Tuesday, March 5, 2013

Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)

FDA believes current regulation protects the public from BSE but reopens comment period due to new studies

 
 
March 4, 2013
 
 
The Food and Drug Administration (FDA) is reopening the comment period for the interim final rule entitled “Use of Materials Derived From Cattle in Human Food and Cosmetics.” The interim final rule protects consumers from exposure to bovine spongiform encephalopathy (BSE) by prohibiting the use of certain cattle parts in human food, including dietary supplements, and cosmetics. Under the interim final rule amended in 2005, the small intestine of cattle can be used in human food, dietary supplements, and cosmetics if the portion of the small intestine known as the distal ileum has been properly removed.
 
 
Since 2005, there have been scientific studies that found trace levels of infectivity in parts of cattle small intestine, other than the distal ileum, from animals with BSE. However, FDA believes that the levels of infectivity are so low that they do not pose a significant health risk to humans or ruminants in the U.S. Consistent with FDA’s position, the World Organization for Animal Health has not changed its definition of “specified risk material” to include any part of the small intestine other than the distal ileum.
 
 
Further, FDA does not believe there would be a measurable reduction in the risk from BSE to the American public by removing additional parts of the cattle small intestine and, as such, it would be appropriate to finalize the interim final rule without changing any provisions related to the small intestine. Nonetheless, FDA is reopening the comment period to give interested parties an opportunity to comment on the studies and on FDA’s tentative conclusion.
Additional information:
 
 
 
 
 
 
 
Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment Period
 
 

 
 
 
This article has a comment period that ends in 60 days (05/03/2013)

Action


Interim Final Rule; Reopening Of The Comment Period.

Summary

 
 
The Food and Drug Administration (FDA or “we”) is reopening the comment period for the interim final rule entitled “Use of Materials Derived From Cattle in Human Food and Cosmetics” that published in the Federal Register of July 14, 2004 (69 FR 42256). The interim final rule prohibited the use of certain cattle material to address the potential risk of bovine spongiform encephalopathy (BSE) in human food, including dietary supplements, and cosmetics. In the Federal Register of September 7, 2005 (70 FR 53063), we amended the interim final rule to make changes, including providing that the small intestine of cattle, formerly prohibited cattle material, could be used in human food and cosmetics if the distal ileum was removed by a specified procedure or one that the establishment could demonstrate is equally effective in ensuring complete removal of the distal ileum. Since 2005, peer-reviewed studies have been published showing the presence of infectivity in the proximal ileum, jejunum, ileocecal junction, and colon of cattle with BSE. Therefore, we are reopening the comment period for the interim final rule to give interested parties an opportunity to comment on the new studies concerning infectivity in parts of the small intestine other than the distal ileum.

 

 


Unified Agenda



Use of Materials Derived From Cattle in Human Food and Cosmetics

 
 
10 actions from July 14th, 2004 to September 2011
 
 
 
 
 
 
 

DATES:


Submit either electronic or written comments by May 3, 2013.

ADDRESSES:


Submit electronic comments to http://www.regulations.gov. Submit written comments to the Division of Dockets Management (HFA-305), Food and Drug Administration, 5630 Fishers Lane, Rm. 1061, Rockville, MD 20852.
 
 
 

FOR FURTHER INFORMATION CONTACT:



Johnny Braddy,Center for Food Safety and Applied Nutrition (HFS-316),Food and Drug Administration,5100 Paint Branch Pkwy.,College Park, MD 20740,240-402-2131.
 
 
 

SUPPLEMENTARY INFORMATION:



I. Background



 
In the Federal Register of July 14, 2004 (69 FR 42256), FDA published an interim final rule entitled “Use of Materials Derived From Cattle in Human Food and Cosmetics.” The interim final rule prohibited the use of certain cattle material to address the potential risk of BSE in human food and cosmetics. The interim final rule designated the small intestine as prohibited cattle material and prohibited its use in human food or cosmetics. In the Federal Register of September 7, 2005 (70 FR 53063), we amended the interim final rule to allow the use of the small intestine if the distal ileum is removed by a procedure that removes at least 80 inches of uncoiled and trimmed small intestine as measured from the ceco-colic junction and progressing proximally towards the jejunum or by a procedure that the establishment can demonstrate is equally effective in ensuring complete removal of the distal ileum.
 
 
 
On January 12, 2004, the U.S. Department of Agriculture, Food Safety and Inspection Service (FSIS), issued an interim final rule to designate materials that could potentially contain BSE infectivity as specified risk materials (SRMs) and prohibit their use for human food (see “Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle”; 69 FR 1862; January 12, 2004). FSIS's interim final rule designated the distal ileum as an SRM but required that the entire small intestine be removed and disposed of as inedible to ensure the effective removal of the distal ileum. On September 7, 2005, FSIS, like FDA, amended its interim final rule to permit the use of the entire small intestine for human food if the distal ileum is removed by a procedure that removes at least 80 inches of the uncoiled and trimmed small intestine as measured from the ceco-colic junction and progressing proximally towards the jejunum or by a procedure that the establishment demonstrates is effective in ensuring complete removal of the distal ileum.
 
 
 
When the FDA and FSIS amendments to the interim final rules were published in 2005, BSE infectivity had been demonstrated in lymphoid tissue of the distal ileum. In naturally occurring cases, sparse immunostaining had also been observed in the myenteric plexus of the distal ileum indicating the presence of PrPSc [,] a TSE-specific protein (Ref. 1). Because the myenteric plexus extends throughout the small intestine, both FDA and FSIS considered that it was possible that infectivity might also exist in the myenteric plexus of the jejunum or the duodenum. We stated in our 2005 amendment to our interim final rule that if we became aware of data indicating that other portions of the small intestine harbored BSE infectivity, we would take action appropriate to the public health risk. FSIS stated in its 2005 amendment to its interim final rule that while it believed that the primary tissues of concern for spreading the BSE agent had been identified, FSIS would use the results of future studies on BSE to further refine its policies with regard to BSE (70 FR 53043 at 53047; September 7, 2005). In 2007, FSIS issued a final rule to make permanent the interim measures implemented in 2004 and amended in 2005 (72 FR 38700; July 13, 2007).
 
 
 
Since we amended our interim final rule in 2005 and FSIS issued its final rule in 2007, peer-reviewed studies have been published showing the presence of some infectivity in the proximal ileum, jejunum, ileocecal junction, and colon of cattle with BSE. The new scientific data confirms the presence of limited amounts of BSE infectivity in the small intestine outside of the distal ileum of classical BSE infected cattle under experimental inoculation and field conditions. The infectivity levels reported in these studies were much lower than the infectivity levels that were previously demonstrated in the distal ileum.
 
 
 
We have added several peer-reviewed studies (Refs. 2 to 6) to the administrative record. We invite comment on those studies.
 
 
 
Additionally, the European Food Safety authority (EFSA) Panel on Biological Hazards (BIOHAZ) has reviewed and evaluated new data as it relates to the BSE epidemiological situation in the European Union. We have added the EFSA documents to the administrative record as well (Refs. 7 and 8). We have evaluated the data from the studies. Only trace amounts of infectivity have been found in the proximal ileum, jejunum, ileocecal junction, and colon of cattle with naturally occurring cases of BSE. We tentatively conclude that the effect of these traces of infectivity on the risk of human or ruminant exposure to BSE in the United States is negligible. The very low levels of infectivity in parts of the intestine other than the distal ileum, the sharp decline in the prevalence of BSE worldwide, FDA's BSE-related restrictions on the contents of animal food and feed (see 21 CFR 589.2000 and 589.2001), and the extremely low prevalence of BSE within cattle in the United States due to the presence of effective mitigations and compliance with international standards suggest that the risk from parts of the intestine other than the distal ileum is extremely low. We also note that the World Organization for Animal Health (formerly known as the Office International des Epizooties or “OIE”) has not changed its definition of SRMs to include any part of the small intestine in addition to the distal ileum. Based on this assessment, we tentatively conclude that requiring the removal of additional parts of the small intestine would not provide a measurable risk reduction compared to that already being achieved by removal of the distal ileum in all cattle and that it would be appropriate to finalize our interim final rule without changing any provisions related to the small intestine. We invite comment on this tentative conclusion.
 
 
 

II. Comments



 
Interested persons may submit either electronic comments regarding this document to http://www.regulations.gov or written comments to the Division of Dockets Management (see ADDRESSES). It is only necessary to send one set of comments. Identify comments with the docket number found in brackets in the heading of this document. Received comments may be seen in the Division of Dockets Management between 9 a.m. and 4 p.m., Monday through Friday, and will be posted to the docket at http://www.regulations.gov.
 
 
 

III. References



 
The following references have been placed on display in the Division of Dockets Management (see ADDRESSES) and may be seen by interested persons between 9 a.m. and 4 p.m., Monday through Friday, and are available electronically at http://www.regulations.gov.
 
 
 
1. Terry, L.A., S. March, S.J. Ryder, et al., “Detection of Disease Specific PrP in the Distal Ileum of Cattle Exposed Orally to the Agent of Bovine Spongiform Encephalopathy,”Veterinary Record, vol. 152, pp. 387-392, 2003.
2. Balkema-Buschmann, A., C. Fast, M. Kaatz, et al., “Pathogenesis of Classical and Atypical BSE in Cattle.”Preventive Veterinary Medicine, vol. 102, pp. 112-117, 2011.
3. Hoffmann, C., M. Eiden, M. Kaatz, et al., “BSE Infectivity in Jejunum, Ileum and Ileocaecal Junction of Incubating Cattle,”Veterinary Research, vol. 42, p. 21, 2011.
4. Kimura K. and M. Haritani, “Distribution of Accumulated Prion Protein in a Cow With Bovine Spongiform Encephalopathy,”The Veterinary Record, vol. 162, pp. 822-825, 2008.
5. Okada H., Y. Iwamaru, M. Imamura, et al. “Detection of Disease-Associated Prion Protein in the Posterior Portion of the Small Intestine Involving the Continuous Peyer's Patch in Cattle Orally Infected With Bovine Spongiform Encephalopathy Agent,”Transboundary and Emerging Diseases, vol. 58(4), pp. 333-343, Aug. 2011.
6. Stack M., S.J. Moore, A. Vidal-Diez, et al. “Experimental Bovine Spongiform Encephalopathy: Detection of PrP(SC) in the Small Intestine Relative to Exposure Dose and Age,”Journal of Comparative Pathology, vol. 145, pp. 289-301, 2011.
7. “European Food Safety Authority (EFSA) Panel on Biological Hazards (BIOHAZ),”EFSA Journal, vol. 1317, pp. 1-9, 2009.
8. “European Food Safety Authority (EFSA) Panel on Biological Hazards (BIOHAZ),”EFSA Journal, vol. 9(3), p. 2104, 2011.
 
 

Dated: February 26, 2013.
Leslie Kux,
Assistant Commissioner for Policy.
[FR Doc. 2013-04869 Filed 3-1-13; 8:45 am]
BILLING CODE 4160-01-P
 
 
 
 
 
 
SUBMIT A FORMAL COMMENT ;
 
 
 
 
 
 
 
 
 
 
 
 
 
Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)
 
 
 
Greetings again FDA et al,
 
 
 
I once again would like to make a comment submission on the same topic BSE aka mad cow disease FDA-2004-N-0188-0051, renewed March 4, 2013 due to new scientific concerns for human health, the same ones of which I have been trying to warn you of since December 14, 1997, when I lost my mother to the hvCJD i.e. the Heidenhain Variant of CJD.
 
 
 
 
I told myself I was not going to do this anymore, because I don’t believe that you care, and that you already have your mind made up, and that no matter how much documented evidence that is brought forth, trade and the almighty dollar will win out again, over a disease that is 100% fatal, once clinical. a disease that has mutated into many strains and variants in many different species, all of which have been fed back livestock producing animals for feed. it’s a vicious cycle of greed, one of which they have already started to repeal and bring back into commerce, i.e. mad cow feed for some species, and if left up to the OIE and the USDA, they will have all these safe guards for the TSE prion disease repealed, because it hurts their bottom dollar.
 
 
 
 
 
The USDA, FSIS, APHIS, FDA, CDC, mad cow follies, or mad cow debacle, as it is known around the world, has and will continue to exist, simply because of the greed and ignorance there from it all. This new science, and other new science in the TSE prion world now, some of which has been around for some time, but yet ignored by the USDA et al, to a point now, where the amplification of the TSE prion agent in the USA and North America is at it’s worst ever, and continues to mount via many species.
 
 
 
 
The USDA et al TRIPLE BSE FIREWALL, as they claim it to be, is and was a farce. ALL of it, the SURVEILLANCE, the TESTING, the FEED BAN, and the SRM removal. 10 years post partial and voluntary mad cow feed ban of August 4, 1997 i.e. 2007 (one decade), 10 MILLION POUNDS OF BLOOD LACED, BANNED MEAT AND BONE MEAL WENT INTO COMMERCE IN THE USA, never to be returned, fed out. The year before that, 2006, was a banner years as well for banned mad cow feed in commerce in the USA. please see the FDA recalls below in source reference. The surveillance and testing for BSE aka mad cow disease in the USA was also hampered with much fraud, from the least likely BSE test to find mad cow disease being used, to only BSE testing the OBEX area of the brain for BSE, to the sad, sad, reality of USDA testing cattle brains that they new were BSE free.
 
 
 
 
until you get the corporate and political science policy making out of the way, you will never stop the TSE prion aka mad cow type disease.
 
 
 
 
the USA must test every cow for the TSE Prion disease.
 
 
 
 
the USA must stop all feeding to all species of ruminant and non ruminant protein.
 
 
 
 
the USA must extend and enhance the mad cow feed ban. this is what was said they would do long ago, if science shows change in tissue infectivity, but they went back on their word, in my opinion.
 
 
 



 
Wednesday, May 2, 2012



 
ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND ANIMAL HEALTH


 
 
 
 
 
 
 
Wednesday, July 28, 2010
 
 
 
 
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010


 
Sent: Wednesday, July 28, 2010 11:42 AM

 
 
Subject: re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE


 
 
Greetings again Ms Williams et al at FOIA USDA,


 
Thank You again for your kind reply on this important information. However, I am concerned that you may not be aware of new transmission studies. You (USDA et al) state Ma'am ;
================================================
 
 
The SCA with Italy was mainly to confirm our respective country’s diagnostic tests would detect the various atypical BSE cases as seen in each country), in the meantime, the Italians have published their transmissibility and pathogenesis work on their BASE cases in the following article:
 
Lombardi G, Casalone C, A DA, Gelmetti D, Torcoli G, Barbieri I, Corona C, Fasoli E, Farinazzo A, Fiorini M, Gelati M, Iulini B, Tagliavini F, Ferrari S, Caramelli M, Monaco S, Capucci L, Zanusso G (2008) Intraspecies transmission of BASE induces clinical dullness and amyotrophic changes. PLoS Pathog 4:e1000075
 
The above mentioned paper concludes, “In all experimentally infected animals, no PrP**TSE was detected in peripheral tissues, including cervical and mesenteric lymph nodes, spleen, thymus, liver, lung, peripheral nerves and forelimb and limb muscles, either by standard Western blot analysis or following phosphotungstic acid precipitation.“
 
 
It is not necessary to change SRM removal due to any different tissue infectivity distribution between classical BSE and atypical BSE. At this time, there is no scientific evidence to suggest a need for expanding the list of tissues included in the Specified Risk Material (SRM) ban as a result of published studies on atypical BSE.
 
 
 
snip...
 
 
Moreover, in the paper by Buschmann A, Groschup MH (2005,) Highly bovine spongiform encephalopathy-sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle. J Infect Dis 192:934-942; the authors, when speaking about the classical BSE food-borne epidemic in Europe, concluded their “results provide further indication that the pathogenesis of BSE in cattle is fundamentally different from that in sheep and mice, due to an exclusive intraneuronal spread of infectivity from the gut to the central nervous system.”
 
 
 
 
end...
================================================
 
 
 
 
Again, in my opinion, the USDA is cherry picking the science they want to use, and in doing so, I believe they are putting human lives at risk.
 
