MAD COW DISEASE, WHO STARTED IT, when and where did it start first ?
Greetings,
I am puzzled by several things. IF I remember correctly, the last two mad cows _documented_ in the U.S.A., this was before the surveillance and testing for BSE was shut down to almost nothing, for obvious reasons i.e. the findings back to back of the two atypical BSE cases, but I am puzzled by the fact that no detailed pathology of _both_ the Texas and the Alabama cow have been released, that I am aware of?
I am also puzzled by the fact that no more attention has been given to the fact of several statements and facts that in fact have come about, to simply go ignored? kind of reminded me of the infamous sporadic CJD in farmers and their wives with BSE herds.
But Confucius is confused again. my questions, who really started mad cow disease and or when and where did it really start? IT seems to me that this is not a questions that has been answered. ONE could look at the U.K. BSE epidemic as the point of origin, but if you go back, typical and atypical TSE in the bovine seems to have started way back. It could go all the way back to the U.S.
HAS the continuous rendering U.K. first theory (continuous rendering technology shipped to U.K. some 5 years and used there first before the U.S.A. started using) been proven, as the key to the start, or just an enhancement of sorts i.e. low temps, minus the oils, and was it true that the U.S. did NOT start using it before the U.K. ? and does it really matter ? could the TSE agent have survived and spread regardless ??? seems from the latest study on the TSE agent surviving the Biodiesel Production process, seems then it would not matter.
Friday, August 15, 2008 Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
http://chronic-wasting-disease.blogspot ... al-is.html
http://organicconsumers.org/forum/index ... topic=1935
Looking further into this 'continuous rendering'. I first wrote about it here ;
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...
2 January 2000
snip...
The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."
A few more factors to consider, page 15;
snip...
http://www.bmj.com/cgi/eletters/320/7226/8/b
NOW, to go back and read this document in full ;
Qualitative Analysis of BSE Risk Factors in the United States February 13, 2000 at 3:37 pm PST (BSE red book)
http://bseusa.blogspot.com/2008/08/qual ... -risk.html
However, going back even further, it seems mad cow disease (a strain BEFORE the U.K. BSE first appeared) was in the U.S.A. spreading for a long time among mink, and after a careful review of the eating habits and diets, it turned out the mink were being fed >95%+ dead stock downer cow ration. the mink developed mad mink disease or what is now called Transmissible Mink Encephalopathy or TME, you can see this data here ;
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
A Quantitative Assessment of the Possible Role of Nonambulatory Cattle in Transmissible Spongiform Encephalopathy in the United States March 6, 2000 at 1:05 pm PST
http://downercattle.blogspot.com/2008/0 ... sible.html
SO, we know some sort of TSE in fact was circulating among the USA cattle as far back as 1985. We can also tie feed of dead stock downer cows i.e. >95%+ dead stock downer cow rations. But these mink were proven to have had TME first in 1965, and shortly after that in 1971 it was proven that sheep scrapie would also transmit to mink. however, it was later found that the minks diet was NOT from sheep, after it was proven what the diet was i.e. dead stock downer cows.
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
Transmissible Mink Encephalopathy TME (MAD MINK DISEASE)
http://transmissible-mink-encephalopathy.blogspot.com/
NOW, in 1979, it was proven that indeed U.S. scrapie strain that was transmitted to U.S. cattle, did NOT produce a Transmissible Spongiform Encephalopathy (TSE) like the U.K. B.S.E., but a TSE unlike the U.K. B.S.E. SO what does all this tell us? it tells me that there is a possibility that a strain of mad cow disease was circulating in the U.S.A. long, long, before originally thought, only left to be ignored, while incubating and spreading.
