BSE and CJD explained

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This presentation outlines how BSE and CJD could have arisen in the United Kingdom.  No attempt has been made to weight the different causes. It should be noted that this is only one way of representing the origins of BSE and CJD.  There are many other explanations for the prion diseases in cows and humans.

The presentation provides a list of possible causes which are:

1)          Organophosphates:

This theory is mentioned because it is interesting and there is some support for it.  The relevance of organophosphates to BSE is outlined in the following book:

            Dying for a Hamburger: Murray Waldman and Marjorie Lamb (2004:187) 

It is stated that "there is a possibility that ... pesticides (organophosphates) could increase the susceptibility of cattle to BSE".  This explanation is likely to be the least plausible.  There was an interesting comment below the video, on you tube.  This comment has been adapted: "the Fore people lived in nature with no pesticide, or any chemicals, yet a very large percentage of them died of Kuru", a form of prion disease. This suggests that a prion disease has been created and spread without any chemical exposure.

2)         The Conventional Explanation:

BSE occurred spontaneously in a cow.  The disease was then spread through the practice of dead cows being fed to other cows.  Humans then ate the cows infected with the BSE. The evidence, from Kuru, provides evidence for the spread of prion disease, within the same (human) species, through the oral route.

3)         The Growth Hormone Explanation:

BSE arose through poorly thought-out experiments using growth hormones.  There is separate evidence that some CJD (human prion disease) has been caused by growth hormones.

A cow, with sporadic BSE, could have been used in the development of a bovine growth hormone.  This growth hormone could then have been transferred into a cow.  The cow then acquired BSE.  Humans could have acquired CJD through meat consumption. 

Alternatively, humans could have acquired the disease through a vaccination.  The weakness of attributing CJD to vaccination, is that it is unclear what type of vaccines could have spread the disease.  It is unclear whether oral vaccines need to be examined or whether a vaccine injected is more relevant. 

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