CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE

CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE

Greetings,

I have put a few of these recalls together from previous SRM recalls. Probably missed some, but i am a bit disturbed that the FSIS has apparently chosen not to list this recall from July 14, 2011 due to SRM spinal cord contamination, that i could find. The state of Ohio made a statement about 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) {see below} ;


Thursday, July 14, 2011

Valley Farm Meats (DBA Strasburg Provision, Inc) Issues Precautionary Recall for Beef Products Due to Possible Contamination with Prohibited Materials SRM Ohio Department of Agriculture and Ohio Department of Health

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/valley-farm-meats-dba-strasburg.html


YET, FSIS seems to find it important enough to list this recall from Ohio ;


Ohio Firm Recalls Various Beef Jerky Products due to Misbranding and Undeclared Allergens

Recall Release CLASS II RECALL FSIS-RC-053-2011 HEALTH RISK: LOW

Congressional and Public Affairs (202) 720-9113 Adam Tarr

WASHINGTON, July 22, 2011 –

http://www.fsis.usda.gov/News_&_Events/Recall_053_2011_Release/index.asp


HOWEVER, look at the recalls of the past (see below), the first two were other voluntary recalls from other Companies, which i am using as an example (and see others that follow), but my question, WHY has the FSIS et al apparently chosen NOT to announce this recall on their website here ;


Valley Farm Meats (DBA Strasburg Provision, Inc) Issues Precautionary Recall for Beef Products Due to Possible Contamination with Prohibited Materials SRM Ohio Department of Agriculture and Ohio Department of Health

http://www.fsis.usda.gov/FSIS_Recalls/Open_Federal_Cases/index.asp


I have written both the FSIS and MEATINGPLACE.COM/, both of which have failed to report this important, life long exposure and human health risk factor for TSE from this voluntary recall, and all it got me was being banned from meatingplace.com/ again, and this time i did not even post anything, just sent them a kind note ;


----- 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


=========================================


----- Original Message -----

From: Terry S. Singeltary Sr.

To: tjohnston@meatingplace.com

Sent: Thursday, July 21, 2011 2:17 PM

Subject: Valley Farm Meats (DBA Strasburg Provision, Inc) Issues Precautionary Recall for Beef Products Due to Possible Contamination with Prohibited Materials SRM


Hello Mr. Johnston !

i have not seen this posted on meatingplace ???

I have stopped commenting on the forum at meatingplace, because everytime i comment or leave some science, i get blocked.

but i thought this important enought to send you you directly.


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

[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.

http://www.agri.ohio.gov/public_docs/recalls/2011/Recall_FS_76-2011.pdf


Valley Farm Meats issues beef recall

TimesReporter.com staff report

Posted Jul 13, 2011 @ 03:18 PM

http://www.timesreporter.com/communities/x401792774/Valley-Farm-Meats-issued-beef-recall


Greetings Friends and Family in Ohio !!!


DON'T let anyone fool you, there would be no immediate health effects from any BSE related contamination for years and years, maybe a decade or more.

FACT is, whomever consumed these banned products will not ever know, until it's too late.

FACT is, TSE prion disease are rampant in North America, and the USA is doing everything in it's power to keep that under lock and key.

FACT is, CJD is spreading in the USA, and sporadic CJD has now been linked to atypical BSE and atypical Scrapie, both of which are in North America.

FACT is, the media has failed us terribly in the complete truth behind the mad cow saga.

FACT is, our fine federal friends have systematically covered the mad cow debacle up, thanks to the help of the USDA and the OIE.

THESE are the facts as i have come to know them since loosing my mother to the Heidenhain Variant of Creutzfeldt Jakob disease.

YOU should know these facts too...

snip...end...tss

blocked...banned again...tss


=========================================


has there been another change in protocol to help cover-up more needless expossure to the TSE in the USA ???

or did i just miss this recall ???

