Feline spongiform encephalopathy: fibril and PrP studies

Pearson, G. R.; Wyatt, J. M.; Gruffydd-Jones, TJ; Hope, James; Chong, Angela; Higgins, Robert; Scott, A. C.; Wells, Gah

doi:10.1136/vr.131.14.307

Cited by 50 publications

(25 citation statements)

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“…Downloaded by [University of Illinois Chicago] at 07: 38 27 November 2014 Introduction Spongy degeneration of the central nervous system has been described by Kelly and Gaskell in 1976 (21) and by Jones et al in 1992 (20). Moreover several cases of Feline Spongiform Encephalopathy (FSE) have been described as a scrapie-like disease (5,26,30,41). It is strongly suspected that FSE is a disease induced by prions.…”

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confidence: 99%

First cases of animal diseases published since 2000. 2. Cats

Elsinghorst¹

2003

Veterinary Quarterly

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In this second article of a series of papers listing first case reports of animal diseases published since 2000, the following nine cases of cat diseases are discussed: Congenital spongiform change in the brain stem nuclei. Enterococcus hirae enteropathy. Focal cerebral angiomatosis. Glomus tumor. Intraocular extramedullary plasmacytoma. Lens epithelial neoplasias. Phaeohyphomycosis due to Fonsecaea pedrosoi. Pulmonary lymphomatoid granulomatosis. Systemic amyloidosis in a Devon rex. After a short introduction, the bibliographical data, the abstract of the author(s) and some additional information derived from the article are given. The article will be regularly updated adding overlooked as well as new first reports.

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confidence: 99%

First cases of animal diseases published since 2000. 2. Cats

Elsinghorst¹

2003

Veterinary Quarterly

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“…That this disease belonged to the group of transmissible SEs was subsequently confirmed by the demonstration of SAF in brain extracts, the presence of modified PrP by immunoblotting (53) and by transmissibility to mice (1). At least 41 (R. Bradley, pers.…”

Section: Feline Spongiform Encephalopathymentioning

confidence: 98%

Animal spongiform encephalopathies ‐ an update part 1. Scrapie and lesser known animal spongiform encephalopathies

Schreuder¹

1994

Veterinary Quarterly

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“…Discussions on viroids and virinos (Kimberlin, 1982) remained (Schreuder, 1998) and even bacterial agents were proposed (Bastian et al, 1981;Wisniewski et al, 1996) until the bovine spongiform encephalopathy (BSE) crisis emerged and transgenic mouse experiments proved the agent replication concept (Scott et al, 1999). Last critics started to vanish after human patients and cats developed a new variant of Creutzfeldt-Jakob's disease (nvCJD) and feline spongiform encephalopathy (FSE) respectively, both caused by the BSE agent (Pearson et al, 1992;Almond and Pattison, 1997;Hill et al, 1997;Bruce et al, 1997).…”

Section: Prions the Bse Crisismentioning

confidence: 99%

Protein folding pathology in domestic animals

Gruys

2004

J. Zheijang Univ.-Sci.

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Fibrillar proteins form structural elements of cells and the extracellular matrix. Pathological lesions of fibrillar microanatomical structures, or secondary fibrillar changes in globular proteins are well known. A special group concerns histologically amorphous deposits, amyloid. The major characteristics of amyloid are: apple green birefringence after Congo red staining of histological sections, and non-branching 7−10 nm thick fibrils on electron microscopy revealing a high content of cross beta pleated sheets. About 25 different types of amyloid have been characterised. In animals, AA-amyloid is the most frequent type. Other types of amyloid in animals represent: AIAPP (in cats), AApoAI, AApoAII, localised AL-amyloid, amyloid in odontogenic or mammary tumors and amyloid in the brain. In old dogs Aβ and in sheep APrP sc -amyloid can be encountered. AA-amyloidosis is a systemic disorder with a precursor in blood, acute phase serum amyloid A (SAA). In chronic inflammatory processes AA-amyloid can be deposited. A rapid crystallization of SAA to amyloid fibrils on small beta-sheeted fragments, the 'amyloid enhancing factor' (AEF), is known and the AEF has been shown to penetrate the enteric barrier. Amyloid fibrils can aggregate from various precursor proteins in vitro in particular at acidic pH and when proteolytic fragments are formed. Molecular chaperones influence this process. Tissue data point to amyloid fibrillogenesis in lysosomes and near cell surfaces. A comparison can be made of the fibrillogenesis in prion diseases and in enhanced AA-amyloidosis. In the reactive form, acute phase SAA is the supply of the precursor protein, whereas in the prion diseases, cell membrane proteins form a structural source. Aβ-amyloid in brain tissue of aged dogs showing signs of dementia forms a canine counterpart of senile dementia of the Alzheimer type (ccSDAT) in man. Misfolded proteins remain potential food hazards. Developments concerning prevention of amyloidogenesis and therapy of amyloid deposits are shortly commented.

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Feline spongiform encephalopathy: fibril and PrP studies

Cited by 50 publications

References 0 publications

First cases of animal diseases published since 2000. 2. Cats

First cases of animal diseases published since 2000. 2. Cats

Animal spongiform encephalopathies ‐ an update part 1. Scrapie and lesser known animal spongiform encephalopathies

Protein folding pathology in domestic animals

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