 
 
 
 
 
 
I disagree for the following reasons. New studies indeed show that ;
 
 
 
July 10, 2010



 
see full text ;
 
 
 
Wednesday, July 28, 2010
 
 
 
 
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010



 
 
 
 
 

Monday, December 26, 2011







*** Prion Uptake in the Gut: Identification of the First Uptake and Replication Sites

 

 
 
 
 
 
 
 
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
 
 
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model
 

 
 
 
 
 
***Infectivity in skeletal muscle of BASE-infected cattle

 
 
 
 
 
 
***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries.

 
 
 
 
 
 
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.
 
 
 
 
 
 
 
 
 
The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission.
 
 
 
In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.
 


 
 
 
 
 
Friday, May 11, 2012
 
 
 
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
 
 
 
***support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE
 

 
 
 
 
Thursday, June 21, 2012
 
 
 
Clinical and Pathologic Features of H-Type Bovine Spongiform Encephalopathy Associated with E211K Prion Protein Polymorphism

 
Justin J. Greenlee1*, Jodi D. Smith1, M. Heather West Greenlee2, Eric M. Nicholson1
 
1 National Animal Disease Center, United States Department of Agriculture, Agricultural Research Service, Ames, Iowa, United States of America, 2 Iowa State University, Ames, Iowa, United States of America
 
 
Abstract
 
 
 
 
The majority of bovine spongiform encephalopathy (BSE) cases have been ascribed to the classical form of the disease. Htype and L-type BSE cases have atypical molecular profiles compared to classical BSE and are thought to arise spontaneously. However, one case of H-type BSE was associated with a heritable E211K mutation in the prion protein gene. The purpose of this study was to describe transmission of this unique isolate of H-type BSE when inoculated into a calf of the same genotype by the intracranial route. Electroretinograms were used to demonstrate preclinical deficits in retinal function, and optical coherence tomography was used to demonstrate an antemortem decrease in retinal thickness. The calf rapidly progressed to clinical disease (9.4 months) and was necropsied. Widespread distribution of abnormal prion protein was demonstrated within neural tissues by western blot and immunohistochemistry. While this isolate is categorized as BSE-H due to a higher molecular mass of the unglycosylated PrPSc isoform, a strong labeling of all 3 PrPSc bands with monoclonal antibodies 6H4 and P4, and a second unglycosylated band at approximately 14 kDa when developed with antibodies that bind in the C-terminal region, it is unique from other described cases of BSE-H because of an additional band 23 kDa demonstrated on western blots of the cerebellum. This work demonstrates that this isolate is transmissible, has a BSE-H phenotype when transmitted to cattle with the K211 polymorphism, and has molecular features that distinguish it from other cases of BSE-H described in the literature.
 
 
snip...
 
 
Most significantly it must be determined if the molecular phenotype of this cattle TSE remains stable when transmitted to cattle without the E211K polymorphism as several other isolates of atypical BSE have been shown to adopt a molecular profile consistent with classical BSE after passage in transgenic mice expressing bovine PrPC [40] or multiple passages in wild type mice [23]. Results of ongoing studies, namely passage of the E211K Htype isolate into wild-type cattle, will lend further insight into what role, if any, genetic and sporadic forms of BSE may have played in the origins of classical BSE. Atypical cases presumably of spontaneous or, in the case of E211K BSE-H, genetic origins highlight that it may not be possible to eradicate BSE entirely and that it would be hazardous to remove disease control measures such as prohibiting the feeding of meat and bone meal to ruminants.
 
 
 
 
 
 
the USA BSE GBR risk assessment, from the evidence I put forth below, in my opinion, should be BSE GBR IV.
 
 
 
The only thing that matters to the USDA and the OIE is trade, nothing else matters. just ask Stanley Prusiner, who won the Nobel prize for the PRION, he said it himself.
 
 
 
 
US SENATOR AND PROFESSOR STANLEY PRUSINER ''DAMNING TESTIMONY''
 
 
Senator Michael Machado from California
 
 
''USDA does not know what's going on''.
 
 
 
 
''USDA is protecting the industry''.
 
 
 
 
''SHOULD the state of California step in''
 
 
 
 
Stanley Prusiner
 
 
 
 
''nobody has ever ask us to comment''
 
 
 
 
''they don't want us to comment''
 
 
 
 
''they never ask''


 
i tried to see Venemon, after Candian cow was discovered with BSE. went to see lyle. after talking with him...


 
absolute ignorance...


 
then thought I should see Venemon...


 
it was clear his entire policy was to get cattle bonless beef prods across the border...


 
nothing else mattered...


 
his aids confirmed this...
 
 
 
 
5 times i tried to see Venemon, never worked...
 
 
 
 
eventually met with carl rove the political...
 
 
 
 
he is the one that arranged meeting with Venemon...


 
just trying to give you a sense of the distance...
 
 
 
 
healh public safety...
 
 
 
 
was never contacted...


 
yes i believe that prions are bad to eat and you can die from them...


 
END
 
 
 
 
PLEASE NOTE THESE VIDEOS HAVE BEEN REMOVED FROM THE INTERNET $$$


 
Dr. Stan bashing Ann Veneman - 3 minutes
 
 
 
Recall Authority and Mad Cow Disease: Is the Current System Good for Californians?

 
Tuesday, February 24, 2004
 
 
 
JOINT HEARING

 
AGRICULTURE AND WATER RESOURCES HEALTH AND HUMAN SERVICES AND SELECT
COMMITTEE ON GOVERNMENT OVERSIGHT - MACHADO, ORTIZ, and SPEIER, Chairs
 
 



 
 
 
please see ;
 


 
 
 
Thursday, January 17, 2013




 
Canada, U.S. agree on animal-disease measures to protect trade, while reducing human and animal health protection

 
 
 
 


 
 
 
 
 


 

Sunday, May 6, 2012

 
 
 

Bovine Spongiform Encephalopathy Mad Cow Disease, BSE May 2, 2012 IOWA State University OIE

 
 
 
 
http://transmissiblespongiformencephalopathy.blogspot.com/2012/05/bovine-spongiform-encephalopathy-mad.html
 
 
 
 
 
 
 
*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS
 
 
 
 
 
 
THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$
 
 
 
 
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
 
 
 
 
 
 
 
 
Saturday, August 14, 2010
 
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

 
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)


 
BANNED MAD COW FEED IN COMMERCE IN ALABAMA


 
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
 
 
 
______________________________
 


 
 
 
 



 
 
 
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
 
 
 
###
 
 
 


 
 
 
 
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
 
 
 
###
 
 
 



 
 
 
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
 
 
 
###
 
 
 
 
 
SPECIFIED RISK MATERIAL SRM BREACHES USA
 
 
 
----- Original Message -----

 
From: Terry S. Singeltary Sr. To: AgRepublicanPress@mail.house.gov
 
 
Sent: Friday, July 22, 2011 4:23 PM
 
 
Subject: Fw: Valley Farm Meats (DBA Strasburg Provision, Inc) Issues Precautionary Recall for Beef Products Due to Possible Contamination with Prohibited Materials SRM

 
Greetings USDA et al,
I have not seen this on the USDA site yet ???
have i missed it ???
thank you, kind regards, terry
 
 
 
 
Ohio Department of Agriculture and Ohio Department of Health
Governor
John R. Kasich
Lieutenant Governor
Mary Taylor
ODA Director
James Zehringer
ODH Director
Theodore E. Wymyslo, M.D.
DT: July 14, 2011
TO: Health Commissioners, Directors of Environmental Health and Interested Parties
RE: Recall Announcement (ODA/ODH) 2011-076
Valley Farm Meats (DBA Strasburg Provision, Inc) Issues Precautionary Recall for Beef Products Due to Possible Contamination with Prohibited Materials
snip...end...TSS
=========================================
 
 
 
Ohio Department of Agriculture and Ohio Department of Health
 
Governor
 
John R. Kasich
 
Lieutenant Governor
 
Mary Taylor
 
ODA Director
 
James Zehringer
 
ODH Director
 
Theodore E. Wymyslo, M.D.
 
DT: July 14, 2011
 
 
TO: Health Commissioners, Directors of Environmental Health and Interested Parties
 
RE: Recall Announcement (ODA/ODH) 2011-076
 
 
Valley Farm Meats (DBA Strasburg Provision, Inc) Issues Precautionary Recall for Beef Products Due to Possible Contamination with Prohibited Materials
 
 
[STRASBURG, Ohio] – Valley Farm Meats (DBA Strasburg Provision, Inc) of Strasburg, OH announces a voluntary recall of an unknown amount of beef products that may contain the spinal cord and vertebral column, which are considered specified risk materials (SRMs). SRMs must be removed from cattle over 30 months of age in accordance with federal and state regulations. SRMs are tissues that are known to contain the infective agent in cattle infected with Bovine Spongiform Encephalopathy (BSE), as well as materials that are closely associated with these potentially infective tissues. Therefore, federal and state regulations prohibit SRMs from use as human food to minimize potential human exposure to the BSE agent.
 
 
The products subject to recall include all beef products slaughtered and processed by or purchased from Valley Farm Meats retail store, 1317 N. Wooster Ave NW, Strasburg, OH 44680 or purchased from Ed Lind Livestock and Poultry, 3333 Church Rd B, Medina, Ohio 44256. These products were produced between 01/28/2011 and 07/05/2011 and offered for sale from 01/28/2011 through 07/11/2011.
 
 
The package labels or beef carcasses may bear the Ohio mark of inspection and “Est. 80”, however products processed through Ed Lind Livestock and Poultry may not contain such markings. The problem was discovered through routine inspection activities by the Ohio Department of Agriculture’s Division of Meat Inspection. The Department has received no reports of illnesses associated with consumption of this product.
 
 
The United States Department of Agriculture’s Food Safety and Inspection Service classifies this type of potential contamination as a low health risk, however individuals concerned about an illness should contact a health care provider.
 
 
Because of potential product contamination, Valley Farm Meats urges its customers who have purchased the suspect product(s) not to eat them and to return them to the company. Customers may bring those designated packages to Valley Farm Meats, 1317 N Wooster Avenue NW, Strasburg, OH 44680 during regular business hours or call the company’s owner, Paul Berry at 330-878-5557.
 
 
 
 
Valley Farm Meats issues beef recall
TimesReporter.com staff report
Posted Jul 13, 2011 @ 03:18 PM
 
 
 
 
 
 
 
see old FSIS example of SRM recalls from the past ;
 
 
 
 
North Dakota Firm Recalls Whole Beef Head Products That Contain Prohibited Materials

 
Recall Release CLASS II RECALL FSIS-RC-023-2010 HEALTH RISK: LOW

 
Congressional and Public Affairs (202) 720-9113 Catherine Cochran
 
 
 
WASHINGTON, April 5, 2010 - North American Bison Co-Op, a New Rockford, N.D., establishment is recalling approximately 25,000 pounds of whole beef heads containing tongues that may not have had the tonsils completely removed, which is not compliant with regulations that require the removal of tonsils from cattle of all ages, the U.S. Department of Agriculture's Food Safety and Inspection Service (FSIS) announced today.

 
Tonsils are considered a specified risk material (SRM) and must be removed from cattle of all ages in accordance with FSIS regulations. SRMs are tissues that are known to contain the infective agent in cattle infected with Bovine Spongiform Encephalopathy (BSE), as well as materials that are closely associated with these potentially infective tissues. Therefore, FSIS prohibits SRMs from use as human food to minimize potential human exposure to the BSE agent.

 
The product subject to recall includes: Various weight cases of "Beef Heads KEEP FROZEN." Each case bears the establishment number "EST. 18859" inside the USDA mark of inspection and a case code number "16999." "North Dakota Natural Beef" is printed in the bottom left-hand corner of each label.

 
The recalled products were produced between June 25, 2009, and February 19, 2010. These products were shipped to distribution centers in Md., Mich., and Minn. for further sale.
 
 
 
The problem was discovered during FSIS inspection activities at the establishment. FSIS routinely conducts recall effectiveness checks to verify recalling firms notify their customers of the recall and that steps are taken to make certain that the product is no longer available to consumers.

 
Media with questions about the recall should contact Philip Wicke, Vice President of Operations, at (701) 356-7723. Consumers with questions about the recall should contact Jeremy Anderson, Director of Customer Service, at (952) 545-2495

 
Consumers with food safety questions can "Ask Karen," the FSIS virtual representative available 24 hours a day at AskKaren.gov. The toll-free USDA Meat and Poultry Hotline 1-888-MPHotline (1-888-674-6854) is available in English and Spanish and can be reached from l0 a.m. to 4 p.m. (Eastern Time) Monday through Friday. Recorded food safety messages are available 24 hours a day. #

 
 
 
 
 
Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials
 
 
 
Recall Release CLASS II RECALL FSIS-RC-021-2008 HEALTH RISK: LOW
 
 
 
Congressional and Public Affairs (202) 720-9113 Amanda Eamich
 
 
 
WASHINGTON, June 26, 2008 – Paradise Locker Meats, a Trimble, Mo., establishment, is voluntarily recalling approximately 120 pounds of fresh cattle heads with tonsils not completely removed, which is not compliant with regulations that require the removal of tonsils from cattle of all ages, the U.S. Department of Agriculture’s Food Safety and Inspection Service announced today.
 
 
 
Tonsils are considered a specified risk material (SRM) and must be removed from cattle of all ages in accordance with FSIS regulations. SRMs are tissues that are known to contain the infective agent in cattle infected with BSE, as well as materials that are closely associated with these potentially infective tissues. Therefore, FSIS prohibits SRMs from use as human food to minimize potential human exposure to the BSE agent.
 
 
 
The products subject to recall include: Boxes of “BEEF HEAD, PARADISE LOCKER MEATS.” Each shipping package bears the establishment numbers “EST. 31865” inside the USDA mark of inspection.
 
 
 
These products were sent to retail establishments and restaurants in the Kansas City, Kansas, area.
 
 
 
The problem was discovered through routine FSIS inspection that verified there had been incomplete removal of the tonsils by the recalling establishment.

 
Media and consumers with questions about the recall should contact company Production Supervisor Louis Fantasma at (816) 370-6328.

 
Consumers with food safety questions can “Ask Karen,” the FSIS virtual representative available 24 hours a day at AskKaren.gov. The toll-free USDA Meat and Poultry Hotline 1-888-MPHotline (1-888-674-6854) is available in English and Spanish and can be reached from l0 a.m. to 4 p.m. (Eastern Time) Monday through Friday. Recorded food safety messages are available 24 hours a day. #
 
 
 


 
 
 
 
 
HAS the greed and money gotten so bad that the FSIS, USDA, APHIS, OIE et al, just decided that not only to exempt the atypical Scrapies and apparently now the BSE's, exempt them all, and just agreed to choose to not even speak about it anymore. i mean...really, the USDA and OIE have systematically covered up mad cow disease i.e. they call it SSS policy. where is USA burying them all at ? i do not accept the star trek like cloaking device that appears to be the only thing left that could be protecting the USA from mad cow disease....really. sadly, Canada has now taken the same low road as the USA in regards to discussing and making public documents on there mad cow cases. all this, 2011, with the science mounting, still follow the global myth of the UKBSEnvCJD only theory, and that all the sporadic CJDs (85%+ of all human TSE) are a mear happenstance of bad luck, when North America is plum full of different strains of the Transmissible Spongiform Encephalopathy in different species, all of which over a period of time, decades, were rendered and fed to food producing animals for human and animal food...really. i really just don't buy it...tss
 
 
 
 
some history on SRM's IN COMMERCE ;
 
 
 
 
SEE FULL TEXT HERE ;




 
Tuesday, July 1, 2008
Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
 
 
 
 
 
 
 
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009
 
 
 
 
 
 
 
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009
 
 


 
 
Thursday, June 26, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials
 
 
 


 
Friday, August 8, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed
 
 
 
 
 
 
 
Saturday, April 5, 2008
SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS
 
 
 


 
Wednesday, April 30, 2008
 
Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings
 
 
 
 
 
 
 
Friday, October 15, 2010

 
BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle
 
 
 
 
 


 
 
SPECIFIED RISK MATERIALS SRMs
 
 
 

 
 
 

 
 
 

 
 
 
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)
 
 
 
PRION DISEASE UPDATE 2010 (11)
 
 
 
 
 
 
 
 
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

 



 
 
USA BSE AKA MAD COW SURVEILLANCE AND TESTING BREACHES
 
 
 
2004, highly suspect stumbling and staggering mad cow reported, however, NO TESTING DONE, ON ORDERS FROM AUSTIN $
May 4, 2004
 
 
Statement on Texas Cow With Central Nervous System Symptoms
 
 
On Friday, April 30th, the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
 
 
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
 
 
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
 
 
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison)...
 
