Potential mad cows that entered food supply without being tested for BSE 2011: UK END OF YEAR REVIEW
Bullock aged over 72 months enters food supply without being tested for BSE
Wednesday 21 December 2011
The Agency has been notified that meat has entered the food supply from a bullock aged over 72 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at over 72 months of age.
It is very unlikely that the bullock was infected with BSE and, as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is the parts of cattle most likely to carry BSE infectivity.
The bullock, aged 75 months and 28 days, was slaughtered at N Bramall & Son Ltd’s abattoir in Oxspring, Nr Sheffield, on 6 October 2011. The error was discovered on 1 December in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested bullock, plus the one slaughtered before and the two after, should not have entered the food supply. However, by the time the failure was discovered, the associated carcasses had left the premises.
One of the carcasses was sent to the Netherlands where the authorities have been informed. The hearts and cheek meat from all the associated carcasses were traced and have since been destroyed. Other checks indicate that the rest of the meat from the carcasses is either no longer in the food supply or traceable and is likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2011/dec/bullockfoodchain
Bullock aged over 72 months enters food supply without being tested for BSE
Monday 14 November 2011
The Agency has been notified that meat has entered the food supply from a bullock aged over 72 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at more than 72 months of age. It is very unlikely that the bullock was infected with BSE and as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is the parts of cattle most likely to carry BSE infectivity.
The bullock, aged 75 months and 7 days, was slaughtered at C&S Meats Ltd’s abattoir in Dorset, on 2 September 2011. The error was discovered on 27 October in the course of routine cross-checks of slaughter and BSE test data. According to BSE regulations, the untested bullock, plus the one slaughtered before should not have entered the food supply. However, by the time the failure was discovered, the associated carcasses had left the premises. Subsequent checks traced a 20kg piece of meat from the untested bullock that has since been destroyed and indicate that the rest of the meat from the carcasses is no longer in the food supply.
http://www.food.gov.uk/news/newsarchive/2011/nov/csmeats
Cow aged over 72 months enters food supply without being tested for BSE
Wednesday 26 October 2011
The Agency has been notified that meat has entered the food supply from a cow aged over 72 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at over 72 months of age. It is very unlikely that the cow was infected with BSE and as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is the parts of cattle most likely to carry BSE infectivity.
The cow, aged 74 months and 11 days, was slaughtered at Anglo Dutch Meats (Charing) Ltd’s abattoir in Kent, on 11 August 2011. The error was discovered on 6 October in the course of routine cross-checks of slaughter and BSE test data. According to BSE regulations, the untested cow, plus the one slaughtered before and the two after should not have entered the food supply. However, by the time the failure was discovered, the associated carcases had left the premises. Subsequent checks indicate that the meat from the carcases was mixed with a large volume of other meat which is no longer in the food supply and is likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2011/oct/anglodutch
Tuesday, April 19, 2011
Bull aged over 48 months enters food supply without being tested for BSE Monday 18 April 2011
Bull aged over 48 months enters food supply without being tested for BSE Monday 18 April 2011
The Agency has been notified that meat has entered the food supply from a bull aged over 48 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at over 48 months of age.
It is very unlikely that the bull was infected with BSE and as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is that part of the animal most likely to contain BSE infectivity.
The bull, aged 88 months, was slaughtered at S J Norman & Sons’ abattoir in Bridport, Dorset on 3 February 2011. The error was discovered on 5 April in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested bull should not have entered the food supply. However, by the time the failure was discovered, the carcass had left the premises.
Subsequent checks indicate that all the meat from the carcass is no longer traceable and is likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2011/apr/otmbull
Imported cow aged over 30 months not tested for BSE
Wednesday 16 February 2011
The Agency has been notified that meat has entered the food supply from an Over Thirty Month (OTM) cow imported from Switzerland that had not been tested for BSE.It is very unlikely that the cow was infected with BSE and, as specified risk material (SRM) was removed, any risk to human health is extremely low.
SRM is those parts of an animal likely to be infected if the animal has BSE.Nevertheless, according to BSE regulations the untested cow, the one slaughtered before and the two slaughtered after must not enter the food supply. Negative BSE test results were received for the 'one before' and 'two after'.
The cow had been imported into the UK in December 2009 and was slaughtered at William Taylor & Son Ltd's abattoir in Bamber Bridge, near Preston, on 15 October 2010 at just over 41 months of age.
BSE testing is mandatory for cattle born in Switzerland if slaughtered for human consumption at over 30 months of age. The missing BSE test result was discovered on 17 November during routine cross checks of slaughter and BSE test data. By the time the failure was discovered, all of the associated carcasses had left the premises.
The Agency has established that the carcase of the Swiss-born bovine was sold as fresh meat and is likely to have been eaten. We also traced the batch of carcases that included the 'one before' and 'two after'. This showed that:
the majority of the meat was no longer in the food supply and is likely to have been eaten a small portion of the batch was found in cold storage and has since been destroyed a small portion of the batch was mixed with a large quantity of meat from other batches and used in Iceland's own brand 1.4kg steak pies with 'best before' dates of 23.11.11 and 26.11.11.
Although any food safety risk from consuming these pies would be extremely low, Iceland has taken the decision to withdraw the affected pies from sale some had been exported to Ireland and the authorities there have been informed.
http://www.food.gov.uk/news/newsarchive/2011/feb/otm160211
Food Standards Agency - 31 Jan 2011 11:53
Two cows aged over 48 months enter food supply without being tested for BSE
The Agency has been notified that meat has entered the food supply from two cows aged over 48 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at over 48 months of age.
It is very unlikely that the cows were infected with BSE and as specified risk material was removed, any risk to human health is extremely low.
One of the cows was just under 52 months of age and the other just over 52 months of age when slaughtered on 2 November 2010 at J V Richards (Reitfontein) Ltd’s abattoir in Truro. The error was discovered on 10 January in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, both the untested cows and the one slaughtered before them should not have entered the food supply. However, by the time the failure was discovered, all three associated carcasses had left the premises.
Subsequent checks indicate that all the meat from the carcasses is no longer in the food supply chain and is likely to have been eaten.
http://www.wired-gov.net/wg/wg-news-1.nsf/lfi/DNWA-8DMFY9
BSE controls explained: Main controls on production
http://www.food.gov.uk/safereating/animaldiseases/bse/what/beef/controls
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report
http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
EFSA Journal 2011 The European Response to BSE: A Success Story
This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip... http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1
http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html
Saturday, November 19, 2011
Novel Prion Protein in BSE-affected Cattle, Switzerland
http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/novel-prion-protein-in-bse-affected.html
Saturday, December 3, 2011
Isolation of Prion with BSE Properties from Farmed Goat
Volume 17, Number 12—December 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/isolation-of-prion-with-bse-properties.html
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
2010-2011
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
2011 Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
http://bse-atypical.blogspot.com/2011/09/l-bse-base-prion-and-atypical-sporadic.html
SEE RISE OF SPORADIC CJD YEAR TO YEAR ;
http://www.cjd.ed.ac.uk/figures.htm
Sunday, December 18, 2011
A blood test for variant Creutzfeldt‐Jakob disease: briefing note for patients, carers and health professionals
http://vcjdtransfusion.blogspot.com/2011/12/blood-test-for-variant-creutzfeldtjakob.html
TSS
Wednesday, December 21, 2011
Monday, November 14, 2011
Bullock aged over 72 months enters food supply without being tested for BSE
Bullock aged over 72 months enters food supply without being tested for BSE
Monday 14 November 2011
The Agency has been notified that meat has entered the food supply from a bullock aged over 72 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at more than 72 months of age.
It is very unlikely that the bullock was infected with BSE and as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is the parts of cattle most likely to carry BSE infectivity.
The bullock, aged 75 months and 7 days, was slaughtered at C&S Meats Ltd’s abattoir in Dorset, on 2 September 2011. The error was discovered on 27 October in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested bullock, plus the one slaughtered before should not have entered the food supply. However, by the time the failure was discovered, the associated carcasses had left the premises.
Subsequent checks traced a 20kg piece of meat from the untested bullock that has since been destroyed and indicate that the rest of the meat from the carcasses is no longer in the food supply.
http://www.food.gov.uk/news/newsarchive/2011/nov/csmeats
a review of other recent bovines entering commerce without being tested for BSE. ...tss
Cow aged over 72 months enters food supply without being tested for BSE
Wednesday 26 October 2011
The Agency has been notified that meat has entered the food supply from a cow aged over 72 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at over 72 months of age.
It is very unlikely that the cow was infected with BSE and as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is the parts of cattle most likely to carry BSE infectivity.
The cow, aged 74 months and 11 days, was slaughtered at Anglo Dutch Meats (Charing) Ltd’s abattoir in Kent, on 11 August 2011. The error was discovered on 6 October in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested cow, plus the one slaughtered before and the two after should not have entered the food supply. However, by the time the failure was discovered, the associated carcases had left the premises.
Subsequent checks indicate that the meat from the carcases was mixed with a large volume of other meat which is no longer in the food supply and is likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2011/oct/anglodutch
Cow aged over 48 months enters food supply without being tested for BSE
Tuesday 23 February 2010
The Agency has been notified that meat from a cow aged over 48 months has entered the food supply without being tested for BSE.
It is very unlikely that the cow was infected with BSE and, as specified risk material (SRM) was removed, any risk to human health is extremely low. However, testing is mandatory for cattle slaughtered for human consumption at over 48 months of age.
The cow was slaughtered at Pickstock Ashby Ltd's abattoir in Hartshorne, Derbyshire, on 4 November 2009 aged almost 57 months. The failure was discovered on 28 January during routine cross checks of slaughter and BSE test data. By the time the failure was discovered all of the affected carcasses and offal had left the premises.
The affected carcasses, some edible co-products and offal had been exported. Some meat returned to Britain after processing and some went to other countries. Other edible co-products remained in Britain. Subsequent checks indicate that all of the meat and edible co-product that remained in Britain or that returned to Britain is no longer in the food supply chain. The authorities in the countries that received the exported material have been informed.
Background to BSE testing The BSE testing age was raised to 48 months at the beginning of last year. Cattle aged over 48 months are allowed to enter the food supply provided they have tested negative for BSE. If there is no BSE test, all parts of the carcase must be condemned.
Specified risk material (SRM) is those parts of the animal that contain almost all BSE infectivity, if the animal is infected with BSE.
http://www.food.gov.uk/news/newsarchive/2010/feb/over48monthcow
Cow aged over 48 months enters food supply without being tested for BSE
Tuesday 14 September 2010
The Agency has been notified that meat has entered the food supply from a cow aged over 48 months that had not been tested for BSE.
It is very unlikely that the cow was infected with BSE and, as specified risk material was removed, any risk to human health is extremely low. Nevertheless, a negative BSE test result is mandatory for cattle over 48 months of age slaughtered for human consumption.
The cow was aged one day over 48 months when slaughtered on 9 July at G & GB Hewitt Ltd abattoir in Chester. The error was discovered on 24 August in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested cow, the animal slaughtered before and the two slaughtered after must not enter the food supply. However, by the time the failure was discovered, all of the associated carcasses had left the premises.
