Hypothesis that BSE originated from a human TSE SEAC

[flounder]

From: TSS ()
Subject: Hypothesis that BSE originated from a human TSE SEAC
Date: October 19, 2005 at 7:11 am PST


SEAC
Position Statement

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Hypothesis that BSE originated from a human TSE
Issue
1. Consideration of a hypothesis that BSE was originally derived from a human TSE.

Background
2. The origins of BSE are unknown. Since the discovery of BSE, SEAC1,2 and others , , have considered a number of hypotheses about the origins of the disease. Recently a further hypothesis has been considered by SEAC, which suggests that BSE may have arisen as a result of UK importation, in the 1960s and 1970s, of mammalian bone and carcass material from the Indian subcontinent, for use in animal feed. Furthermore, this hypothesis suggests that this material may have been contaminated with human remains harbouring a strain of CJD, which could have been transmitted to cattle.

Contamination of animal feed with human remains
3. It is not possible to establish with any certainty whether feed given to animals in the 1960s and 1970s was contaminated with human remains. However it is possible that carcass material, which may have inadvertently included human remains, was imported into the UK from the Indian subcontinent (particularly the Ganges region) during that period, and used in animal feed. Professor Colchester provides indirect evidence to suggest that this may have occurred.

4. It is likely that similar material was imported into other countries, such as Australia, that have not detected BSE in their livestock. Furthermore, the amount of human remains that may have contaminated animal feed would have been a very small fraction of the amount of sheep and cattle material that was incorporated into animal feed in the past. Thus, there was a much greater opportunity for cattle to have been exposed to an animal TSE rather than a human TSE. Current control measures implemented across the EU and in the UK has prevented the importation of such material for either animal feed or fertilizer.

Properties of BSE and other TSEs
5. BSE may have originated as a result of misfolding of the prion protein in cattle, the amplification via feed of a rare or new spontaneous mutation in cattle or transmission of a TSE from another species. There are barriers to transmission from one host species to another and there appears to be an appreciable barrier to transmission between cattle and humans. It is not currently possible to predict the ability, or likelihood, of transmission between species based on current understanding of strain characteristics.

6. Prion strains can be characterised by their properties in biochemical and infectivity tests. Generally, prion strains are transformed as a result of transmission to a new host, with consequent changes in their biochemical properties. However, BSE is somewhat unusual in that it appears to retain its strain characteristics when passaged through a new host. Experiments in transgenic mice expressing human, bovine and ovine forms of the prion protein gene have been designed to determine the likelihood of a strain passing to a new host but can also shed light on possible relationships between prion strains.

7. Nevertheless it is difficult, and often impossible with current technologies, to establish whether one strain is related to another following transmission to another species. It may therefore, never be possible to determine the true origin of BSE.

Summary of SEAC's discussion
8. SEAC considered it unlikely that the origins of BSE would ever be determined conclusively.

9. It is not possible to determine, from current knowledge of the characteristics of prion strains, whether BSE originated from CJD or other animal prion strains.

10. There was evidence to suggest that human remains may have been included in animal feed derived from the Indian subcontinent in the past, and the hypothesis presented by Professor Colchester was therefore considered plausible, but ultimately untestable.

11. Very much larger quantities of cattle and sheep remains historically had entered animal feed, compared with putative human remains. There is also likely to be a significant species barrier between humans and cattle, as there is known to be such a barrier in the opposite direction. It is therefore very much more likely that the origins of BSE are related to a TSE that originated in cattle or sheep, rather than a TSE from humans.

12. In conclusion, although Professor Colchester's hypothesis can never be ruled out, SEAC considered that, on the balance of possibilities, human TSE-contaminated material in animal feed was unlikely to have been the origin of BSE.

13. Although further experiments suggested by Professor Colchester would be of some scientific interest, SEAC did not consider them essential as they are unlikely to yield conclusive results on the origin of BSE, and because current control measures now prevent possible transmission via the route proposed in this hypothesis.

SEAC
September 2005


1 http://www.seac.gov.uk/summaries/summ_0901.htm
2 http://www.seac.gov.uk/papers/paper_inf81-8.pdf
3 http://www.defra.gov.uk/animalh/bse/science-research/epidem.html
4 http://www.bseinquiry.gov.uk/report/volume2/chapta10.htm
5 http://www.defra.gov.uk/animalh/bse/publications/bseorigin.pdf
6 Colchester AC, Colchester NT (2005). The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet. 366, 856-61.

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Page updated:19 October, 2005

http://www.seac.gov.uk/statements/state191005.htm

TSS

 

[Kathy]

Statements quoted from the above, by SEAC:

5....There are barriers to transmission from one host species to another and there appears to be an appreciable barrier to transmission between cattle and humans. It is not currently possible to predict the ability, or likelihood, of transmission between species based on current understanding of strain characteristics.

