Prions: detection of bovine spongiform encephalopathy and links to variant Creutzfeldt–Jakob disease

Konold, Timm; Arnold, Mark; Adkin, Amie

doi:10.1016/b978-0-12-819470-6.00042-1

Cited by 1 publication

(1 citation statement)

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“…Bovine spongiform encephalopathy (BSE), first described as a neurological disease in cattle in 1987 [ 1 ], was caused by the feeding of cattle with meat and bone meal (MBM) contaminated with a transmissible spongiform encephalopathy (TSE) agent that led to an epidemic affecting more than 180 000 cattle in the United Kingdom (UK) alone and is responsible for currently 178 cases of variant Creutzfeldt-Jakob disease in humans in the UK [ 2 ]. One of the measures introduced to monitor the epidemic was enhanced surveillance for TSEs, not only in cattle but also in sheep and goats, which were known to be affected by a TSE called scrapie.…”

Section: Introductionmentioning

confidence: 99%

Experimental transmission of ovine atypical scrapie to cattle

Konold,

Spiropoulos,

Hills

et al. 2023

Vet Res

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Classical bovine spongiform encephalopathy (BSE) in cattle was caused by the recycling and feeding of meat and bone meal contaminated with a transmissible spongiform encephalopathy (TSE) agent but its origin remains unknown. This study aimed to determine whether atypical scrapie could cause disease in cattle and to compare it with other known TSEs in cattle. Two groups of calves (five and two) were intracerebrally inoculated with atypical scrapie brain homogenate from two sheep with atypical scrapie. Controls were five calves intracerebrally inoculated with saline solution and one non-inoculated animal. Cattle were clinically monitored until clinical end-stage or at least 96 months post-inoculation (mpi). After euthanasia, tissues were collected for TSE diagnosis and potential transgenic mouse bioassay. One animal was culled with BSE-like clinical signs at 48 mpi. The other cattle either developed intercurrent diseases leading to cull or remained clinical unremarkable at study endpoint, including control cattle. None of the animals tested positive for TSEs by Western immunoblot and immunohistochemistry. Bioassay of brain samples from the clinical suspect in Ov-Tg338 and Bov-Tg110 mice was also negative. By contrast, protein misfolding cyclic amplification detected prions in the examined brains from atypical scrapie-challenged cattle, which had a classical BSE-like phenotype. This study demonstrates for the first time that a TSE agent with BSE-like properties can be amplified in cattle inoculated with atypical scrapie brain homogenate.

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Section: Introductionmentioning

confidence: 99%