3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE.339 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture.340 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre.341 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle,
*** did not produce the same clinical signs of brain lesions characteristic of BSE. ***
3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988,342 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988–89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA.343 It was also felt that the results of such an experiment would be hard to interpret. While a negative result 337 Fraser, H., Bruce, M., Chree, A., McConnell, I. and Wells, G. (1992) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice, Journal of General Virology, 73, 1891–7; Bruce, M., Chree, A., McConnell, I., Foster, J., Pearson, G. and Fraser, H. (1994) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice: Strain Variation and the Species Barrier, Philosophical Transactions of the Royal Society of London, Series B, Biological Sciences, 343, 405–11 338 Bruce, M., Will, R., Ironside, J., McConell, I., Drummond, D., Suttie, A., McCordie, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. (1997) Transmissions to Mice Indicate that 'New Variant' CJD is Caused by the BSE Agent, Nature, 389, 498–501 339 Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle Experimentally Infected with the Scrapie Agent, American Journal of Veterinary Research, 56, 606–12 340 YB88/10.00/1.1 341 Cutlip, R., Miller, J., Race, R., Jenny, A., Katz, J., Lehmkuhl, H., Debey, B. and Robinson, M. (1994) Intracerebral Transmission of Scrapie to Cattle, Journal of Infectious Diseases, 169, 814–20 342 YB88/6.21/1.2 343 YB88/11.17/2.4 SCIENCE 84 would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE.344 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest.345 3.59 Nevertheless, from the first demonstration of transmissibility of BSE in 1988, the possibility of differences in the transmission properties of BSE and scrapie was clear. Scrapie was transmissible to hamsters, but by 1988 attempts to transmit BSE to hamsters had failed. Subsequent findings increased that possibility.
http://www.bseinquiry.gov.uk/pdf/volume2/chapter3.pdf
doi:10.1016/S0021-9975(97)80022-9 Copyright © 1997 Published by Elsevier Ltd. Second passage of a US scrapie agent in cattle
R.C. Cutlip, J.M. Miller and H.D. Lehmkuhl
United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Ames, Iowa, USA
Received 10 September 1996; accepted 31 July 1997. Available online 25 May 2006.
Summary
Scrapie and bovine spongiform encephalopathy are similar chronic neurodegenerative diseases of sheep and cattle. An earlier study showed that, on first passage in cattle, a US scrapie agent caused an encephalopathy that was distinct from bovine spongiform encephalopathy (BSE). The present report describes a second passage in cattle, carried out because diseases caused by the spongiform encephalopathy agents often change in character with additional passages in abnormal hosts. For this work, young calves were inoculated intracerebrally with a pooled suspension of brain from cattle that had died of encephalopathy after experimental inoculation with brain from scrapie-affected sheep. The second passage disease was essentially identical with the first passage disease, as judged by clinical signs, histopathological findings and distribution of "prion protein scrapie" (PrPsc). This represents additional evidence to suggest that the US sheep scrapie agent tested is incapable of causing BSE in cattle.
http://www.sciencedirect.com/science?_o ... c4305a4752
IT seems that Cutlip, Miller, Lehmkuhl et al, it seems by this statement ;
'suggest that the US sheep scrapie agent tested is incapable of causing BSE in cattle.'
THAT the USA is home free from TSEs, however, how many scrapie strains are in the USA, including the atypical. we know atypical scrapie Nor-98 has been in the USA for a while, only detected recently. but did this study include all USA scrapie strains typical and atypical ??? I dont think so. also, this TSE strain that is produced by USA scrapie, could it be more virulent, and how many phenotypes are there ??? we know that the atypical BSE is more virulent, so I dont understand what seems to be 'jubilation' of the small study that shows that in fact the USA scrapie DOES produce a Transmissible Spongiform Encephalopathy TSE, it just happens to be unlike that of the UK BSE phenotype, and I would have expected nothing less, considering the many different strains. but I don't think these findings makes the USA mad cow free. IN fact, I find that by these findings, TSE in the USA bovine could have gone way back before the UK BSE epidemic, and I think it's just possible that the USA started this epidemic of TSEs.
