Although scrapie is cited as one of the reasons for the unseemly haste of this bill, (i.e. Animal Health (amendment) bill) scrapie has been in Britain for at least two centuries, is of no danger to human health - nor, as recent fiascos have shown, is there any proof whatsoever that sheep can develop BSE. NOR has any link between BSE and vCJD ever been properly proved. The precise relationship between genotypes and resistance to scrapie is not properly understood, and decisions are being made in ignorance.
Lawrence Alderson, Director of Rare Breeds International : Meeting in House of Commons, Nov 29

"Decisions are being made in ignorance." Roger Green B.Vet Med MRCVS President Royal College of Veterinary Surgeons, addressing a question at the meeting in the House of Commons on Thursday 29th November 200, had this to say:

" There are several types of scrapie; what they are doing at the moment is selecting for just one thing - a bad thing to do - The proposal is to select for those sheep not resistant to scrapie "A". There is evidence to show that by doing that there will be more susceptibility to scrapie "C"; that those destined to be culled will have more resistance to scrapie "C". The science is not clear. And therefore it needs to be made clear."


BSE/CJD? Prion disease - extract from Hansard - what numbers are we talking about? - 3 knowledgeable correspondents write about scrapie - ten further examples of scientific comment about scrapie
2. Prion diseases by Dr Susan Haywood

The relationship between BSE, scrapie and variant CJD is unclear and largely conjectural. There is no firm evidence to relate BSE to a mutant prion ingested from scrapie-affected ovine material. Neither has the transmissibility of BSE affected meat to people who later develop vCJD been unequivocally established.

The hypothesis that a conformational change (mutation) of the prion protein PrP to PrPsc which then causes the disease has been challenged by Brown, Wong and colleagues who have established a role for metal substitution in the genesis of the disease.

These investigators have established PrPc as a metal (Cu) binding protein which functions as an antioxidant in the normal brain (Brown et al, 2001). The conformational change of PrPc to PrPsc is associated with changes in metal occupancy - Mn, Zn replacing Cu (Wong et al, 2001). This suggests that genetically derived changes in brain metal-binding or metal -transporter dysfunction is at least as credible a hypothesis as the current one. If the prion diseases were to be confirmed as a consequence of aberrant metal binding in the brain this would bring them into the general fold of metallochemico-neurogenerative diseases such as Alzheimers and others.

Conclusions
In all, the present lack of knowledge concerning the causation, development and relationship of the human and animal prion diseases one to another, coupled with the limitations inherent in the detection of predisposition to disease, the utmost care is needed based on present knowledge in formulating control and eradication policies

A law which allows the implementation of such policies without any legal redress runs the risk of ruining our agricultural heritage for no sound reason.

References Brown D R, Clive C & Haswell S J. (2001) J Neurochem 76; 69-76 Haywood S, Fuentealba I C & Kemp S J (2001) J small Anim Pract 42; 181-185 Holmes N, G, Herrtage M E, Ryder E J & Binns M M (1998) Vet Rec142;351-352 Wong B-S, Brown D R et al, (2001) J Neurochem 78; 1400-08 Ibid (2001) 79;689-698

Susan Haywood November 2001


Extracts from Hansard, 12th November - Animal Health Bill second reading:

12 Nov 2001 : Column 578 Mrs. Browning: The right hon. Lady is talking about the theoretical risk of BSE in sheep. Will she share with the House what is clearly new scientific advice to the Government? I noticed that, in a statement on 21 October, Sir John Krebs said that, if BSE in sheep were proven, the Food Standards Agency would advise banning the consumption of all dairy and milk products from sheep and goats. Clearly, there has been transmissible spongiform encephalopathy in bovines, but the idea is that, in a different species, TSE will mean a ban on the milk supply. On what scientific basis was that statement made?

Margaret Beckett: I am afraid that I cannot do so. The hon. Lady might raise the question with the Food Standards Agency. I am not totally familiar with the statement that she quotes, and I am not aware on what scientific advice it might be based.

