Transmissible Mink Encephalopathy TME
Subject: In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
Gerald Wells: Report of the Visit to USA, April-May 1989
snip...
The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...
snip...
It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...
snip...
3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought
this was a fanatical incident to be _avoided_ in the US _at all costs_...
snip...please read this old full text document !
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
Sunday, December 10, 2006
Transmissible Mink Encephalopathy TME Subject: In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
Gerald Wells: Report of the Visit to USA, April-May 1989
snip...
The general opinion of those present was that BSE, as an overt disease phenomenon, _could exist in the USA, but if it did, it was very rare. The need for improved and specific surveillance methods to detect it as recognised...
snip...
It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US...
snip...
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a _very low profile indeed_. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be _avoided_ in the US _at all costs_...
snip...please read this old full text document !
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
R.F. Marsh* and G.R. Hartsough
•Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092
ABSTRACT
Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England.
INTRODUCTION
Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough and Burger who demonstrated that the disease was transmissible with a long incubation period, and that affected mink had a spongiform encephalopathy similar to that found in scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965). Because of the similarity between TME and scrapie, and the subsequent finding that the two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was concluded that TME most likely resulted from feeding mink scrapie-infecied sheep. The experimental transmission of sheep scrapie to mink (Hanson et al., 1971) confirmed the close association of TME and scrapie, but at the same time provided evidence that they may be different. Epidemiologic studies on previous incidences of TME indicated that the incubation periods in field cases were between six months and one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be transmitted to mink in less than one year. To investigate the possibility that TME may be caused by a (particular strain of scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie agent, including their sheep or goat sources, were inoculated into a total of 61 mink. Only one mink developed a progressive neurologic disease after an incubation period of 22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent from an unidentified source.
OBSERVATIONS AND RESULTS
A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were "acting funny", and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death. 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.
Experimental Transmission.
The clinical diagnosis of TME was confirmed by histopaihologic examination and by experimental transmission to mink after incubation periods of four months. To investigate the possible involvement of cattle in this disease cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally with a brain suspension from affected mink. Each developed a fatal spongiform encephalopathy after incubation periods of 18 and 19 months.
DISCUSSION
These findings suggest that TME may result from feeding mink infected cattle and we have alerted bovine practitioners that there may exist an as yet unrecognized scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has recently been reported in England (Wells et al., 1987), and investigators are presently studying its transmissibility and possible relationship to scrapie. Because this new bovine disease in England is characterized by behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be confused with rabies in the United Stales and not be diagnosed. Presently, brains from cattle in the United States which are suspected of rabies infection are only tested with anti-rabies virus antibody and are not examined histopathologically for lesions of spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible involvement of cattle in the epidemiology of TME. One of these is the backpassage of our experimental bovine encephalopathy to mink. Because (here are as yet no agent- specific proteins or nucleic acids identified for these transmissible neuropathogens, one means of distinguishing them is by animal passage and selection of the biotype which grows best in a particular host. This procedure has been used to separate hamster- adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral backpassage of the experimental bovine agent resulted in incubations of only four months indicating no de-adaptation of the Stetsonville agent for mink after bovine passage. Mink fed infected bovine brain remain normal after six months. It will be essential to demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic association is to be confirmed.
ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United States Department of Agriculture. The authors also wish to acknowledge the help and encouragement of Robert Hanson who died during the course of these investigations.
REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and natural transmission. J. Infec. Dis. 115:393-399. Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861. Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392. Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the transmissible mink encephalopathy agent. 3. ViroL 3:176-180. Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460. Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle? Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary Medicine. University of Arizona, pp 20. Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121:419-420.
MARSH
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
In Confidence - Perceptions of unconventional slow virus diseases
of animals in the USA - APRIL-MAY 1989 - G A H Wells
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
Title: Experimental Transmission of Transmissible Mink Encephalopathy (Tme) to Cattle by Intracerebral Inoculation
http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=191825
Subject: USA MINK FARMS AND TSE TESTING ???
