Inconsistent detection of PrP in extraneural tissues of cats with feline spongiform encephalopathy

Ryder, S. J.; Wells, Gah; Bradshaw, John; Pearson, G. R.

doi:10.1136/vr.148.14.437

Cited by 33 publications

(39 citation statements)

References 23 publications

(27 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Dietary exposure to beef contaminated with the BSE agent is believed to have caused nearly 200 cases of variant CJD (vCJD) in humans (12)(13)(14)(15) as well as spongiform encephalopathies in domestic cats and British zoo animals (16)(17)(18)(19). Prion transmission across species barriers has been replicated experimentally and typically leads to incomplete attack rates and to prolonged, highly variable ips (20).…”

Section: Introductionmentioning

confidence: 99%

A molecular switch controls interspecies prion disease transmission in mice

Sigurdson¹,

Nilsson²,

Hornemann³

et al. 2010

J. Clin. Invest.

130

139

View full text Add to dashboard Cite

Transmissible spongiform encephalopathies are lethal neurodegenerative disorders that present with aggregated forms of the cellular prion protein (PrP C ), which are known as PrP Sc . Prions from different species vary considerably in their transmissibility to xenogeneic hosts. The variable transmission barriers depend on sequence differences between incoming PrP Sc and host PrP C and additionally, on strain-dependent conformational properties of PrP Sc . The β 2 -α 2 loop region within PrP C varies substantially between species, with its structure being influenced by the residue types in the 2 amino acid sequence positions 170 (most commonly S or N) and 174 (N or T). In this study, we inoculated prions from 5 different species into transgenic mice expressing either disordered-loop or rigid-loop PrP C variants. Similar β 2 -α 2 loop structures correlated with efficient transmission, whereas dissimilar loops correlated with strong transmission barriers. We then classified literature data on cross-species transmission according to the 170S/N polymorphism. Transmission barriers were generally low between species with the same amino acid residue in position 170 and high between those with different residues. These findings point to a triggering role of the local β 2 -α 2 loop structure for prion transmissibility between different species.

show abstract

Section: Introductionmentioning

confidence: 99%

A molecular switch controls interspecies prion disease transmission in mice

Sigurdson¹,

Nilsson²,

Hornemann³

et al. 2010

J. Clin. Invest.

130

139

View full text Add to dashboard Cite

show abstract

“…Ninety cases have been identified in Great Britain, 11 1 in Northern Ireland (Federal Register, 1997), 1 in Norway, 1 5 Domestic cats with FSE are generally 4 to 9 years of age (mean, 6.6 years). 38 FSE has also been reported in other felids, 24 including the cheetah (Acinonyx jubatus), 19 ocelot (Felis pardalis), puma (Felis concolor), 36 lion (Felis leo), and tiger (Panthera tigris). 16 The clinical signs and pathologic features of the disease are similar in all susceptible species of Felidae.…”

Section: Introductionmentioning

confidence: 98%

“…23 Spongiosis is widespread in the brain and most marked in the medial geniculate nucleus and the basal nuclei. 24,37 The degree of vacuolation in the neuropil can be marked, progressing to status spongiosis in some cases. Vacuolation is also present in neuronal perikarya, particularly in the raphe nucleus, the dorsal motor nucleus of the vagus nerve, and the red nucleus.…”

Section: Introductionmentioning

confidence: 99%

“…PrP sc is typically detectable throughout the brain of cats with FSE as small aggregates, with punctate, particulate, and linear strands of immunoreactivity. 24 In 1998, Zanusso et al reported the simultaneous occurrence of spongiform encephalopathy in a 60-year-old Italian man and his cat. The prion strain in the brain of the cat was similar to that in the man, but distinct from the UK strain of BSE (new variant Creutzfeldt-Jakob disease and its feline counterpart).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Neuropathology of Italian Cats in Feline Spongiform Encephalopathy Surveillance

et al. 2008

View full text Add to dashboard Cite

Abstract. Feline spongiform encephalopathy (FSE) is a transmissible spongiform encephalopathy associated with the consumption of feedstuffs contaminated with tissue from bovine spongiform encephalopathy-affected cattle and characterized by the accumulation in the central nervous system of an abnormal isoform of the prion protein (PrP sc ). Clinically, it presents as a progressive fatal neurologic syndrome that is not easily distinguished from other feline neurologic conditions. Most cases of FSE have been reported in England, where it was first detected in 1990, but a few cases have been reported from other European countries. To identify possible cases of FSE in Italy, the Italian Ministry of Health funded a 2-year surveillance project during which the brains from 110 domestic cats with neurologic signs were evaluated histologically for spongiform encephalopathy and immunohistochemically to detect PrP sc . Although no cases of FSE were found, the study proved useful in monitoring the Italian cat population for other neurologic diseases: neoplasia (21.8%), toxic-metabolic encephalopathy (18.2%), granulomatous encephalitis (15.5%), suppurative encephalitis (4.6%), trauma (3.6%), circulatory disorders (3.6%), degeneration (2.7%), nonsuppurative encephalitis (2.7%), and neuromuscular diseases (1.8%). No histologic lesions were found in 20% of the brains, and samples from 5.5% of the cats were rejected as unsuitable.

show abstract

“…Feline spongiform encephalopathy first appeared in the United Kingdom (UK) in the 1990s during the epizootic of bovine spongiform encephalopathy (BSE), and since then approximately 90 cases of FSE have been seen in the UK and in Europe. 7 Feline spongiform encephalopathy is thought to have been transmitted by consumption of food contaminated with BSE, which is suspected to have resulted from consumption of food contaminated with scrapie. 1 In the United States, at least 2 experiments have been conducted to show that intracerebral inoculations of sheep scrapie into cattle produces a form of TSE, but the experimental disease is clinicopathologically different from BSE.…”

mentioning

confidence: 99%

Resistance of Domestic Cats to a US Sheep Scrapie Agent by Intracerebral Route

et al. 2002

View full text Add to dashboard Cite

Feline spongiform encephalopathy (FSE) is thought to have resulted from consumption of food contaminated with bovine spongiform encephalopathy and the latter is believed to result from the consumption of food contaminated with scrapie. However, no direct experimental documentation exists to indicate that the scrapie agent is capable of amplifying in cats, and, therefore, crossing the species barrier. During 1979, 6 cats ranging in age from 3.5 to 18 months were intracerebrally inoculated with sheep scrapie (inoculum G-639-PP) and were observed for an extended period. Inoculated cats did not develop neurologic disease, and microscopic lesions of spongiform encephalopathy were not evident. Immunohistochemistry and Western blot techniques failed to detect the abnormal form of prion protein (PrPres). These results indicate that the sheep scrapie agent (G-639-PP) used in this study was not capable of amplifying in cats and therefore was unable to cross the species barrier to produce FSE.

show abstract

Inconsistent detection of PrP in extraneural tissues of cats with feline spongiform encephalopathy

Cited by 33 publications

References 23 publications

A molecular switch controls interspecies prion disease transmission in mice

A molecular switch controls interspecies prion disease transmission in mice

Neuropathology of Italian Cats in Feline Spongiform Encephalopathy Surveillance

Resistance of Domestic Cats to a US Sheep Scrapie Agent by Intracerebral Route

Contact Info

Product

Resources

About