12 Nov 2001 : Column 615

Rt Hon David Curry: I do not want the scrapie issue to be entirely lost. I draw the Minister's attention to an article on the back page of Farmers Guardian, a journal to which I have warmed considerably since it invited me to write a column. The article refers to Professor Malcolm Ferguson-Smith of Cambridge university, who argues:

"The Government is drafting a Bill to completely remove those sheep that are susceptible to scrapie--that could mean culling three quarters of the national flock as that is the proportion susceptible to it . . . We need to know if those sheep resistant to scrapie are resistant to the development of the disease or resistant to infection, as if it is the latter they could pass the disease on".

The professor also said that it had already been shown

"that sheep resistant to scrapie are susceptible to BSE so the culling policy as a BSE measure did not make any scientific sense at all."

Those are the professor's claims. As I said, I am not a scientist, and do not know whether he is right or wrong. If he is right, some serious questions need to be asked about the course along which the Government are about to embark. I hope that the Minister will deal with that point.


It is to prevent how many cases per annum out of a national flock of 40 million that the Ministry want the power to slaughter or neuter our sheep?

I rang our vets this morning and was told that scrapie is 'very rare' in the farms covered by the practice - 'very few cases' - and the vets ought to hear of any cases going because it is a 'notifiable disease'. So the Ministry must keep statistics showing incidence. I have asked the SVS Devon if they can tell me what was the incidence in Devon over whatever defined period suits their record keeping.

And more:

The SVS rang me back to tell me that in Devon the records regarding scrapie are as follows:

In 2000:
78 sheep reported as showing symptoms which could indicate scrapie, of which 8 were rejected on inspection, 5 were negative on PM examination, leaving 65 cases of scrapie recorded. In 2001 so far:
48 sheep reported as showing symptoms which could indicate scrapie, of which 6 were rejected on inspection, 2 were negative on PM examination, leaving 37 cases of scrapie recorded. The SVS officer doesn't have statistics for overall numbers of sheep, but he cited 48,000 sheep slaughtered on FMD farms in Devon to illustrate that sheep with scrapie represent a tiny proportion of the sheep population in Devon.


Three knowledgeable correspondents write about scrapie.

1. Scrapie - by a Devon sheep farmer

I have never seen a case of scrapie in my sheep, but aware that I have only about 130 sheep and have only been keeping sheep for the last ten years, I checked with Michael, who has lived on the neighbouring farm all his life [he must be in his sixties now] and has been farming considerably more sheep all his working life. He had never seen a case of scrapie either. He reinforced this by saying that in the days when sheep were worth money and we could afford to take them to the vet, the vet had never ever diagnosed scrapie.

I looked up scrapie in 'The Veterinary Book for Sheep Farmers' published in 1990, by David C Henderson.

He describes it as a slow-developing disease of sheep and goats which can occur at any time of the year, but which spreads particularly at lambing time. It has been recognised for more than two centuries in Britain and other European countries, and despite 60 years of research it is still incompletely understood.

"It is an infectious disease, and although the causative agent has not yet been identified, much is known about its properties. Usually referred to as the 'scrapie agent', it is a virus-like particle (or virion) which exists in at least 20 different forms or strains. It is a tough organism which can resist many of the chemical and physical conditions that would kill viruses and is able to survive many months on pastures or in buildings."

The symptoms "are nervous in character" but generally involve the sheep scatching, biting or rubbing themselves as though in response to intense irritation: hence the name 'scrapie'.

On susceptibility and resistance, he says "Sheep do not necessarily succumb to the disease simply because they become infected with the scrapie agent. Individual sheep react to infection with one or other of the agents in a way which is determined by the animal's genetic make-up. Sheep are said to be either susceptible or resistant to scrapie, although this is probably rather simplistic. The incubation period of the disease ... is measured in years. It is thought that resistance to scrapie simply means that some individuals are able to prolong the incubation period, perhaps for so long that the animal dies of other natural causes or is culled befor it has time to develop clinical signs of scrapie. On the other hand, susceptible sheep are probably unable to do this and will therefore develop clinical signs much sooner." [ the farmer comments - if this is the case, the resistant sheep might turn out to be more dangerous - because they merely mask the symptoms and carry infection longer!]

