Prions?

[cowman]

I think everyone can agree that what allowed this BSE thing to flourish was probably the feeding of infected cattle to other cattle?
Now as I understand it Prions are not the culprit as such. Apparently all animals have prions including man. But somewhere along the line a prion folds or mutates or something and then it becomes the deadly BSE/scrapie/cjd prion. So how come this prion changes? Is it a totally fluke type of thing? Or is something causing it to change?
I believe Purdys theory(as I understand it)is that a mineral immbalance causes the change. And perhaps certain pesticides can cause the mineral immbalance? And that makes sense to me, how about you? Why has so much of the research been about what happens after the BSE prion is present and hardly any on why the radical prion forms?
I would assume if an animal ate BSE prions they would shortly have enough multiplying in their brains to test positive...perhaps it takes up to 24 months to get large enough numbers to test positive? But does it not make sense that if the animal ate the BSE prion then the animal has the BSE prion? Probably up to the brain within about a day? Or also if the chemical immbalance occurs and the prion mutates/folds then at that time the BSE prion is present?
Maybe I think too much!

[rsomer]

I agree with much of your comments. I do not believe prions are the culprit as such. The reading I have done suggest prions are a result not the cause of BSE. Prions are dead, they have no DNA. The more credible research I see being conducted is looking for the real infectious agent or cause.
Sheep producers have long known a relationship between copper deficiency and scrapies. I suspect Purdy’s theories about minerals being a causative agent may be valid. In Alberta, areas of the province are known to be copper deficient, especially areas of the Peace country and around Leduc.
Where Purdy looses me is his theory that sonic booms from the Concorde are a probable cause of BSE. Purdy is now drawing a relationship between the two cases in Alberta and their proximity to Camp Wainwright where he claims heavy shelling is taking place. That may be but even though Camp Wainwright looks close to Leduc/Calmar and the Peace Country on a map, it is way too far away for sonic booms from Camp Wainwright to be a cause in these cases.
Mark Purdy’s website is found at: http://www.purdeyenvironment.com

[pandiana]

Actually, I do believe that the prion is coded for by the host dna. I also believe that the dna forms the basis of the GeneThera test. They use a technique to amplify the abnormal dna so that it can be more readily detected. The normal alpha form of the protein is soluable, the beta form which seems to be universally associated with transmissible spongiform encephalopathies TSE, combines with other prions to form sheets. This has been described as a cascade effect. One analogy I heard was that it was like the albumin in egg whites which is liquid but when heated becomes a solid. You can also visualize how sugar crystals grow when concentrations become high. I think this part of the model fits Purdey's hypothesis alright as the normal prion is associated with a Cu ion. When these ions are depleted and Mn are substituted he thinks this is what causes the abnormal folding and sheeting. I am not sure how the variants of the protein associated with different pathalogical outcomes fit (BSE, CJD,) The article by Ricketts (1997) that looks at the possibly infectivity of blood, has a good review of the literature to that date and explains a mutuation found in a codon associated with some variants. http://www.cdc.gov/ncidod/EID/vol3no2/ricketts.htm

The problem I have with Purdey's hypothesis is that there does seem to be sufficient evidence to suggest that the agent can become infections when ingested. His theory does not seem to address this. To my knowledge, he is working stricly on empirical data from observations of occurances, i.e. clumping of cases around airports, shell ranges, etc. and the use of organophospates.

[cowman]

Thank you very much for the info. You are both obviously more up on this than me.
I will relate to you breifly once again about my own "mad cow". About 1986 I had a heifer that I believe had mad cow! The blood tests showed she had high levels of magnesium. The vet was completely baffled and in the end we shot her and let the coyotes eat her. A comprehensive feed test showed an extremely low copper content. Since then we have added some copper to the fertilizer and of course the mineral. Just about all the farmers add copper to the fertilizer in this area as the low levels were beginning to affect production. Never had this problem again.