Subsequent checks traced one small batch of meat that has since been destroyed and indicate that the rest of the meat from the carcasses is no longer in the food supply chain.
http://www.food.gov.uk/news/newsarchive/2010/sep/otmuntested
Cow aged over 48 months enters food supply without being tested for BSE
Monday 2 November 2009
The Agency has been notified that a 58 months old cow has entered the food supply without being tested for BSE. BSE testing is mandatory for cattle slaughtered for human consumption at over 48 months of age.
However, as all the specified risk material (SRM) was removed, and it is unlikely that the cow was infected with BSE, any risk to human health is very low. SRM is those parts of the animal that contain almost all BSE infectivity.
The cow was slaughtered on 28 July 2009 at Dunbia abattoir in Dungannon. The error was discovered by Northern Ireland's Department of Agriculture and Rural Development (DARD) when a routine annual herd TB test revealed that the cow had been misidentified.
DARD has now established the correct identity and age of the cow slaughtered on 28 July. Checks indicate that all the meat and other products from the untested cow are likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2009/nov/over48
Monday, May 12, 2008
BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS
http://bseyoungestage.blogspot.com/
Tuesday, November 01, 2011
Could we face the return of CJD? Experts fear it may lie dormant in thousands
http://creutzfeldt-jakob-disease.blogspot.com/2011/11/could-we-face-return-of-cjd-experts.html
EFSA Journal 2011 The European Response to BSE: A Success Story
This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1
http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html
Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
http://bse-atypical.blogspot.com/2011/09/l-bse-base-prion-and-atypical-sporadic.html
tss
Monday 14 November 2011
The Agency has been notified that meat has entered the food supply from a bullock aged over 72 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at more than 72 months of age.
It is very unlikely that the bullock was infected with BSE and as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is the parts of cattle most likely to carry BSE infectivity.
The bullock, aged 75 months and 7 days, was slaughtered at C&S Meats Ltd’s abattoir in Dorset, on 2 September 2011. The error was discovered on 27 October in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested bullock, plus the one slaughtered before should not have entered the food supply. However, by the time the failure was discovered, the associated carcasses had left the premises.
Subsequent checks traced a 20kg piece of meat from the untested bullock that has since been destroyed and indicate that the rest of the meat from the carcasses is no longer in the food supply.
http://www.food.gov.uk/news/newsarchive/2011/nov/csmeats
a review of other recent bovines entering commerce without being tested for BSE. ...tss
Cow aged over 72 months enters food supply without being tested for BSE
Wednesday 26 October 2011
The Agency has been notified that meat has entered the food supply from a cow aged over 72 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at over 72 months of age.
It is very unlikely that the cow was infected with BSE and as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is the parts of cattle most likely to carry BSE infectivity.
The cow, aged 74 months and 11 days, was slaughtered at Anglo Dutch Meats (Charing) Ltd’s abattoir in Kent, on 11 August 2011. The error was discovered on 6 October in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested cow, plus the one slaughtered before and the two after should not have entered the food supply. However, by the time the failure was discovered, the associated carcases had left the premises.
Subsequent checks indicate that the meat from the carcases was mixed with a large volume of other meat which is no longer in the food supply and is likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2011/oct/anglodutch
Cow aged over 48 months enters food supply without being tested for BSE
Tuesday 23 February 2010
The Agency has been notified that meat from a cow aged over 48 months has entered the food supply without being tested for BSE.
It is very unlikely that the cow was infected with BSE and, as specified risk material (SRM) was removed, any risk to human health is extremely low. However, testing is mandatory for cattle slaughtered for human consumption at over 48 months of age.
The cow was slaughtered at Pickstock Ashby Ltd's abattoir in Hartshorne, Derbyshire, on 4 November 2009 aged almost 57 months. The failure was discovered on 28 January during routine cross checks of slaughter and BSE test data. By the time the failure was discovered all of the affected carcasses and offal had left the premises.
The affected carcasses, some edible co-products and offal had been exported. Some meat returned to Britain after processing and some went to other countries. Other edible co-products remained in Britain. Subsequent checks indicate that all of the meat and edible co-product that remained in Britain or that returned to Britain is no longer in the food supply chain. The authorities in the countries that received the exported material have been informed.
Background to BSE testing The BSE testing age was raised to 48 months at the beginning of last year. Cattle aged over 48 months are allowed to enter the food supply provided they have tested negative for BSE. If there is no BSE test, all parts of the carcase must be condemned.
Specified risk material (SRM) is those parts of the animal that contain almost all BSE infectivity, if the animal is infected with BSE.
http://www.food.gov.uk/news/newsarchive/2010/feb/over48monthcow
Cow aged over 48 months enters food supply without being tested for BSE
Tuesday 14 September 2010
The Agency has been notified that meat has entered the food supply from a cow aged over 48 months that had not been tested for BSE.
It is very unlikely that the cow was infected with BSE and, as specified risk material was removed, any risk to human health is extremely low. Nevertheless, a negative BSE test result is mandatory for cattle over 48 months of age slaughtered for human consumption.
The cow was aged one day over 48 months when slaughtered on 9 July at G & GB Hewitt Ltd abattoir in Chester. The error was discovered on 24 August in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested cow, the animal slaughtered before and the two slaughtered after must not enter the food supply. However, by the time the failure was discovered, all of the associated carcasses had left the premises.
Subsequent checks traced one small batch of meat that has since been destroyed and indicate that the rest of the meat from the carcasses is no longer in the food supply chain.
http://www.food.gov.uk/news/newsarchive/2010/sep/otmuntested
Cow aged over 48 months enters food supply without being tested for BSE
Monday 2 November 2009
The Agency has been notified that a 58 months old cow has entered the food supply without being tested for BSE. BSE testing is mandatory for cattle slaughtered for human consumption at over 48 months of age.
However, as all the specified risk material (SRM) was removed, and it is unlikely that the cow was infected with BSE, any risk to human health is very low. SRM is those parts of the animal that contain almost all BSE infectivity.
The cow was slaughtered on 28 July 2009 at Dunbia abattoir in Dungannon. The error was discovered by Northern Ireland's Department of Agriculture and Rural Development (DARD) when a routine annual herd TB test revealed that the cow had been misidentified.
DARD has now established the correct identity and age of the cow slaughtered on 28 July. Checks indicate that all the meat and other products from the untested cow are likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2009/nov/over48
Monday, May 12, 2008
BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS
http://bseyoungestage.blogspot.com/
Tuesday, November 01, 2011
Could we face the return of CJD? Experts fear it may lie dormant in thousands
http://creutzfeldt-jakob-disease.blogspot.com/2011/11/could-we-face-return-of-cjd-experts.html
EFSA Journal 2011 The European Response to BSE: A Success Story
This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1
http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html
Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
http://bse-atypical.blogspot.com/2011/09/l-bse-base-prion-and-atypical-sporadic.html
tss
Friday, June 10, 2011
Board advises on increase in BSE testing age FSA
The Agency has advised Ministers that it would be acceptable to increase the age at which BSE tests are carried out on healthy cattle slaughtered for human consumption.
http://www.wired-gov.net/wg/wg-news-1.nsf/lfi/DNWA-8HPHBS
Food Standards Agency - 10 Jun 2011 15:15
Board advises on increase in BSE testing age
The Agency has advised Ministers that it would be acceptable to increase the age at which BSE tests are carried out on healthy cattle slaughtered for human consumption.
The advice was given following a discussion on proposed changes to BSE testing held at the Board’s open meeting in Belfast on 25 May. The proposal is that the age threshold for healthy cattle slaughtered for human consumption born in the UK and 24 other member states should be increased from 48 to 72 months.
BSE testing requirements for 'risk' cattle (those most likely to test positive for BSE, but not BSE suspects) would remain largely the same and those for BSE suspects (cattle with clinical symptoms of the disease) would not change.
Commenting on the proposed change, FSA director of food safety Alison Gleadle said: 'Numbers of BSE cases have dropped dramatically since the height of the UK's BSE epidemic. In 1992 there were more than 37,000 clinical cases reported. Last year there were just 11 detected via the testing programme – none of which were in cattle slaughtered for human consumption.
'Subject to effective surveillance for BSE continuing to be in place, the Agency believes that increasing the threshold for BSE testing of healthy slaughtered cattle to 72 months would be acceptable on grounds of food safety. The main protection for consumers is through the removal of specified risk material.'
If Ministers agree to proceed with the change, which could take place from 1 July this year, it will be the third major relaxation in BSE controls in the last six years.
In November 2005, the ban on cattle aged over thirty months (OTM) from entering the food chain was replaced with BSE testing of all OTM cattle entering the food chain.
In January 2009, the age threshold at which cattle had to be tested for BSE was increased from 30 months to 48 months.
The latest change would mean that almost all healthy cattle slaughtered for human consumption will not have to be tested until the age of 72 months.
http://www.wired-gov.net/wg/wg-news-1.nsf/lfi/DNWA-8HPHBS
SEAC
POSITION STATEMENT ON THE REQUIREMENTS FOR BSE TESTING OF HEALTHY CATTLE
SEAC was asked by the Food Standards Agency to consider the change in risk to consumers from exposure to BSE that would result if (a) from 2011, the age threshold for BSE testing healthy slaughter cattle was raised from 48 to 72 months and (b) BSE testing of healthy slaughter cattle was to stop altogether.
FSA presented to SEAC an analysis carried out by the Veterinary Laboratories Agency (VLA) assessing the impact of reducing the level of BSE testing of healthy cattle slaughtered for human consumption, using a mathematical model developed at VLA. The model predicts the number of additional infected cattle that would be consumed if monitoring is reduced and estimates the consequent impact on the amount of infectivity entering the food supply.
SEAC advises that in the short-term there is an insignificant additional risk to human health that would result from raising the age for healthy slaughter cattle from 48 to 72 months. The VLA modelling results concur with the low numbers of cattle now being identified with BSE. However, SEAC notes that this conclusion is only valid if the prevalence of BSE in the UK cattle population remains at or decreases from its current value. The current and future validity of this analysis therefore depends critically on the nature and quality of BSE surveillance within the cattle population, and in particular its capacity to ensure the early detection of any re-emerging epidemic. This assessment would equally apply to any proposal to cease altogether the testing of healthy slaughter cattle. SEAC considers that any change in the incidence of BSE is most likely to be detected in fallen stock and casualty animals because of the currently higher likelihood of detecting BSE in these sub-populations. Provided that surveillance of fallen stock and casualty animals is sufficient to provide the necessary information about disease incidence and prevalence, the additional risk to consumers of reducing testing of healthy cattle will remain small.
In addition, SEAC offers the following observations that the FSA and other interested Government Departments might wish to consider:
(a) Surveillance is the only effective means of monitoring changes in the incidence or prevalence of BSE. It is therefore important that current surveillance protocols are kept under review, to ensure that they are capable of detecting an increase in BSE prevalence both in an appropriate time frame and at a suitable sensitivity to detect an
increase in prevalence that would warrant reintroduction of testing healthy slaughtered cattle.
(b) It is not clear that testing a sample of healthy slaughter cattle older than 72 months would provide much useful information: this age group might be sub-optimal. The arguments for random testing of healthy slaughter cattle at this age, compared to other ages, should be considered carefully, taking account of the purpose of this sampling, the sample size and test sensitivity (by incubation period) amongst other considerations.
(c) UK data should continue to be used to demonstrate a decline in the prevalence of BSE in the UK herd, rather than relying on EU-wide figures.
