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Chronic wasting disease (CWD) is a form of transmissible spongiform encephalopathy (TSE) that infects members of the cervid family. It is caused by infection with a unique pathogen known as a prion protein (PrP CWD). Infection results in the normal version of the protein, a component of the membrane of cells in nervous tissue (neurons), being transformed into the infectious form of the prion protein (PrP CWD). This protein cannot be broken down in the same way and accumulates in nervous tissue, impairing function and resulting in the neurodegenerative condition, CWD.
In the United States CWD has been identified in mule deer, white-tailed deer, Rocky Mountain Elk, and Shira’s moose. In Europe, CWD cases have been reported in Elk (European moose) and reindeer in Norway. Based on their genetic relationship to the cervid species that have been affected by CWD in America, it is thought that European red dear and the Finnish white-tailed deer population (imported from the US nearly a centruy ago) are also susceptible to infection.
It is not thought that other species can be naturally infected with the causative agent of CWD (PrP CWD).
Once the PrP CWD enters the brain (showing a preference for certain sites including nerves in the brain stem) it starts to accumulate and affected neurons show degenerative changes which appear under the microscope as holes or spaces in the cells and their processes. This holey appearance underlies the use of the term ‘spongiosis’ in the name of this group of diseases. Clinical signs typically reflect this damage to nervous tissue which causes behavioural changes such as depression, aggression and separation from the group. In addition, the animals may have difficulty with swallowing and locomotion, both of which can lead to weight loss. The average time between infection and the development of clinical signs is nearly two years.
CWD is transmitted horizontally by direct contact between infected and non-infected cervids, and via the environment; grazing, herding and bedding areas contaminated with the feces, saliva or carcass of infected animals act as a source of infection. Additionally, PrP CWD survives in water making shared water sources a potential route of transmission.
After ingestion the PrP CWD replicates in the lymphoid tissue and is thought to enter the brain either via the blood or along nerve tracts. Later in infection the prion is found throughout the body and is shed in feces, urine and saliva.
To date, no cases of the human form of TSE (Creutzfeld Jakob disease) associated with ingestion of venison have been reported. Furthermore, an increased rate of CJD amongst hunters, their families or venison eaters has not been found. Despite these finding, avoiding consumption of CWD-infected meat is advised.
Until recently, based on a Europe-wide survey carried out between 2007 and 2009 in which nearly 15000 wild and farmed cervids were tested, it was thought that CWD was restricted to the North American continent, with a single case report of CWD in a moose in South Korea that had been exported from Canada. However, in 2016 the Norwegian authorities reported cases of CWD in free-living elk and a reindeer.
Infectious Diseases of Wild Mammals and Birds in Europe (1). Somerset, GB: Wiley-Blackwell, 2012. ProQuest ebrary. Web. 6 October 2016.
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