 
 
 
 
 
 
USDA regulations, any cow that exhibits signs of central nervous system (CNS)
 
 
According to a 1997 Animal and Plant Health Inspection Service (NHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "it is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."
 
 
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
 
 
May 13,2004
Page 2
snip...
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
 
 
This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:
 
 
 
 
 
-------- Original Message --------
 
 
 
Subject: re-USDA's surveillance plan for BSE aka mad cow disease

 
Date: Mon, 02 May 2005 16:59:07 -0500
 
 
 
From: "Terry S. Singeltary Sr."
 
 
 
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us
 
 
 
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............
 
 
 
 
snip...
 
 
 
 
There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...


 
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 xxx xxx xxxx



 
Date: June 14, 2005 at 1:46 pm PST In

 
Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results posted by TSS on June 13, 2005 at 7:33 pm:
 
 
 
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS
 
 
 
 
 
MAD COW IN TEXAS NOVEMBER 2004. ...TSS
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
 
 
 
 
Date: Mon, 22 Nov 2004 17:12:15 –0600
 
 
From: "Terry S. Singeltary Sr."
 
 
To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>
 
 
 
 
Greetings Carla,still hear a rumor;
 
 
Texas single beef cow not born in Canada no beef entered the food chain?
 
 
and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???
 
 
 
terry
 
 
 
-------- Original Message --------
 
 
 
 
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
 
 
 
Date: Fri, 19 Nov 2004 11:38:21 –0600
 
 
 
From: Carla Everett
 
 
 
To: "Terry S. Singeltary Sr." References: <[log in to unmask]>
 
 
 
 
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas. Carla At 09:44 AM 11/19/2004, you wrote:>Greetings Carla,>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from>TEXAS. can you comment on this either way please?>>thank you,>Terry S. Singeltary Sr.>>
 
 
 
 
-------- Original Message --------
 
 
 
 
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
 
 
 
Date: Mon, 22 Nov 2004 18:33:20 -0600 From: Carla Everett
 
 
 
To: "Terry S. Singeltary Sr."
 
 
 
 
References: ...sniptss
 
 
 
 
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something. At 06:05 PM 11/22/2004,
 
 
 
 
you wrote:
 
 
 
 
>why was the announcement on your TAHC site removed?
 
 
 
 
>>Bovine Spongiform Encephalopathy:
 
 
 
 
>November 22: Press Release title here
 
 
 
 
>>star image More BSE information
 
 
 
 
>>>>terry
 
 
 
 
>>Carla Everett wrote:
 
 
 
 
>>>no confirmation on the U.S.' inconclusive test...
 
 
 
 
>>no confirmation on location of animal.>>>>>>
 
 
 
 
==========================


 
 
 
-------- Original Message --------
 
 
 
 
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
 
 
 
 
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
 
 
 
 
Date: Mon, 22 Nov 2004 17:12:15 –0600
 
 
 
 
From: "Terry S. Singeltary Sr."
 
 
 
 

To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>



Greetings Carla,



still hear a rumor;

Texas single beef cow not born in Canada no beef entered the food chain?


and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???


terry


==============================
 
 




 
USDA did not test possible mad cows
 
 
 
By Steve Mitchell
 
 
 
United Press International

 
Published 6/8/2004 9:30 PM
 
 
 
 
WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims ittested 500 cows with signs of a brain disorder for mad cow disease last year, but agency documents obtained by United Press International show the agency tested only half that number.
 
 
 
 
 
 
 
 
 
 
 
 
""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."
 
 
 
THIS WAS DONE FOR A REASON!
 
 
 
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS
 
 
 
 
TEXAS 2ND MAD COW THAT WAS COVERED UP, AFTER AN ACT OF CONGRESS, AND CALLS FROM TSE PRION SCIENTIST AROUND THE GLOBE, THIS 2ND MAD COW IN TEXAS WAS CONFIRMED
 
 
 
THE USDA MAD COW FOLLIES POSITIVE TEST COVER UP
 
 
 
JOHANNS SECRET POSTIVE MAD COW TEST THAT WERE IGNORED

 
OIG AND THE HONORABLE FONG CONFIRMS TEXAS MAD AFTER AN ACT OF CONGRESS 7 MONTHS LATER
 
 
 
TEXAS MAD COW
 
 
 
THEY DID FINALLY TEST AFTER SITTING 7+ MONTHS ON A SHELF WHILE GW BORE THE BSE MRR POLICY, i.e. legal trading of all strains of TSE. now understand, i confirmed this case 7 months earlier to the TAHC, and then, only after i contacted the Honorable Phyllis Fong and after an act of Congress, this animal was finally confirmed ;


 
During the course of the investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE. 200 adult animals of interest were determined to have left the index farm. Of these 200, APHIS officials determined that 143 had gone to slaughter, two were found alive (one was determined not to be of interest because of its age and the other tested negative), 34 are presumed dead, one is known dead and 20 have been classified as untraceable. In addition to the adult animals, APHIS was looking for two calves born to the index animal. Due to record keeping and identification issues, APHIS had to trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter channels, four are presumed to have entered feeding and slaughter channels and one calf was untraceable.
 
 
 
 
 
 
 
 
Executive Summary In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.
 
 
 
 
snip...
 
 
 
 
Trace Herd 3 The owner of Trace Herd 3 was identified as possibly having received an animal of interest. The herd was placed under hold order on 7/27/05. The herd inventory was conducted on 7/28/05. The animal of interest was not present within the herd, and the hold order was released on 7/28/05. The person who thought he sold the animal to the owner of Trace Herd 3 had no records and could not remember who else he might have sold the cow to. Additionally, a search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. The animal of interest traced to this herd was classified as untraceable because all leads were exhausted.



 
Trace Herd 4 The owner of Trace Herd 4 was identified as having received one of the COI through an order buyer. Trace Herd 4 was placed under hold order on 7/29/05. A complete herd inventory was conducted on 8/22/05 and 8/23/05. There were 233 head of cattle that were examined individually by both State and Federal personnel for all man-made identification and brands. The animal of interest was not present within the herd. Several animals were reported to have died in the herd sometime after they arrived on the premises in April 2005. A final search of GDB records yielded no further results on the eartag of interest at either subsequent market sale or slaughter. With all leads having been exhausted, this animal of interest has been classified as untraceable. The hold order on Trace Herd 4 was released on 8/23/05.
 



 
Trace Herd 5 The owner of Trace Herd 5 was identified as having received two COI and was placed under hold order on 8/1/05. Trace Herd 5 is made up of 67 head of cattle in multiple pastures. During the course of the herd inventory, the owner located records that indicated that one of the COI, a known birth cohort, had been sold to Trace Herd 8 where she was subsequently found alive. Upon completion of the herd inventory, the other animal of interest was not found within the herd. A GDB search of all recorded herd tests conducted on Trace Herd 5 and all market sales by the owner failed to locate the identification tag of the animal of interest and she was subsequently classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 5 was released on 8/8/05.
 
 
 
 
 
Trace Herd 6 The owner of Trace Herd 6 was identified as possibly having received an animal of interest and was placed under hold order on 8/1/05. This herd is made up of 58 head of cattle on two pastures. A herd inventory was conducted and the animal of interest was not present within the herd. The owner of Trace Herd 6 had very limited records and was unable to provide further information on where the cow might have gone after he purchased her from the livestock market. A search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. Additionally, many of the animals presented for sale by the owner of the herd had been re-tagged at the market effectually losing the traceability of the history of that animal prior to re-tagging. The animal of interest traced to this herd was classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 6 was released on 8/3/05.



 
Trace Herd 7 The owner of Trace Herd 7 was identified as having received an animal of interest and was placed under hold order on 8/1/05. Trace Herd 7 contains 487 head of cattle on multiple pastures in multiple parts of the State, including a unit kept on an island. The island location is a particularly rough place to keep cattle and the owner claimed to have lost 22 head on the island in 2004 due to liver flukes. Upon completion of the herd inventory, the animal of interest was not found present within Trace Herd 7. A GDB search of all recorded herd tests conducted on Trace Herd 7 and all market sales by the owner failed to locate the identification tag of the animal of interest. The cow was subsequently classified as untraceable. It is quite possible though that she may have died within the herd, especially if she belonged to the island unit. The hold order on Trace Herd 7 was released on 8/8/05.
 
 
 
 
 
 
 
 
 
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...




 
 
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
 
 
 
 
 
 
 
 
 
 
 
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."
 
 
 
 
 
end...tss



 
Saturday, May 26, 2012

 
 
Are USDA assurances on mad cow case 'gross oversimplification'?
 
 
 
SNIP...
 
 
 
What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”
 
 
 
The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”
 
 
 
“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.
 
 
 
In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the origins of atypical cases of BSE,” she said
 
 
 
The argument about feed is critical because if feed is the cause, not a spontaneous mutation, the California cow could be part of a larger outbreak.
 
 
 
SNIP...
 
 
 
Saturday, August 4, 2012
 
 
 
*** Final Feed Investigation Summary - California BSE Case - July 2012
 
 
 
 
 
 
 
 
 
in the url that follows, I have posted
 
 
 
SRM breaches first, as late as 2011.
 
 
 
then
 
 
 
MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until 2007, when they ceased posting them.
 
 
 
then,
 
 
 
MAD COW SURVEILLANCE BREACHES.
 
 
 
Friday, May 18, 2012
 
 
 
Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States Friday May 18, 2012
 
 
 
 
 
 
 
 
 
 
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006


 
 
 
 
 
 
 
 
 
 
 
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
 
 
 
 
 
 
 
 
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"
 
 
 
 
 
 
 
 
Wednesday, December 22, 2010

 
Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle and what about mad cow disease ?
 
 
 
 
 
 
 
 
USDA ET AL SECRET TEST THEY USE ON HOW NOT TO FIND MAD COW DISEASE IN USA
 
 
 
 
 
Tuesday, November 02, 2010
 
 
 
IN CONFIDENCE
 
 
 
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".

 
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
 
 
 
 
 
 
 
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006

 
 
 
 
Comments on technical aspects of the risk assessment were then submitted to FSIS.
 
 
 
Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.

 
This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:
 
 
 
 
 
 
Owens, Julie
 
 
 
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
 
 
 
Sent: Monday, July 24, 2006 1:09 PM

 
To: FSIS RegulationsComments

 
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)

 
Page 1 of 98
 
 
 
 
 
 
*** FSIS, USDA, REPLY TO SINGELTARY
 
 
 
 
 
 
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
 
 
 
 
 
 
 
 
 
 
2012 atypical L-type BSE BASE California reports
 
 
 
Saturday, August 4, 2012
 
 
 
Final Feed Investigation Summary - California BSE Case - July 2012
 
 
 
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012
 
 
 
Summary Report BSE 2012
 
 
 
Executive Summary
 
 
 
 
 
 
 
Saturday, August 4, 2012

 
Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation
 
 
 
 
 
 
 
 
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...



 
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model
 
 
 
 
 
 
***Infectivity in skeletal muscle of BASE-infected cattle
 
 
 
 
 
 
***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries.
 
 
 
 
 
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.
 
 
 
 
 
 
The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission.
 
 
 
In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.
 
 
 
 
 
 
 
Thursday, June 21, 2012
 
 
 
Clinical and Pathologic Features of H-Type Bovine Spongiform Encephalopathy Associated with E211K Prion Protein Polymorphism

 
Justin J. Greenlee1*, Jodi D. Smith1, M. Heather West Greenlee2, Eric M. Nicholson1
 
 
 
1 National Animal Disease Center, United States Department of Agriculture, Agricultural Research Service, Ames, Iowa, United States of America, 2 Iowa State University, Ames, Iowa, United States of America
 
 
 
Abstract
 
 
 
The majority of bovine spongiform encephalopathy (BSE) cases have been ascribed to the classical form of the disease. Htype and L-type BSE cases have atypical molecular profiles compared to classical BSE and are thought to arise spontaneously. However, one case of H-type BSE was associated with a heritable E211K mutation in the prion protein gene. The purpose of this study was to describe transmission of this unique isolate of H-type BSE when inoculated into a calf of the same genotype by the intracranial route. Electroretinograms were used to demonstrate preclinical deficits in retinal function, and optical coherence tomography was used to demonstrate an antemortem decrease in retinal thickness. The calf rapidly progressed to clinical disease (9.4 months) and was necropsied. Widespread distribution of abnormal prion protein was demonstrated within neural tissues by western blot and immunohistochemistry. While this isolate is categorized as BSE-H due to a higher molecular mass of the unglycosylated PrPSc isoform, a strong labeling of all 3 PrPSc bands with monoclonal antibodies 6H4 and P4, and a second unglycosylated band at approximately 14 kDa when developed with antibodies that bind in the C-terminal region, it is unique from other described cases of BSE-H because of an additional band 23 kDa demonstrated on western blots of the cerebellum. This work demonstrates that this isolate is transmissible, has a BSE-H phenotype when transmitted to cattle with the K211 polymorphism, and has molecular features that distinguish it from other cases of BSE-H described in the literature.
 
 
 
 
snip...
 
 
 
 
Most significantly it must be determined if the molecular phenotype of this cattle TSE remains stable when transmitted to cattle without the E211K polymorphism as several other isolates of atypical BSE have been shown to adopt a molecular profile consistent with classical BSE after passage in transgenic mice expressing bovine PrPC [40] or multiple passages in wild type mice [23]. Results of ongoing studies, namely passage of the E211K Htype isolate into wild-type cattle, will lend further insight into what role, if any, genetic and sporadic forms of BSE may have played in the origins of classical BSE. Atypical cases presumably of spontaneous or, in the case of E211K BSE-H, genetic origins highlight that it may not be possible to eradicate BSE entirely and that it would be hazardous to remove disease control measures such as prohibiting the feeding of meat and bone meal to ruminants.
 
 
 
 
 
 
 
 
Sunday, May 18, 2008
 
 
 
BSE, CJD, and Baby foods (the great debate 1999 to 2005)

 
 
 
 
 
Thursday, July 22, 2010


 
 
BSE INQUIRY DFA 18 COSMETICS


 
 
From: TSS


 
 
Subject: Use of Materials Derived From Cattle in Human Food and Cosmetics [Docket No. 2004N-0081] RIN 0910-AF47
 
 
 
 
 
Date: April 17, 2008 at 2:41 pm PST


 
 
 



 
 
Sunday, May 18, 2008

 
MAD COW DISEASE BSE CJD CHILDREN VACCINES
 
 



 
Sunday, May 18, 2008







BSE Inquiry DRAFT FACTUAL ACCOUNT DFA

 


 
 
 
 
 
 
 
 
 
1999




15 November 1999


British Medical Journal



vCJD in the USA * BSE in U.S.


http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us




 



2 January 2000






British Medical Journal
 


U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
 
 
 



 
 
 
2001
 


 
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...


 
 
 
 
 
 
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001


 
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########


 
Greetings List Members,
I was lucky enough to sit in on this BSE conference call today and even managed to ask a question. that is when the trouble started.
I submitted a version of my notes to Sandra Blakeslee of the New York Times, whom seemed very upset, and rightly so.
"They tell me it is a closed meeting and they will release whatever information they deem fit. Rather infuriating."
and i would have been doing just fine, until i asked my question. i was surprised my time to ask a question so quick.
 
 
 
 
(understand, these are taken from my notes for now. the spelling of names and such could be off.)