"In most infected flocks the number of deaths from scrapie each year usually averages less than one in twenty, but in highly susceptible flocks this may rise to a third or even half the flock." [ comment: the fact that neither Michael nor I have seen any cases in our sheep suggests that our flocks are free of scrapie whether or not they are resistant.]


2. And...from another farmer in Wales...

I think that we need to launch another offensive in the direction of the totally misinformed cretins who seem determined to wreck farming.

1. As we all know, there is no proven link between CJD and BSE.

2. There is also no proof of a link between BSE and prions produced by Scrapie infected animal protein in animal feed. I was aware some while ago that extensive tests were underway in various parts of the World to try to replicate the BSE effect by feeding cows with feed that was purposely contaminated and they were failing to get the BSE result. I am sure these tests have continued as it represents good science but WHERE ARE THE RESULTS ?

3. Now we have a new attack based upon Scrapie "masking" BSE in Sheep. Theoretically, the same "scrapie infected" protein could have been fed to sheep. Also, again extremely theoretically, BSE infected cattle protein could have been fed to sheep.

4.The odds are infinitessimal that any feed could have got BSE infected protein into it as so little was ever likely to have been produced before the problem was recognised and the whole practice stopped.

5. Something no-one ever considers - is the enormous amount of animal feed that goes into the pig and poultry sectors anyway.

6. Of even more significance is the fact that, amongst cattle, it was virtually only the dairy cattle that ever got BSE. To the best of my knowledge all the cattle in the beef industry that got it had been bred in the dairy industry and were victims of maternal transmission. It is vital to know that dairy cattle consume up to 1.5 tonnes of cake feed p.a. The only other use is for finishing beef.

7. Similarly, in the sheep industry the mass of cake feed used is for finishing - so no problem. Amongst ewes, many hill ewes get none at all and the greatest use is a kilo/day for 6 weeks before and after lambing which is 25% of the year.

8. Again , to the best of my knowledge, any Scrapie infected sheep are dispatched by the farmer and not used for further breeding.

9. In conclusion, the clowns are saying that amongst the sheep flock are animals carrying BSE that are going into the food chain. These animals would have had to get it by maternal transmission from ewes before the farmer spotted them.These ewes must have been bred from a long line of similarly infected ewes ( kept for breeding ) back to the 80's before the feed rules were changed. The original ewes would have had to be fed from this incredibly small supply of potentially BSE infected material. The amount of feed that is fed to breeding ewes is similarly incredibly small compared with all the other sectors e.g. dairy cows.

The odds are so microscopically infinitessimal that we should challenge the mathematicians to calculate it. I would guess it would be like one person winning the National Lottery for every week of his life.


And from a third

....the article in Science re the theoretical possibility of there being 20 sheep (out of 36 MILLION) being infected with BSE caused steam to issue forth!!!

Not content with nearly causing the slaughter of the entire British flock by testing the wrong sort of brains - this collection of fund-hungry scientists are now trying to regain their damaged reputations by manufacturing some kind of pseudo-epidemic via their computers!

BSE was noted in cows in the mid 1980s. We are now 18 years on.

We have not had a case of BSE in sheep that has occurred naturally outside the highly artificial confines of a laboratory.

Given the far shorter lifespan of sheep and the lower amounts of feed they are given, is it not likely that any infection would have been very limited and shortlived? If it is there, surely one of the "scrapie" cases would have tested positive - so why has it not been seen? The answer couldn't possibly be because BSE isn't in the national flock - could it? No - because that would be far too boring and there would be no need for research!

Computer modelling may have its uses but attempting to make a real life disaster out of a "virtual" situation and report it as eminent science is reprehensible and irresponsible in the extreme . I am afraid it appears to be a rather cheap attempt to attract funding by sensationalist headlines without a single thought for the consequences of their ill-considered statements. Unfortunately our political masters indulge in considerably less critical analysis than the average ovine , and so are taken in by such pronouncements.