Date: July 15, 2006 at 5:52 am PST
Pelt Production Up 3 Percent Mink pelt production in the United States in 2005 totaled 2.63 million pelts, up 3 percent from 2004. Wisconsin, the largest mink producing State, produced 778,000 pelts. Utah the second largest producing State, produced 600,000 pelts. The number of pelts by color class as a percent of the total U.S.production in 2005 is as follows: Black at 47.6 percent, Mahogany at 20.9 percent, Blue Iris at 11.3 percent, Demi/Wild at 6.3 percent, Sapphire at 4.0 percent, and White at 3.8 percent. The remaining color classes accounted for 6.1 percent. Value of Pelt Production Up 33 Percent Mink pelts produced during the 2005 crop year were valued at $160 million, up 33 percent from $120 million a year ago. The average price per pelt for the 2005 crop year was $60.90, up from $47.10 in 2004. .....snip.......end
http://usda.mannlib.cornell.edu/reports/nassr/other/zmi-bb/mink0706.pdf
TME
http://www.aphis.usda.gov/lpa/pubs/fsheet_faq_notice/fs_ahtme.html
3.9.11 Mink Producers Mink offal is now rendered with other species and will decline in value under the first four regulatory options.
http://www.fda.gov/cvm/Documents/bse3.pdf
2.8 PROFILE OF MINK PRODUCERS Mink are raised for their pelts and oil. Most mink farmers kill and pelt their own animals once a year near the end of November or in early December. Once the pelts are removed, the fat is then scrapped from the hide. This fat is used to manufacture mink oil that is sought for cosmetic uses because of its hypoallergenic qualities and in leather treatments. The total value of mink production in 1995 was $143 million, an increase of 72 percent from 1994. In 1995, 446 mink farms produced a total of 2.69 million pelts (NASS, 1996b). Mink producers vary in size but most are small operations. Mink farming is concentrated in Utah (130 2-11 farms), Wisconsin (77 farms), and Minnesota (52 farms). There has been recent consolidation within the industry, with the number of farms decreasing by 8 percent from 1993 to 1994 and 3 percent from 1994 to 1995. The market price for mink pelts is subject to wide demand fluctuations based on fashion and weather. Once the pelt and fat are removed, the entire carcass is then rendered. Mink carcasses sent to rendering (minus the pelt and fat) weigh an average of 2.5 pounds, so the total estimated offal produced per year is 6.7 million pounds. Mink farmers are reported to have difficulty with getting renderers to pick-up their material because of its low volume and the infrequency of offal generation.
http://www.fda.gov/cvm/Documents/bse2.pdf
WHAT sort of TME surveillance program is in place now, if any??? DO they test for TSE in Mink and what are these figures if so ???
ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bare with me)
THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals or human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted blood from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.
These are the facts as i have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species. ...
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
Gerald Wells: Report of the Visit to USA, April-May 1989
snip...
The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...
snip...
It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...
snip...
3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought
this was a fanatical incident to be _avoided_ in the US _at all costs_...
snip...please read this old full text document !
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
Sunday, December 10, 2006
Transmissible Mink Encephalopathy TME Subject: In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
Gerald Wells: Report of the Visit to USA, April-May 1989
snip...
The general opinion of those present was that BSE, as an overt disease phenomenon, _could exist in the USA, but if it did, it was very rare. The need for improved and specific surveillance methods to detect it as recognised...
snip...
It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US...
snip...
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a _very low profile indeed_. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be _avoided_ in the US _at all costs_...
snip...please read this old full text document !
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
R.F. Marsh* and G.R. Hartsough
•Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092
ABSTRACT
Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England.
INTRODUCTION
Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough and Burger who demonstrated that the disease was transmissible with a long incubation period, and that affected mink had a spongiform encephalopathy similar to that found in scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965). Because of the similarity between TME and scrapie, and the subsequent finding that the two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was concluded that TME most likely resulted from feeding mink scrapie-infecied sheep. The experimental transmission of sheep scrapie to mink (Hanson et al., 1971) confirmed the close association of TME and scrapie, but at the same time provided evidence that they may be different. Epidemiologic studies on previous incidences of TME indicated that the incubation periods in field cases were between six months and one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be transmitted to mink in less than one year. To investigate the possibility that TME may be caused by a (particular strain of scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie agent, including their sheep or goat sources, were inoculated into a total of 61 mink. Only one mink developed a progressive neurologic disease after an incubation period of 22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent from an unidentified source.
OBSERVATIONS AND RESULTS
A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were "acting funny", and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death. 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.
Experimental Transmission.
The clinical diagnosis of TME was confirmed by histopaihologic examination and by experimental transmission to mink after incubation periods of four months. To investigate the possible involvement of cattle in this disease cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally with a brain suspension from affected mink. Each developed a fatal spongiform encephalopathy after incubation periods of 18 and 19 months.