 
[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
from this point, i was still connected, got to listen and tape the whole conference. at one point someone came on, a woman, and ask again;
[unknown woman] what group are you with?
[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD and other human TSE's world wide. i was invited to sit in on this from someone inside the USDA/APHIS and that is why i am here. do you intend on banning me from this conference now?
at this point the conference was turned back up, and i got to finish listening. They never answered or even addressed my one question, or even addressed the issue. BUT, i will try and give you a run-down for now, of the conference.
IF i were another Country, I would take heed to my notes, BUT PLEASE do not depend on them. ask for transcript from;
RBARNS@ORA.FDA.GOV 301-827-6906
he would be glad to give you one ;-)
Rockville Maryland, Richard Barns Host
BSE issues in the U.S., How they were labelling ruminant feed? Revising issues.
The conference opened up with the explaining of the U.K. BSE epidemic winding down with about 30 cases a week.
although new cases in other countries were now appearing.
Look at Germany whom said NO BSE and now have BSE.
BSE increasing across Europe.
Because of Temporary Ban on certain rendered product, heightened interest in U.S.
A recent statement in Washington Post, said the New Administration (old GW) has a list of issues. BSE is one of the issues.
BSE Risk is still low, minimal in U.S. with a greater interest in MBM not to enter U.S.
HOWEVER, if BSE were to enter the U.S. it would be economically disastrous to the render, feed, cattle, industries, and for human health.
(human health-they just threw that in cause i was listening. I will now jot down some figures in which they told you, 'no need to write them down'. just hope i have them correct. hmmm, maybe i hope i don't ???)
80% inspection of rendering
*Problem-Complete coverage of rendering HAS NOT occurred.
sizeable number of 1st time FAILED INITIAL INSPECTION, have not been reinspected (70% to 80%).
Compliance critical, Compliance poor in U.K. and other European Firms.
Gloria Dunason Major Assignment 1998 goal TOTAL compliance. This _did not_ occur. Mixed level of compliance, depending on firm.
Rendering FDA license and NON FDA license
system in place for home rendering & feed 76% in compliance 79% cross contamination 21% DID NOT have system 92% record keeping less than 60% total compliance
279 inspectors 185 handling prohibited materials
Renderer at top of pyramid, significant part of compliance. 84% compliance
failed to have caution statement render 72% compliance & cross contamination caution statement on feed, 'DO NOT FEED TO CATTLE'
56 FIRMS NEVER INSPECTED
1240 FDA license feed mills 846 inspected
"close to 400 feed mills have not been inspected"
80% compliance for feed.
10% don't have system.
NON-FDA licensed mills There is NO inventory on non licensed mills. approximately 6000 to 8000 Firms ??? 4,344 ever inspected. "FDA does not have a lot of experience with"
40% do NOT have caution statement 'DO NOT FEED'.
74% Commingling compliance
"This industry needs a lot of work and only half gotten to"
"700 Firms that were falitive, and need to be re-inspected, in addition to the 8,000 Firms."
Quote to do BSE inspection in 19 states by end of January or 30 days, and other states 60 days. to change feed status??? Contract check and ask questions and pass info.
At this time, we will take questions.
[I was about the third or fourth to ask question. then all B.S.eee broke loose, and i lost my train of thought for a few minutes. picked back up here]
someone asking about nutritional supplements and sourcing, did not get name. something about inspectors not knowing of BSE risk??? the conference person assuring that Steve Follum? and the TSE advisory Committee were handling that.
Some other Dr. Vet, whom were asking questions that did not know what to do???
[Dennis Wilson] California Food Agr. Imports, are they looking at imports?
[Conference person] they are looking at imports, FDA issued imports Bulletin.
[Linda Singeltary ??? this was a another phone in question, not related i don't think] Why do we have non-licensed facilities?
(conference person) other feed mills do not handle as potent drugs???
Dennis Blank, Ken Jackson licensed 400 non FDA 4400 inspected of a total of 6000 to 8000, (they really don't know how many non licensed Firms in U.S. they guess 6000 to 8000??? TSS)
Linda Detwiler asking everyone (me) not to use emergency BSE number, unless last resort. (i thought of calling them today, and reporting the whole damn U.S. cattle herd ;-) 'not'
Warren-Maryland Dept. Agr. Prudent to re-inspect after 3 years. concerned of Firms that have changed owners.
THE END
TSS


 
 
 
 
 
 
snip...
 


 
see full text and more here on tissue donor herds and the TSE Prion disease ;




U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
 
 
 
 
 
 
 
 



Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al.



JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA




Diagnosis and Reporting of Creutzfeldt-Jakob Disease



To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.





Terry S. Singeltary, Sr Bacliff, Tex




1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT




http://jama.jamanetwork.com/article.aspx?articleid=1031186





26 March 2003



Terry S. Singeltary, retired (medically) CJD WATCH



I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?


http://www.neurology.org/content/60/2/176/reply#neurology_el_535
 
 
 
 
2009




 
 

14th ICID International Scientific Exchange Brochure -


 








Final Abstract Number: ISE.114
 


Session: International Scientific Exchange
 



Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

 

T. Singeltary

 

Bacliff, TX, USA

 

Background:

 

An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

 

Methods:
 



12 years independent research of available data
 



Results:
 


I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

 

Conclusion:

 

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
 






 
 
 
 
 
 
 


re-Human Prion Diseases in the United States Posted by flounder on 01 Jan 2010 at 18:11 GMT


 




I kindly disagree with your synopsis for the following reasons ;



 








 
 

 







Wednesday, May 16, 2012
 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
 


Proposal ID: 29403



 










 
Wednesday, August 24, 2011

 








*** There Is No Safe Dose of Prions



Monday, December 26, 2011






 


*** Prion Uptake in the Gut: Identification of the First Uptake and Replication Sites



 

 
 
 
Thursday, February 14, 2013
 
 
 
*** The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease
 
 
 
 
 
 
Wednesday, February 20, 2013
 
 
 
*** World Organization for Animal Health Recommends United States' BSE Risk Status Be Upgraded
 
 
 
Statement from Agriculture Secretary Tom Vilsack:
 
 
 
 
 
 
 


Monday, January 14, 2013








*** Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe





 
Thursday, February 21, 2013
*** National Prion Disease Pathology Surveillance Center Cases Examined January 16, 2013
 
 
 
 
 
Monday, May 30, 2011
 
 
 
 
*** CEPs for gelatin and impact of the revised EU Note for Guidance on the TSE risk EMEA/410/01 Rev.3) will come into force in July 2011
 
 
 
 
 
 
Monday, February 01, 2010
 
 
 
Import Alert 17-04 BSE CJD HIGH RISK TISSUES, Nutritional Supplements and Cosmetics
 
 
 
snip...
 
 
 
1998 MY SUBMISSION TO THE BSE INQUIRY ENGLAND
 
 
 
Sender: "Patricia Cantos"
 
 
 
To: "Terry S Singeltary Sr. (E-mail)"
 
 
 
Subject: Your submission to the Inquiry
 
 
 
Date: Fri, 3 Jul 1998 10:10:05 +0100
 
 
 
3 July 1998 Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.net Ref: E2979
 
 
 
Dear Mr Singeltary,
 
 
 
Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died.
 
 
 
As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments.
 
 
 
Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD. I would refer you to the transcripts of evidence we have already heard which are found on our internet site at http://www.bse.org.uk. Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on 0171 261 8332 should you have any queries.
 
 
 
 
Yours sincerely Patricia Cantos Families Team Leader Attachments TSS
 
 
 
==============
 
 
 
 
My neighbors Mom also died from CJD. She had been taking a nutritional supplement which contained the following; vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. As I said, this woman taking these nutritional supplements, died from CJD. The particular batch of pills that was located, in which she was taking, was tested. From what I have heard, they came up negative, for the prion protein. But, in the same breath, they said their testing, may not have been strong enough to pick up the infectivity. Plus, she had been taking these type pills for years, so, could it have come from another batch?
 
 
 
 
 
 
 
IPLEX, mad by standard process;
vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach.
also;


 
i will only list animal ingredients of the following Nutritional Supplements by only ONE company;
 
 
Standard Process Co.
 
 
 
 
IPLEX; bovine EYE PMG Extract, veal bone PMG Extract, bovine liver powder, vaccuum dried porcine stomach, vacuum dried bovine adrenal, vacuum dried bovine kidney, bovine adrenal, vacuum dried BOVINE BRAIN, bone meal, vacuum dried veal bone.
 
 
 
 
A-FBetafood R vacuum dried bovine prostate, bovine liver powder, vacuum dried bovine kidney, bovine orchic glandular extract, bovine liver fat extract.
 
 
 
 
Arginex R bovine liver powder.
 
 
 
 
Adrenal, Desiccated TM Vacuum dried bovine adrenal.
 
 
 
 
Albaplex R bovine liver PMG Extract, vacuum dried bovine adrenal, bovine kidney PMF Extract, bovine thymus Cytosol Extract, bovine liver powder, bone meal, vacuum dried bovine kidney, veal bone meal.
 
 
 
 
Allerplex TM bovine lung PMF Extract, bovine adrenal PMF Extract, bovine liver fat extract (yakriton), bone meal, vacuum dried bovine kidney, vacuum dried veal bone.
 
 
 
 
Immuplex R Bovine liver PMG Extract, bovine liver powder, veal bone PMF Extract, bovine spleen PMF Extract, vacuum dried bovine and ovine spleen, bovine thymus PMF Extract, bovine thymus Cytosol Extract.


 
Vasculin R Bovine Heart PMG Extract, veal bone PMF Extract, bovine liver powder, vacuum dried porcine duodenum, bovine adrenal Cytosol Extract, vacuum dried bovine and ovine spleen.
 
 
 
 
Zypan R bovine pancreas Cytosol Extract, vacuum dried bovine and ovine spleen.
 
 
 
last i heard, they were getting sued;
 
 
 
 
Suit Filed Over Mad Cow Disclaimer

 
By Jason Hoppin The Recorder March 23, 2001
 
 
snip...see full text ;
 
 
 
 
 
 
 
 

Volume 15, Number 5—May 2009

 
 

Research

 
 

Chronic Wasting Disease Prions in Elk Antler Velvet

 
 
 
 
 
 
 
 
 
 
 
Thursday, January 31, 2008
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft minutes of the 99th meeting held on 14th December 2007
snip...
 
 
 
ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION
 
 
 
 
40. The Chair explained that the purpose of the question and answer session was to give members of the public an opportunity to ask questions related to the work of SEAC. Mr Terry Singeltary (Texas, USA) had submitted a question prior to the meeting, asking: “With the Nor-98 now documented in five different states so far in the USA in 2007, and with the two atypical BSE H-base
 
 
 
 
13 © SEAC 2007
 
 
 
 
cases in Texas and Alabama, with both scrapie and chronic wasting disease (CWD) running rampant in the USA, is there any concern from SEAC with the rise of sporadic CJD in the USA from ''unknown phenotype'', and what concerns if any, in relations to blood donations, surgery, optical, and dental treatment, do you have with these unknown atypical phenotypes in both humans and animals in the USA? Does it concern SEAC, or is it of no concern to SEAC? Should it concern USA animal and human health officials?”
 
 
 
 
41. A member considered that this question ............
 
 
 
 
 
 
 
 
 

Comment from Terry S Singletary Sr

 
 
Document ID: APHIS-2006-0041-0006 Document Type: Public Submission
This is comment on Proposed Rule: Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines
Docket ID:






RIN:0579-AC01
Topics: No Topics associated with this document
 



 
----- Original Message -----
 
 
 
 
 
 
 
 
 
Sent: Wednesday, November 29, 2006 1:24 PM
 
 
 
Subject: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION]

 
November 29, 2006
 
 
 
Greetings FDA, DHH, Dr. Freas, and Dr. Harvey et al,

 
a kind and warm Holiday Greetings to you all.

 
i kindly wish to submit the following to the TSE advisory committee for the meeting December 15, 2006,
about the assessment for potential exposure to vCJD in human plasma-derived antihemophilic factor (FVIII) products manufactured from U.S. plasma donors and related communication material ;
 
 


 
i see the media picked up on this as a 'low risk', from what the gov. agency perceived to be to them;





 






 
 
 
however, i seem to disagree. from my primitive ciphering, i see it another way. this is a huge catastrophic risk. 3 in 160 is 1.9%. so call that 2% which is 1 in 50 or twenty per thousand or 20,000 per million. also, what about the mixed genotypes/mixed susceptibility? what about the silent carriers that donated tainted blood? what about the sporadic CJDs of UNKNOWN strain or phenotype? this risk assessment is just more BSe to me. Just another in a long line of industry fed crap. i pray that my assessment is the one that is wrong. but it is THEY who roll the dice with your life. It is THEY who refuse to regulate an industry that has run amok. just from a recall aspect of potentially tainted blood, and these are just recent recalls ;
 
 
 
Attachment to Singletary comment
SNIP...SEE FULL TEXT IN THE ATTACHMENT SOURCE REFERENCES AT THE BOTTOM OF THIS SUBMISSION ;
 
 
 
Attachment to Singletary comment


 


 
Response to Public Comments
 
 
 
on the
 
 
 
Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005
 
 
 
INTRODUCTION
 
 
 
 
The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website: http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp).
 
 
 
Comments on technical aspects of the risk assessment were then submitted to FSIS.


 
Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.

 
This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:
 
 
 
 
 
 
 
Suppressed peer review of Harvard study October 31, 2002.
 
 
 
 
October 31, 2002 Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Conducted by the Harvard Center for Risk Analysis, Harvard School of Public Health and Center for Computational Epidemiology, College of Veterinary Medicine, Tuskegee University Final Report Prepared for U.S. Department of Agriculture Food Safety and Inspection Service Office of Public Health and Science Prepared by RTI Health, Social, and Economics Research Research Triangle Park, NC 27709 RTI Project Number 07182.024
 
 
 
 
 
 
 
 
 
 
 
 
2005
 
 
 
 
----- Original Message -----
 
 
 
 
From: Terry S. Singeltary Sr.
 
 
 
 
 
 
 
 
Sent: Wednesday, September 07, 2005 9:44 PM


 
Subject: Use of Materials Derived From Cattle in Human Food and Cosmetics [Docket No. 2004N-0081] RIN 0910-AF47
 
 
 
 
-------- Original Message --------
 
 
 
 
Subject: Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)
 
 
 
 
Date: Sun, 11 Jul 2004 21:34:22 –0500
 
 
 
 
From: "Terry S. Singeltary Sr."
 
 
 
 
 
 
 
 
CC: regulations@aphis.usda.gov, burt.pritchett@fda.gov
 
 
 
 
Docket No. 04-047-l No. 04-021ANPR No. 2004N-0264 NEW BSE SAFEGUARDS Federal Measures to Mitigate BSE Risks: Considerations for Further Action



 
 
Greetings FDA,
 
 
 
 
USDA and APHIS et al, I would kindly like to comment on the continued delay of the regulations that have been proposed for years to reduce the risk of BSE/TSE in the USA. Each day that is wasted debating this issue allows this agent to spread, and many many more humans and animals become needlessly exposed to this agent via a multitude of potential routes and sources right here in the USA. TO continue to ignore the new findings from several scientists about the fact that BSE is not the only strain of TSE in cattle, the fact that new atypical strains of TSE are showing up in not only cattle, but sheep and the fact that the new strain of TSE in cattle seems to be more similar to sporadic CJD as opposed to the nv/v CJD, to continue to ignore these findings will only further spread this agent. CWD and Scrapie have been running rampant in the USA for decades. BOTH of which have been rendered and fed back to animals for human/animal consumption for decades. All of which transmits to primates by the natural and non-forced oral consumption of TSE scrapie, CJD, Kuru agent (and CWD by inoculation). Strong Scientific evidence discovered back in the 80s support the fact that a TSE has been prevalent in the USA bovine for decades, either undetected or ignored. IF you consider the recent stumbling and staggering TEXAS cow that was showing all signs of a CNS/TSE disorder that was ordered to be rendered without BSE/TSE test, brains, spinal cord, head and all (as to no possible evidence left of TSE), I would think the 'ignored' or 'covered up' to be the better terminology. Then you have the Downer in Washington state that was actually a good walker and then all the banned Canadian products that some how found it's way across the border into the USA, considering all this, it is very difficult for me to believe that the FDA/USDA/APHIS et al are doing everything possible to protect the 'consumer'. Hardly the case;
 
 
 
 
Congressman Henry Waxmans Letter to the Honorable Ann Veneman
 



(updated links 2013...tss)

 
 

http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2004/ucm108292.htm



http://oversight-archive.waxman.house.gov/documents/20040608105007-72922.pdf



http://oversight-archive.waxman.house.gov/documents/20040607142914-86912.pdf



http://oversight-archive.waxman.house.gov/documents/20040817120642-85052.pdf



http://oversight-archive.waxman.house.gov/documents/20040817120805-51929.pdf



http://www.usda.gov/oig/webdocs/Testimony7-2004.pdf



http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/bse_final_epi_report8-05.pdf



http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/06/0235.xml



http://www.cidrap.umn.edu/cidrap/content/other/bse/news/june3005bse.html



http://www.fda.gov/downloads/ICECI/EnforcementActions/EnforcementStory/EnforcementStoryArchive/UCM091074.pdf



http://www.fda.gov/ICECI/EnforcementActions/EnforcementStory/EnforcementStoryArchive/ucm107472.htm
 
 
 
 
 
 
 
 
snip...
 