Regrettably , it won't be virtual sheep that may end up being slaughtered.

Betty from Holland sent this selection of relevant pieces about scrapie/BSE to Alan Beat. I reproduce them here with gratitude to both Betty and Alan. References to each are at the bottom of the page.

Extract
"'I am sure that a lot of research that has been done is not made public yet and never will be. You came to the conclusion that there is no reason backed by any science to kill millions of animals. I agree with this because, after years of research they are not even close to answers, hence again slaughter of millions for purely market driven reasons and a lot of scaremongering."

Reading all the articles of scientists lately I was struck by the many points of differences. Being aware of the consequences for our animals I got a little information from the internet and spend last week reading. The differences are so enormous that in my opinion it would be unjustifiable to proceed with whatever plans that could kill millions of sheep.

I started off with the report of Stanley B.Prusiner: The Prion Diseases. (1)

'The source of the emerging epidemic was soon traced to a food supplement that included meat an bone meal from dead sheep.'

But we read in a report from the United States Department of Agriculture: (2)

' Because scrapie occurs in most countries of the world and initial indications are that BSE originated from sheep, we were concerned that scrapie or CWD might transmit to cattle in the U.S. and cause BSE. Five years ago, we demonstrated that scrapie would cause a neurologic disease when given by injecting the agent into the brain, but the disease induced was different from BSE as it occurs in the United Kingdom and Europe. In this study, we found that cattle fed raw brain or meat and bone meal (MBM) and tallow prepared from sheep with scrapie remained normal for eight years after exposure. This work indicates that cattle are highly resistant to scrapie but does not totally exclude the possibility that genetic differences might allow transmission. These results lend assurance to the cattle and sheep industries that the U.S. form of sheep scrapie will not cause BSE in cattle as implicated in Europe.'

Further with Stanley B.Prusiner:

'Prion Diseases Can Be Inherited. In many cases, the scrapielike illnesses of humans seemed to occur without having been spread from one host to another, and in some families they appeared to be inherited. (Today researchers know that about 10 percent of human prion diseases are familial, felling half of the members of the affected families.) It was this last pattern that drew our attention. Could it be that prions were more unusual than we originally thought? Were they responsible for the appearance of both hereditary and transmissible illnesses? In 1988 Karen Hsiao in my laboratory and I uncovered some of the earliest data showing that human prion diseases can certainly be inherited. We acquired clones of a PrP gene obtained from a man who had Gerstmann-Str|ssler- Scheinker disease in his family and was dying of it himself. Then we compared his gene with PrP genes obtained from a healthy population and found a tiny abnormality known as a point mutation. To grasp the nature of this mutation, it helps to know something about the organization of genes. Genes consist of two strands of the DNA building blocks called nucleotides, which differ from one another in the bases they carry. The bases on one strand combine with the bases on the other strand to form base pairs: the "rungs" on the familiar DNA "ladder." In addition to holding the DNA ladder together, these pairs spell out the sequence of amino acids that must be strung together to make a particular protein. Three base pairs together-a unit called a codon-specify a single amino acid. In our dying patient, just one base pair (out of more than 750) had been exchanged for a different pair. The change, in turn, had altered the information carried by codon 102, causing the amino acid leucine to be substituted for the amino acid proline in the man's PrP protein. With the help of Tim J. Crow of Northwick Park Hospital in London and Jurg Ott of Columbia University and their colleagues, we discovered the same mutation in genes from a large number of patients with Gerstmann-Str...ussler-Scheinker disease, and we showed that the high incidence in the affected families was statistically significant. In other words, we established genetic linkage between the mutation and the disease-a finding that strongly implies the mutation is the cause. Over the past six years work by many investigators has uncovered 18 mutations in families with inherited prion diseases; for five of these mutations, enough cases have now been collected to demonstrate genetic linkage'

We read in Nature (3)

'Of 50 patients with vCJD-about half of those know to have the disease- only 12% have a gene called DQ7, John Collinge of Imperial College School of Medicine in London and his colleagues have found. In contrast, 36% of the normal population has the gene.'