(d) It is instructive to use the VLA model to examine a range of hypothetical rates of increase in BSE infection and the ability of current surveillance measures to detect the change, and this should be repeated as necessary when significant changes to current practices are envisaged.
(e) Changing one BSE control measure can have knock-on effects on other control measures and it is important that the possibility of such interactions is fully taken into account when a proposal such as this is considered.
30 MARCH 2011
http://www.food.gov.uk/multimedia/pdfs/seacstatment.pdf
Related links
BSE
http://www.food.gov.uk/safereating/animaldiseases/bse/
Chair's letters to ministers
http://www.food.gov.uk/multimedia/pdfs/letterstominst.pdf
(pdf 696KB)
Letter from the Chief Medical Officer
http://www.food.gov.uk/multimedia/pdfs/lettermedpfficer.pdf
(pdf 110KB)
Paper considered by SEAC
http://www.food.gov.uk/multimedia/pdfs/paperseac.pdf
(pdf 250KB)
SEAC position statement
http://www.food.gov.uk/multimedia/pdfs/seacstatment.pdf
(pdf 23KB)
END...TSS
Monday, May 12, 2008
BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS
http://bseyoungestage.blogspot.com/
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
Friday, May 13,
2011 EFSA Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/efsa-joint-scientific-opinion-on-any.html
Monday, May 23, 2011
Atypical Prion Diseases in Humans and Animals 2011
Top Curr Chem (2011)
DOI: 10.1007/128_2011_161
# Springer-Verlag Berlin Heidelberg 2011
Michael A. Tranulis, Sylvie L. Benestad, Thierry Baron, and Hans Kretzschmar
Abstract
Although prion diseases, such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie in sheep, have long been recognized, our understanding of their epidemiology and pathogenesis is still in its early stages. Progress is hampered by the lengthy incubation periods and the lack of effective ways of monitoring and characterizing these agents. Protease-resistant conformers of the prion protein (PrP), known as the "scrapie form" (PrPSc), are used as disease markers, and for taxonomic purposes, in correlation with clinical, pathological, and genetic data. In humans, prion diseases can arise sporadically (sCJD) or genetically (gCJD and others), caused by mutations in the PrP-gene (PRNP), or as a foodborne infection, with the agent of bovine spongiform encephalopathy (BSE) causing variant CJD (vCJD). Person-to-person spread of human prion disease has only been known to occur following cannibalism (kuru disease in Papua New Guinea) or through medical or surgical treatment (iatrogenic CJD, iCJD). In contrast, scrapie in small ruminants and chronic wasting disease (CWD) in cervids behave as infectious diseases within these species. Recently, however, so-called atypical forms of prion diseases have been discovered in sheep (atypical/Nor98 scrapie) and in cattle, BSE-H and BSE-L. These maladies resemble sporadic or genetic human prion diseases and might be their animal equivalents. This hypothesis also raises the significant public health question of possible epidemiological links between these diseases and their counterparts in humans.
M.A. Tranulis (*)
Norwegian School of Veterinary Science, Oslo, Norway
e-mail: Michael.Tranulis@nvh.no
S.L. Benestad
Norwegian Veterinary Institute, Oslo, Norway
T. Baron
Agence Nationale de Se´curite´ Sanitaire, ANSES, Lyon, France
H. Kretzschmar
Ludwig-Maximilians University of Munich, Munich, Germany
Keywords Animal Atypical Atypical/Nor98 scrapie BSE-H BSE-L Human Prion disease Prion strain Prion type
http://resources.metapress.com/pdf-preview.axd?code=f433r34h34ugg617&size=largest
snip...SEE MORE HERE ;
http://bse-atypical.blogspot.com/2011/05/atypical-prion-diseases-in-humans-and.html
Thursday, June 2, 2011
USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California
http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the USA Question number: EFSA-Q-2003-083
Adopted: 1 July 2004
Summary
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1211902594180.htm
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 1 - European Food Safety Authority Scientific Expert Working Group on GBR Working Group Report on the Assessment of the Geographical BSE-Risk (GBR) of UNITED STATES OF AMERICA 2004
http://www.efsa.europa.eu/en/scdocs/doc/3rax1.pdf
Sunday, May 01, 2011
STUDY OF ATYPICAL BSE 2010 Annual Report May 2011
http://bse-atypical.blogspot.com/2011/05/study-of-atypical-bse-2010-annual.html
What is the potential cost of pre- and post-slaughter testing? The estimated cost of post-mortem testing is $40 per head. This amount is comprised almost entirely of the cost of the test kit and sample analysis. It is expected that ante-mortem tests (live animal), if a test is developed, will reduce BSE testing costs to approximately $15 per head.
http://www.prionetcanada.ca/detail.aspx?menu=12&dt=293720&app=70&cat1=211&tp=12&lk=no
Monday, May 23, 2011
CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/cdc-assesses-potential-human-exposure.html
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report
http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html
IBNC
"All of the 15 cattle tested showed that the brains had abnormally accumulated prion protein."
Saturday, February 28, 2009
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009
SEAC 102/2
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
Tuesday, April 26, 2011
sporadic CJD RISING Text and figures of the latest annual report of the NCJDRSU covering the period 1990-2009 (published 11th March 2011)
http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
Tuesday, April 26, 2011
sporadic CJD RISING Text and figures of the latest annual report of the NCJDRSU covering the period 1990-2009 (published 11th March 2011)
http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html
something that disturbs me very much, iatrogenic prion TSE exposure and accumulation there from all of the above ???
Tuesday, March 29, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY EXPOSURE SPREADING VIA HOSPITALS AND SURGICAL PROCEDURES AROUND THE GLOBE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/transmissible-spongiform-encephalopathy.html
TSS
http://www.wired-gov.net/wg/wg-news-1.nsf/lfi/DNWA-8HPHBS
Food Standards Agency - 10 Jun 2011 15:15
Board advises on increase in BSE testing age
The Agency has advised Ministers that it would be acceptable to increase the age at which BSE tests are carried out on healthy cattle slaughtered for human consumption.
The advice was given following a discussion on proposed changes to BSE testing held at the Board’s open meeting in Belfast on 25 May. The proposal is that the age threshold for healthy cattle slaughtered for human consumption born in the UK and 24 other member states should be increased from 48 to 72 months.
BSE testing requirements for 'risk' cattle (those most likely to test positive for BSE, but not BSE suspects) would remain largely the same and those for BSE suspects (cattle with clinical symptoms of the disease) would not change.
Commenting on the proposed change, FSA director of food safety Alison Gleadle said: 'Numbers of BSE cases have dropped dramatically since the height of the UK's BSE epidemic. In 1992 there were more than 37,000 clinical cases reported. Last year there were just 11 detected via the testing programme – none of which were in cattle slaughtered for human consumption.
'Subject to effective surveillance for BSE continuing to be in place, the Agency believes that increasing the threshold for BSE testing of healthy slaughtered cattle to 72 months would be acceptable on grounds of food safety. The main protection for consumers is through the removal of specified risk material.'
If Ministers agree to proceed with the change, which could take place from 1 July this year, it will be the third major relaxation in BSE controls in the last six years.
In November 2005, the ban on cattle aged over thirty months (OTM) from entering the food chain was replaced with BSE testing of all OTM cattle entering the food chain.
In January 2009, the age threshold at which cattle had to be tested for BSE was increased from 30 months to 48 months.
The latest change would mean that almost all healthy cattle slaughtered for human consumption will not have to be tested until the age of 72 months.
http://www.wired-gov.net/wg/wg-news-1.nsf/lfi/DNWA-8HPHBS
SEAC
POSITION STATEMENT ON THE REQUIREMENTS FOR BSE TESTING OF HEALTHY CATTLE
SEAC was asked by the Food Standards Agency to consider the change in risk to consumers from exposure to BSE that would result if (a) from 2011, the age threshold for BSE testing healthy slaughter cattle was raised from 48 to 72 months and (b) BSE testing of healthy slaughter cattle was to stop altogether.
FSA presented to SEAC an analysis carried out by the Veterinary Laboratories Agency (VLA) assessing the impact of reducing the level of BSE testing of healthy cattle slaughtered for human consumption, using a mathematical model developed at VLA. The model predicts the number of additional infected cattle that would be consumed if monitoring is reduced and estimates the consequent impact on the amount of infectivity entering the food supply.
SEAC advises that in the short-term there is an insignificant additional risk to human health that would result from raising the age for healthy slaughter cattle from 48 to 72 months. The VLA modelling results concur with the low numbers of cattle now being identified with BSE. However, SEAC notes that this conclusion is only valid if the prevalence of BSE in the UK cattle population remains at or decreases from its current value. The current and future validity of this analysis therefore depends critically on the nature and quality of BSE surveillance within the cattle population, and in particular its capacity to ensure the early detection of any re-emerging epidemic. This assessment would equally apply to any proposal to cease altogether the testing of healthy slaughter cattle. SEAC considers that any change in the incidence of BSE is most likely to be detected in fallen stock and casualty animals because of the currently higher likelihood of detecting BSE in these sub-populations. Provided that surveillance of fallen stock and casualty animals is sufficient to provide the necessary information about disease incidence and prevalence, the additional risk to consumers of reducing testing of healthy cattle will remain small.
In addition, SEAC offers the following observations that the FSA and other interested Government Departments might wish to consider:
(a) Surveillance is the only effective means of monitoring changes in the incidence or prevalence of BSE. It is therefore important that current surveillance protocols are kept under review, to ensure that they are capable of detecting an increase in BSE prevalence both in an appropriate time frame and at a suitable sensitivity to detect an
increase in prevalence that would warrant reintroduction of testing healthy slaughtered cattle.
(b) It is not clear that testing a sample of healthy slaughter cattle older than 72 months would provide much useful information: this age group might be sub-optimal. The arguments for random testing of healthy slaughter cattle at this age, compared to other ages, should be considered carefully, taking account of the purpose of this sampling, the sample size and test sensitivity (by incubation period) amongst other considerations.
(c) UK data should continue to be used to demonstrate a decline in the prevalence of BSE in the UK herd, rather than relying on EU-wide figures.
(d) It is instructive to use the VLA model to examine a range of hypothetical rates of increase in BSE infection and the ability of current surveillance measures to detect the change, and this should be repeated as necessary when significant changes to current practices are envisaged.
(e) Changing one BSE control measure can have knock-on effects on other control measures and it is important that the possibility of such interactions is fully taken into account when a proposal such as this is considered.