let's look at the new atypical scrapie that has been in the U.S.A. i.e. the NOR-98-like;-) strain ;
PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**
http://www.aphis.usda.gov/animal_health ... ie_rpt.pps
NOT to forget the 5 cases of the NOR-98 atypical scrapie documented in the USA in 2007, in five different states. WHICH pathologically looks like some sub-types of sporadic CJD, of which Stanely Prusiner warns of a public health risk ;
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
http://www.prion2007.com/pdf/Prion%20Bo ... tracts.pdf
Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)
http://www.pnas.org/cgi/content/abstract/0502296102v1
Tuesday, June 3, 2008 SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA
http://nor-98.blogspot.com/2008/06/scra ... or-98.html
NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 007
http://nor-98.blogspot.com/2008/04/seac ... isory.html
http://nor-98.blogspot.com/
SCRAPIE USA
http://scrapie-usa.blogspot.com/
Sunday, June 15, 2008
A descriptive study of the prevalence of atypical and classical scrapie in sheep in 20 European countries
Research article
http://nor-98.blogspot.com/2008/06/desc ... ce-of.html
another question, just how long have these atypical BSE TSEs been around in the bovine ???
let's look at another case of atypical BSE in Germany way back in 1992 ;
Subject: atypical BSE reported in 1992 and conviently slaughterd and incinerated and then swept under rug for about 12 years Date: April 26, 2007 at 1:08 pm PST 1992
NEW BRAIN DISORDER
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE?
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN THE HISTOPATHOLOGY AND INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS NOT BSE.
4. IS THIS NEW BRAIN DISORDER A THREAT?
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE, AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. .......
http://www.bseinquiry.gov.uk/files/yb/1 ... 001001.pdf
2. The Collinge/Will dispute appears to rumble on. Dr. Collinge had told Dr. Tyrrell that Dr. Will's response to his criticism about sharing material had been ''quite unacceptable'' (in spite of it's apparently conciliatory tone). Apparently Professor Allen was now going to try and arrange a meeting to resolve the dispute. No action here for MAFF, although Mr. Murray may be interested.
3. Dr. Tyrrell regretted that the Committee had not seen the article on BBD. However he felt that for the time being NO specific action was called for. The most important need was to consider the possibility that the condition might be transmissible. As we have discussed, I suggested that we might circulate a paper to the members of the committee giving our appreciation of this condition (and perhaps of other non-BSE neurological conditions that had been identified in negative cases) and of any necessary follow up action. IF any Committee member felt strongly about this, or if the issue CAME TO A HEAD, we would call an interim meeting. He was happy with this approach. I would be grateful if Mr. Maslin could, in discussion with CVL and veterinary colleagues draft such a note, which will presumably very largely follow what Mr. Bradley's briefing paper has already said, taking account of DOH comments, We can then clear a final version with DOH before circulating it to Committee members.
http://www.bseinquiry.gov.uk/files/yb/1 ... 005001.pdf
IN CONFIDENCE
This is a highly competitive field and it really will be a pity if we allow many of the key findings to be published by overseas groups while we are unable to pursue our research findings because of this disagreement, which I hope we can make every effort to solve.
http://www.bseinquiry.gov.uk/files/yb/1 ... 002001.pdf
COLLINGE THREATENS TO GO TO MEDIA
http://www.bseinquiry.gov.uk/files/yb/1 ... 005001.pdf
2. The discovery might indicate the existence of a different strain of BSE from that present in the general epidemic or an unusual response by an individual host.
3. If further atypical lesion distribution cases are revealed in this herd then implications of misdiagnosis of 'negative' cases in other herds may not be insignificant.
snip...
This minute is re-issued with a wider distribution. The information contained herein should NOT be disseminated further except on the basis of ''NEED TO KNOW''.