 
 
 
 
From: TSS Subject:
 
 
 
 
Re: Docket No. 2004N-0081 Use of Materials Derived From Cattle in Human Food and Cosmetics [TSS SUBMISSION]
 
 
 
 
Date: September 7, 2005 at 7:35 pm PST
 
 
 
 
In Reply to:
 
 
 
 
 
Docket No. 2004N-0081 Use of Materials Derived From Cattle in Human Food and Cosmetics posted by TSS on September 7, 2005 at 7:07 am:
 
 
 
 
----- Original Message -----
 
 
 
 
From: Terry S. Singeltary Sr.
 
 
 
 
To: fdadockets@oc.fda.gov





Sent: Wednesday, September 07, 2005 9:44 PM
 
 
 
 
Subject: Use of Materials Derived From Cattle in Human Food and Cosmetics [Docket No. 2004N-0081] RIN 0910-AF47
Greetings FDA,
 
 
 
I would kindly like to comment on ;
 
 
 
Use of Materials Derived From Cattle in Human Food and Cosmetics [Docket No. 2004N-0081] RIN 0910-AF47
 
 
 
SUMMARY: The Food and Drug Administration (FDA) is amending the interim final rule on use of materials derived from cattle in human food and cosmetics published in the Federal Register of July 14, 2004. In the July 14, 2004, interim final rule, FDA designated certain materials from cattle, including the entire small intestine, as ``prohibited cattle materials'' and banned the use of such materials in human food, including dietary supplements, and in cosmetics. FDA is taking this action in response to comments received on the interim final rule. Information was provided in comments that persuaded the agency that the distal ileum, one of three portions of the small intestine, could be consistently and effectively removed from the small intestine, such that the remainder of the small intestine, formerly a prohibited cattle material, could be used for human food or cosmetics. We (FDA) are also clarifying that milk and milk products, hide and hide-derived products, and tallow derivatives are not prohibited cattle materials. Comments also led the agency to reconsider the method cited in the interim final rule for determining insoluble impurities in tallow and to cite instead a method that is less costly to use and requires less specialized equipment. FDA issued the interim final rule to minimize human exposure to materials that scientific studies have demonstrated are highly likely to contain the bovine spongiform encephalopathy (BSE) agent in cattle infected with the disease. FDA believes that the amended provisions of the interim final rule provide the same level of protection from human exposure to the agent that causes BSE as the original provisions. ...
 
 
 
I would kindly like to submit the following ;
 
 
 
I find it very very disturbing that FDA now takes the position;
 
 
 
 
>>>Information was provided in comments that persuaded the agency that the distal ileum, one of three portions of the small intestine, could be consistently and effectively removed from the small intestine, such that the remainder of the small intestine, formerly a prohibited cattle material, could be used for human food or cosmetics. <<<
 
 
 
 
TSE science is emerging and the old testing techniques for TSEs are becoming much more sensitive than when some of these old BSE tissue bio-assays were done in the distant past. I urge once again for the FDA and the USDA to put forth sound science instead of the political and corporate science they have floundered with for the last 3 decades. THERE is much new data out that dispute the position the FDA/USDA have taken on SRMs.
 
 
 
 
STATEMENT ON INFECTIVITY IN BOVINE TONSIL
 
 
 
 
Background


 
1. The views of the Committee were sought on unpublished results from an
ongoing long-term study of the pathogenesis of BSE in cattle. This study is
being carried out by the Veterinary Laboratory Agency and is funded by the
Food Standards Agency (FSA).
 
 
 
 
2. In this study, cattle were orally dosed with 100g of BSE-infected bovine
brain material. At various times after oral dosing, cattle were killed and
different tissues tested for infectivity. In the first instance, the presence of
infectivity was assessed by injection of various tissues into inbred mice
("mouse bioassay "). In this research infectivity was detected in:
 
 
 
 
• distal ileum (the earliest infectivity was detected at 6 months after
inoculation.)
 
 
 
 
• brain and spinal cord and closely associated nervous tissue
(infectivity was detected in the months just prior to the clinical onset
of BSE in cattle)
 
 
 
 
• at a single time point (around the time of clinical onset) bone marrow
was also found to contain infectivity. ...snip
 
 
 
 
 
 
 
 
 
 
UPDATE OF THE OPINION ON
 
 
 
 
TSE INFECTIVITY DISTRIBUTION IN RUMINANT TISSUES
 
 
 
 
INITIALLY ADOPTED BY
 
 
 
 
THE SCIENTIFIC STEERING COMMITTEE
 
 
 
 
AT ITS MEETING OF 10-11 JANUARY 2002
 
 
 
 
AND AMENDED AT ITS MEETING OF 7-8 NOVEMBER 2002
 
 
 
 
following the submission of (1) a risk assessment by the German Federal Ministry of
Consumer Protection, food and Agriculture and (2) new scientific evidence
regarding BSE infectivity distribution in tonsils
 
 
 
 
 
 
 
3. New work, work still in progress and future work
The infectivity of neural and non-neural tissues by intracerebral inoculation of cattle is being
assayed in projects M03006 and M03007. These studies are important since it is possible
that some tissues may not yet have been found to be infective, due to the fact that
infectivity in these tissues is below the detection limits of the tests applied so far. To date,
this study has shown infectivity in CNS tissues, the distal ileum, tonsil tissue and the
nictitating membrane (the nictitating membrane is also known as the third eyelid). Other
challenged and control cattle continue to be closely monitored for clinical signs of BSE.
 
 
 
 
Research is ongoing to determine the susceptibility of other food animal species to TSEs.
These include a project to determine the susceptibility of pigs to scrapie through oral
exposure (M03005) and a project to further study the transmission of BSE to pigs (M03010).
Project M03024 aims to determine whether UK red deer are susceptible to BSE by oral
exposure. These studies are important since it is highly probable that pigs and deer were
historically exposed to ruminant derived meat and bone meal (MBM). ...
 
 
 
 
 
 
 
 
TSEs And The Environment
 
 
 
The LANCET Volume 351, Number 9110 18 April 1998
 
 
 
BSE: the final resting place
 
 
 
snip...
 
 
 
The first matter to consider is the distribution of infectivity in the bodies of infected animals. The brain (and more generally, the central nervous system) is the primary target in all transmissible spongiform encephalopathies (TSE), and it contains by far the highest concentration of the infectious agent. In naturally occuring disease, infectivity may reach levels of up to about one million lethal doses per gram of brain tissue, whether the disease be kuru, CJD, scrapie, or BSE. The infectious agent in BSE-infected cattle has so far been found only in brain, spinal cord, cervical and thoracic dorsal root ganglia, trigeminal ganglia, distal ileum, and bone marrow.4 However, the much more widespread distribution of low levels of infectivity in human beings with kuru or CJD, and in sheep and goats with scrapie, suggests that caution is advisable in prematurely dismissing as harmless other tissues of BSE-infected cattle.
 
 
 
 
snip...end...TSS
 
 
 
 
snip...
 
 
 
 
BY reducing or weakening the SRM list due to the Economic Impact of BSE on the U.S. Beef Industry and while doing so, ignoring all 'sound science', again the FDA/USDA et al are willing to put every human and animal out there at risk to further exposure to this TSE agent, all for a buck. this is not 'sound science' this is what i call 'corporate science', and it is and will continue to expose people. some of these people will die from this agent either directly or indirectly via a multitude of scientific proven routes and sources. WE must remove all political and corporate science from TSE research.
 
 
 
 
I find it disturbing that products that carry SRMs are still on the market for humans such as nutritional supplements ;
 
 
 
 
ODD, I just picked up a catalog from STANDARD PROCESS INC. 2003 - 2004 Product Catalog (a chiropractor had just left this catalog in my wife's foot doctors office 4/5/05) and it's full of THOSE SRMS FOR HUMANS. I wonder how much is still left on the market, and how much is still in production, how much crosses the borders? 5 pages of products full of SRMs for humans. THIS is a really fine catalog, i am just now going over. LOADED with SRMs for humans. NO wonder my neighbors mom died from CJD while taking these damn mad cow pills. THEY even have a candy bars loaded with SRMs. HERE is one ;
 
 
 
 
NATURAL COCOA STANDARDBAR (mad cow candy bar) (i will just list animal organs)
 
 
 
bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney...
 
 
 
NATURAL PEANUT BUTTER STANDARDBAR
 
 
 
bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney...
 
 
 
USF (MAD COW) OINTMENT (RUB A DUB DUB, KURU ETC) ;
 
 
 
bovine orhic glandular extract
 
 
 
UTROPHIN PMG
 
 
 
bovine uterus PMG
 
 
 
VASCULIN
 
 
 
bovine heart PMG extract, veal bone PMG extract, bovine liever, porcine duodenum, bovine adrenal Cytosol extract, bovine spleen, ovine spleen (some yummy stuff)
 
 
 
IPLEX (neighbors mom died from CJD while taking these pills for years)
 
 
 
bovine eye PMG extract, veal bone PMG, bovine liver, porcine stomach, bovine adrenal, bovine kidney, bovine adrenal Cytosol extract, BOVINE BRAIN, bovine bone, veal bone meal
 
 
 
MYO-PLUS
 
 
 
bovine heart PMG, bovine liver, porcine stomach, bovine orchic extract, bovine spleen, ovine spleen, bovine adrenal Cytosol extract, BOVINE BRAIN
 
 
 
NEUROPLEX
 
 
 
bovine orchic Cytosol extract, bovine spleen, BOVINE BRAIN PMG EXTRACT, BOVINE ANTERIOR PITUITARY, bovine liver, BOVINE PITUITARY PMG EXTRACT, AND MORE BOVINE BRAIN... HOLY MAD COW IN A PILL !!!
 
 
 
NEUROTROPHIN PMG
 
 
 
BOVINE BRAIN PMG
 
 
 
NIACINAMIDE B6 VM
 
 
 
bovine liver, porcine stomach, bovine spleen ovine spleen, BOVINE BRAIN
 
 
 
OCULOTROPHIN PMG BOVINE EYE PMG
 
 
 
ORCHEX
 
 
 
bovine liver, bovine orchic Cytosol extract, porcine stomch, bovine spleen, ovine spleen, BOVINE BRAIN
 
 
 
OSTARPLEX
 
 
 
veal bone PMG extract, veal bone PMG extract, bovine liver, porcine stomach, bovine adrenal, bovine spleen, ovine spleen, BOVINE BRAIN
 
 
 
PARAPLEX
 
 
 
bovine pancreas PMG extract, porcine duodenum, bovine adrenal PMG, BOVINE PITUITARY PMG EXTRACT, bovine thyroid PMG extract
 
 
 
PITUITROPHIN PMG
 
 
 
RUMAPLEX
 
 
 
BOVINE BRAIN, veal bone PMG extract, bovine adrenal, bovine prostate Cytosol extract, veal bone meal, bovine liver PMG extract, bovine spleen, ovine spleen, bovine liver
 
 
 
SENAPLEX
 
 
 
bovine liver PMG extract, bovine adrenal, BOVNE BRAIN, veal bone meal, bovine kidney, bovine orchic extract, bovine spleen, ovine spleen ..........
 
 
 
THESE are just a few of MANY of just this ONE COMPANY.
 
 
 
Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice in Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number: EC -2 Accepted - Volume 7
 
 
 
253 1 DR. BOLTON:
 
 
 
I have an additional question about 2 that. What is the assurance that additional locally sourced 3 tracheas are not added into that manufacturing process, thus 4 boosting the yield, if you will, but being returned to the 5 U.S. as being produced from U.S.-sourced raw material? 6 DR. McCURDY: Are there data to indicate how many 7 grams, or whatever, of infected brain are likely to infect 8 an organism, either animal or man, when taken orally? 9 DR. BROWN: If I am not mistaken, and I can be 10 corrected, I think a half a gram is enough in a cow, orally; 11 in other words, one good dietary-supplement pill. 12 DR. McCURDY: What I am driving at is the question 13 we are asked is really not do we wish to regulate these 14 things coming in. I think the statements about difficulties 15 in regulating things in the future or near future for new 16 regulations were probably accurate. 17 But I think that we could exhibit some quite 18 reasonable concern about blood donors who are taking dietary 19 supplements that contain a certain amount of unspecified- 20 origin brain, brain-related, brain and pituitary material. 21 If they have done this for more than a sniff or something 22 like that, then, perhaps, they should be deferred as blood 23 donors. 24 That is probably worse than spending six months in 25 the U.K. 254 1 DR. BROWN: That is exactly right. I think that 2 is why the discussion has apparently been on things that are 3 not directly related to these questions because, in order to 4 think about deferrals for blood donors who are taking 5 dietary supplements with things like bovine brain in them, 6 it is very important that we know that those products are 7 safe. 8 I think we have heard enough to suggest that they 9 may not be. 10 DR. McCURDY: There is one other item that needs 11 to be considered and that is what proportion of blood donors 12 are doing this; that is, how many blood donors would you 13 lose, and I don't know what the demographics--there is 14 fairly good information on the demography of blood donors. 15 I have no idea what the demography of people who take these 16 supplements is. Maybe they are old men like me and aren't 17 going to be blood donors anymore. 18 DR. BROWN: The wording of the question is not as 19 demanding as the wording of other deferral questions; that 20 is, the question here is consider recommending. We are 21 not even recommending at this point. We are saying to the 22 FDA, please think about this. It is worth thinking about. 23 DR. DETWILER: One point about brain from Europe, 24 and Jean Philippe is still here, those are considered 25 specified risk material and it is not correct to be 255 1 incinerated; correct? Or destroyed? Brain and spinal cord 2 and other high-risk tissues in Europe? 3 DR. NORTON: In tomorrow morning's British Medical 4 Journal, which has appeared on-line today, there is an 5 article called U.S. Takes Precautions against BSE. One 6 paragraph says, Even though the U.S. and U.K. governments 7 ban the practice of feeding cattle products to cows, in the 8 early 1990s, some U.K. renderers continued to manufacture 9 and ship contaminated meat and bonemeal around the world. 10 British export statistics show that thirty-seven tons of 11 meal made from offal was sent to the United States in 1997, 12 well after the U.S. government banned imports of such risky 13 meat. The ultimate use of these imports has not been 14 identified. 15 That will appear tomorrow morning. 16 DR. DETWILER: That actually was in The New York 17 Times. That is a direct quote out of The New York Times 18 article. We called the reporter on that. That statement, 19 the thirty-seven tons, was taken out of the U.S. 20 Geographical BSE Risk Assessment. What they didn't put in 21 there, in the statement, was the remainder of the GBR is at 22 that time, the big labeling for that category in the U.K., 23 because it was illegal for them to ship it to us from their 24 own regs. It is illegal for us to get that. 25 We did go and try and trace that so that wasn't [FULL TEXT ABOUT 600 PAGES] 3681t2.rtf
 
 
 
 
 
 
 
 
 
 
 
IN fact, we are now finding that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE ;
 
 
 
Published online
 
 
 
January 27, 2005
 
 
 
Risk of oral infection with bovine spongiform
 
 
 
encephalopathy agent in primates
 
 
 
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia,
 
 
 
Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
 
 
 
The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)—which can lead to variant Creutzfeldt-Jakob disease (vCJD)—is compounded by incomplete knowledge about the ef.ciency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these .ndings and data from other studies, we made a
preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
 
 
 
 
snip...
 
