Feline spongiform encephalopathy

Pearson, G. R.; Gruffydd-Jones, TJ; Wyatt, J. M.; Hope, Jim; Chong, Angela; Scott, AC; Dawson, Margaret; Wells, G.

doi:10.1136/vr.128.22.532-b

Cited by 38 publications

(15 citation statements)

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“…Prion diseases are typically observed in man and ruminants, but outbreaks of feline spongiform encephalopathy (FSE) in various feline species [12] and transmissible mink encephalopathy (TME) in farmed mink ( Neovision ( mustela ) vison ) [13] have shown that species of the Order Carnivora can be infected with prions under natural conditions, i.e. through contaminated feed.…”

Section: Introductionmentioning

confidence: 99%

Genetic Predictions of Prion Disease Susceptibility in Carnivore Species Based on Variability of the Prion Gene Coding Region

et al. 2012

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Mammalian species vary widely in their apparent susceptibility to prion diseases. For example, several felid species developed prion disease (feline spongiform encephalopathy or FSE) during the bovine spongiform encephalopathy (BSE) epidemic in the United Kingdom, whereas no canine BSE cases were detected. Whether either of these or other groups of carnivore species can contract other prion diseases (e.g. chronic wasting disease or CWD) remains an open question. Variation in the host-encoded prion protein (PrPC) largely explains observed disease susceptibility patterns within ruminant species, and may explain interspecies differences in susceptibility as well. We sequenced and compared the open reading frame of the PRNP gene encoding PrPC protein from 609 animal samples comprising 29 species from 22 genera of the Order Carnivora; amongst these samples were 15 FSE cases. Our analysis revealed that FSE cases did not encode an identifiable disease-associated PrP polymorphism. However, all canid PrPs contained aspartic acid or glutamic acid at codon 163 which we propose provides a genetic basis for observed susceptibility differences between canids and felids. Among other carnivores studied, wolverine (Gulo gulo) and pine marten (Martes martes) were the only non-canid species to also express PrP-Asp163, which may impact on their prion diseases susceptibility. Populations of black bear (Ursus americanus) and mountain lion (Puma concolor) from Colorado showed little genetic variation in the PrP protein and no variants likely to be highly resistant to prions in general, suggesting that strain differences between BSE and CWD prions also may contribute to the limited apparent host range of the latter.

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Section: Introductionmentioning

confidence: 99%

Genetic Predictions of Prion Disease Susceptibility in Carnivore Species Based on Variability of the Prion Gene Coding Region

et al. 2012

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“…It has been shown that BSE can either naturally or experimentally infect a wide range of species, including mice, sheep, goats, cats, macaques, mink, red deer, and humans (9)(10)(11)(12)(13)(14)(15). Until BSE is eliminated, it will remain a threat to susceptible species, including cervids, which could potentially act as a reservoir of the agent.…”

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confidence: 99%

Assessing the Susceptibility of Transgenic Mice Overexpressing Deer Prion Protein to Bovine Spongiform Encephalopathy

Vickery

Lockey

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et al. 2014

J Virol

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cSeveral transgenic mouse models have been developed which facilitate the transmission of chronic wasting disease (CWD) of cervids and allow prion strain discrimination. The present study was designed to assess the susceptibility of the prototypic mouse line, Tg(CerPrP)1536 ؉/؊ , to bovine spongiform encephalopathy (BSE) prions, which have the ability to overcome species barriers. Tg(CerPrP)1536 ؉/؊ mice challenged with red deer-adapted BSE resulted in 90% to 100% attack rates, and BSE from cattle failed to transmit, indicating agent adaptation in the deer.

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“…In 1991, BSE was reported in a domestic cat that presumably was contaminated via pet food 6) . Transmission of scrapie from small ruminants to cats had never been described, raising concern that BSE might be more pathogenic than scrapie not only for cats, but also for humans.…”

Section: Vcjd In Humans and Transmission Of Bse To Non-human Primatesmentioning

confidence: 99%

Modeling Variant Creutzfeldt-Jakob Disease and Its Pathogenesis in Non-human Primates

Lasmézas

2017

Food Safety

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In the early 90s', Europe was shaken by the fear that the prions from "mad cow disease" (bovine spongiform encephalopathy) would transmit the disease to humans via beef products. In 1996, the first variant Creutzfeldt-Jakob (vCJD) patients were described, and the same year our Bovine Spongiform Encephalopathy (BSE) transmission studies to cynomolgus macaques demonstrated that the BSE prion was highly infectious for primates, inducing brain lesions identical to those observed in vCJD patients. These studies provided the first experimental evidence that vCJD was BSE in humans. Subsequent studies established the BSE/vCJD-infected cynomolgus macaque as a robust model to study the pathogenesis of vCJD. We showed rapid adaptation of BSE prions to primates upon subsequent passage, and their distribution in peripheral tissues and blood. Some key studies are summarized in the present paper.

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Feline spongiform encephalopathy

Cited by 38 publications

References 0 publications

Genetic Predictions of Prion Disease Susceptibility in Carnivore Species Based on Variability of the Prion Gene Coding Region

Genetic Predictions of Prion Disease Susceptibility in Carnivore Species Based on Variability of the Prion Gene Coding Region

Assessing the Susceptibility of Transgenic Mice Overexpressing Deer Prion Protein to Bovine Spongiform Encephalopathy

Modeling Variant Creutzfeldt-Jakob Disease and Its Pathogenesis in Non-human Primates

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