30 MARCH 2011
http://www.food.gov.uk/multimedia/pdfs/seacstatment.pdf
Related links
BSE
http://www.food.gov.uk/safereating/animaldiseases/bse/
Chair's letters to ministers
http://www.food.gov.uk/multimedia/pdfs/letterstominst.pdf
(pdf 696KB)
Letter from the Chief Medical Officer
http://www.food.gov.uk/multimedia/pdfs/lettermedpfficer.pdf
(pdf 110KB)
Paper considered by SEAC
http://www.food.gov.uk/multimedia/pdfs/paperseac.pdf
(pdf 250KB)
SEAC position statement
http://www.food.gov.uk/multimedia/pdfs/seacstatment.pdf
(pdf 23KB)
END...TSS
Monday, May 12, 2008
BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS
http://bseyoungestage.blogspot.com/
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
Friday, May 13,
2011 EFSA Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/efsa-joint-scientific-opinion-on-any.html
Monday, May 23, 2011
Atypical Prion Diseases in Humans and Animals 2011
Top Curr Chem (2011)
DOI: 10.1007/128_2011_161
# Springer-Verlag Berlin Heidelberg 2011
Michael A. Tranulis, Sylvie L. Benestad, Thierry Baron, and Hans Kretzschmar
Abstract
Although prion diseases, such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie in sheep, have long been recognized, our understanding of their epidemiology and pathogenesis is still in its early stages. Progress is hampered by the lengthy incubation periods and the lack of effective ways of monitoring and characterizing these agents. Protease-resistant conformers of the prion protein (PrP), known as the "scrapie form" (PrPSc), are used as disease markers, and for taxonomic purposes, in correlation with clinical, pathological, and genetic data. In humans, prion diseases can arise sporadically (sCJD) or genetically (gCJD and others), caused by mutations in the PrP-gene (PRNP), or as a foodborne infection, with the agent of bovine spongiform encephalopathy (BSE) causing variant CJD (vCJD). Person-to-person spread of human prion disease has only been known to occur following cannibalism (kuru disease in Papua New Guinea) or through medical or surgical treatment (iatrogenic CJD, iCJD). In contrast, scrapie in small ruminants and chronic wasting disease (CWD) in cervids behave as infectious diseases within these species. Recently, however, so-called atypical forms of prion diseases have been discovered in sheep (atypical/Nor98 scrapie) and in cattle, BSE-H and BSE-L. These maladies resemble sporadic or genetic human prion diseases and might be their animal equivalents. This hypothesis also raises the significant public health question of possible epidemiological links between these diseases and their counterparts in humans.
M.A. Tranulis (*)
Norwegian School of Veterinary Science, Oslo, Norway
e-mail: Michael.Tranulis@nvh.no
S.L. Benestad
Norwegian Veterinary Institute, Oslo, Norway
T. Baron
Agence Nationale de Se´curite´ Sanitaire, ANSES, Lyon, France
H. Kretzschmar
Ludwig-Maximilians University of Munich, Munich, Germany
Keywords Animal Atypical Atypical/Nor98 scrapie BSE-H BSE-L Human Prion disease Prion strain Prion type
http://resources.metapress.com/pdf-preview.axd?code=f433r34h34ugg617&size=largest
snip...SEE MORE HERE ;
http://bse-atypical.blogspot.com/2011/05/atypical-prion-diseases-in-humans-and.html
Thursday, June 2, 2011
USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California
http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the USA Question number: EFSA-Q-2003-083
Adopted: 1 July 2004
Summary
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1211902594180.htm
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 1 - European Food Safety Authority Scientific Expert Working Group on GBR Working Group Report on the Assessment of the Geographical BSE-Risk (GBR) of UNITED STATES OF AMERICA 2004
http://www.efsa.europa.eu/en/scdocs/doc/3rax1.pdf
Sunday, May 01, 2011
STUDY OF ATYPICAL BSE 2010 Annual Report May 2011
http://bse-atypical.blogspot.com/2011/05/study-of-atypical-bse-2010-annual.html
What is the potential cost of pre- and post-slaughter testing? The estimated cost of post-mortem testing is $40 per head. This amount is comprised almost entirely of the cost of the test kit and sample analysis. It is expected that ante-mortem tests (live animal), if a test is developed, will reduce BSE testing costs to approximately $15 per head.
http://www.prionetcanada.ca/detail.aspx?menu=12&dt=293720&app=70&cat1=211&tp=12&lk=no
Monday, May 23, 2011
CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/cdc-assesses-potential-human-exposure.html
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report
http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html
IBNC
"All of the 15 cattle tested showed that the brains had abnormally accumulated prion protein."
Saturday, February 28, 2009
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009
SEAC 102/2
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
Tuesday, April 26, 2011
sporadic CJD RISING Text and figures of the latest annual report of the NCJDRSU covering the period 1990-2009 (published 11th March 2011)
http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
Tuesday, April 26, 2011
sporadic CJD RISING Text and figures of the latest annual report of the NCJDRSU covering the period 1990-2009 (published 11th March 2011)
http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html
something that disturbs me very much, iatrogenic prion TSE exposure and accumulation there from all of the above ???
Tuesday, March 29, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY EXPOSURE SPREADING VIA HOSPITALS AND SURGICAL PROCEDURES AROUND THE GLOBE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/transmissible-spongiform-encephalopathy.html
TSS
Tuesday, May 3, 2011
Bovine spongiform encephalopathy, Switzerland O.I.E. report
Bovine spongiform encephalopathy, Switzerland
Information received on 03/05/2011 from Mr Hans Wyss, Chief Veterinary Officer, Schwarzenburgstrasse 161, Swiss Federal Veterinary Office, LIEBEFELD BERNE, Switzerland
Summary
Report type Immediate notification (Final report) Start date 08/04/2011 Date of first confirmation of the event 18/04/2011 Report date 03/05/2011 Date submitted to OIE 03/05/2011 Date event resolved 03/05/2011 Reason for notification Reoccurrence of a listed disease Date of previous occurrence 10/2006 Manifestation of disease Sub-clinical infection Causal agent Prion Nature of diagnosis Laboratory (advanced) This event pertains to the whole country
New outbreaks Summary of outbreaks Total outbreaks: 1 Location(s) SANKT GALLEN (Sankt Gallen)
Total animals affected Species Susceptible Cases Deaths Destroyed Slaughtered Cattle 32 1 0 1 0
Outbreak statistics Species Apparent morbidity rate Apparent mortality rate Apparent case fatality rate Proportion susceptible animals lost* Cattle 3.13% 0.00% 0.00% 3.13%
* Removed from the susceptible population through death, destruction and/or slaughter
Epidemiology Source of the outbreak(s) or origin of infection Unknown or inconclusive
Control measures Measures applied No vaccination No treatment of affected animals
Measures to be applied No other measures
Diagnostic test results Laboratory name and type National Reference Laboratory (National laboratory) Tests and results Species Test Test date Result Cattle western blotting 18/04/2011 Positive
Future Reporting The event is resolved. No more reports will be submitted.
http://web.oie.int/wahis/public.php?page=single_report&pop=1&reportid=10546
Switzerland sporadic CJD ; Swiss rise in CJD raises concerns over possible BSE link [LONDON]
THE LANCET
Plaque attack: Swiss patients have spongiform patterns in the brain typical of sporadic CJD. The number of people dying from Creutzfeldt-Jakob disease (CJD) has risen sharply in Switzerland -- sparking fears of a possible link with bovine spongiform encephalopathy (BSE). BSE is thought to be the cause of a distinctive form of the brain-wasting disease known as variant CJD. The Swiss cases, in contrast, are standard 'sporadic' CJD. Each year between 1997 and 2000, no more than 11 Swiss people developed CJD. But 19 cases were reported in 2001, and seven were recorded in the first quarter of this year. This is some four times higher than the incidence elsewhere, reports a team led by Adriano Aguzzi of the University Hospital Zurich (M. Glatzel et al. Lancet 360, 139-141; 2002). The increase could be a mere statistical blip, or it may be due to increased awareness of the disease leading to more diagnoses. More disturbing is the possibility that the cases are linked to the consumption of BSE-infected meat products -- which would mean that the BSE agent can cause two distinct forms of CJD. Possible links between the Swiss CJD cases and BSE will now be explored by strain-typing experiments in which the disease is transmitted to mice. These tests will take at least a year to complete. "It's the best way to establish or exclude any suspected link," says Moira Bruce of the UK Institute for Animal Health's Neuropathogenesis Unit in Edinburgh.
======================================
Experiences in England and Switzerland -- two countries that discovered mad cow disease in their cattle -- have heightened concerns about the possibility some cases of sporadic CJD are due to consuming mad-cow-tainted beef. Both countries have reported increases in sporadic CJD since mad cow was first detected in British herds in 1986. Switzerland discovered last year its CJD rate was twice that of any other country in the world. Switzerland had been seeing about eight to 11 cases per year from 1997 to 2000. Then the incidence more than doubled, to 19 cases in 2001 and 18 cases in 2002.
http://www.upi.com/view.cfm?StoryID=20030721-102924-4786r
Mouse model sheds new light on human prion disease
snip...
Professor John Collinge said We are not saying that all or even most cases of sporadic CJD are as a result of BSE exposure, but some more recent cases may be the incidence of sporadic CJD has shown an upward trend in the UK over the last decade. While most of this apparent increase may be because doctors are now more aware of CJD and better at diagnosing it, serious consideration should be given to a proportion of this rise being BSE-related. Switzerland, which has had a substantial BSE epidemic, has noted a sharp recent increase in sporadic CJD.
snip...
http://www.mrc.ac.uk/txt/index/public-interest/public-news-4/public-news_archive/public-news-archive_nov_dec_02/public-bse_and_sporadic_cjd.htm
Monday, May 19, 2008
SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS
http://bseinquiry.blogspot.com/
Thursday, August 12, 2010
Seven main threats for the future linked to prions First threat The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
Sunday, May 01, 2011
STUDY OF ATYPICAL BSE 2010 Annual Report May 2011
http://bse-atypical.blogspot.com/2011/05/study-of-atypical-bse-2010-annual.html
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5–May 2011
http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html
"THE OIE has now shown they are nothing more than a National Trading Brokerage for all strains of animal TSE. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization."
NOW, some history on the failed OIE BSE/TSE policy, and why the OIE allowed BSE and other TSE to spread around the globe $$$
while i applaud Switerland for reporting this case of BSE, i must say again that the OIE is a failed organization. to have a reporting system set up for TSE that only reports a case of TSE when a country sees fit to report a case, and only relies on the GOOD WORD of a country, is a failed system. apparently, the USA and Canada and Mexico i.e. North America, is exempt from the OIE reporting base of TSE on the OIE news feed. ...tss
Scrapie
The two Commissions discussed the issue of ‘atypical’ scrapie in terms of notification requirements and the issue of the host genetic resistance. In response to questions of Members, the Code Commission clarified that ‘classical’ scrapie is reportable to the OIE but that ‘atypical’ scrapie is not reportable (in accordance with the recommendations made by the ad hoc Group on Atypical Scrapie and Atypical BSE, which met in November 2007). However, the sharing of scientific information on ‘atypical’ scrapie is encouraged. At this time, the Code Commission considered that more scientific information would be needed to fully address the issues associated with host genotype.
EU comment
4
OIE Terrestrial Animal Health Standards Commission / September 2010
The EU takes note of the fact that atypical scrapie is not an OIE listed disease. Nevertheless, it will remain notifiable in the EU. Moreover it must be stressed that any emergence of this disease should be notified to the OIE by Members and that scientific data should continue to be gathered.
snip...
Zoonotic Potential
Has transmission to humans been proven? (with the exception of artificial circumstances) AND Is human infection associated with severe consequences? (death or prolonged illness)
http://ec.europa.eu/food/international/organisations/docs/EU_comments_OIE_terrestrial_animal_health_code_en.pdf
What is Nor98-Like (Nonclassical) Scrapie?
