Abstract
European red deer (Cervus elaphus elaphus) are susceptible to the agent of bovine spongiform encephalopathy, one of the transmissible spongiform encephalopathies, when challenged intracerebrally but their susceptibility to alimentary challenge, the presumed natural route of transmission, is unknown. To determine this, eighteen deer were challenged via stomach tube with a large dose of the bovine spongiform encephalopathy agent and clinical signs, gross and histological lesions, presence and distribution of abnormal prion protein and the attack rate recorded. Only a single animal developed clinical disease, and this was acute with both neurological and respiratory signs, at 1726 days post challenge although there was significant (27.6%) weight loss in the preceding 141 days. The clinically affected animal had histological lesions of vacuolation in the neuronal perikaryon and neuropil, typical of transmissible spongiform encephalopathies. Abnormal prion protein, the diagnostic marker of transmissible encephalopathies, was primarily restricted to the central and peripheral nervous systems although a very small amount was present in tingible body macrophages in the lymphoid patches of the caecum and colon. Serial protein misfolding cyclical amplification, an in vitro ultra-sensitive diagnostic technique, was positive for neurological tissue from the single clinically diseased deer. All other alimentary challenged deer failed to develop clinical disease and were negative for all other investigations. These findings show that transmission of bovine spongiform encephalopathy to European red deer via the alimentary route is possible but the transmission rate is low. Additionally, when deer carcases are subjected to the same regulations that ruminants in Europe with respect to the removal of specified offal from the human food chain, the zoonotic risk of bovine spongiform encephalopathy, the cause of variant Creutzfeldt-Jakob disease, from consumption of venison is probably very low.
Highlights
Bovine spongiform encephalopathy (BSE) is infectious to, primarily, domestic cattle and wild bovids, several species of antelope, sheep and felids and is considered to be the cause of variant Creutzfeldt-Jakob disease in humans [1,2]. It is a member of the transmissible spongiform encephalopathies (TSE) group of diseases, known as prion diseases, which include, amongst others, scrapie in sheep and goats, sporadic, familial and iatrogenic Creutzfeldt-Jakob disease (CJD) and kuru in humans, transmissible mink encephalopathy in ranched mink and chronic wasting disease (CWD) in farmed and free-living cervids [3]
None of the animals subjected to post-mortem examinations at either 190 or 365 dpc showed any clinical signs of disease
The increase in incubation period compared to European red deer challenged with BSE intra-cerebrally (1060 days) [33] compared to oral challenge (1727 days) is approximately 60% and similar to the differences observed in incubation periods for sheep or goats when challenged with TSE agents by these two routes [40,41]
Summary
Bovine spongiform encephalopathy (BSE) is infectious to, primarily, domestic cattle and wild bovids, several species of antelope, sheep and felids and is considered to be the cause of variant Creutzfeldt-Jakob disease (vCJD) in humans [1,2]. It is a member of the transmissible spongiform encephalopathies (TSE) group of diseases, known as prion diseases, which include, amongst others, scrapie in sheep and goats, sporadic, familial and iatrogenic Creutzfeldt-Jakob disease (CJD) and kuru in humans, transmissible mink encephalopathy in ranched mink and chronic wasting disease (CWD) in farmed and free-living cervids [3]. Following scrapie exposure it has been shown experimentally, with respect to both attack rate and incubation period, pre-weaned lambs are at greater risk of infection, possibly due to patent gut epithelium [10]
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