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. #

http://www.fsis.usda.gov/News_&_Events/Recall_023_2010_Release/index.asp


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. #

http://www.fsis.usda.gov/News_&_Events/Recall_021_2008_Release/index.asp


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

http://madcowfeed.blogspot.com/2008/07/missouri-firm-recalls-cattle-heads-that.html


Sunday, October 18, 2009

Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009

http://madcowfeed.blogspot.com/2009/10/wisconsin-firm-recalls-beef-tongues.html


Thursday, October 15, 2009

Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009

http://madcowfeed.blogspot.com/2009/10/nebraska-firm-recalls-beef-tongues-that.html


Thursday, June 26, 2008

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials

http://madcowfeed.blogspot.com/2008/06/texas-firm-recalls-cattle-heads-that.html


Friday, August 8, 2008

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed

http://madcowfeed.blogspot.com/2008/08/texas-firm-recalls-cattle-heads-that.html


Saturday, April 5, 2008

SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/srm-mad-cow-recall-406-thousand-pounds.html


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

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/consumption-of-beef-tongue-human-bse.html


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

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/consumption-of-beef-tongue-human-bse.html


Friday, October 15, 2010

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

http://bseusa.blogspot.com/2010/10/bse-infectivity-in-absence-of.html



SPECIFIED RISK MATERIALS SRMs


http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html



http://madcowfeed.blogspot.com/



http://madcowspontaneousnot.blogspot.com/




Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation

http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html



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

PRION DISEASE UPDATE 2010 (11)

http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129



Tuesday, May 3, 2011


PRION, TSE, typical, atypical BSE, aka mad cow disease, spray dried blood, feed, and a recipe for disaster

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/prion-tse-typical-atypical-bse-aka-mad.html



NOW, what about that mad cow feed from atypical BSE in commerce and SRM regulations ???


Research Project: Study of Atypical Bse Location: Virus and Prion Research Unit

Project Number: 3625-32000-086-05 Project Type: Specific Cooperative Agreement

Start Date: Sep 15, 2004 End Date: Sep 14, 2009

Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.

Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate.

Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.

http://www.ushrl.saa.ars.usda.gov/research/projects/projects.htm?accn_no=408490



Saturday, June 12, 2010

PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse

http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html



Wednesday, July 28, 2010

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

http://bse-atypical.blogspot.com/2010/07/re-freedom-of-information-act-project.html



Friday, October 8, 2010

Scientific reasons for a feed ban of meat-and-bone meal, applicable to all farmed animals including cattle, pigs, poultry, farmed fish and pet food

http://madcowfeed.blogspot.com/2010/10/scientific-reasons-for-feed-ban-of-meat.html



Wednesday, July 06, 2011

Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation

http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html



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.

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf



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 ;



http://web.archive.org/web/20060517074958/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf




2011


ANNEX

Major categories of infectivity

The tables below are taken from the WHO Guidelines on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies (2010).

Data entries are shown as follows:

http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:C:2011:073:0001:0018:EN:PDF




THE LATEST DATA ON TISSUE INFECTIVITY

WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies Updated 2010

MAJOR CATEGORIES OF INFECTIVITY: TABLES IA, IB, IC

The assignment of tissues to high, low, and undetected infectivity categories is based exclusively upon observations of naturally occurring disease, or primary experimental infection by the oral route (in ruminants). The Tables do not include results from disease models using strains of TSE that have been adapted to experimental animals, because passaged strain phenotypes can differ significantly and unpredictably from those of naturally occurring disease. However, for tissues and fluids of exceptional public health interest, such as muscle, intestine, skin, secretions and excretions, experimental results have been indicated in footnotes.

Because the detection of misfolded prion protein (PrPTSE) broadly parallels infectivity titers in various tissues [Beekes et al 1996; Andreoletti et al 2004], PrPTSE testing results are presented in parallel with bioassay data.

Although a given tissue may be positive or negative in different varieties of TSE, the expert group considered a tissue to be potentially infectious even if a positive result occurred in only a single disease. The categorical assignment of tissues will almost certainly undergo further revision as new data accumulate from increasingly sensitive tests.

IA: High-infectivity tissues: CNS tissues that attain a high titer of infectivity in the later stages of all TSEs, and certain tissues that are anatomically associated with the CNS.