Nor98-like scrapie is a prion disease. The prion diseases include classical scrapie in sheep and goats, Bovine Spongiform Encephalopathy (BSE) primarily of cattle, chronic wasting disease (CWD) of deer and elk, and in humans Creutzfeldt-Jakob Disease (CJD) and variant Creutzfeldt-Jakob Disease (vCJD). What each of these diseases has in common is that they cause a progressive and ultimately fatal degeneration of the nervous system. While the underlying cause(s) are still debated, the theory most widely accepted in the scientific community is that the agent is a prion – an abnormal form of a normally occurring cellular protein.
Unlike BSE, classical scrapie and Nor98-like scrapie have not been shown to be a threat to human health. Classical scrapie has been known to exist for over 250 years, and cases have occurred in the United States since 1947. It is likely that Nor98-like scrapie has also existed for a long time; however, it was first identified in Norway in 1998, hence the name Nor98. This type of scrapie is referred to as “atypical scrapie”, “Nor98 scrapie”, “Nor98-like scrapie”, or “nonclassical scrapie” in the literature.
Since 1998, almost every country in Europe, as well as the Falkland Islands, New Zealand, Canada, and the United States have found similar cases. The first cases in the United States were identified in 2007.
Nor98-like (nonclassical) scrapie and classical scrapie are separate diseases with distinct features.
Transmission
Classical scrapie is an infectious disease that is transmitted to other sheep and goats under natural conditions.
Nor98-like scrapie is either not transmitted or is poorly transmitted, under natural conditions. Many scientists believe that Nor98-like scrapie is not an infectious disease under natural conditions and that it is instead caused by a random conversion of the normal prion protein into the abnormal form (often referred to as “sporadic”).
Distribution
Nor98-like scrapie has been found in all countries where extensive surveillance has been conducted using sensitive test methods; whereas, classical scrapie has not been reported in some of these countries.
Nor98-like scrapie cases are widely distributed and proportionate with sheep/goat populations; whereas, classical scrapie cases often occur in clusters.
Number of affected sheep or goats in a flock or herd
Classical scrapie usually infects more than one animal in an infected flock. In the US, approximately 18 percent of the mature, genetically susceptible sheep in an infected flock are infected.
Nor98-like scrapie is rarely found in more than one animal in a flock or herd. When an additional case is found, it is usually in flocks with more than 500 sheep.
Average age of onset of clinical signs in animals
With classical scrapie, clinical signs typically first appear and result in death in animals that are between 3-5 years of age.
In Nor98-like scrapie, clinical signs are rarely documented and the animals are typically diagnosed when they are sampled at slaughter, usually at greater than 5 years of age.
Variations in protection against disease conferred by genotype
Sheep with genotypes that are resistant to classical scrapie are susceptible to Nor98-like scrapie.
Clinical signs associated with disease
Unlike classical scrapie, clinical signs are rarely reported in Nor98-like scrapie cases.
In the few Nor98-like scrapie cases where clinical signs were reported, the signs observed were indistinguishable from those described for classical scrapie. These include incoordination, gait abnormalities, collapse while running, tremors, loss of condition, leg biting, nibble response and/or behavioral changes.
One potential clinical difference is that intense rubbing is a frequently occurring clinical sign in classical scrapie cases; whereas, it has not been reported in Nor98-like scrapie cases.
Laboratory findings readily distinguish Nor98-like scrapie from classical scrapie.
In 2009, the World Animal Health Organization (OIE) recognized Nor98-like scrapie as a separate disease from classical scrapie because of differences in laboratory findings, transmissibility, and distribution. This determination means that Nor98-like scrapie is not a reportable disease to OIE, and should be of no trade concern.
How has APHIS’ policy changed regarding Nor98-like scrapie?
APHIS will no longer require the depopulation or movement restriction of Nor98-like scrapie exposed sheep and goats. APHIS will propose changes to the Code of Federal Regulations (CFR) in 2010 to allow the APHIS Administrator to eliminate or reduce post exposure requirements for certain scrapie types (or certain/specific types of scrapie)-- such as Nor98-like scrapie -- that are determined to pose minimal risk of lateral transmission under natural conditions.
In the meantime, APHIS is conducting a national scrapie control pilot project for Nor98-like scrapie. The project is for flocks and herds in which animals positive to Nor98-like scrapie were born, lambed, or kidded.
What will the pilot project do for producers?
The pilot project will allow producers that have sheep and goats exposed to Nor98-like (nonclassical) scrapie to retain, sell, exhibit or move them for any purpose.
What will happen if Nor98-like scrapie case is found on or traced back to an owner’s flock or herd?
The owner will be contacted by a Federal or State veterinarian who will schedule a visit to the farm with the owner. The activities listed below will be performed.
Confirm the identification of the positive animal.
Provide the owner with information about scrapie and its control.
Determine if the positive animal was born in or gave birth in the flock/herd. If so, the veterinarian will:
Work with state animal health authority to ensure animals are not moved from the premises until they have been officially identified;
Develop a Nor98-like scrapie flock plan and a 5 year monitoring plan with the producer;
If not already officially identified, apply official eartags to sheep and goats exposed to Nor98-like scrapie; and
Inventory all sheep and goats, and any sheep or goat embryos.
The officially identified sheep and goats will then be classified and handled as low-risk exposed animals, allowing the owner to move the animals from the premises for any purpose including sale.
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/nor98-like_information.pdf
SCRAPIE The United States is unable to support the proposed new draft Code Chapter on Scrapie. The draft chapter, as written, departs significantly from the existing chapter, is confusing and is difficult to understand. This version of the scrapie chapter uses much of the same wording as the BSE chapter and is written as if the predominance of evidence revealed that scrapie was a food-borne disease similar to BSE in cattle which is inappropriate. Moreover, several of the new changes are not supported by current scientific evidence. As a result, detailed comments on individual articles would not meaningful at this time. The United States is not supportive of the proposed draft chapter for the following reasons: 1. Inclusion of “atypical” scrapie: The scientific evidence indicates that “atypical” scrapie, also referred to as Nor-98, Nor-98-like, or non-classical scrapie, is not the same disease as classical scrapie. Further, “atypical” scrapie does not meet the criteria for listing diseases of trade concern by the OIE, as described in Chapter 2.1.1 of the Code. The United States recommends that the scope of this chapter be limited to classical scrapie in sheep and goats. Further, the United States recommends that OIE clearly adopt the position that “atypical” scrapie represents a distinct disease entity from classical scrapie and that it not be a listed disease. • There is no evidence that “atypical” scrapie is a contagious disease. If it is contagious, available evidence suggests that it has a much lower transmission efficiency. (Hopp, et al, 2006; Green, et al, 2007; Benestad, et al 2008; McIntyre, et al, 2008) • The disease appears to be ubiquitous in that it has been found wherever sufficient surveillance has been conducted. (Buschmann et al, 2004; De Bosschere et al, 2004; Orge, et al, 2004; Everest et al, 2006; Arsac, 2007; Benestad, et al 2008; Fediaevsky, et al, 2008) • The disease does not appear to be economically significant in that the prevalence of clinical disease is low and it typically occurs in older animals. (Luhken, et al., 2007; Benestad, et al 2008). • The disease is as likely as not to be the result of a spontaneous conversion of normal prion protein. (Benestad, et al 2008, De Bosschere et al 2007) • Removal of exposed sheep is unlikely to reduce the prevalence of “atypical” scrapie infection and removing only those exposed sheep that are phenylalanine (F) at codon 141 is scientifically unsound since the disease is known to affect sheep of most other genotypes. Further, sheep with AHQ alleles have a similar risk of infection with “atypical” strains as sheep with F at codon 141. (Luhken, et al., 2007). • If “atypical” scrapie is included as a listed disease, the surveillance and diagnostic requirements which are needed to identify these cases should be described in detail in both this Chapter and the Manual of Diagnostic Tests and Vaccines for Terrestrial 2 Animals. Data from Europe illustrates that using the proper test(s) is essential for the identification of atypical scrapie (Fediaevsky et al., 2008).
SNIP...
6. Overemphasis on importation and use of bovine meat and bone meal as a route of scrapie transmission: Given that the draft Chapter is not intended to address risk mitigation for BSE in small ruminants, we believe there is an over-emphasis on this potential route of transmission in the current draft. The United States recommends that the requirements in this chapter be limited to the inclusion of products from sheep and goats (instead of from all ruminants) in feed or feed ingredients intended for consumption by animals • The use of products from sheep and goats as feed or feed ingredients for ruminant or non-ruminant animals represent one possible route of transmission (Philippe, et al, 2005) and a source of environmental contamination with the classical scrapie agent. However, this is not the primary route of transmission for the scrapie agent. • The need for the exclusion of cattle-derived protein or other animal protein to mitigate BSE risk should be based on a country’s BSE risk status and should be addressed in Chapter 2.3.13 of the Code.
SNIP...
14. Failure to provide scientific justification for the list of permitted commodities in Item 1 of Article 2.4.8.1. . We recommend that the list be re-evaluated and those items that have not been substantiated as presenting no risk be excluded or those with some risk but where the intended use mitigates the risk the use be specified. • There is no known human health risk associated with scrapie. As such, if meat and meat products for human consumption are included in this list, sheep and/or goat milk intended for human consumption should also be added to the list of permitted commodities in Item 1 of Article 2.4.8.1. • In the vast majority of sheep infected with classical scrapie, actual infectivity or PrPres has been identified in most tissues including the lymphoreticular system (tonsils, spleen, lymph nodes), the gastrointestinal tract, brain, and spinal cord (Hadlow et. al. 1979; Hadlow et al., 1980; van Kuelen et al., 1996; van Kuelen et al., 1999, Andreoletti et al., 2000; Heggebø et al., 2002; Caplazi et al., 2004). Infectivity and/or PrPres has also been identified in the placenta (see Hourrigan et al., 1979; Onodera et al., 1993; Pattison et al., 1972; Pattison et al., 1974; Race et al., 1998), blood (Hunter et al., 2002; Houston et al. 2008); peripheral nerves (Groschup et al., 1996), muscle (Pattison and Millson, 1962; Andreoletti et al., 2004; Casalone et al., 2005), salivary gland (Hadlow et al., 1980; Vascellari et al., 2007), kidney (Siso et al., 2006), and skin ( Thomzig et al., 2007). In addition, recent work has shown milk and/or colostrum from scrapie infected ewes transmitted the disease to 17 of 18 lambs (Konold et al., 2008). • The data on the risk of low protein tallow made from scrapie infected tissues particularly for use in milk replacer is limited and some epidemiologic studies suggest an association of milk replacer use with scrapie risk. Taylor et al., 1997 examined the inactivation capacity of different rendering system in regards to scrapie. The presence of infectivity was determined by bioassay into mice. From the onset of this study, it was assumed that tallow was not the vehicle for the transmission of TSE. Hence only 2 tallow samples were examined.
http://www.aphis.usda.gov/import_export/animals/oie/downloads/tahc_mar-sep08/tahc-scrapie-77-mar08_cmt.pdf
Increased Atypical Scrapie Detections
Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.
http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf
Saturday, December 18, 2010
OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5–May 2011
http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 a nd how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
i wonder if CFIA Canada uses the same OBEX ONLY diagnostic criteria as the USDA ?