If this is the case, how is that BSE is catagorically blamed for causing vCJD? And now media is even blaming it for causing sporadic CJD.

7.... Nevertheless it is difficult, and often impossible with current technologies, to establish whether one strain is related to another following transmission to another species. It may therefore, never be possible to determine the true origin of BSE.

It may never be possible to find the true origin of any prion disease, especially if you don't investigate deeper, and if you ignore the species barrier, as well as research conducted by those venturing out on different limbs of the research tree.

9. It is not possible to determine, from current knowledge of the characteristics of prion strains, whether BSE originated from CJD or other animal prion strains.

Once again, the opposite can be stated.

10...the hypothesis presented by Professor Colchester was therefore considered plausible, but ultimately untestable.

Now why would we want to do experiments to see if human prion diseases can be transmitted to transgenetic bovine PrPC mice or transgenetic sheep PrPC expressing mice. What possible purpose would that serve?

Once again, the powers that be have determined what is best for us. To say his hypothesis is untestable is ludicrous. Perhaps, it would show that by using experimental models, similar to the present homogenate transmission procedures used for BSE and CWD, some human forms of prion disease could iatrogenically be transmitted to cattle and sheep.

11...There is also likely to be a significant species barrier between humans and cattle, as there is known to be such a barrier in the opposite direction. It is therefore very much more likely that the origins of BSE are related to a TSE that originated in cattle or sheep, rather than a TSE from humans.

It is most likely that the origins of BSE in cattle were spontaneous. The Born After the Reinforced Ban (BARB) cases continue increase. The word spontaneous is for fools, as there is always a reason. For now we are just arguing over who to believe, or not to believe.

13. Although further experiments suggested by Professor Colchester would be of some scientific interest, SEAC did not consider them essential as they are unlikely to yield conclusive results on the origin of BSE, and because current control measures now prevent possible transmission via the route proposed in this hypothesis.

SEAC
September 2005

The current measures cannot prevent contamination of the animal, or human, with the true original causative agent. But SEAC considers this research non-essential. Yesh!!

 

[Kathy]

Apparently, there is nothing more flounder has to say about the comments which I have made, above, in regards to the SEAC justification for not researching further the hypothesis of Professor Colchester (which was that human prion disease could spread to cattle, and possibly initiated the BSE in the UK).

While I do not believe this is what happened; I would not shut the door on experimentation into it, which should be similar to the transmission experiments currently done to convict the poor rancher, and his cow, of causing vCJD.

The SEAC statement can be turned on them, and the same arguements made for BSE causing vCJD. Further research into intracranial inoculation of human prion disease into cattle or sheep, etc., would likely result in at least some animals becoming sick with human prion diseases. That is because the iatrogenic experimental transmission experiments over-ride the species barrier, which SEAC so fervently points out:

"There are barriers to transmission from one host species to another and there appears to be an appreciable barrier to transmission between cattle and humans."

 

[flounder]

hello kathy,


kathy writes;

[[[Apparently, there is nothing more flounder has to say about the comments which I have made,]]]


correctamundo.


no need to continue to argue just to hear one argue.
i said what i had to say. you cannot or would not show us the documents that show what you claim to be true about ops causing the bse in the UK cattle. i show you transmission studies of TSEs that have nothing to do with ops and you still want to argue. put up or moove on.
transmission studies do not lie.


apparently it is now kathy that cannot read


i will post again what i already posted once here in another thread.



Sunday, October 16, 2005 10:48 AM


Also, what is your take on this theory?


i have always tried to stay neutral, because i just do not know, nor does anyone else, the 'origin' of the 'agent'. this is what i have most always called 'tse agent' as opposed to the 'prion disease'. i have never concentrated my efforts on the origin. my efforts have always been ''amplification and transmission'', this we know and have known for decades. its been well documented, but corporate interests have kept any substantial strict regulations/guidelines/enforcement from coming about. from the cattle industry, sheep, deer and elk industry, feed industry, pharmaceutical industry, surgical/medical industry, cosmetic industry, nutritional supplements industry, etc. they all are and have been involved with this campaign to make the regulations the most 'industry friendly' as possible. the incubation period of this agent is what has allowed this to happen, and the fact that very few are documented (human TSE), due to lack of credible surveillance and very few elderly demented are autopsied. the cards are and have been stacked heavily against us. i bitch about GW alot, and this administration _has_ been more blatant about secrecy and have been _caught_ more about lying about feed bans and triple firewalls etc, but let us face the facts, it's been going on for decades. The harvest that you reap depends on the kind of seeds you sow. If you sow corn, you reap a bountiful harvest, if you sow mad cow disease (i.e. human/animal TSEs) via a multitude of routes, sources and strains, due to nothing more than greed, and through that greed you go against all of Gods giving's from an industry so fraught with greed i.e. the rendering industry and factory farming (hence, i am still a meat eater, kinda) then you reap Gods wrath. This is the basic nature of God's Justice: "YOU REAP WHAT YOU SOW" ! it's been around for thousands of years. amen.

hallelujah, it's Sunday morning and i'm sounding like a preacher now. frightening isn't it ;-) ... with kindest regards, terry/TSS

 

[Kathy]

Quotes from flounder:

i show you transmission studies of TSEs that have nothing to do with ops

What do my above comments have to do with organophosphates?

i have never concentrated my efforts on the origin

then why did YOU post this thread about the hypothesized origins of BSE?