DISCUSSION
These findings suggest that TME may result from feeding mink infected cattle and we have alerted bovine practitioners that there may exist an as yet unrecognized scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has recently been reported in England (Wells et al., 1987), and investigators are presently studying its transmissibility and possible relationship to scrapie. Because this new bovine disease in England is characterized by behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be confused with rabies in the United Stales and not be diagnosed. Presently, brains from cattle in the United States which are suspected of rabies infection are only tested with anti-rabies virus antibody and are not examined histopathologically for lesions of spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible involvement of cattle in the epidemiology of TME. One of these is the backpassage of our experimental bovine encephalopathy to mink. Because (here are as yet no agent- specific proteins or nucleic acids identified for these transmissible neuropathogens, one means of distinguishing them is by animal passage and selection of the biotype which grows best in a particular host. This procedure has been used to separate hamster- adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral backpassage of the experimental bovine agent resulted in incubations of only four months indicating no de-adaptation of the Stetsonville agent for mink after bovine passage. Mink fed infected bovine brain remain normal after six months. It will be essential to demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic association is to be confirmed.
ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United States Department of Agriculture. The authors also wish to acknowledge the help and encouragement of Robert Hanson who died during the course of these investigations.
REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and natural transmission. J. Infec. Dis. 115:393-399. Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861. Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392. Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the transmissible mink encephalopathy agent. 3. ViroL 3:176-180. Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460. Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle? Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary Medicine. University of Arizona, pp 20. Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121:419-420.
MARSH
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
In Confidence - Perceptions of unconventional slow virus diseases
of animals in the USA - APRIL-MAY 1989 - G A H Wells
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
Title: Experimental Transmission of Transmissible Mink Encephalopathy (Tme) to Cattle by Intracerebral Inoculation
http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=191825
Subject: USA MINK FARMS AND TSE TESTING ???
Date: July 15, 2006 at 5:52 am PST
Pelt Production Up 3 Percent Mink pelt production in the United States in 2005 totaled 2.63 million pelts, up 3 percent from 2004. Wisconsin, the largest mink producing State, produced 778,000 pelts. Utah the second largest producing State, produced 600,000 pelts. The number of pelts by color class as a percent of the total U.S.production in 2005 is as follows: Black at 47.6 percent, Mahogany at 20.9 percent, Blue Iris at 11.3 percent, Demi/Wild at 6.3 percent, Sapphire at 4.0 percent, and White at 3.8 percent. The remaining color classes accounted for 6.1 percent. Value of Pelt Production Up 33 Percent Mink pelts produced during the 2005 crop year were valued at $160 million, up 33 percent from $120 million a year ago. The average price per pelt for the 2005 crop year was $60.90, up from $47.10 in 2004. .....snip.......end
http://usda.mannlib.cornell.edu/reports/nassr/other/zmi-bb/mink0706.pdf
TME
http://www.aphis.usda.gov/lpa/pubs/fsheet_faq_notice/fs_ahtme.html
3.9.11 Mink Producers Mink offal is now rendered with other species and will decline in value under the first four regulatory options.
http://www.fda.gov/cvm/Documents/bse3.pdf
2.8 PROFILE OF MINK PRODUCERS Mink are raised for their pelts and oil. Most mink farmers kill and pelt their own animals once a year near the end of November or in early December. Once the pelts are removed, the fat is then scrapped from the hide. This fat is used to manufacture mink oil that is sought for cosmetic uses because of its hypoallergenic qualities and in leather treatments. The total value of mink production in 1995 was $143 million, an increase of 72 percent from 1994. In 1995, 446 mink farms produced a total of 2.69 million pelts (NASS, 1996b). Mink producers vary in size but most are small operations. Mink farming is concentrated in Utah (130 2-11 farms), Wisconsin (77 farms), and Minnesota (52 farms). There has been recent consolidation within the industry, with the number of farms decreasing by 8 percent from 1993 to 1994 and 3 percent from 1994 to 1995. The market price for mink pelts is subject to wide demand fluctuations based on fashion and weather. Once the pelt and fat are removed, the entire carcass is then rendered. Mink carcasses sent to rendering (minus the pelt and fat) weigh an average of 2.5 pounds, so the total estimated offal produced per year is 6.7 million pounds. Mink farmers are reported to have difficulty with getting renderers to pick-up their material because of its low volume and the infrequency of offal generation.
http://www.fda.gov/cvm/Documents/bse2.pdf
WHAT sort of TME surveillance program is in place now, if any??? DO they test for TSE in Mink and what are these figures if so ???
ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bare with me)
THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals or human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted blood from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.
These are the facts as i have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species. ...
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
Labels: PRION, TME, TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY
posted by Terry S. Singeltary Sr. at
11:48 AM
1 Comments