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Sunday, March 27, 2011
SCRAPIE USA UPDATE FEBRUARY 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/scrapie-usa-update-february-2011.html
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html
Wednesday, March 9, 2011
27 U.S. Senators want to force feed Japan Highly Potential North America Mad Cow Beef TSE PRION CJD
March 8, 2011
President Barack Obama The White House
1600 Pennsylvania Avenue, W Washington, DC 20500
Dear President Obama:
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/27-us-senators-want-to-force-feed-japan.html
TSS
Information received on 03/05/2011 from Mr Hans Wyss, Chief Veterinary Officer, Schwarzenburgstrasse 161, Swiss Federal Veterinary Office, LIEBEFELD BERNE, Switzerland
Summary
Report type Immediate notification (Final report) Start date 08/04/2011 Date of first confirmation of the event 18/04/2011 Report date 03/05/2011 Date submitted to OIE 03/05/2011 Date event resolved 03/05/2011 Reason for notification Reoccurrence of a listed disease Date of previous occurrence 10/2006 Manifestation of disease Sub-clinical infection Causal agent Prion Nature of diagnosis Laboratory (advanced) This event pertains to the whole country
New outbreaks Summary of outbreaks Total outbreaks: 1 Location(s) SANKT GALLEN (Sankt Gallen)
Total animals affected Species Susceptible Cases Deaths Destroyed Slaughtered Cattle 32 1 0 1 0
Outbreak statistics Species Apparent morbidity rate Apparent mortality rate Apparent case fatality rate Proportion susceptible animals lost* Cattle 3.13% 0.00% 0.00% 3.13%
* Removed from the susceptible population through death, destruction and/or slaughter
Epidemiology Source of the outbreak(s) or origin of infection Unknown or inconclusive
Control measures Measures applied No vaccination No treatment of affected animals
Measures to be applied No other measures
Diagnostic test results Laboratory name and type National Reference Laboratory (National laboratory) Tests and results Species Test Test date Result Cattle western blotting 18/04/2011 Positive
Future Reporting The event is resolved. No more reports will be submitted.
http://web.oie.int/wahis/public.php?page=single_report&pop=1&reportid=10546
Switzerland sporadic CJD ; Swiss rise in CJD raises concerns over possible BSE link [LONDON]
THE LANCET
Plaque attack: Swiss patients have spongiform patterns in the brain typical of sporadic CJD. The number of people dying from Creutzfeldt-Jakob disease (CJD) has risen sharply in Switzerland -- sparking fears of a possible link with bovine spongiform encephalopathy (BSE). BSE is thought to be the cause of a distinctive form of the brain-wasting disease known as variant CJD. The Swiss cases, in contrast, are standard 'sporadic' CJD. Each year between 1997 and 2000, no more than 11 Swiss people developed CJD. But 19 cases were reported in 2001, and seven were recorded in the first quarter of this year. This is some four times higher than the incidence elsewhere, reports a team led by Adriano Aguzzi of the University Hospital Zurich (M. Glatzel et al. Lancet 360, 139-141; 2002). The increase could be a mere statistical blip, or it may be due to increased awareness of the disease leading to more diagnoses. More disturbing is the possibility that the cases are linked to the consumption of BSE-infected meat products -- which would mean that the BSE agent can cause two distinct forms of CJD. Possible links between the Swiss CJD cases and BSE will now be explored by strain-typing experiments in which the disease is transmitted to mice. These tests will take at least a year to complete. "It's the best way to establish or exclude any suspected link," says Moira Bruce of the UK Institute for Animal Health's Neuropathogenesis Unit in Edinburgh.
======================================
Experiences in England and Switzerland -- two countries that discovered mad cow disease in their cattle -- have heightened concerns about the possibility some cases of sporadic CJD are due to consuming mad-cow-tainted beef. Both countries have reported increases in sporadic CJD since mad cow was first detected in British herds in 1986. Switzerland discovered last year its CJD rate was twice that of any other country in the world. Switzerland had been seeing about eight to 11 cases per year from 1997 to 2000. Then the incidence more than doubled, to 19 cases in 2001 and 18 cases in 2002.
http://www.upi.com/view.cfm?StoryID=20030721-102924-4786r
Mouse model sheds new light on human prion disease
snip...
Professor John Collinge said We are not saying that all or even most cases of sporadic CJD are as a result of BSE exposure, but some more recent cases may be the incidence of sporadic CJD has shown an upward trend in the UK over the last decade. While most of this apparent increase may be because doctors are now more aware of CJD and better at diagnosing it, serious consideration should be given to a proportion of this rise being BSE-related. Switzerland, which has had a substantial BSE epidemic, has noted a sharp recent increase in sporadic CJD.
snip...
http://www.mrc.ac.uk/txt/index/public-interest/public-news-4/public-news_archive/public-news-archive_nov_dec_02/public-bse_and_sporadic_cjd.htm
Monday, May 19, 2008
SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS
http://bseinquiry.blogspot.com/
Thursday, August 12, 2010
Seven main threats for the future linked to prions First threat The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
Sunday, May 01, 2011
STUDY OF ATYPICAL BSE 2010 Annual Report May 2011
http://bse-atypical.blogspot.com/2011/05/study-of-atypical-bse-2010-annual.html
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5–May 2011
http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html
"THE OIE has now shown they are nothing more than a National Trading Brokerage for all strains of animal TSE. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization."
NOW, some history on the failed OIE BSE/TSE policy, and why the OIE allowed BSE and other TSE to spread around the globe $$$
while i applaud Switerland for reporting this case of BSE, i must say again that the OIE is a failed organization. to have a reporting system set up for TSE that only reports a case of TSE when a country sees fit to report a case, and only relies on the GOOD WORD of a country, is a failed system. apparently, the USA and Canada and Mexico i.e. North America, is exempt from the OIE reporting base of TSE on the OIE news feed. ...tss
Scrapie
The two Commissions discussed the issue of ‘atypical’ scrapie in terms of notification requirements and the issue of the host genetic resistance. In response to questions of Members, the Code Commission clarified that ‘classical’ scrapie is reportable to the OIE but that ‘atypical’ scrapie is not reportable (in accordance with the recommendations made by the ad hoc Group on Atypical Scrapie and Atypical BSE, which met in November 2007). However, the sharing of scientific information on ‘atypical’ scrapie is encouraged. At this time, the Code Commission considered that more scientific information would be needed to fully address the issues associated with host genotype.
EU comment
4
OIE Terrestrial Animal Health Standards Commission / September 2010
The EU takes note of the fact that atypical scrapie is not an OIE listed disease. Nevertheless, it will remain notifiable in the EU. Moreover it must be stressed that any emergence of this disease should be notified to the OIE by Members and that scientific data should continue to be gathered.
snip...
Zoonotic Potential
Has transmission to humans been proven? (with the exception of artificial circumstances) AND Is human infection associated with severe consequences? (death or prolonged illness)
http://ec.europa.eu/food/international/organisations/docs/EU_comments_OIE_terrestrial_animal_health_code_en.pdf
What is Nor98-Like (Nonclassical) Scrapie?
Nor98-like scrapie is a prion disease. The prion diseases include classical scrapie in sheep and goats, Bovine Spongiform Encephalopathy (BSE) primarily of cattle, chronic wasting disease (CWD) of deer and elk, and in humans Creutzfeldt-Jakob Disease (CJD) and variant Creutzfeldt-Jakob Disease (vCJD). What each of these diseases has in common is that they cause a progressive and ultimately fatal degeneration of the nervous system. While the underlying cause(s) are still debated, the theory most widely accepted in the scientific community is that the agent is a prion – an abnormal form of a normally occurring cellular protein.
Unlike BSE, classical scrapie and Nor98-like scrapie have not been shown to be a threat to human health. Classical scrapie has been known to exist for over 250 years, and cases have occurred in the United States since 1947. It is likely that Nor98-like scrapie has also existed for a long time; however, it was first identified in Norway in 1998, hence the name Nor98. This type of scrapie is referred to as “atypical scrapie”, “Nor98 scrapie”, “Nor98-like scrapie”, or “nonclassical scrapie” in the literature.
Since 1998, almost every country in Europe, as well as the Falkland Islands, New Zealand, Canada, and the United States have found similar cases. The first cases in the United States were identified in 2007.
Nor98-like (nonclassical) scrapie and classical scrapie are separate diseases with distinct features.
Transmission
Classical scrapie is an infectious disease that is transmitted to other sheep and goats under natural conditions.
Nor98-like scrapie is either not transmitted or is poorly transmitted, under natural conditions. Many scientists believe that Nor98-like scrapie is not an infectious disease under natural conditions and that it is instead caused by a random conversion of the normal prion protein into the abnormal form (often referred to as “sporadic”).
Distribution
Nor98-like scrapie has been found in all countries where extensive surveillance has been conducted using sensitive test methods; whereas, classical scrapie has not been reported in some of these countries.
Nor98-like scrapie cases are widely distributed and proportionate with sheep/goat populations; whereas, classical scrapie cases often occur in clusters.
Number of affected sheep or goats in a flock or herd
Classical scrapie usually infects more than one animal in an infected flock. In the US, approximately 18 percent of the mature, genetically susceptible sheep in an infected flock are infected.
Nor98-like scrapie is rarely found in more than one animal in a flock or herd. When an additional case is found, it is usually in flocks with more than 500 sheep.
Average age of onset of clinical signs in animals
With classical scrapie, clinical signs typically first appear and result in death in animals that are between 3-5 years of age.
In Nor98-like scrapie, clinical signs are rarely documented and the animals are typically diagnosed when they are sampled at slaughter, usually at greater than 5 years of age.
Variations in protection against disease conferred by genotype
Sheep with genotypes that are resistant to classical scrapie are susceptible to Nor98-like scrapie.
Clinical signs associated with disease
Unlike classical scrapie, clinical signs are rarely reported in Nor98-like scrapie cases.
In the few Nor98-like scrapie cases where clinical signs were reported, the signs observed were indistinguishable from those described for classical scrapie. These include incoordination, gait abnormalities, collapse while running, tremors, loss of condition, leg biting, nibble response and/or behavioral changes.
One potential clinical difference is that intense rubbing is a frequently occurring clinical sign in classical scrapie cases; whereas, it has not been reported in Nor98-like scrapie cases.
Laboratory findings readily distinguish Nor98-like scrapie from classical scrapie.
In 2009, the World Animal Health Organization (OIE) recognized Nor98-like scrapie as a separate disease from classical scrapie because of differences in laboratory findings, transmissibility, and distribution. This determination means that Nor98-like scrapie is not a reportable disease to OIE, and should be of no trade concern.
How has APHIS’ policy changed regarding Nor98-like scrapie?
APHIS will no longer require the depopulation or movement restriction of Nor98-like scrapie exposed sheep and goats. APHIS will propose changes to the Code of Federal Regulations (CFR) in 2010 to allow the APHIS Administrator to eliminate or reduce post exposure requirements for certain scrapie types (or certain/specific types of scrapie)-- such as Nor98-like scrapie -- that are determined to pose minimal risk of lateral transmission under natural conditions.
In the meantime, APHIS is conducting a national scrapie control pilot project for Nor98-like scrapie. The project is for flocks and herds in which animals positive to Nor98-like scrapie were born, lambed, or kidded.
What will the pilot project do for producers?
The pilot project will allow producers that have sheep and goats exposed to Nor98-like (nonclassical) scrapie to retain, sell, exhibit or move them for any purpose.
What will happen if Nor98-like scrapie case is found on or traced back to an owner’s flock or herd?