If you believe that BSE only occurs in animals that consumed other animals, how do you explain how cattle raised on grass with no access to MBM, developed BSE at the UK government's experimental farm at Liscombe. Or how four of the original five kudu antelope that developed BSE at the London zoo, had not had any possible access to MBM containing feeds.

I have only commented about SEAC's statement because you posted it here for us to read. Otherwise I wouldn't have known about it. SEAC is stating, categorically, that there is a species barrier.


-you posted this not me.

SEAC Position Statement

--------------------------------------------------------------------------------

Hypothesis that BSE originated from a human TSE
Issue
1. Consideration of a hypothesis that BSE was originally derived from a human TSE.

Background
2. The origins of BSE are unknown. Since the discovery of BSE, SEAC1,2 and others , , have considered a number of hypotheses about the origins of the disease. Recently a further hypothesis has been considered by SEAC, which suggests that BSE may have arisen as a result of UK importation, in the 1960s and 1970s, of mammalian bone and carcass material from the Indian subcontinent, for use in animal feed. Furthermore, this hypothesis suggests that this material may have been contaminated with human remains harbouring a strain of CJD, which could have been transmitted to cattle.

Contamination of animal feed with human remains
3. It is not possible to establish with any certainty whether feed given to animals in the 1960s and 1970s was contaminated with human remains. However it is possible that carcass material, which may have inadvertently included human remains, was imported into the UK from the Indian subcontinent (particularly the Ganges region) during that period, and used in animal feed. Professor Colchester provides indirect evidence to suggest that this may have occurred.

4. It is likely that similar material was imported into other countries, such as Australia, that have not detected BSE in their livestock. Furthermore, the amount of human remains that may have contaminated animal feed would have been a very small fraction of the amount of sheep and cattle material that was incorporated into animal feed in the past. Thus, there was a much greater opportunity for cattle to have been exposed to an animal TSE rather than a human TSE. Current control measures implemented across the EU and in the UK has prevented the importation of such material for either animal feed or fertilizer.

Properties of BSE and other TSEs
5. BSE may have originated as a result of misfolding of the prion protein in cattle, the amplification via feed of a rare or new spontaneous mutation in cattle or transmission of a TSE from another species. There are barriers to transmission from one host species to another and there appears to be an appreciable barrier to transmission between cattle and humans. It is not currently possible to predict the ability, or likelihood, of transmission between species based on current understanding of strain characteristics.

6. Prion strains can be characterised by their properties in biochemical and infectivity tests. Generally, prion strains are transformed as a result of transmission to a new host, with consequent changes in their biochemical properties. However, BSE is somewhat unusual in that it appears to retain its strain characteristics when passaged through a new host. Experiments in transgenic mice expressing human, bovine and ovine forms of the prion protein gene have been designed to determine the likelihood of a strain passing to a new host but can also shed light on possible relationships between prion strains.

7. Nevertheless it is difficult, and often impossible with current technologies, to establish whether one strain is related to another following transmission to another species. It may therefore, never be possible to determine the true origin of BSE.

Summary of SEAC's discussion
8. SEAC considered it unlikely that the origins of BSE would ever be determined conclusively.

9. It is not possible to determine, from current knowledge of the characteristics of prion strains, whether BSE originated from CJD or other animal prion strains.

10. There was evidence to suggest that human remains may have been included in animal feed derived from the Indian subcontinent in the past, and the hypothesis presented by Professor Colchester was therefore considered plausible, but ultimately untestable.

11. Very much larger quantities of cattle and sheep remains historically had entered animal feed, compared with putative human remains. There is also likely to be a significant species barrier between humans and cattle, as there is known to be such a barrier in the opposite direction. It is therefore very much more likely that the origins of BSE are related to a TSE that originated in cattle or sheep, rather than a TSE from humans.

12. In conclusion, although Professor Colchester's hypothesis can never be ruled out, SEAC considered that, on the balance of possibilities, human TSE-contaminated material in animal feed was unlikely to have been the origin of BSE.

13. Although further experiments suggested by Professor Colchester would be of some scientific interest, SEAC did not consider them essential as they are unlikely to yield conclusive results on the origin of BSE, and because current control measures now prevent possible transmission via the route proposed in this hypothesis.

SEAC
September 2005