And: (4)

'Like vCJD, kuru is a neurodegenarative disease caused by infection with a rogue 'prion' protein. The disease spread among the Fore people of Papua New Guinea in the 1940s and 1959s as a result of their cannibalistic funerary rituals. They found that the first in the population to develop kuru shared the genetic feature common to most vCJD victims- an amino-acid combination linking tow methionine molecules (dubbed M/M) at a specific position in the gene coding for the protein PrP. This protein is the one modified by prions to such devastating effects in kuru and vCJD. In the UK, two third of people have a different amino-acid combination at this point in the PrP gene-methionine and valine (M/V) of valine and valine (V/V)- and so, some believe, are less susceptible to prion disease. Further cases of vCJD may show longer incubation periods an occur in older individuals with the M/V and V/V genotypes, notes Goldfarb.'

We read in report of a Case-control study of risk factors of Creutzfeldt-Jacob disease in Europe during 1993-95: (5)

' Discussion In our collaborative study of risk factors of CJD, we found evidence for familial aggregation of CJD with dementia due to causes other than CJD. We did not find significant evidence for iatrogenic transmission of CJD. With regard to the exposures to animals and animal products studied, a significant increase in risk of CJD was found for cases exposed to leather products and fertiliser containing hoofs and horns. Of the dietary factors studied, the consumption of brain and raw meat were associated with an increased risk of CJD. No association was found with the consumption of beef, veal, lamb, cheese, or milk in these analyses.'

And:

' Table 3 shows that the consumption of raw meat products is significantly associated overall with an increased risk of CJD. Although risks did not differ significantly between countries, risks were found to be significantly increased in Netherlands/Belgium (RR 3735 [1735-8731]) and Germany (2730 [1739-3779]) but not in other countries.'

And:

'Brain consumption (animal source unspecified) was associated with an increased risk of CJD (RR 1768 [1718-2739]; table 3) but this increase was not, by conditional regression analysis, significant (p=0718). The number of exposures at each site was too small for interpretation, but the association was found consistently in each subgroup analysis. None of the dairy, organ, or meat products such as sausage or black pudding was associated with increased CJD risk in an analysis testing for a trend with increasing frequency of consumption. Finally, there was no evidence for a significant association of CJD with the consumption of beef, veal, lamb, or pork (table 4). The only evidence for an increase in risk of CJD with increasing consumption was found for pork consumption (p for trend 0702). Further, in the analysis for trend, the frequency of consumption of pork was found to be associated to the risk of CJD, despite the lack of evidence for an increased frequency of spongiform encephalopathy in pigs. Each of these three findings lack a plausible biological explanation and need to be confirmed. From a public-health perspective several of the negative findings are especially relevant. In the overall analyses, no evidence was found for an increase in risk of CJD associated with occupational exposure to cows. There was no association of CJD with the consumption of beef, veal, lamb, or milk products.'

Back to Further with Stanley B.Prusiner:

'SPECIES BARRIER Since the mid-1980s we have also sought insight into a phenomenon known as the species barrier. This concept refers to the fact that something makes it dificult for prions made by one species to cause disease in animals of another species. The cause of this diUculty is of considerable interest today because of the epidemic of mad cow disease in Britain. We and others have been trying to find out whether the species barrier is strong enough to prevent the spread of prion disease from cows to humans. The attraction of scrapie PrP for cellular PrP having the same sequence probably explains why scrapie managed to spread to cows in England from food consisting of sheep tissue: sheep and bovine PrP differ only at seven positions. In contrast, the sequence difference between human and bovine PrP is large: the molecules diverge at more than 30 positions. Because the variance is great, the likelihood of transmission from cows to people would seem to be low. Consistent with this assessment are epidemiological studies by W. Bryan Matthews, a professor emeritus at the University of Oxford. Matthews found no link between scrapie in sheep and the occurrence of Creutzfeldt-Jakob disease in sheep-farming countries.'