R Bradley
http://www.bseinquiry.gov.uk/files/yb/1 ... 001001.pdf
IN CONFIDENCE
BSE ATYPICAL LESION DISTRIBUTION
http://www.bseinquiry.gov.uk/files/yb/1 ... 001001.pdf
snip... please see full text ;
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
August 20, 2008
http://bse-atypical.blogspot.com/2008/0 ... y-mad.html
TSS
Greetings,
I am puzzled by several things. IF I remember correctly, the last two mad cows _documented_ in the U.S.A., this was before the surveillance and testing for BSE was shut down to almost nothing, for obvious reasons i.e. the findings back to back of the two atypical BSE cases, but I am puzzled by the fact that no detailed pathology of _both_ the Texas and the Alabama cow have been released, that I am aware of?
I am also puzzled by the fact that no more attention has been given to the fact of several statements and facts that in fact have come about, to simply go ignored? kind of reminded me of the infamous sporadic CJD in farmers and their wives with BSE herds.
But Confucius is confused again. my questions, who really started mad cow disease and or when and where did it really start? IT seems to me that this is not a questions that has been answered. ONE could look at the U.K. BSE epidemic as the point of origin, but if you go back, typical and atypical TSE in the bovine seems to have started way back. It could go all the way back to the U.S.
HAS the continuous rendering U.K. first theory (continuous rendering technology shipped to U.K. some 5 years and used there first before the U.S.A. started using) been proven, as the key to the start, or just an enhancement of sorts i.e. low temps, minus the oils, and was it true that the U.S. did NOT start using it before the U.K. ? and does it really matter ? could the TSE agent have survived and spread regardless ??? seems from the latest study on the TSE agent surviving the Biodiesel Production process, seems then it would not matter.
Friday, August 15, 2008 Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
http://chronic-wasting-disease.blogspot ... al-is.html
http://organicconsumers.org/forum/index ... topic=1935
Looking further into this 'continuous rendering'. I first wrote about it here ;
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...
2 January 2000
snip...
The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."
A few more factors to consider, page 15;
snip...
http://www.bmj.com/cgi/eletters/320/7226/8/b
NOW, to go back and read this document in full ;
Qualitative Analysis of BSE Risk Factors in the United States February 13, 2000 at 3:37 pm PST (BSE red book)
http://bseusa.blogspot.com/2008/08/qual ... -risk.html
However, going back even further, it seems mad cow disease (a strain BEFORE the U.K. BSE first appeared) was in the U.S.A. spreading for a long time among mink, and after a careful review of the eating habits and diets, it turned out the mink were being fed >95%+ dead stock downer cow ration. the mink developed mad mink disease or what is now called Transmissible Mink Encephalopathy or TME, you can see this data here ;
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
A Quantitative Assessment of the Possible Role of Nonambulatory Cattle in Transmissible Spongiform Encephalopathy in the United States March 6, 2000 at 1:05 pm PST
http://downercattle.blogspot.com/2008/0 ... sible.html
SO, we know some sort of TSE in fact was circulating among the USA cattle as far back as 1985. We can also tie feed of dead stock downer cows i.e. >95%+ dead stock downer cow rations. But these mink were proven to have had TME first in 1965, and shortly after that in 1971 it was proven that sheep scrapie would also transmit to mink. however, it was later found that the minks diet was NOT from sheep, after it was proven what the diet was i.e. dead stock downer cows.
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
Transmissible Mink Encephalopathy TME (MAD MINK DISEASE)
http://transmissible-mink-encephalopathy.blogspot.com/
NOW, in 1979, it was proven that indeed U.S. scrapie strain that was transmitted to U.S. cattle, did NOT produce a Transmissible Spongiform Encephalopathy (TSE) like the U.K. B.S.E., but a TSE unlike the U.K. B.S.E. SO what does all this tell us? it tells me that there is a possibility that a strain of mad cow disease was circulating in the U.S.A. long, long, before originally thought, only left to be ignored, while incubating and spreading.
