cow to her calf is not conclusive, and if it does occur it only does so at a frequency of about 10 % (Wilesmith et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…inoculation of brain homogenate from humans affected by Creutzfeldt-Jakob disease (Hadlow et al, 1980). Natural scrapie in sheep has been shown to transmit laterally to goats if they are closely confined for a long time with a succession of sheep natural scrapie cases (Brotherston et al, 1968). It is now thought probable that scrapie is an endemic disease of goats, which apparently propagate the infection at least partly by maternal transmission (Hourrigan et al, 1979).…”

Section: Introductionmentioning

confidence: 99%

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Experimentally induced bovine spongiform encephalopathy did not transmit via goat embryos.

Foster

McKelvey

Fraser

et al. 1999

Journal of General Virology

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Experimentally induced bovine spongiform encephalopathy did not transmit via goat embryos.

Foster

McKelvey

Fraser

et al. 1999

Journal of General Virology

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“…In scrapie, the infectious agent is present in the environment and taken up orally during grazing on scrapie contaminated pastures [8,13,14]. In the case of BSE in cattle, infection has occurred through feeding concentrates with meat and bone meal derived from BSE infected cattle [75][76][77].…”

Section: Crossing the Mucosal Barriermentioning

confidence: 99%

TSE pathogenesis in cattle and sheep

2008

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-Many studies have been undertaken in rodents to study the pathogenesis of transmissible spongiform encephalopathies (TSE). Only a few studies have focused on the pathogenesis of bovine spongiform encephalopathy (BSE) and scrapie in their natural hosts. In this review, we summarize the most recent insights into the pathogenesis of BSE and scrapie starting from the initial uptake of TSE agents and crossing of the gut epithelium. Following replication in the gut-associated lymphoid tissues (GALT), TSE agents spread to the enteric nervous system (ENS) of the gut. Infection is then carried through the efferent fibers of the post-ganglionic neurons of the parasympathetic and sympathetic nervous system to the pre-ganglionic neurons in the medulla oblongata of the brain and the thoracic segments of the spinal cord. The differences between the pathogenesis of BSE in cattle and scrapie in sheep are discussed as well as the possible existence of additional pathogenetic routes.

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“…Scrapie in sheep was the first disease to be recognized within the group of the transmissible spongiform encephalopathies (TSE), which affect several mammalian species, including man and cattle. Naturally-occurring scrapie in goats was first reported in France [5], and although this and other subsequent descriptions [3,16,34] record contact with scrapie-infected sheep, some others do not [15,29,34]. In most cases, the disease in goats has been reported to closely resemble that in sheep, although differences in clinical manifestation between the two species have been described [4].…”

Section: Introductionmentioning

confidence: 99%

High prevalence of scrapie in a dairy goat herd: tissue distribution of disease-associated PrP and effect ofPRNPgenotype and age

González¹,

Martin²,

Sisó³

et al. 2009

Vet. Res.

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-Following a severe outbreak of clinical scrapie in 2006-2007, a large dairy goat herd was culled and 200 animals were selected for post-mortem examinations in order to ascertain the prevalence of infection, the effect of age, breed and PRNP genotype on the susceptibility to scrapie, the tissue distribution of diseaseassociated PrP (PrP d ), and the comparative efficiency of different diagnostic methods. As determined by immunohistochemical (IHC) examinations with Bar224 PrP antibody, the prevalence of preclinical infection was very high (72/200; 36.0%), with most infected animals being positive for PrP d in lymphoreticular system (LRS) tissues (68/72; 94.4%) compared to those that were positive in brain samples (38/72; 52.8%). The retropharyngeal lymph node and the palatine tonsil showed the highest frequency of PrP d accumulation (87.3% and 84.5%, respectively), while the recto-anal mucosa-associated lymphoid tissue (RAMALT) was positive in only 30 (41.7%) of the infected goats. However, the efficiency of rectal and palatine tonsil biopsies taken shortly before necropsy was similar. The probability of brain and RAMALT being positive directly correlated with the spread of PrP d within the LRS. The prevalence of infection was influenced by PRNP genetics at codon 142 and by the age of the goats: methionine carriers older than 60 months showed a much lower prevalence of infection (12/78; 15.4%) than those younger than 60 months (20/42; 47.6%); these last showed prevalence values similar to isoleucine homozygotes of any age (40/80; 50.0%). Two of seven goats with definite signs of scrapie were negative for PrP d in brain but positive in LRS tissues, and one goat showed biochemical and IHC features of PrP d different from all other infected goats. The results of this study have implications for surveillance and control policies for scrapie in goats.scrapie / goat / prion disease / transmissible spongiform encephalopathy

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Spread of scrapie by contact to goats and sheep

Cited by 95 publications

References 13 publications

Experimentally induced bovine spongiform encephalopathy did not transmit via goat embryos.

Experimentally induced bovine spongiform encephalopathy did not transmit via goat embryos.

TSE pathogenesis in cattle and sheep

High prevalence of scrapie in a dairy goat herd: tissue distribution of disease-associated PrP and effect ofPRNPgenotype and age

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