Epidemiology and control of bovine spongiform encephalopathy (BSE)

Bradley, R.; Wilesmith, J. W.

doi:10.1093/oxfordjournals.bmb.a072654

Cited by 66 publications

(29 citation statements)

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“…C-BSE was likely caused primarily by widespread prion contamination of cattle feed (17). After peaking in the early 1990s, the incidence of C-BSE has now been greatly reduced by regulatory measures that limit its horizontal spread.…”

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confidence: 99%

Detection of Atypical H-Type Bovine Spongiform Encephalopathy and Discrimination of Bovine Prion Strains by Real-Time Quaking-Induced Conversion

et al. 2016

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Many mammalian species can be afflicted with prion diseases or transmissible spongiform encephalopathies. Prion diseases are neurodegenerative, transmissible, untreatable, and fatal (reviewed in references 1 and 2). The underlying pathogenesis of prion diseases involves the conversion of the host's normal prion protein, PrP C , to abnormal forms that are usually more protease resistant, multimeric, and insoluble. The multimeric and insoluble forms have been generically called PrP Sc (PrP-scrapie), or more functionally PrP Res (protease resistant) and PrP D (disease associated). At least some of these forms comprise the transmissible agent or prion (3-10). Multiple prion strains can be propagated within a given host species, giving consistently different clinical, pathological, and molecular phenotypes (11-16).The first prion disease to be recognized in cattle was classical bovine spongiform encephalopathy (C-BSE). C-BSE was likely caused primarily by widespread prion contamination of cattle feed (17). After peaking in the early 1990s, the incidence of C-BSE has now been greatly reduced by regulatory measures that limit its horizontal spread. C-BSE is the only known zoonotic prion disease, having caused variant Creutzfeldt-Jakob disease (vCJD) in humans who presumably consumed contaminated beef. Although new clinical cases of vCJD are rare (http://www.cjd.ed.ac .uk/documents/figs.pdf), a recent survey of appendices in the United Kingdom suggests a high incidence of subclinical vCJD infections, at ϳ1:2,000 of the population born between 1941 and 1985 (18).Since the C-BSE epidemic, two atypical strains of BSE, H-type BSE (H-BSE) and L-type BSE (L-BSE), have also been identified in cattle. PrPRes is usually composed of a mixture of glycosylated and unglycosylated molecules, and the various BSE strains can be differentiated biochemically using Western blotting of postmortem brain tissue samples by comparing the proteinase K (PK)-treated PrPRes banding patterns (19)(20)(21)(22). The H and L types of BSE are classified by their respective high and low apparent molecular masses of the unglycosylated PrP Res band. These atypical BSE strains, which are rare (Ͻ100 cases identified worldwide), tend to affect older animals (23) and appear to represent sporadic forms of bovine prion diseases (24). Despite the apparent rarity of the various types of BSE, the facts that H-and L-BSE appear to arise spontaneously and have distinct transmissibilities (20, 25-32) make it important to be able to detect and differentiate them to reduce the risk of transmission to cattle or other species, such as humans.Several in vitro methods have been developed to detect C-, L-, and H-BSE. Commercially available rapid immunochemical tests for PrP D can, in the best cases, give positive responses from 10 Ϫ3 to 10 Ϫ4 dilutions of postmortem brain tissues with high levels of PrP D (33, 34). Immunoblotting for PrP Res can detect BSE-infected tissues with similar sensitivity and also discriminate between the bovine strains based on the relative electro...

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Detection of Atypical H-Type Bovine Spongiform Encephalopathy and Discrimination of Bovine Prion Strains by Real-Time Quaking-Induced Conversion

et al. 2016

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“…Indeed there is now convincing evidence from interspecies transmission studies in animals (Lasmézas et al, 1996(Lasmézas et al, , 2001Bruce et al, 1997) and transgenic mice (Hill et al, 1997;Scott et al, 1999) that cattle BSE prions have been transmitted to humans (Table 1). Hamsters have not been successfully inoculated with bovine PrP (Bradley and Wilesmith, 1993), and Creutzfeldt-Jakob disease was only serially transmitted to Syrian hamsters via guinea pigs (Manuelidis et al, 1978; Table 1). In the latter case, incubation times varied depending on the CJD strain used.…”

Section: Heterodimerization Of Prion Proteins Of Different Speciesmentioning

confidence: 99%

Intra- and Interspecies Interactions between Prion Proteins and Effects of Mutations and Polymorphisms

Hundt¹,

Gauczynski²,

Leucht³

et al. 2003

Biological Chemistry

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“…Until today, no evidence of BSE infectivity in semen, embryos, placenta or milk (Bradley and Wilesmith, 1993;Buschmann and Groschup, 2005;Taylor et al, 1995;Wrathall et al, 2002) have been determined although increased risk of BSE development has been reported for the offspring of infected cows. The practice of feeding cattle with meat and bone meal (MBM) contaminated with infectious prions was proposed as the most likely responsible for the BSE epidemic and some hypotheses on the origin of BSE were considered: (i) the primary existence of sporadic or genetic BSE in cattle before its transmission via MBM Capobianco et al, 2007;Nicholson et al, 2008;Richt and Hall, 2008;Torres et al, 2013); (ii) sheep or goat-scrapie transmission to cattle through MBM (Hill et al, 1998); and (iii) human CJD (Colchester and Colchester, 2005).…”

Section: Bovine Spongiform Encephalopathy (Bse)mentioning

confidence: 99%