 
 
BSE bovine brain inoculum
 
 
 
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
 
 
 
Primate (oral route)* 1/2 (50%)

 
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
 
 
 
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

 
PrPres biochemical detection
 
 
 
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the .rst positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
 
 
 
 
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
snip...end
www.thelancet.com Published online January 27, 2005
 
THEN you must consider cross contamination at feed mills and such. this has been well proven in both the UK and the USA to date via r-to-r feed ban violations. IT was proven in the UK that they indeed put profits before human health;
 
 
 
 
[PDF] The BSE Inquiry / Statement No. 14 Issued 20 March 1998 THE ...



The BSE Inquiry / Statement No. 14. Issued 20 March 1998 ... number of feed compounders and it became clear that cross contamination of feeds could occur. ...
 
 
 
 
 
 
[PDF] The BSE Inquiry / Statement No 76F (Supplementary) Mr Alan ...
But the mainbut the main problem was probably cross-contamination. ...
 
 
 
 
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
 
 
 
snip...
 
 
 
To minimise the risk of farmers' claims for compensation from feed compounders.
 
 
 
To minimise the potential damage to compound feed markets through adverse publicity.
 
 
 
To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.

 
snip...
 
 
 
 
 
THE FUTURE
 
 
 
4..........
 
 
 
 
MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.
 
 
 
 
5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.
 
 
 
 
6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...
 
 
 
 
SEE full text ;
 
 
 
 
 
 
snip...
From: TSS
 
 
 
Subject: Inspector to file charges against USDA for them charging him with misconduct on telling the truth about SRM mad cow violations
 
 
 
Date: September 7, 2005 at 1:37 pm PST

 
Consumer Health
 
 
 
Inspector to file charges against USDA By Steve Mitchell Sep 6, 2005, 22:46 GMT
 
 
 
WASHINGTON, DC, United States (UPI) -- The federal meat inspector who was charged with misconduct by the U.S. Department of Agriculture after he claimed mad cow disease safeguards were being violated at slaughterhouses told United Press International he plans to file charges against the agency.
 
 
 
Stan Painter, a USDA inspector and chair of the National Joint Council of Food Inspection Locals, the inspectors union, notified the agency`s management in a letter last December he was aware of instances where the riskiest parts of older cows were not being marked or removed from processing.
 
 
 
Painter worried these risky parts -- known as specified risk materials, or SRMs -- could enter the food supply and infect people, causing a fatal brain illness called variant Creutzfeldt Jakob disease.
 
 
 
Two cases of mad cow have been detected in U.S. herds, and some suspect there are more. The USDA put the SRM safeguards in place in 2004 to protect the public from mad cow disease -- also known as bovine spongiform encephalopathy or BSE -- if more cases are detected.
 
 
 
The USDA did not respond to Painter`s concerns until he made his letter known to news outlets.
 
 
 
On Dec. 28, 2004, the agency charged Painter with personal misconduct for not revealing the names of the inspectors who told him of the SRM violations. Officials also told him he was under a formal investigation, which was dropped last month after the release of internal documents revealing more than 1,000 violations of the USDA`s SRM regulations.
 
 
 
Painter said he thinks the USDA was attempting 'to harass and intimidate him (and) to have a chilling effect' on other inspectors.
 
 
 
'I plan to file charges against the agency,' he told UPI, adding he has not yet decided if he will go through the legal system, through internal USDA procedures or another avenue.

 
Asked about Painter`s intent to bring charges, agency spokesman Steven Cohen told UPI the documents -- called noncompliance reports, or NRs -- demonstrate 'that BSE safeguard regulations are being enforced and prohibited materials did not reach the public.'
 
 
 
Mad cow disease remains a sensitive topic for the USDA because it can have significant economic ramifications. The U.S. beef industry lost billions of dollars because more than 60 nations closed their borders in 2003 to American beef after the report of the first detected case in U.S. herds. Japan, formerly the largest importer of American beef, still has not reopened its borders.
 
 
 
For months, USDA officials denied Painter`s allegations in media reports, saying they had investigated and found no evidence to substantiate his claims. The NRs released last month under the Freedom of Information Act, however, showed 1,036 violations of SRM regulations in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. The USDA delayed releasing the documents for eight months despite a federal law mandating a response within 30 days.
 
 
 
Patty Lovera, of the watchdog group Public Citizen, which requested the USDA documents, said some of the violations cited in the NRs are egregious. In one, an employee at a plant in Michigan was not properly marking older cows to have their SRMs removed because he did not have a pencil. In another, an employee in a Missouri plant was loading cow heads onto his pickup truck to take home to feed to his dog.
 
 
 
Lovera charged the USDA with attempting to silence Painter and failing to address problems with the SRM ban.
 
 
 
'Their behavior through this whole thing is appalling,' she told UPI. 'Stan brought them concerns about a policy and instead of investigating the policy, they investigated him.'
 
 
 
Last December, after Painter made his letter known publicly, the USDA sent an officer to Painter`s house while he was on leave to question him about the allegations in his letter. Later, USDA officials interrogated Painter twice, asking him for the names of the inspectors who told him about the violations.
 
 
 
Painter said he intentionally was kept ignorant of the inspectors` names because he feared the agency would retaliate against them. Painter also said USDA officials did not need the inspectors` names because they could determine where the infractions were occurring by looking at their database of NRs.
 
 
 
Sometime around June the U.S. Embassy in Japan posted a notice on its Web site stating USDA officials had found no evidence to substantiate Painter`s claims and had requested a criminal investigation into his actions. The notice was removed in July after UPI reported its existence.
 
 
 
Although Cohen acknowledged more than 1,000 NRs were written by USDA inspectors, he minimized their significance, saying they 'amount to less than one-half of one percent of the total written for all reasons by (USDA) inspection program personnel.'
 
 
 
Lovera said any infraction of mad cow safeguards should be of concern, because this disease always is fatal in humans and cooking does not destroy the pathogen.
 
 
 
'You have very little margin of error for something you don`t want to get because you can`t cook it away and you can`t disinfect it,' she said.
 
 
 
Painter said his concern now is what the agency will do to fix what he sees as shortcomings in the SRM policy.
 
 
 
'It`s a failed policy,' he said. 'It doesn`t protect the consumer.'
 
 
 
Cohen did not respond to whether the USDA planned to change the SRM regulations.
 
 
 
The USDA`s Office of Inspector General has launched an investigation to determine whether the regulations are being implemented effectively, and results are due out soon.
 
 
 
 
 
 
 
Copyright 2005 by United Press International
 
 
 
 
 
 
makes no difference, GW will change the SRM rules like he has the BSE GBR risk assessment to the terribly flawed BSE MRR policy, the legal trading of all strains of TSE, the 'gold card'. ...TSS
 
 
 
IN a time when FDA/USDA et al should be strengthening the TSE regulations, it seems corporate interest has won out again over sound science and consumer protection from an agent that is 100% fatal for the ones that go clinical. With the many different atypical TSEs showing up in different parts of the world, and with GWs BSE MRR policy (the legal policy of trading all strains of TSEs), the battle that has waged for the last 25 years to eradicate this agent from this planet will be set back decades, if not lost for good. ...TSS
 
 
 
 
snip...
 
 
 
 
 
 
 
 
 
 
 
 
APHIS-2006-0041-0006 TSE advisory committee for the meeting December 15, 2006
 
 
 
 
 
 
 
 
 
 
Thursday, April 17, 2008
 
 
 
Use of Materials Derived From Cattle in Human Food and Cosmetics [Docket No. 2004N-0081] RIN 0910-AF47
 
 
 
[Federal Register: April 17, 2008 (Volume 73, Number 75)] [Rules and Regulations] [Page 20785-20794] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr17ap08-7]
 
 
 
 
 
 
 
Scientific Opinion on BSE Risk in Bovine Intestines Question number: EFSA-Q-2009-00226
 
 
 
Adopted: 10 September 2009 Summary (0.1Mb)
 
 
 
Opinion (0.1Mb)
 
 
 
Summary
 
 
 
Following a request from the European Commission (EC), the Panel on Biological Hazards (BIOHAZ) was asked to deliver a scientific opinion on the BSE related risk of bovine intestines used for casings. Regulation (EC) No 999/2001 of the European Parliament and of the Council stipulates that certain tissues from bovine, ovine and caprine animals must be considered as Specified Risk Material (SRM) and must be removed from the food and feed chain to protect the health of consumers against the risk of bovine transmissible spongiform encephalopathies (BSE). The intestines, from the duodenum to the rectum, of bovine animals of all ages are currently included in the list of SRM. The "TSE roadmap" prepared by the EC details the short, middle and long term actions on TSE measures such as SRM removal and sets the objectives to ensure and maintain the existing high level of consumer protection. It allows for amendments of the current SRM list based on new evolving scientific knowledge while ensuring and maintaining a high level of consumer protection.
 
 
 
 
Specifically, the mandate asked the BIOHAZ panel to evaluate the scientific validity of a report prepared by Det Norske Veritas Ltd" (DNV) for the Swiss Cervelas task force. This report provides an assessment of the current potential human exposure to BSE infectivity that could result from eating sausages made with EU bovine casings. The BIOHAZ panel was further requested to evaluate the conclusions of the DNV report and, if it was considered necessary based on the report and any other new relevant scientific information, to provide a re-assessment of the BSE related risk of bovine intestines after processing into natural sausage casings.
 
 
 
 
The BIOHAZ panel evaluated the risk assessment as described in the DNV report, and took into account the relevant previous EFSA opinions as well as new scientific data on the same subject.
 
 
 
 
New but limited experimental scientific data demonstrate that in addition to ileum, also jejunum may harbour infectivity when a large BSE inoculum dose was used to experimentally infect cattle. With regard to the DNV Report, the BIOHAZ Panel considers its approach (concept and methodology) scientifically sound, whereas the interpretation of the results as obtained is not shared by the Panel. Its assumptions were based on limited scientific data obtained from a single morphometric study (which was already found to be inadequate in the previous EFSA Opinion on bovine casings) and on limited and earlier data on the presence of PrPsc/infectivity in bovine gut after experimental oral BSE inoculation. There is uncertainty about the relative BSE risk of neural and lymphoid tissues in casings compared to CNS that might have significant impact on the calculated results of the DNV Report. The Panel notes that the DNV Report considers the individual human BSE exposure risk from bovine casings, excluding ileum, to be "very low". However, when the upper confidence limits are taken into account, along with the uncertainties in key parameter assumptions, the calculated total human exposure per year in the EU from bovine casings, even when ileum is excluded (based on the calculated BSE prevalence in 2007) is 11.000 cattle oral ID50 units per year (when all casings would have been sourced in the UK) and about 1.000 cattle oral ID50 units per year (when all casings would have been sourced in the Netherlands) and therefore cannot be considered negligible. Thus the conclusion in the DNV report that sausage casings sourced from intestines of cattle in EU Member States would lead to a negligible risk for human consumption cannot be considered valid. Moreover, when considering other new relevant scientific information it is concluded that the previous EFSA assessment of the BSE related risk of bovine intestines after processing into natural sausage casings remains valid. The Panel recommends that future considerations on the risk in bovine casings should take into account the BSE prevalence in cattle at that time.
 
 
 
 
 
Published: 22 September 2009
 
 
 
 
 
 
 
 
 
 
 
SUMMARY
 
 
 
 
 
 
 
OPINION
 
 
 
 
snip...
 
 
 
 
6. Overview of current scientific knowledge on BSE risk in Bovine Intestines. The previous EFSA Opinion on BSE risk from bovine intestine summarised the scientific knowledge that was available until early 2007. Since then, additional publications have become available on a natural BSE case in Japan (Kimura and Haritani, 2008) and two experimental studies that examined
 
 
 
 
presence of PrPsc and/or infectivity in the intestines of cattle challenged orally with 100g (Espinosa et al., 2007; Hoffmann et al., 2007). Moreover, a new study performed by the VLA in the UK on PrPsc in BSE-infected cattle (Stack, 2009) and preliminary results from the German BSE pathogenesis study have recently be made available to EFSA and were also taken into account.
 
 
 
6.1. New experimental studies on intestines of BSE infected cattle
 
 
 
 
Espinosa et al. (2007) examined pooled tissues from 13 cattle inoculated at ages between 4 and 6 months and culled at ages between 24 and 39 months. Infectivity in Tgbov mice but not PrPsc by ELISA/WB was found in Peyer's patches dissected from distal ileum at all ages. Hoffmann et al (2007) demonstrated PrPsc by IHC in Peyer's patches of distal ileum in one of two preclinical animals sacrificed at 24 and 28 months post inoculation (mpi). Most recently, Arnold et al. (2009) estimated the titre of infectivity in the distal ileum from the incubation time found by bioassay in wild type mice. Over time, the infectivity in the distal ileum showed an initial increase up to 14-18 months post exposure, followed by a decrease, which was likely to be highly variable between animals. However, these estimates were based on mouse titration of brain material, while the incubation period to dose relationship may differ between brain and intestines (Robinson et al., 1990).
 
 
 
6.2. Infectivity of intestines in cattle with natural BSE infection
 
 
 
 
Data on presence of PrPsc or infectivity in intestines of natural BSE cases are sparse. The immunohistochemistry (IHC) and Western blot examinations of three BSE infected cattle detected in Japan in the course of active surveillance (but showing locomotor deficits) found PrPsc in distal ileum of two (by IHC confined to the myenteric plexus) (Iwata et al., 2006). No PrPsc was detected in Peyer's patches of distal ileum, or in samples of other regions of small and large intestine, or in a range of other lymphoid tissues. Labelling of myenteric plexus was also detected in 9/29 confirmed field cases of BSE examined in the UK (Terry et al., 2003). Infectivity by wild-type mouse assay or the presence of PrPsc has not been found in the distal ileum, or other levels of intestine in a total of some six natural BSE cases studied (Fraser and Foster, 1994; Buschmann and Groschup 2005; Iwata et al., 2006). In one of these cases in Germany, however, infectivity was detected in the distal ileum by bioassay in TgBov XV mice (Buschmann and Groschup, 2005). More recently, another BSE case (94 months of age) in Japan showed definite or equivocal immunoreactivity in nerve cells of the myenteric plexus in ileum, caecum and colon, and in Schwann cells of the myenteric plexus in duodenum, jejunum, ileum, caecum and colon (Kimura and Haritani, 2008).
 
 
 
6.3. Study commissioned by ENSCA
 
 
 
This ENSCA commissioned study investigated the presence of BSE PrPsc in small intestines of cattle that had been orally challenged at 4-6 months of age with 100g or 1 g doses of BSE affected brain tissue. These animals were culled and examined 18-30 months post inoculation (p.i.). Three methods to identify PrPsc were applied: a commercial ELISA test, Western immunoblotting, and IHC. Results confirmed previous observations that PrPsc was mainly confined to lymphoid tissue of the ileum, whereas the duodenum was negative and no part of the enteric nervous system tested positive. The lymphoid tissue of the jejunum of one high-dosed animal tested positive. As expected, the low-dosed animals had a much lower frequency of positive ileum samples (1/18 vs. 15/18 in the high-dose group) and some longer incubation times (24 months in the one animal with positive ileum), whereas the high-dose group included animals positive at all ages examined.
 