We read in Nature: (9)

'Diseases like BSE could be harder to catch than some people think, Jessa Netting discovers. Prion diseases like BSE seem unlikely to cross between distant species, a new study indicates. Abnormal 'chronic wasting disease' prions from deer wreak havoc with elk protein but hardly affect protein from sheep, cows or people, the study by Gregory Ramond and colleagues in the Rocky Mountains laboratory of the US National Institute ofHealth, Hamilton, Montana, shows.'

Sheep: We read in Transmissible Spongiform Encephalopathies: (6)

'Scrapie: a genetic disease? In the NPU Cheviot flock, natural scrapie occurs spontaneously in animals of PrP genotypes VV136RR154QQ171 and VA136RR154QQ171 at around 800 days and 1200 days of age respectively. Suffolk sheep are different genetically, in that the V136R154Q171 PrP allele is rare. Suffolks do, however, contract scrapie, in the genotype AA136RR154QQ171.

We have already shown that these scrapie-susceptible PrP genotypes can be found in sheep in Australia and New Zealand, countries which are free of scrapie. Scrapie cannot therefore be a simple PrP-related spontaneous genetic disease and PrP genotype most likely determines susceptibility to an infection which is absent in scrapie-free countries. In a new study PrP genotypes were investigated in a flock of Poll Dorset sheep which had been born in New Zealand (NZ) and brought to the UK as young adults (between 15 and 15 months of age). In UK-born Poll Dorsets, scrapie can occur in VV136RR154QQ171, VA136RR154QQ171 and AA136RR154QQ171 genotypes and these genotypes were found in the NZ-born animals at frequencies of 3%, 7% and 11% respectively. These scrapie-susceptible sheep lived for between 43 and 54 months, with no signs of scrapie, after being brought to the UK. These results strengthen the evidence that scrapie is not a genetic disease.'

>From the same source:

'BSE in sheep: The genotype at codon 136 is also of importance as those animals carrying valine (V136) have a slightly longer BSE incubation period than alanine/alanine (AA136) homozygotes. This is unlike the majority of natural scrapie cases which carry V136, 60% as heterozygotes. It follows from this, that those sheep dying of natural scrapie and with a PrP genotype AA136QQ171 will have the most chance of having picked up BSE infection rather than sheep scrapie, if indeed BSE has got into the national sheep flock.'

We read in Minutes of NPU: (7)

'Scrapie depends on codon 136, if it codes for valine the sheep is susceptible but if the sheep is homozygous for alanine at this locus it is not susceptible- following subutaneous challenge.

THERE IS NO BSE LINKAGE TO VALINE AT 136. ANIMALS WITH HOMOZYGOUS GLUTAMINE AT 171 WERE SUSCEPTIBLE IN CONTRAST TO HETEROZYGOTES GLUTAMINE+ARGININE WHICH WERE RESISTANT. WITHIN SHEEP WITH HOMOZYGOUS GLUTAMINE AT 171 THOSE HOMNOZYGOUS FOR ALANINE AT 136 HAD SHORTER INCUBATION PERIODS THAT HETEROZYGOUS ALANINE AND VALINE AT 136.'

And again in Transmissible Spongiform Encephalopathies: (6)