The owner will be contacted by a Federal or State veterinarian who will schedule a visit to the farm with the owner. The activities listed below will be performed.
Confirm the identification of the positive animal.
Provide the owner with information about scrapie and its control.
Determine if the positive animal was born in or gave birth in the flock/herd. If so, the veterinarian will:
Work with state animal health authority to ensure animals are not moved from the premises until they have been officially identified;
Develop a Nor98-like scrapie flock plan and a 5 year monitoring plan with the producer;
If not already officially identified, apply official eartags to sheep and goats exposed to Nor98-like scrapie; and
Inventory all sheep and goats, and any sheep or goat embryos.
The officially identified sheep and goats will then be classified and handled as low-risk exposed animals, allowing the owner to move the animals from the premises for any purpose including sale.
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/nor98-like_information.pdf
SCRAPIE The United States is unable to support the proposed new draft Code Chapter on Scrapie. The draft chapter, as written, departs significantly from the existing chapter, is confusing and is difficult to understand. This version of the scrapie chapter uses much of the same wording as the BSE chapter and is written as if the predominance of evidence revealed that scrapie was a food-borne disease similar to BSE in cattle which is inappropriate. Moreover, several of the new changes are not supported by current scientific evidence. As a result, detailed comments on individual articles would not meaningful at this time. The United States is not supportive of the proposed draft chapter for the following reasons: 1. Inclusion of “atypical” scrapie: The scientific evidence indicates that “atypical” scrapie, also referred to as Nor-98, Nor-98-like, or non-classical scrapie, is not the same disease as classical scrapie. Further, “atypical” scrapie does not meet the criteria for listing diseases of trade concern by the OIE, as described in Chapter 2.1.1 of the Code. The United States recommends that the scope of this chapter be limited to classical scrapie in sheep and goats. Further, the United States recommends that OIE clearly adopt the position that “atypical” scrapie represents a distinct disease entity from classical scrapie and that it not be a listed disease. • There is no evidence that “atypical” scrapie is a contagious disease. If it is contagious, available evidence suggests that it has a much lower transmission efficiency. (Hopp, et al, 2006; Green, et al, 2007; Benestad, et al 2008; McIntyre, et al, 2008) • The disease appears to be ubiquitous in that it has been found wherever sufficient surveillance has been conducted. (Buschmann et al, 2004; De Bosschere et al, 2004; Orge, et al, 2004; Everest et al, 2006; Arsac, 2007; Benestad, et al 2008; Fediaevsky, et al, 2008) • The disease does not appear to be economically significant in that the prevalence of clinical disease is low and it typically occurs in older animals. (Luhken, et al., 2007; Benestad, et al 2008). • The disease is as likely as not to be the result of a spontaneous conversion of normal prion protein. (Benestad, et al 2008, De Bosschere et al 2007) • Removal of exposed sheep is unlikely to reduce the prevalence of “atypical” scrapie infection and removing only those exposed sheep that are phenylalanine (F) at codon 141 is scientifically unsound since the disease is known to affect sheep of most other genotypes. Further, sheep with AHQ alleles have a similar risk of infection with “atypical” strains as sheep with F at codon 141. (Luhken, et al., 2007). • If “atypical” scrapie is included as a listed disease, the surveillance and diagnostic requirements which are needed to identify these cases should be described in detail in both this Chapter and the Manual of Diagnostic Tests and Vaccines for Terrestrial 2 Animals. Data from Europe illustrates that using the proper test(s) is essential for the identification of atypical scrapie (Fediaevsky et al., 2008).
SNIP...
6. Overemphasis on importation and use of bovine meat and bone meal as a route of scrapie transmission: Given that the draft Chapter is not intended to address risk mitigation for BSE in small ruminants, we believe there is an over-emphasis on this potential route of transmission in the current draft. The United States recommends that the requirements in this chapter be limited to the inclusion of products from sheep and goats (instead of from all ruminants) in feed or feed ingredients intended for consumption by animals • The use of products from sheep and goats as feed or feed ingredients for ruminant or non-ruminant animals represent one possible route of transmission (Philippe, et al, 2005) and a source of environmental contamination with the classical scrapie agent. However, this is not the primary route of transmission for the scrapie agent. • The need for the exclusion of cattle-derived protein or other animal protein to mitigate BSE risk should be based on a country’s BSE risk status and should be addressed in Chapter 2.3.13 of the Code.
SNIP...
14. Failure to provide scientific justification for the list of permitted commodities in Item 1 of Article 2.4.8.1. . We recommend that the list be re-evaluated and those items that have not been substantiated as presenting no risk be excluded or those with some risk but where the intended use mitigates the risk the use be specified. • There is no known human health risk associated with scrapie. As such, if meat and meat products for human consumption are included in this list, sheep and/or goat milk intended for human consumption should also be added to the list of permitted commodities in Item 1 of Article 2.4.8.1. • In the vast majority of sheep infected with classical scrapie, actual infectivity or PrPres has been identified in most tissues including the lymphoreticular system (tonsils, spleen, lymph nodes), the gastrointestinal tract, brain, and spinal cord (Hadlow et. al. 1979; Hadlow et al., 1980; van Kuelen et al., 1996; van Kuelen et al., 1999, Andreoletti et al., 2000; Heggebø et al., 2002; Caplazi et al., 2004). Infectivity and/or PrPres has also been identified in the placenta (see Hourrigan et al., 1979; Onodera et al., 1993; Pattison et al., 1972; Pattison et al., 1974; Race et al., 1998), blood (Hunter et al., 2002; Houston et al. 2008); peripheral nerves (Groschup et al., 1996), muscle (Pattison and Millson, 1962; Andreoletti et al., 2004; Casalone et al., 2005), salivary gland (Hadlow et al., 1980; Vascellari et al., 2007), kidney (Siso et al., 2006), and skin ( Thomzig et al., 2007). In addition, recent work has shown milk and/or colostrum from scrapie infected ewes transmitted the disease to 17 of 18 lambs (Konold et al., 2008). • The data on the risk of low protein tallow made from scrapie infected tissues particularly for use in milk replacer is limited and some epidemiologic studies suggest an association of milk replacer use with scrapie risk. Taylor et al., 1997 examined the inactivation capacity of different rendering system in regards to scrapie. The presence of infectivity was determined by bioassay into mice. From the onset of this study, it was assumed that tallow was not the vehicle for the transmission of TSE. Hence only 2 tallow samples were examined.
http://www.aphis.usda.gov/import_export/animals/oie/downloads/tahc_mar-sep08/tahc-scrapie-77-mar08_cmt.pdf
Increased Atypical Scrapie Detections
Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.
http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf
Saturday, December 18, 2010
OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5–May 2011
http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 a nd how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
i wonder if CFIA Canada uses the same OBEX ONLY diagnostic criteria as the USDA ?
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Sunday, March 27, 2011
SCRAPIE USA UPDATE FEBRUARY 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/scrapie-usa-update-february-2011.html
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html
Wednesday, March 9, 2011
27 U.S. Senators want to force feed Japan Highly Potential North America Mad Cow Beef TSE PRION CJD
March 8, 2011
President Barack Obama The White House
1600 Pennsylvania Avenue, W Washington, DC 20500
Dear President Obama:
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/27-us-senators-want-to-force-feed-japan.html
TSS
Tuesday, April 19, 2011
Bull aged over 48 months enters food supply without being tested for BSE Monday 18 April 2011
Bull aged over 48 months enters food supply without being tested for BSE Monday 18 April 2011
The Agency has been notified that meat has entered the food supply from a bull aged over 48 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at over 48 months of age.
It is very unlikely that the bull was infected with BSE and as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is that part of the animal most likely to contain BSE infectivity.
The bull, aged 88 months, was slaughtered at S J Norman & Sons’ abattoir in Bridport, Dorset on 3 February 2011. The error was discovered on 5 April in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested bull should not have entered the food supply. However, by the time the failure was discovered, the carcass had left the premises.
Subsequent checks indicate that all the meat from the carcass is no longer traceable and is likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2011/apr/otmbull
Wednesday, April 13, 2011
Joint consultation by the FSA, Defra and Welsh Assembly Government on proposed changes to BSE testing of cattle slaughtered for human consumption
http://madcowtesting.blogspot.com/2011/04/joint-consultation-by-fsa-defra-and.html
The drawbacks of allowing testing relate to the potential to negatively impact consumer attitudes toward untested beef, lack of support from regulators, and the prospect that testing, especially under a future ante mortem test, might identify positive cases and adversely impact Canada‘s BSE risk status.
SEE FULL TEXT ;
http://prioninstitute.ca/forms/BSE%20Testing%20Final-revised%20%20Plus%20App%20C%20AM%20Mar%2029.pdf
Saturday, January 29, 2011
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Jpn. J. Infect. Dis., 64 (1), 81-84, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
Monday, May 11, 2009
Rare BSE mutation raises concerns over risks to public health
http://bse-atypical.blogspot.com/2009/05/rare-bse-mutation-raises-concerns-over.html
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
i wonder if CFIA Canada uses the same OBEX ONLY diagnostic criteria as the USDA ? they could not have found a mad cow if they were standing beside the stumbling and staggering bovine $$$, using the diagnostic criteria they were using, AND TOLD SO, but they kept on doing it anyway. ...
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Wednesday, November 17, 2010
MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE
http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html
Friday, February 18, 2011
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS ''PLEADS GUILTY"
http://bse-atypical.blogspot.com/2011/02/united-states-of-america-vs-galen-j.html
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE) Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1 include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
http://www.usda.gov/oig/webdocs/sarc070619.pdf
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
In an article today for United Press International, science reporter Steve Mitchell writes:
Analysis: What that mad cow means
By STEVE MITCHELL UPI Senior Medical Correspondent
WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.
Despite this, Brown said the U.S. prevalence of mad cow, formally known as bovine spongiform encephalopathy, or BSE, did not significantly threaten human or cattle health.
"Overall, my view is BSE is highly unlikely to pose any important risk either in cattle feed or human feed," he said.
However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers should be troubled by the USDA's secrecy and its apparent plan to dramatically cut back the number of mad cow tests it conducts.
"Consumers should be very concerned about how little we know about the USDA's surveillance program and the failure of the USDA to reveal really important details," Halloran told UPI. "Consumers have to be really concerned if they're going to cut back the program," she added.
Last year the USDA tested more than 300,000 animals for the disease, but it has proposed, even in light of a third case, scaling back the program to 40,000 tests annually.
"They seem to be, in terms of actions and policies, taking a lot more seriously the concerns of the cattle industry than the concerns of consumers," Halloran said. "It's really hard to know what it takes to get this administration to take action to protect the public."
The USDA has insisted that the safeguards of a ban on incorporating cow tissue into cattle feed (which is thought to spread the disease) and removal of the most infectious parts of cows, such as the brain and spinal cord, protect consumers. But the agency glosses over the fact that both of these systems have been revealed to be inadequately implemented.
The feed ban, which is enforced by the Food and Drug Administration, has been criticized by the Government Accountability Office in two reports, the most recent coming just last year. The GAO said the FDA's enforcement of the ban continues to have weaknesses that "undermine the nation's firewall against BSE."