 
 
As the ENSCA commissioned study was performed retrospectively on archival tissue, sampling was limited by availability, and the study authors themselves concede that "it is possible tissue sampling was not optimal" for duodenum and jejunum of low-dosed animals. The 1g-dosed group included 6 animals sampled at 18 months p.i., 6 at 24 months, and 6 at 30 months. The 100g-dosed group included 6 animals sampled for ileum at 18 months p.i., 6 at 24 months, and 6 at 30 months;
 
 
 
 
duodenum and jejunum, however, were sampled only in 2 animals each at 18, 24 and 30 months p.i., respectively. From each level of the intestine, three sections were examined by IHC per case. While at least two of the three sections of the ileum per case contained lymphoid follicles, in 36% of the duodenum cases, and in 39% of the jejunum cases lymphoid follicles were absent in any of the examined sections. The frequency of positive follicles per section ranged between 1% and 14% in ileum of the high-dose group, and 0,7% in the one positive ileum of the low-dose group, and was 6,7% and 11,1% in the two positive jejunum sections of one high-dosed animal.
 
 
 
Conclusions on the ENSCA commissioned study:
 
 
 
 
. This study confirms that detectable PrPsc is mainly confined to lymphoid tissue of the ileum in cattle orally challenged with 100g of BSE brain and culled at 18, 24 and 30 months postinoculation (p.i.)
 
 
 
 
. One out of 18 animals challenged orally with 1g of BSE brain was positive in ileum.
 
 
 
 
. One out of 18 animals challenged orally with 100g of BSE brain was positive in jejunum.
 
 
 
 
. The duodenum was always negative.
 
 
 
 
. However, the sampling in particular of duodenum and jejunum was limited and contained lymphoid tissue only in a part of sections examined.
 
 
 
 
. In contrast to previous reports on natural BSE cases in older animals, the enteric nervous system was always negative.
 
 
 
 
. In consideration of the previous EFSA opinion on bovine intestine that gives detailed advice for future studies, in particular concerning the lower frequency of lymphoid follicles in parts of the intestine other than the distal ileum, the present ENSCA commissioned study meets some but not all recommendations; in particular the mostly negative results obtained for jejunum and duodenum should not be over-interpreted when tissue sampling was limited.
 
 
 
 
6.4. New preliminary data on bovine intestine from the German BSE Pathogenesis study
 
 
 
 
In the German BSE pathogenesis study performed at the Friedrich-Loeffler-Institute (FLI), 56 Simmental cross-breed calves aged about four months were challenged orally with 100g brainstemhomogenate pooled out of clinically BSE diseased cattle. The infectivity load in the homogenate was about 106.1 ID50 (grams of tissue)-1 as determined by end-point titration in Tgbov XV mice (Buschmann & Groschup, 2005, Hoffmann et al., 2007). Furthermore, as controls, 18 calves were inoculated orally with a BSE-negative brainstem homogenate. Four to five animals were selected randomly and euthanised every four months. More than 150 tissue and body fluid samples were sampled at subsequent necropsies from each animal under TSE-sterile conditions.
 
 
 
 
After oral exposure with the TSE agent, previous studies had demonstrated consistently early prion accumulation in the gut associated lymphatic tissue, about six months post infection (mpi) in cattle (Terry et al., 2003), and at two mpi in scrapie infected sheep (van Keulen et al., 2002) and in 21 days old lambs (Andreoletti et al., 2002). In contrast to scrapie, the accumulation of PrPd in the distal ileum of BSE-infected cattle was confined to an only minor proportion of follicles respectively neurons/glial cells of the enteric nervous system (Terry et al., 2003).
 
 
 
 
Normally when performing IHC, a three micrometer section per paraffin block is used, reflecting a very small proportion of the tissue sample. Therefore a serial section procedure was newly established at the FLI to increase the total amounts of tissue structures examined per sample and consequently increasing the probability of detecting PrPsc accumulation. Thereby, five sections per paraffin block with a plane distance of about 25-30 µm were examined. Hence, a tissue depth of about 150-200 µm per block was screened for positive immunosignals. Additionally two different PrP-specific monoclonal antibodies, highly sensitive for the detection of bovine PrPsc were used.
 
 
 
 
According to this method, representative samples of the small intestine, in particular Peyer's patches of the distal ileum but also the ileo-caecal junction from most of the infected animals of the German BSE Pathogenesis study were examined by IHC. From 4 mpi until 44 mpi in most animals (38/43), PrPsc was detectable, initially in the follicles of the Peyer's patches and at later stages of the incubation period in the enteric nervous system too.
 
 
 
 
Conclusions on the German pathogenesis study
 
 
 
 
. With improved sampling, nearly all animals dosed with 100 g of BSE brain tissue showed PrPsc in distal ileum between 4 and 44 mpi, first in lymphoid tissue and later in enteric nervous system.
 
 
 
 
7. Review of the DNV report
 
 
 
 
7.1. Summary of the report
 
 
 
 
DNV makes an attempt to quantify the amount of BSE infectious load in bovine sausage casings. This is then extrapolated to the risk carried in an individual sausage, a normal persons risk per year and the overall exposure within the EU in a year. The key points of the DNV Report are as follows:
 
 
 
 
. The DNV Report assumes that the ileum is not used for the production of casings and is removed and discarded.
 
 
 
 
. The DNV Report is based on the assumption that potential infectivity in bovine intestine used for sausage casing production would be 2 logs less than in the ileum. Based on experimental data, the infectivity in the distal ileum was considered to be at a titre equivalent to that in the CNS at the late stage of infection. Thus infectivity in non-ileal parts of the intestines used for casings production was assumed to be 100 fold less than in the CNS.
 
 
 
 
. The DNV Report uses a value of 0.43g/m (obtained from Wijnker et al.) of casing to quantify the amount of lymphoid and neural tissue that might harbour infectivity in a sausage casing,
 
 
 
 
. The results of the DNV Report calculate that an exposure per person per year from bovine casings produced in the Netherlands "would be very low" even when a high consumption pattern like in Germany is assumed (upper range 7 x 10-6 cattle oral (CO) ID50 units). For casings sourced in the UK, the exposure would be about one log higher.
 
 
 
 
. When the calculated total amount of cumulative human exposure per year in the EU is considered, the following scenario emerges: 11.000 CO ID50 units per year when all casings would have been sourced in the UK, and about 1.000 CO ID50 units when all casings would have been sourced in the Netherlands, a country with an about average prevalence of BSE in the EU4.
 
 
 
 
4 How can the output of the DNV calculations be interpreted in terms of potential human infections? If we follow, as in the previously adopted EFSA Opinions on Tallow and MBM (EFSA 2005 a and b) the cautionary advice of the original QRA WG and assume the species barrier is 1 as a worst case scenario, then there would be up to 5500 infected person in the EU per year in the first scenario, and up to about 500 in the second. This would have to assume a linear dose-response curve of infectivity at very low doses. If the species barrier was given a more realistic value obtained from the analysis carried out on the exposure of the British population to the BSE agent (EFSA, 2006) of around 1000 - 4000, this would mean that there might be up to around 1 to 5 infected person in the EU per year in the first scenario, and less than 1 in the second.
 
 
 
 
snip... see full text ;
 
 
 
 
 
 
 
 
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
 
 
 
 
 
 
 
Tuesday, September 14, 2010

 
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
 
 
 
 
 
 
 
Monday, February 7, 2011
 
 
 
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???
 
 
 
 
 
 
 
Monday, May 30, 2011
 
 
 
CEPs for gelatin and impact of the revised EU Note for Guidance on the TSE risk EMEA/410/01 Rev.3) will come into force in July 2011
 
 
 
Note concerning CEPs for gelatin and impact of the revised EU Note for Guidance on the TSE risk
 
 
 
 
 
 
 
Thursday, December 22, 2011
 
 
 
Risk of Prion Disease Transmission through Bovine-Derived Bone Substitutes: A Systematic Review Clin Implant Dent Relat Res. 2011 Dec 15. doi: 10.1111/j.1708-8208.2011.00407.x. [Epub ahead of print]
 
 
 
 
 
 
 
Volume 18, Number 1—January 2012 Dispatch
Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model
 
 
 
 
Nadine Mestre-Francés , Simon Nicot, Sylvie Rouland, Anne-Gaëlle Biacabe, Isabelle Quadrio, Armand Perret-Liaudet, Thierry Baron, and Jean-Michel Verdier Author affiliations: Institut National de la Santé et de la Recherche Médicale (INSERM) U710, Montpellier, France (N. Mestre-Francés, S. Rouland, J.-M. Verdier); Université Montpellier 2, Montpellier (N. Mestre-Francés, S. Rouland, J.-M. Verdier); École Pratique des Hautes Etudes, Paris, France (N. Mestre-Francés, S. Rouland, J.-M. Verdier); Agence Nationale de Sécurité Sanitaire, Lyon, France (S. Nicot, A.-G. Biacabe, T. Baron); Hopitaux Civils de Lyon, Lyon, France (I. Quadrio, A. Perret-Liaudet); Université Lyon 1, Lyon (I. Quadrio, A. Perret-Liaudet); INSERM U1028, Lyon (I. Quadrio, A. Perret-Liaudet); Centre National de la Recherche Scientifique, Lyon (I. Quadrio, A. Perret-Liaudet)
 
 
 
Abstract
 
 
 
We report transmission of atypical L-type bovine spongiform encephalopathy to mouse lemurs after oral or intracerebral inoculation with infected bovine brain tissue. After neurologic symptoms appeared, transmissibility of the disease by both inoculation routes was confirmed by detection of disease-associated prion protein in samples of brain tissue.
 
 
 
 
SNIP...


 
The Study A total of 12 mouse lemurs of both sexes (Center for Breeding and Experimental Conditioning of Animal Models, University Montpellier 2, Montpellier, France) were maintained in animal Biosafety Level 3 facilities, according to requirements of the French ethics committee (authorization CE-LR-0810). Young and adult lemurs were fed (8 animals) or IC inoculated (4 animals) with 5 or 50 mg of L-BSE–infected brain tissue (10% homogenate in 5% glucose) (Table). The isolate for the L-BSE agent (02–2528) was derived from cattle in France (11). When progression of prion disease was evident, the lemurs were euthanized and their brains were isolated. Brains were processed for Western blot analysis with SHa31 monoclonal antibody against PrP for PrPres detection, as described in mice (11); for histologic examination by using hematoxylin and eosin staining; and for disease-associated prion protein (PrPd) immunochemical detection by using the paraffin-embedded tissue blot method or immunohistochemical analysis with monoclonal antibody 3F4 against PrP.
 
 
 
 
Beginning ≈3 months before the terminal stage of the disease (19–22 months after inoculation), neurologic symptoms developed in the 4 mouse lemurs that received IC inoculations (Table). In all 4 animals, initial clinical signs and symptoms were blindness, thigmotaxic behavior, and poor appearance of the fur. Appetite and general fitness were maintained; anxiety and aggressiveness were not observed. Next, locomotion became slower, followed by incoordination and loss of balance in the last month of life. Ipsilateral circling behavior was reported, indicating unilateral degeneration of the striatum. This behavior stopped 15 days after onset, suggesting damage to the contralateral striatum. Disequilibrium, with frequent falls, became more noticeable. At the terminal stage of the disease, the animals were prostrate.
 
 
 
 
One orally inoculated lemur, which was fed 5 mg of infected brain and euthanized 27 months later, had signs and symptoms of disease similar to those in IC-inoculated animals, except for the ipsilateral circling behavior. In 2 lemurs fed 50 mg and 2 others fed 5 mg of L-BSE–infected brain, clinical signs and symptoms of prion disease developed just a few weeks before the animals were euthanized (18 and 32 months and 33 and 34 months after inoculation, respectively). Disease was characterized by progressive prostration, loss of appetite, and poor appearance of the fur, without incoordination or disequilibrium. The 3 remaining lemurs were orally inoculated at 2 years of age and were still alive and healthy 28 months after inoculation (Table).
 
 
 
 
snip...
 
 
 
 
Conclusions
 
 
 
 
We demonstrated that the agent of L-BSE can be transmitted by the oral route from cattle to mouse lemurs. As expected, orally inoculated animals survived longer than IC-inoculated animals. Orally inoculated lemurs had less severe clinical signs and symptoms, with no evidence of motor dysfunction. It was previously suggested that the agent of L-BSE might be involved in the foodborne transmission of a prion disease in mink (11,12), a species in which several outbreaks of transmissible mink encephalopathy had been identified, notably in the United States (13).
 
 
 
 
Our study clearly confirms, experimentally, the potential risk for interspecies oral transmission of the agent of L-BSE. In our model, this risk appears higher than that for the agent of classical BSE, which could only be transmitted to mouse lemurs after a first passage in macaques (14). We report oral transmission of the L-BSE agent in young and adult primates. Transmission by the IC route has also been reported in young macaques (6,7). A previous study of L-BSE in transgenic mice expressing human PrP suggested an absence of any transmission barrier between cattle and humans for this particular strain of the agent of BSE, in contrast to findings for the agent of classical BSE (9). Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.
 
 
 
 
Dr Mestre-Francés is an assistant professor at the École Pratique des Hautes Études. Her research focuses on neurodegenerative diseases (Alzheimer disease, prion diseases) in the nonhuman primate model Microcebus murinus.
 
 
 
 
 
 
 
 
October 2009 O.11.3 Infectivity in skeletal muscle of BASE-infected cattle
 
 
 
 
Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1, Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3, Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5, Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS Torino, Italy; 5University of Verona, Italy




 
Background: BASE is an atypical form of bovine spongiform encephalopathy caused by a prion strain distinct from that of BSE. Upon experimental transmission to cattle, BASE induces a previously unrecognized disease phenotype marked by mental dullness and progressive atrophy of hind limb musculature. Whether affected muscles contain infectivity is unknown. This is a critical issue since the BASE strain is readily transmissible to a variety of hosts including primates, suggesting that humans may be susceptible.


 
Objectives: To investigate the distribution of infectivity in peripheral tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and i.p. with 10% homogenates of a variety of tissues including brain, spleen, cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from cattle intracerebrally infected with BASE. No PrPres was detectable in the peripheral tissues used for inoculation either by immunohistochemistry or Western blot.
 
 
 
 
Results: Mice inoculated with BASE-brain homogenates showed clinical signs of disease with incubation and survival times of 175±15 and 207±12 days. Five out of seven mice challenged with skeletal muscle developed a similar neurological disorder, with incubation and survival times of 380±11 and 410±12 days. At present (700 days after inoculation) mice challenged with the other peripheral tissues are still healthy. The neuropathological phenotype and PrPres type of the affected mice inoculated either with brain or muscle were indistinguishable and matched those of Tgbov XV mice infected with natural BASE.
 
 
 
 
Discussion: Our data indicate that the skeletal muscle of cattle experimentally infected with BASE contains significant amount of infectivity, at variance with BSE-affected cattle, raising the issue of intraspecies transmission and the potential risk for humans. Experiments are in progress to assess the presence of infectivity in skeletal muscles of natural BASE.
 
 
 
 
 
 
 
 
see much more here ;
 
 
 
Friday, December 23, 2011
 
 
 
 
Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model
 
 
 
Volume 18, Number 1—January 2012 Dispatch
 
 
 
 
 
 
 
 
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"
 
 
 
 
 
 
 
 
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...
 
 
 
 
 
 
 
 
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.
 
 
 
 
 
 
 
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.
 
 
 
 
 
 
 
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...
 
 
 
 
 
 
P.9.21 Molecular characterization of BSE in Canada
 
 
 
 
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
 
 
 
 
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
 
 
 
 
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.
 
 
 
 
Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis. Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
 
 
 
 
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *** It also suggests a similar cause or source for atypical BSE in these countries.
 
 
 
 
 
 
 
 
 
Saturday, July 23, 2011
 
 
 
 
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
 
 
 
 
 
 
 
 
 
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
 
 
 
 
 
 
 
 
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>
 
 
 
Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)
 
 
 
 
 
 
 
P.4.23
 
 
 
Transmission of atypical BSE in humanized mouse models
 
 
 
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA
 
 
 
 
Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.
 
 
 
 
Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.
 
 
 
 
Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time.*** The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.
 
 
 
 
Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.
 