' Maternal transmission of BSE in sheep: This study is designed to investigate whether it is possible for experimentally induced BSE to be maternally transmitted in sheep. To achieve this the following protocol has been devised. Ewes from the NPU Cheviot negative line were selected according to PrP genotype, for artificial insemination prior to oral challenge with BSE. Twelve ewes (AA136RR154QQ171) were inseminated from a AA136RR154QQ171 sire, and six each of AA136RR154RQ171 and AA136RR154RR171 ewes were inseminated from a AA136RR154RQ171 sire on the same day. The spread of ewe and sire genotypes will ensure a similar mix in the progeny with a bias towards AA136RR154QQ171, which appears the most susceptible to BSE challenge. Three weeks later, eight of the AA136RR154QQ171 and all of the AA136RR154RQ171 and AA136RR154RR171 ewes were challenged orally with BSE. Four AA136RR154QQ171 ewes were left unchallenged to act as monitors for the possibility of BSE cross-contamination from the challenged sheep. At lambing all ewes were penned individually a few days prior to parturition. A total of 28 lambs were born with 19 surviving to date. Ewes and lambs are segregated and housed away from other sheep. Ram lambs have been left entire. Ewes are being mated naturally to sires of the same genotypes as used for AI and should lamb in 1998. A final lamb crop will be taken in 1999. Thereafter ewes and lambs will be monitored for clinical signs of TSE. All sheep in this experiment are being housed and strictly segregated from other stock.'

>From Fred Horak a Jacob breeder (13)

' There are other "complex breeds" which have complex PrP genetics: Swaledale and Shetlands, for example, have 4 PrP gene alleles: VRQ, ARQ, ARR, AHQ. In this case the VRQs seem to be extremely susceptible. Texels are thought to have 5 PrP gene alleles and thus even more complicated. If resistance to natural scrapie were bred solely on genotype an absolute disaster could occur: a Suffolk ARQ/ARQ is a scrapie high risk; a Swaledale ARQ/ARQ is "resistant". That is, selecting on an allele without regard to the number of alleles and genotype susceptibility, could be chaos. Studies (?) suggest that ARR/ARR at codon 171 is thought to be "resistant" to scrapie and BSE for most genotypes. There are also strains of prion diseases and I don't know if "resistance" means resistance to all strains.'

>From Medline: (8)

' The development of clinical signs of scrapie in sheep has been linked to polymorphisms in the prion protein (PrP) gene. The most important polymorphisms appear to be at codons 136, 154 and 171. The objective of this study was to investigate polymorphisms at these codons in five native (Belclare, Galway, Wicklow Cheviot, Donegal Blackface Mountain and Mayo Blackface Mountain) and five imported (Texel, Bleu du Maine, Rouge de l'Ouest, Vendeen and Charollais) sheep breeds in Ireland. A total of 13 genotypes were found. The percentage of the most resistant genotype AA(136)RR(154)RR(171)varied from 1.8 per cent in the Vendeen breed, 3.1 per cent in Donegal Blackface Mountain, 10.0 per cent in Texel, 11.1 per cent in Wicklow Cheviot, 12.9 per cent in Belclare, 22.0 per cent in Charollais, 25.6 per cent in Mayo Blackface Mountain, 33.3 per cent in Galway, 46.4 per cent in Bleu du Maine to 62.5 per cent in Rouge de l'Ouest. The results indicate that a significant amount of variation exists between the breeds analysed in this study. Copyright 2001 Harcourt Publishers Ltd.'

And we have to mention the report from Professor Alan Ebringer which has only recently been sent to the Department of Environment, supporting the theory that BSE is an auto-immune disease caused by a common bacteria. Alan Ebringer is professor of immunology at Kint's College, London. Further studies are not funded.

And also: (10)

'A number of researchers have found that organophosphate (OP) in systemic warble fly insecticide can deform the prion molecule, rendering it ineffective at buffering free radical effects in the body. Worse still, the prion is then partial to bond with manganese and become a 'rogue' prion. A chain reaction whereby rogue prions turn others to rogues also, can explain the bovine spongiform disease mechanism.

>From FAQ; (11)

'Organophoshates (Ops) and TSEs: The OP Phosmet used at 4 times the ecommended max dose on cows in Britain in the 80s to control warble fly is a dithiophosphate systemic OP.'

BBC: (12)

'The variant form of CJD may simply be a rare type which existed long before the BSE epidemic in cows- but was simply not diagnosed and catalogued properly until the 1990s. If his theory is correct it would mean victims of the condition did not get it by eating infected meat.'