3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE.339 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture.340 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre.341 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle,
*** did not produce the same clinical signs of brain lesions characteristic of BSE. ***
3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988,342 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988–89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA.343 It was also felt that the results of such an experiment would be hard to interpret. While a negative result 337 Fraser, H., Bruce, M., Chree, A., McConnell, I. and Wells, G. (1992) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice, Journal of General Virology, 73, 1891–7; Bruce, M., Chree, A., McConnell, I., Foster, J., Pearson, G. and Fraser, H. (1994) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice: Strain Variation and the Species Barrier, Philosophical Transactions of the Royal Society of London, Series B, Biological Sciences, 343, 405–11 338 Bruce, M., Will, R., Ironside, J., McConell, I., Drummond, D., Suttie, A., McCordie, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. (1997) Transmissions to Mice Indicate that 'New Variant' CJD is Caused by the BSE Agent, Nature, 389, 498–501 339 Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle Experimentally Infected with the Scrapie Agent, American Journal of Veterinary Research, 56, 606–12 340 YB88/10.00/1.1 341 Cutlip, R., Miller, J., Race, R., Jenny, A., Katz, J., Lehmkuhl, H., Debey, B. and Robinson, M. (1994) Intracerebral Transmission of Scrapie to Cattle, Journal of Infectious Diseases, 169, 814–20 342 YB88/6.21/1.2 343 YB88/11.17/2.4 SCIENCE 84 would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE.344 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest.345 3.59 Nevertheless, from the first demonstration of transmissibility of BSE in 1988, the possibility of differences in the transmission properties of BSE and scrapie was clear. Scrapie was transmissible to hamsters, but by 1988 attempts to transmit BSE to hamsters had failed. Subsequent findings increased that possibility.
http://www.bseinquiry.gov.uk/pdf/volume2/chapter3.pdf
doi:10.1016/S0021-9975(97)80022-9 Copyright © 1997 Published by Elsevier Ltd. Second passage of a US scrapie agent in cattle
R.C. Cutlip, J.M. Miller and H.D. Lehmkuhl
United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Ames, Iowa, USA
Received 10 September 1996; accepted 31 July 1997. Available online 25 May 2006.
Summary
Scrapie and bovine spongiform encephalopathy are similar chronic neurodegenerative diseases of sheep and cattle. An earlier study showed that, on first passage in cattle, a US scrapie agent caused an encephalopathy that was distinct from bovine spongiform encephalopathy (BSE). The present report describes a second passage in cattle, carried out because diseases caused by the spongiform encephalopathy agents often change in character with additional passages in abnormal hosts. For this work, young calves were inoculated intracerebrally with a pooled suspension of brain from cattle that had died of encephalopathy after experimental inoculation with brain from scrapie-affected sheep. The second passage disease was essentially identical with the first passage disease, as judged by clinical signs, histopathological findings and distribution of "prion protein scrapie" (PrPsc). This represents additional evidence to suggest that the US sheep scrapie agent tested is incapable of causing BSE in cattle.
http://www.sciencedirect.com/science?_o ... c4305a4752
IT seems that Cutlip, Miller, Lehmkuhl et al, it seems by this statement ;
'suggest that the US sheep scrapie agent tested is incapable of causing BSE in cattle.'
THAT the USA is home free from TSEs, however, how many scrapie strains are in the USA, including the atypical. we know atypical scrapie Nor-98 has been in the USA for a while, only detected recently. but did this study include all USA scrapie strains typical and atypical ??? I dont think so. also, this TSE strain that is produced by USA scrapie, could it be more virulent, and how many phenotypes are there ??? we know that the atypical BSE is more virulent, so I dont understand what seems to be 'jubilation' of the small study that shows that in fact the USA scrapie DOES produce a Transmissible Spongiform Encephalopathy TSE, it just happens to be unlike that of the UK BSE phenotype, and I would have expected nothing less, considering the many different strains. but I don't think these findings makes the USA mad cow free. IN fact, I find that by these findings, TSE in the USA bovine could have gone way back before the UK BSE epidemic, and I think it's just possible that the USA started this epidemic of TSEs.