 
 
 
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
 
 
 
 
 
 
 
 
P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS
 
 
 
 
Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA
 
 
 
Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C.*** The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.
 
 
 
 
III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)
 
 
 
 
 
 
 
 
I ask Professor Kong ;
 
 
 
Thursday, December 04, 2008 3:37 PM
 
 
 
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
 
 
 
 
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
 
 
 
 
Professor Kong reply ;
 
 
 
.....snip
 
 
 
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''
 
 
 
Best regards,
 
 
 
Qingzhong Kong,
 
 
 
 
 
PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
 
 
 
END...TSS
 
 
 
Tuesday, November 02, 2010
 
 
 
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
 
 
 
 
 
 
 
Thursday, December 04, 2008 2:37 PM
 
 
"we have found that H-BSE can infect humans."
 
 
personal communication with Professor Kong. ...TSS
 
 
 
BSE-H is also transmissible in our humanized Tg mice.
 
 
 
The possibility of more than two atypical BSE strains will be discussed.
 
 
 
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
 
 
 
 
 
 
 
 
 
 
Thursday, June 23, 2011
 
 
 
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
 
 
 
 
 
 
 
Thursday, December 22, 2011
 
 
 
Risk of Prion Disease Transmission through Bovine-Derived Bone Substitutes: A Systematic Review
 
 
 
Clin Implant Dent Relat Res. 2011 Dec 15. doi: 10.1111/j.1708-8208.2011.00407.x. [Epub ahead of print]
 
 
 
 
 
 
 
Friday, December 16, 2011
 
 
 
Creutzfeldt-Jacob Disease Question Asked by Lord Walton of Detchant P-Capt filter
 
 
 
 
 
 
 
Saturday, December 3, 2011
 
 
 
Candidate Cell Substrates, Vaccine Production, and Transmissible Spongiform Encephalopathies
 
 
 
Volume 17, Number 12—December 2011
 
 
 
 
 
 
 
Wednesday, August 24, 2011
 
 
 
All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD

 
 
 
 
 
Wednesday, August 24, 2011
 
 
 
There Is No Safe Dose of Prions
 
 
 
 
 
 
 
2011
 


 
 
Monday, September 26, 2011
 


 
 
L-BSE BASE prion and atypical sporadic CJD
 


 
 
 
 
 
 
 
 
 
Tuesday, November 08, 2011
 
 
 
Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011
 
 
 
Original Paper
 
 
 
Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.
 
 
 
 
 
 
 
Editorial: The European Response to BSE: A Success Story
 
 
 
EFSA Journal 2011; 9(9):e991 [3 pp.]. doi:10.2903/j.efsa.2011.e991 Author Herbert Budka, Member and Vice-Chair of EFSA's Panel on Biological Hazards (BIOHAZ)Contact
 
 
 
 
 
 
Type: Editorial Published: 02 September 2011 Affiliation: European Food Safety Authority (EFSA), Parma, Italy Article
 
 
 
Editorial Bovine spongiform encephalopathy (BSE, "mad cow disease") was officially first reported in November 1986 in the UK. It became quickly interpreted as likely counterpart in bovines of scrapie, the paramount transmissible spongiform encephalopathy (TSE, prion disease) in sheep and goats. A landmark epidemiological study by John Wilesmith and co-workers (Wilesmith et al., 1988) identified in 1988 cattle feedstuffs containing ruminant-derived protein (meat-bone meal, MBM) as source for the evolving epidemic that numbered almost 185.000 diagnosed cases in total in the UK and a further 5.500 elsewhere in the EU, with some 2 million infected bovines estimated to have entered the human food chain in the UK. The first UK response was a ban on feeding MBM to ruminants, as a measure that significantly curbed but did not eliminate the epidemic.
 
 
 
A likely link between BSE and the human disease variant Creutzfeldt-Jakob disease (vCJD) was published in early April 1996 (Will et al., 1996), followed by a media outbreak of apocalyptic scenarios sketching a man-made disaster of then unpredictable proportions. Health authorities were frantically acting to limit damage from BSE not only to human health, but also to agriculture, economies, political credibility and public confidence. In the UK, the Phillips Inquiry (Lord Phillips et al., 2000) took two and a half years to accrue insight into why and how the BSE saga developed. The key conclusions depicted BSE as a consequence of intense farming practices, with significant shortcomings in the way things were done, with sensible measures taken that were not always timely and adequately implemented and enforced, and implicitly guided by the belief that BSE was not a real threat to human health. Moreover, there was too much secrecy and unjustified reassurance by governmental bodies in order to protect the agricultural industry.
 
 
 
Almost simultaneously with publication of the Phillips Report, the second public BSE crisis started in 2000 when first results of active BSE surveillance on the European continent confirmed scientists' opinion that political claims of "freedom from BSE" in several countries were wishful thinking rather than reality. As a result, the EU TSE Regulation of 2001[1] laid down a comprehensive set of harmonised rules for the prevention, control and eradication of TSEs, including an EU-wide total ban on the feeding of animal proteins to farmed animals. More or less independent national food safety authorities were now established in most EU countries, and the need to separate risk assessment from risk management could no longer be ignored.
 
 
 
Since the first BSE crisis of 1996, the European Commission (EC) has embarked on a science-guided response, establishing a TSE/BSE ad hoc Group of their Scientific Steering Committee (SSC) that provided up to 2003 a plethora of opinions on all aspects of BSE and other TSEs (SSC, 1997-2003). The SSC was a risk assessment and risk advisory body, separated from risk management which remained with the EC Directorate General for Health & Consumers (DG SANCO). From December 1997, the SSC adopted their first important documents on the scientific basis to protect human health from BSE, such as the definition of tissues containing most of infectious TSE agents (prions), termed Specific Risk Materials (SRM). Regrettably, politicians in several EU Member States (MS) were then unwilling to translate this into legislation, still sticking to their "freedom from BSE" illusion. It was only after a delay of almost 3 years that the EU-wide SRM ban, the most important measure to protect public health from BSE, became implemented.
 
 
 
Since 2003, EFSA has taken over the role of science-based advice to the EC on BSE/TSE-related matters, with the BIOHAZ Panel producing an equally impressive amount of opinions and reports (EFSA, 2003-2011) as the former SSC. As a whole, these scientific risk assessments - first by the SCC, then by EFSA - and their translation into adequate measures by national and EC risk managers were the basis of the European response to BSE, which has been a spectacular success story. This is evident from quantitative data on both the animal and human disease. First, the prevalence of BSE as detected by current surveillance has come down steadily in the EU to a trickle, from several thousands of cases in the early 2000s, to 44 in 2010 in the EU (11 in the UK) (OIE, 2011). Second, surveillance of vCJD in the UK indicates that the epidemic, having reached a peak in the year 2000 when there were 28 deaths, has declined to a current incidence of about one diagnosis/death per year (Andrews, 2011). Clearly, it is now time to be re-assured but still too early for complacency (Budka et al., 2008).
 
 
 
Given the quantitative indicators of what seems, in the EU, to be the near-extinction of the animal epidemic and control of cattle-to-human transmission, is there anything left for concern? Unfortunately, there is. With BSE, the global disease burden is far from clear in countries with less well-developed surveillance. In humans, the potential continuing person to person spread by blood and blood products remains a problem as seen with the four cases of transfusion-associated vCJD infection to date (Andrews, 2011). With BSE and other TSEs in animals, the recognition of the wide diversity of prion strains in the field, including three new forms of animal TSEs (L-type Atypical BSE, H-type Atypical BSE and Atypical scrapie), has complicated disease diagnosis and surveillance, as well as scientific assessment of their potential risks to humans. 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. In particular the L-type Atypical BSE agent might be similarly or even more virulent to humans than the Classical BSE agent. While mankind has been in contact with the major TSE of small ruminants for centuries, there is no epidemiological evidence to suggest that classical scrapie is zoonotic; however, experimental transmission data on humanised mice and non-human primates have been very scarce so far.
 
 
 
 
 
What does this mean for the future? The decline of the BSE epidemic seen by 2005 led to consideration of some relaxation of costly BSE control measures as depicted in the EU TSE Roadmap (EC, 2005), and will inevitably be followed by further relaxation as already outlined in another EU TSE Roadmap 2 of 2010 (EC, 2010). It remains critical that current levels of consumer protection are maintained and all future changes from well established and highly effective current risk management measures are based upon sound scientific advice that EFSA will continue to provide.
 
 
 
Which old issues will remain, and which new issues will become relevant? For Atypical BSE, the most widely accepted hypothesis is that of a spontaneously arising ("sporadic") disease in relatively old bovines. If this holds true, it will be impossible to eradicate such a disease which originates de novo; probably we then have to live forever with a ban on SRMs, in particular the central nervous system (CNS), of older cattle. Given our insufficient knowledge about the true prevalence of atypical animal prion strains in the field, it will be important to continue and improve the systematic surveillance of animal TSEs, and to refine our diagnostic and laboratory methods and experiments. As some scientific data suggest that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011), the issue of a zoonotic potential of prions is likely to remain with us a time. For human TSEs including sporadic CJD, it will be important to continue systematic surveillance that should be able, as clearly shown with vCJD in the past, eventually to identify emerging new phenotypes or new prion strains. In sum, at a time when many scientists and most decision makers are no longer interested in prions and their risk, it will be prudent to stay vigilant, although this must be in a way that is balanced with other risks to human and animal health. In the risk assessment area, this will continue to be a challenge for EFSA in the years to come.
 
 
 
--------------------------------------------------------------------------------
 
 
 
[1] Regulation (EC) No 999/2001 of the European Parliament and of the Council of 22 May 2001 laying down rules for the prevention, control and eradication of certain transmissible spongiform encephalopathies. OJ L 147, 31.05.2001, p. 1-40.
 
 
 
 
 
 
 
 
 
see full text and more here ;
 
 
 
 
 
 
 
 
Tuesday, October 4, 2011
 
 
 
De novo induction of amyloid-ß deposition in vivo
 
 
 
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
 
 
 
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
 
 
 
De novo induction of amyloid-ß deposition in vivo
 
 
 
R Morales1,2, C Duran-Aniotz1,3, J Castilla2,4, L D Estrada2,5 and C Soto1,2
 
 
 
1Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Houston Medical School, Houston, TX, USA 2University of Texas Medical Branch at Galveston, Galveston, TX, USA 3Universidad de Los Andes, Facultad de Medicina. Av. San Carlos de Apoquindo 2200, Las Condes, Santiago, Chile 4CIC bioGUNE, Parque Tecnologico de Biskaia, Ed 800, 48160 Derio and IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Spain
 
 
 
Correspondence: Dr C Soto, Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Houston Medical School, 6431 Fannin St, Houston, TX 77030, USA. E-mail: Claudio.Soto@uth.tmc.edu
 
 
 
5Current address: Laboratorio de Señalización Celular, Centro de Envejecimiento y Regeneración. P. Universidad Catolica de Chile, Santiago, Chile.
 
 
 
Received 8 March 2011; Revised 15 August 2011; Accepted 25 August 2011; Published online 4 October 2011.
 
 
 
 
 
Abstract
 
 
 
Alzheimer's disease (AD), the most common type of senile dementia, is associated to the build-up of misfolded amyloid-ß (Aß) in the brain. Although compelling evidences indicate that the misfolding and oligomerization of Aß is the triggering event in AD, the mechanisms responsible for the initiation of Aß accumulation are unknown. In this study, we show that Aß deposition can be induced by injection of AD brain extracts into animals, which, without exposure to this material, will never develop these alterations. The accumulation of Aß deposits increased progressively with the time after inoculation, and the Aß lesions were observed in brain areas far from the injection site. Our results suggest that some of the typical brain abnormalities associated with AD can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding. These findings may have broad implications for understanding the molecular mechanisms responsible for the initiation of AD, and may contribute to the development of new strategies for disease prevention and intervention.
 
 
 
Keywords:
 
 
 
amyloid; prion; protein misfolding; disease transmission
 
 
 
 
 
see more here ;
 
 
 
 
 
 
 
 
 
 
 
Wednesday, September 21, 2011
 
 
 
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
 
 
 
 
 
 
Monday, September 26, 2011
 
 
 
Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI, GSS, gCJD, hvCJD, sCJD, TSE, PRION, update 2011
 
 
 
 
 
 
Friday, November 23, 2012
 
 
 
sporadic Creutzfeldt-Jakob Disease update As at 5th November 2012 UK, USA, AND CANADA
 
 
 
 
 
 
Monday, January 14, 2013
 
 
 
 
Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe
 
 
 
 
 
 
 
 
Thursday, February 21, 2013
 
 
 
National Prion Disease Pathology Surveillance Center Cases Examined January 16, 2013
 
 
 
 
 
 
 
Sunday, February 10, 2013
 
 
 
Creutzfeldt-Jakob disease (CJD) biannual update (February 2013) Infection report/CJD
 
 
 
 
 
 
 
Mad Cow Scaremongers
 
 
 
Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent 2003-2011
 
 
 
re-2003
 
 
 
"he also blindly insists upon a mad-cow with Alzheimer's, Parkinson's, and Lou Gehrig's disease."
 
 
 
 
 
 
 
 
 
 
SNIP...SEE FULL TEXT ;
 
 
 
 
 
 
 
 
layperson
TSS
 
 
 
 
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
 
 
 
 
 
-------- Original Message --------
 
 
 
Subject: [Docket No. 04-116-1] USE of veterinary biological products on the topic of Transmissible Spongiform Encephalopathies (TSS SUBMISSION)


 
Date: Fri, 05 Nov 2004 11:49:49 -0600
 
 
 
 
From: "Terry S. Singeltary Sr."


 
CC: Nicole.L.Ruffcorn@aphis.usda.gov, Questa.R.Glenn@aphis.usda.gov, BSE-L
 
 
 
 
> Meeting topics and proposed presentation titles should be submitted

> to Steven A. Karli, director, CVB, APHIS, Veterinary Services, 510

> South 17 St., Suite 104, Ames, IA 50010-8197; phone (515) 232-5785,

> fax (515) 232-7120 or e-mail CVB@aphis.usda.gov. For registration

> information contact Nicole Ruffcorn at the same address and fax number

 
> or via phone dial (515) 232-5785 extension 127 or e-mail
 
 
 
 
 
 
 
 
 
 
I wish to kindly submit the following to Mr. Steven A. Karli for the 13th public meeting to discuss regulatory and policy issues related to the manufacture, distribution, and use of veterinary biological products on the topic of Transmissible Spongiform Encephalopathies (all of them).
 
 
 
 
[Docket No. 04-116-1]
 
 
 
 
 
Greetings APHIS/USDA et al,
 
 
 
INOCULATION of the TSE agent is the most effected mode of transmission, or so it seems.
 
 
 
MOST people have forgotten the medicines act of 1968 where they state not to use scrapie associated fibers SAF for any pharmaceuticals for animals in vet products;
 
 
 
June 1983 MEDICINES ACT 1968
 
 
 
''Unless there is a risk from a heat-resistant pathogen such as the scrapie agent, no restrictions are placed on substances sterilized by autoclaving provided that the complete mass is held at a minimum of 115°C for at least 15 minutes''...
 
 
 
 
 
 
 
PLEASE do not forget the infamous 'Louping-ill vaccine' incident;
 
 
 
 
SNIP...END
 
 
 
 
 
-------- Original Message --------
 
 
 
Subject: Bovine-derived Products Used in the Manufacture and Formulation of Vaccines: Current Policies and Issues for the Future
 
 
 
Date: Fri, 5 Nov 2004 15:06:53 –0600
 
 
 
From: "Terry S. Singeltary Sr."

 
Reply-To: Bovine Spongiform Encephalopathy

 
 
 
 
 
##################### Bovine Spongiform Encephalopathy #####################
 
 
 
 
 
2004 PDA/FDA Joint Regulatory Conference - 9/20-22/2004
 
 
 
 
 
SNIP...END
 
 
 
layperson
 
 
 
 
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
 
 
 

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Use of Materials Derived from Cattle in Human Food and Cosmetics (FDA-2004-N-0188-0051)

 

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