Abstract
Small ruminant post-mortem testing programs were initially designed for monitoring the prevalence of prion disease. They are now considered as a potential alternative to genetic selection for eradicating/controlling classical scrapie at population level. If such policy should be implemented, its success would be crucially dependent on the efficiency of the surveillance system used to identify infected flocks. In this study, we first determined the performance of post-mortem classical scrapie detection in eight naturally affected goat herds (total n = 1961 animals) according to the age at culling. These results provided us with necessary parameters to estimate, through a Monte Carlo simulation model, the performance of scrapie detection in a commercial population. According to this model, whatever the number of tests performed, post mortem surveillance will have limited success in identifying infected herds. These data support the contention that scrapie eradication programs relying solely on post mortem testing in goats will probably fail. Considering the epidemiological and pathological similarities of scrapie in sheep and goats, the efficiency of scrapie surveillance in both species is likely to be similar.
Highlights
Transmissible Spongiform Encephalopathies (TSE), or prion diseases, are fatal neurodegenerative disorders occurring in a number of mammal species like sheep and goats, cattle, or humans (Creutzfeldt-Jakob disease–CJD)
Our results provides a basis for discussing the effectiveness of policies that would rely solely on TSE testing for controlling and eradicating classical scrapie in small ruminants
These observations support the contention that both ELISA (PrPSc rapid detection test) and IHC, display similar performances for PrPSc detection in the posterior brainstem and lymphoid tissues from classical scrapie infected small ruminants
Summary
Transmissible Spongiform Encephalopathies (TSE), or prion diseases, are fatal neurodegenerative disorders occurring in a number of mammal species like sheep and goats (scrapie), cattle (bovine spongiform encephalopathy–BSE), or humans (Creutzfeldt-Jakob disease–CJD). PrPSc is currently considered to be the only TSE biochemical marker. According to the prion concept, abnormal PrP would be the causative agent of TSE [2]. Following the BSE epidemics in the UK and the identification of BSE zoonotic properties [3,4], the control of human and animal exposure to TSE agents has become a priority. A sanitary policy has been implemented based on both eradication of TSE in food producing animals and exclusion of known infectious materials (Specified Risk Materials, SRM) from the food chain. Whereas the SRM retrieval policy is considered to be highly efficient in preventing dietary exposure to cattle BSE, it has a more limited impact on the entry into the food chain of small ruminants’ classical or atypical TSE agents [5]
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