USDA documents released last year showed more than 1,000 violations of the regulations requiring the removal of brains and spinal cords in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. In addition, a violation of similar regulations that apply to beef exported to Japan is the reason why Japan closed its borders to U.S. beef in January six weeks after reopening them.
Other experts also question the adequacy of the USDA's surveillance system. The USDA insists the prevalence of mad cow disease is low, but the agency has provided few details of its surveillance program, making it difficult for outside experts to know if the agency's monitoring plan is sufficient.
"It's impossible to judge the adequacy of the surveillance system without having a breakdown of the tested population by age and risk status," Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments, told UPI.
"Everybody would be happier and more confident and in a sense it might be able to go away a little bit for (the USDA) if they would just publish a breakdown on the tests," Mumford added.
UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.
Mumford said the prevalence of the disease in U.S. herds is probably quite low, but there have probably been other cases that have so far gone undetected. "They're only finding a very small fraction of that low prevalence," she said.
Mumford expressed surprise at the lack of concern about the deadly disease from American consumers. "I would expect the U.S. public to be more concerned," she said.
Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.
"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.
© Copyright 2006 United Press International, Inc. All Rights Reserved
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
http://www.upi.com/Science_News/2003/12/30/Mad-Cow-Linked-to-thousands-of-CJD-cases/UPI-47861072816318/
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS
http://madcowtesting.blogspot.com/2009/07/mad-cow-cover-up-usa-masked-as-sporadic.html
OR, what the Honorable Phyllis Fong of the OIG found ;
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program  Phase II and Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
Tuesday, January 1, 2008
BSE OIE USDA
STATEMENT BY DR. RON DEHAVEN REGARDING OIE RISK RECOMMENDATION
March 9, 2007
http://madcowtesting.blogspot.com/2008/01/bse-oie-usda.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
BANNED MAD COW FEED IN COMMERCE IN ALABAMA (where h-g-BSEalabama mad cow was documented)
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
Monday, January 17, 2011
MAD COW Update on Feed Enforcement Activities to Limit the Spread of BSE January 13, 2011
January 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/mad-cow-update-on-feed-enforcement.html
Friday, January 7, 2011
MEAT AND BONE MEAL AND MINERAL FEED ADDITIVES MAY INCREASE THE RISK OF ORAL PRION DISEASE TRANSMISSION
Journal of Toxicology and Environmental Health, Part A, 74:161–166, 2011 Copyright © Taylor & Francis Group, LLC ISSN: 1528-7394 print / 1087-2620 online DOI: 10.1080/15287394.2011.529066
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/meat-and-bone-meal-and-mineral-feed.html
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html
Wednesday, March 9, 2011
27 U.S. Senators want to force feed Japan Highly Potential North America Mad Cow Beef TSE PRION CJD
March 8, 2011
President Barack Obama The White House
1600 Pennsylvania Avenue, W Washington, DC 20500
Dear President Obama:
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/27-us-senators-want-to-force-feed-japan.html
Sunday, April 17, 2011
Transmission of Prion Strains in a Transgenic Mouse Model Overexpressing Human A53T Mutated [alpha]-Synuclein
Journal of Neuropathology & Experimental Neurology:
POST AUTHOR CORRECTIONS, 8 April 2011 doi: 10.1097/NEN.0b013e318217d95f
http://bse-atypical.blogspot.com/2011/04/transmission-of-prion-strains-in.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
another by-product of ignorance and the industries $$$
Tuesday, March 29, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY EXPOSURE SPREADING VIA HOSPITALS AND SURGICAL PROCEDURES AROUND THE GLOBE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/transmissible-spongiform-encephalopathy.html
Friday, April 15, 2011
PRION TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PROJECTS, RESEARCH FUNDING, BSE VOLUNTARY TESTING UPDATE IN NORTH AMERICA 2011
http://prionunitusaupdate2008.blogspot.com/2011/04/prion-transmissible-spongiform.html
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
TSS
The Agency has been notified that meat has entered the food supply from a bull aged over 48 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at over 48 months of age.
It is very unlikely that the bull was infected with BSE and as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is that part of the animal most likely to contain BSE infectivity.
The bull, aged 88 months, was slaughtered at S J Norman & Sons’ abattoir in Bridport, Dorset on 3 February 2011. The error was discovered on 5 April in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested bull should not have entered the food supply. However, by the time the failure was discovered, the carcass had left the premises.
Subsequent checks indicate that all the meat from the carcass is no longer traceable and is likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2011/apr/otmbull
Wednesday, April 13, 2011
Joint consultation by the FSA, Defra and Welsh Assembly Government on proposed changes to BSE testing of cattle slaughtered for human consumption
http://madcowtesting.blogspot.com/2011/04/joint-consultation-by-fsa-defra-and.html
The drawbacks of allowing testing relate to the potential to negatively impact consumer attitudes toward untested beef, lack of support from regulators, and the prospect that testing, especially under a future ante mortem test, might identify positive cases and adversely impact Canada‘s BSE risk status.
SEE FULL TEXT ;
http://prioninstitute.ca/forms/BSE%20Testing%20Final-revised%20%20Plus%20App%20C%20AM%20Mar%2029.pdf
Saturday, January 29, 2011
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Jpn. J. Infect. Dis., 64 (1), 81-84, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
Monday, May 11, 2009
Rare BSE mutation raises concerns over risks to public health
http://bse-atypical.blogspot.com/2009/05/rare-bse-mutation-raises-concerns-over.html
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
i wonder if CFIA Canada uses the same OBEX ONLY diagnostic criteria as the USDA ? they could not have found a mad cow if they were standing beside the stumbling and staggering bovine $$$, using the diagnostic criteria they were using, AND TOLD SO, but they kept on doing it anyway. ...
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Wednesday, November 17, 2010
MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE
http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html
Friday, February 18, 2011
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS ''PLEADS GUILTY"
http://bse-atypical.blogspot.com/2011/02/united-states-of-america-vs-galen-j.html
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE) Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1 include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
http://www.usda.gov/oig/webdocs/sarc070619.pdf
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
In an article today for United Press International, science reporter Steve Mitchell writes:
Analysis: What that mad cow means
By STEVE MITCHELL UPI Senior Medical Correspondent
WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.
Despite this, Brown said the U.S. prevalence of mad cow, formally known as bovine spongiform encephalopathy, or BSE, did not significantly threaten human or cattle health.
"Overall, my view is BSE is highly unlikely to pose any important risk either in cattle feed or human feed," he said.
However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers should be troubled by the USDA's secrecy and its apparent plan to dramatically cut back the number of mad cow tests it conducts.
"Consumers should be very concerned about how little we know about the USDA's surveillance program and the failure of the USDA to reveal really important details," Halloran told UPI. "Consumers have to be really concerned if they're going to cut back the program," she added.
Last year the USDA tested more than 300,000 animals for the disease, but it has proposed, even in light of a third case, scaling back the program to 40,000 tests annually.
"They seem to be, in terms of actions and policies, taking a lot more seriously the concerns of the cattle industry than the concerns of consumers," Halloran said. "It's really hard to know what it takes to get this administration to take action to protect the public."
The USDA has insisted that the safeguards of a ban on incorporating cow tissue into cattle feed (which is thought to spread the disease) and removal of the most infectious parts of cows, such as the brain and spinal cord, protect consumers. But the agency glosses over the fact that both of these systems have been revealed to be inadequately implemented.
The feed ban, which is enforced by the Food and Drug Administration, has been criticized by the Government Accountability Office in two reports, the most recent coming just last year. The GAO said the FDA's enforcement of the ban continues to have weaknesses that "undermine the nation's firewall against BSE."
USDA documents released last year showed more than 1,000 violations of the regulations requiring the removal of brains and spinal cords in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. In addition, a violation of similar regulations that apply to beef exported to Japan is the reason why Japan closed its borders to U.S. beef in January six weeks after reopening them.
Other experts also question the adequacy of the USDA's surveillance system. The USDA insists the prevalence of mad cow disease is low, but the agency has provided few details of its surveillance program, making it difficult for outside experts to know if the agency's monitoring plan is sufficient.
"It's impossible to judge the adequacy of the surveillance system without having a breakdown of the tested population by age and risk status," Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments, told UPI.
"Everybody would be happier and more confident and in a sense it might be able to go away a little bit for (the USDA) if they would just publish a breakdown on the tests," Mumford added.
UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.
Mumford said the prevalence of the disease in U.S. herds is probably quite low, but there have probably been other cases that have so far gone undetected. "They're only finding a very small fraction of that low prevalence," she said.
Mumford expressed surprise at the lack of concern about the deadly disease from American consumers. "I would expect the U.S. public to be more concerned," she said.
Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.
"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.
© Copyright 2006 United Press International, Inc. All Rights Reserved
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
http://www.upi.com/Science_News/2003/12/30/Mad-Cow-Linked-to-thousands-of-CJD-cases/UPI-47861072816318/
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS
http://madcowtesting.blogspot.com/2009/07/mad-cow-cover-up-usa-masked-as-sporadic.html
OR, what the Honorable Phyllis Fong of the OIG found ;
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program  Phase II and Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
Tuesday, January 1, 2008
BSE OIE USDA
STATEMENT BY DR. RON DEHAVEN REGARDING OIE RISK RECOMMENDATION
March 9, 2007
http://madcowtesting.blogspot.com/2008/01/bse-oie-usda.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
BANNED MAD COW FEED IN COMMERCE IN ALABAMA (where h-g-BSEalabama mad cow was documented)
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
Monday, January 17, 2011
MAD COW Update on Feed Enforcement Activities to Limit the Spread of BSE January 13, 2011
January 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/mad-cow-update-on-feed-enforcement.html
Friday, January 7, 2011
MEAT AND BONE MEAL AND MINERAL FEED ADDITIVES MAY INCREASE THE RISK OF ORAL PRION DISEASE TRANSMISSION
Journal of Toxicology and Environmental Health, Part A, 74:161–166, 2011 Copyright © Taylor & Francis Group, LLC ISSN: 1528-7394 print / 1087-2620 online DOI: 10.1080/15287394.2011.529066
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/meat-and-bone-meal-and-mineral-feed.html
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html
Wednesday, March 9, 2011
27 U.S. Senators want to force feed Japan Highly Potential North America Mad Cow Beef TSE PRION CJD
March 8, 2011
President Barack Obama The White House
1600 Pennsylvania Avenue, W Washington, DC 20500
Dear President Obama:
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/27-us-senators-want-to-force-feed-japan.html
Sunday, April 17, 2011
Transmission of Prion Strains in a Transgenic Mouse Model Overexpressing Human A53T Mutated [alpha]-Synuclein
Journal of Neuropathology & Experimental Neurology:
POST AUTHOR CORRECTIONS, 8 April 2011 doi: 10.1097/NEN.0b013e318217d95f
http://bse-atypical.blogspot.com/2011/04/transmission-of-prion-strains-in.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
another by-product of ignorance and the industries $$$
Tuesday, March 29, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY EXPOSURE SPREADING VIA HOSPITALS AND SURGICAL PROCEDURES AROUND THE GLOBE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/transmissible-spongiform-encephalopathy.html
Friday, April 15, 2011
PRION TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PROJECTS, RESEARCH FUNDING, BSE VOLUNTARY TESTING UPDATE IN NORTH AMERICA 2011
http://prionunitusaupdate2008.blogspot.com/2011/04/prion-transmissible-spongiform.html
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
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