let's look at the new atypical scrapie that has been in the U.S.A. i.e. the NOR-98-like;-) strain ;
PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**
http://www.aphis.usda.gov/animal_health ... ie_rpt.pps
NOT to forget the 5 cases of the NOR-98 atypical scrapie documented in the USA in 2007, in five different states. WHICH pathologically looks like some sub-types of sporadic CJD, of which Stanely Prusiner warns of a public health risk ;
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
http://www.prion2007.com/pdf/Prion%20Bo ... tracts.pdf
Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)
http://www.pnas.org/cgi/content/abstract/0502296102v1
Tuesday, June 3, 2008 SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA
http://nor-98.blogspot.com/2008/06/scra ... or-98.html
NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 007
http://nor-98.blogspot.com/2008/04/seac ... isory.html
http://nor-98.blogspot.com/
SCRAPIE USA
http://scrapie-usa.blogspot.com/
Sunday, June 15, 2008
A descriptive study of the prevalence of atypical and classical scrapie in sheep in 20 European countries
Research article
http://nor-98.blogspot.com/2008/06/desc ... ce-of.html
another question, just how long have these atypical BSE TSEs been around in the bovine ???
let's look at another case of atypical BSE in Germany way back in 1992 ;
Subject: atypical BSE reported in 1992 and conviently slaughterd and incinerated and then swept under rug for about 12 years Date: April 26, 2007 at 1:08 pm PST 1992
NEW BRAIN DISORDER
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE?
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN THE HISTOPATHOLOGY AND INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS NOT BSE.
4. IS THIS NEW BRAIN DISORDER A THREAT?
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE, AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. .......
http://www.bseinquiry.gov.uk/files/yb/1 ... 001001.pdf
2. The Collinge/Will dispute appears to rumble on. Dr. Collinge had told Dr. Tyrrell that Dr. Will's response to his criticism about sharing material had been ''quite unacceptable'' (in spite of it's apparently conciliatory tone). Apparently Professor Allen was now going to try and arrange a meeting to resolve the dispute. No action here for MAFF, although Mr. Murray may be interested.
3. Dr. Tyrrell regretted that the Committee had not seen the article on BBD. However he felt that for the time being NO specific action was called for. The most important need was to consider the possibility that the condition might be transmissible. As we have discussed, I suggested that we might circulate a paper to the members of the committee giving our appreciation of this condition (and perhaps of other non-BSE neurological conditions that had been identified in negative cases) and of any necessary follow up action. IF any Committee member felt strongly about this, or if the issue CAME TO A HEAD, we would call an interim meeting. He was happy with this approach. I would be grateful if Mr. Maslin could, in discussion with CVL and veterinary colleagues draft such a note, which will presumably very largely follow what Mr. Bradley's briefing paper has already said, taking account of DOH comments, We can then clear a final version with DOH before circulating it to Committee members.
http://www.bseinquiry.gov.uk/files/yb/1 ... 005001.pdf
IN CONFIDENCE
This is a highly competitive field and it really will be a pity if we allow many of the key findings to be published by overseas groups while we are unable to pursue our research findings because of this disagreement, which I hope we can make every effort to solve.
http://www.bseinquiry.gov.uk/files/yb/1 ... 002001.pdf
COLLINGE THREATENS TO GO TO MEDIA
http://www.bseinquiry.gov.uk/files/yb/1 ... 005001.pdf
2. The discovery might indicate the existence of a different strain of BSE from that present in the general epidemic or an unusual response by an individual host.
3. If further atypical lesion distribution cases are revealed in this herd then implications of misdiagnosis of 'negative' cases in other herds may not be insignificant.
snip...
This minute is re-issued with a wider distribution. The information contained herein should NOT be disseminated further except on the basis of ''NEED TO KNOW''.
R Bradley
http://www.bseinquiry.gov.uk/files/yb/1 ... 001001.pdf
IN CONFIDENCE
BSE ATYPICAL LESION DISTRIBUTION
http://www.bseinquiry.gov.uk/files/yb/1 ... 001001.pdf
snip... please see full text ;
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
August 20, 2008
http://bse-atypical.blogspot.com/2008/0 ... y-mad.html
TSS
