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The wasting lands - The CWD epidemic in deer

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The WASTING LANDS - the CWD epidemic in deer

Mark Purdey

Chronic Wasting Disease of deer is much the same as scrapie in sheep. It is a traditional variant  of the spongiform encephalopathy (TSE) range of diseases; a previously unheard of neurodegenerative syndrome made famous by the outbreak of mad cow disease in the UK .

Seven per cent of the free ranging/captive deer and elk population residing along a 100 mile length of the Front Range of the Rocky Mountains in North Colorado and South East Wyoming have been affected with this disease for several years now. Originally identified as a TSE in the late 1970's by veterinary neuropathologist, Professor Beth Williams, the disease could have been endemic for many decades. Any rancher or hunter who had noticed these ailing deer hobbling around the place, had probably put such cases down to premature ageing or some ‘weakling’ wasting condition.   

The origins of  hyper infectious hysteria.

Despite the long term tradition of CWD haunting the Front Range foothills, a surge of near hysteria has bestruck the official US wildlife departments whose job it is to preside over CWD. Following in the footsteps of the official furore over mad cow disease in Europe, the US government has sadly adopted the same unproven hypothetical mindset on the origins of these diseases; that TSEs stem from exposure to hyper infectious ‘prions’ that are readily transmitted via body to body contact (saliva, etc), or via ‘prion’ contaminated feed. In this respect, blame has been conveniently offloaded onto the deer themselves – for sharing the same feed troughs, etc, – or onto the hunters for transporting the ‘infectious’ agent around with them from shooting region to region.

But why has such a deeply flawed and scientifically inept theoretical consensus been permitted ‘gospel’ status for such an unusually protracted period of time? The launch of any new theory into the notoriously sceptical scientific establishment invariably attracts a fair degree of  healthy challenge. But strangely enough with TSEs, there has been an exception to this rule. This is largely because the UK government has been actively engaged in tailoring or outright suppressing, any publicity surrounding dissident scientific studies that invalidate or even begin to threaten any aspect of the official hypothesis. Furthermore, it is strange to witness the same old ‘masters of complacency’ in the higher echelons of UK officialdom, suddenly adopting a high degree of hypersensitivity over the way that they deal with their affairs. Such an incongruous style of official behaviour has betrayed a deep level of insecurity over anything that they are telling us on BSE.

For instance, nobody has been told that the British meat and bone meal (MBM) feed that was held responsible for the massive BSE epidemic in the UK has been exported by the cargo boat load, to cattle herds all over the world since the 1960s - yet the majority of those countries have never suffered a single case of BSE in their cattle herds to date. Nor does anyone know about the 40,000 cases of BSE that have appeared in UK cows that were born after the 1988 ban on MBM going into UK cattle feed. In this respect, nearly a quarter of the total cases of BSE in Britain cannot be explained by the conventional causal theory! In some BSE endemic countries, more than half of their total BSE cases were born after their respective MBM bans.  Even my five year old son can see the stupidity of  such an obvious ‘cover story’.

To escape the embarrassment of the outright failure of control measures, the UK government set about hoodwinking the British public and their foreign interests by creating a second feed ban in 1996;  whereupon they instructed their spin doctor journalists to misappropriate blame for the unaccountable 40,000 cases of BSE onto ‘leakage of micro amounts of MBM left over in the feed silos getting into cattle feed’. They then gave full coverage to the fact that the government were now banning the inclusion of MBM going into feeds destined for all types of farm livestock. The 1988 ban was subsequently forgotten and conveniently erased from the public memory banks. But today, 22 cases of BSE have now emerged that were born after this second 1996 ban!

This whole hyper infectious myth has been based on the fact that TSEs can be transmitted in the laboratory; whereby TSE affected brain tissue is injected into misfortunate laboratory animals that subsequently contract TSE. The fact that classes of Alzheimer’s and other neurodegenerative diseases can be transmitted in this way is completely ignored. But these transmission experiments prove nothing in terms of demonstrating whether TSEs are caused by a microbiological infectious agent or not. After all TSEs do not fulfil Koch’s postulates; the conventional yardstick for assessing whether a given disease stems from infectious origins.

The ‘all important’ success of these ‘trumped up’ transmission experiments could have equally easily represented the fact that a highly toxic chemical or metal species which had originally contaminated and killed the initial TSE diseased animal was then being transmitted into a secondary host. Once again, this equally feasible alternative explanation has been ignored.

But one of the first lines of epidemiological inquiry aimed at investigating the origins of CWD ought to have addressed the question why the disease has not spread like wildfire, wiping out susceptible individuals of the deer population residing right across the entire Rocky mountain ranges. But whenever the likes of rancher and hunting folk who live and breathe with the deer has attempted to infiltrate the CWD debate, their intuitive and practical perspectives on the disease have invariably been rebuffed by the official and scientific policy makers.  

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Last updated 11th April 2008