>From Sabine Zentis:

'I am sure that a lot of research that has been done is not made public yet and never will be. You came to the conclusion that there is no reason backed by any science to kill millions of animals. I agree with this because, after years of research they are not even close to answers, hence again slaughter of millions for purely market driven reasons and a lot of scaremongering. Here are some background informations on points you raised in your paper : Leave the US, they have never done proper surveillance on TSE's and the scientific papers by Prusiner have, IMHO , to be read with caution for the following reasons: In 1978 a lady called Patricia Merz did a lot of work with brain and spleens from scrapie infected sheep. She was the first to detect the socalled SAF= Scrapie associated fibrilles after staining tissues with kongo red under the electronic microscope. And guess who, some years later, made the 'discovery' of the PRION? And was honoured with the Nobel price? Right, Prusiner. What this guy just forgot to mention that P. Merz was the one to discover the SAF's which are nothing else than his Prions. Every time a new horror story emerged with regard to BSE, vCJD etc. he came up with his latest research and promised a life test, a cure for vCJD etc. Now, where are his solutions to the problems ? Not very successful so far. TSE's , developed naturally in a specific host, are species-specific. There is no natural transmission between i.e. humans, cows, sheep or others. ( By patting a sheep with scrapie or a cow with BSE you won't contract vCJD). But if 'unnatural' practices are used, i.e. feeding infected material (ruminant to ruminant/ ruminant to human) there might an infection be triggered. But this is a 'forced' infection. And I think there are a lot more things involved. It is not as simple as feeding a calf with infected feed and it will go down with BSE 4-5 years later. I think it is a multifactorial development with genetics influencing the susceptibility or length of incubation period, OP's ( which are not only in warble fly treatments but are also fed to cattle when using the remains from citrus fruits in cattle feed. And even the Purdey theory of an imbalance of copper/mangan levels can contribute to the development of TSE's. This in itself poses no problem. The problems occur with the challenge. If you don't 'force' infected material on the host you will only come about the one in a million 'sporadic' case. And I am sure BSE is not sheep scrapie in cattle but recycling of infected cattle into cattle feed. This is about BSE. Scrapie in sheep shows some distinct patterns. There are different strains, different tissues have been shown to be infective interestingly there has so far never been found infectivity in the spleen or the afterbirth (cleansings) of BSE cattle, but in scrapie affected sheep this has been found). There seems to be vertical and horizontal transmission of scrapie in sheep which has never been proven in cattle.

In humans CJD has been transmitted through surgery, growth hormones and transplants. And through cannibalism. (Fore/Kuru)

Living with someone with CJD under one roof poses no risk of infection.

So, in my opinion, everything that includes industrial processes, treatments or 'unnatural' habits is a risk, not the disease itself. Eating meat is not a problem, but producing mechanically recovered meat and stripping every bit of carcasses including tissues one would normally never touch is the danger. Cannibalism in animals and man is a danger. Xenotransplants will be the next big thread.

And interestingly, when in 1996 the article on the vCJD was published it showed slides of brain samples of affected people. This samples showed the same patterns- 'floral plaques'- like the brains of the Fore people that had died of KURU.'

I rest my case, hoping scientist will start working together. Betty Stikkers

(1) http://www.sciam.com/0896issue/prion.html
(2) http://www.nal.usda.gov/ttic/tektran/data/000010/86/0000108646.html
(3) http://www.nature.com/nsu/011115/011115-6.html
(4) http://www.nature.com/nsu/010208/010208-5.html
(5) http://www.eurocjd.ed.ac.uk/lancet3.html
(6) http://www.iah.bbsrc.ac.uk/reports/1997/tse.html
(7) http://www.vegsource.com/talk/lyman/messages/7617.html
(8) if needed, I can forward this
(9) http://www.nature.com/nsu/000928/000928-3.html
(10) http://www.eionews.addr.com/organop/organop.html
(11) http://www.warmwell.com/ventersoct12.html
(12) http://www.warmwell.com/ventersoct12.html
(13) http://www.pairlist.net/pipermail/jacob-list/2000-November/000920.html

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