IB: Lower-infectivity tissues: peripheral tissues that have tested positive for infectivity and/or PrPTSE in at least one form of TSE.

IC: Tissues with no detectable infectivity: tissues that have been examined for infectivity and/or PrPTSE with negative results.

Data entries are shown as follows:

+ Presence of infectivity or PrPTSE

- Absence of detectable infectivity or PrPTSE

NT Not tested

NA Not applicable ?

Uncertain interpretation

( ) Limited or preliminary data

[ ] Infectivity or PrPTSE data based exclusively on bioassays in transgenic

(Tg)mice over-expressing the PrP-encoding gene or PrPTSE amplification methods.

A word of caution is offered about tissues in Table IB for which positive results are so far limited to either detection of PrPTSE using amplification techniques (PMCA), or infectivity bioassays in Tg mice that over-express PrP. The amounts of pathological protein or infectious agent detected by these exquisitely sensitive assays may well fall below the threshold of transmissibility for normal animals and humans. WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies 5

A good example is illustrated in the studies of urine and feces from deer infected with CWD: bioassays using normal deer as recipient subjects were negative; subsequent bioassays performed in Tg mice were positive. A similar discordance was observed for BSE muscle inoculated into cattle and Tgmice. Until more evidence is compiled showing that positive results in experimental PMCA and Tg mouse assays equate to a risk of transmitting disease under natural conditions, it cannot be assumed that such results imply the existence of a substantial risk to the health of animals or humans.

Considering the succession of updated Tables of the past few years, and the fact that inflammation has been shown to result in PrPTSE deposition in tissues that are not normally involved in TSE pathogenesis, it is evident that as testing continues, more tissues will find their way from Table IC into Table IB (but probably not from either Table IC or IB into Table IA). It is also evident that the data generated to date are far from complete, and that a great deal more work needs to be done if conclusions about the tissue distribution and significance of infectivity in a given TSE are to be based on direct measurements rather than by analogy to other forms of the disease.

Finally, it is critically important to understand that categories of infectivity are not the same as categories of risk, which require consideration not only of the level of infectivity in tissue, but also of the amount of tissue to which a person or animal is exposed, and the route by which infection is transmitted. For example, although the level of tissue infectivity is the most important factor in estimating the risk of transmission by instrument crosscontamination during surgical procedures (e.g., neurosurgery versus general surgery), it will be only one determinant of the risk of transmission by blood transfusions, in which a large amount of low-infectivity blood is administered intravenously, or the risk of transmission by foodstuffs that, irrespective of high or low infectivity, involve a comparatively inefficient oral route of infection.

snip...

Table IC: Tissues with no detected infectivity or PrPTSE

snip...

Musculo-skeletal tissues

Bone NT - NT - - NT NT NT NT NT

Tendon NT - NT - - NT NT NT NT NT

snip...

please see full text with tables here ;

WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies Updated 2010

also in the references at bottom i saw ;

12. A single positive marrow in multiple transmission attempts from cattle orally dosed with BSE-infected brain [Wells et al., 1999; Wells et al., 2005; Sohn et al., 2009].

http://www.who.int/bloodproducts/tablestissueinfectivity.pdf



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)

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html



URGENT DATA ON ATYPICAL BSE RISK FACTORS TO HUMANS AND ANIMALS OIE REFUSE TO ACKNOWLEDGE $

position: Post Doctoral Fellow | Atypical BSE in Cattle

Closing date: December 24, 2009

Anticipated start date: January/February 2010

Employer: Canadian and OIE Reference Laboratories for BSE CFIA Lethbridge Laboratory, Lethbridge/Alberta

snip...

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.

snip...

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2


please see full text ;

Wednesday, March 31, 2010

Atypical BSE in Cattle

http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html


14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)

18.173 page 189

Experimental Challenge of Cattle with H-type and L-type Atypical BSE

A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada

Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.

Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.

Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.

http://www.isid.org/14th_icid/


http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf


http://www.isid.org/publications/ICID_Archive.shtml


Tuesday, July 19, 2011

Neuroanatomical Distribution of Disease-Associated Prion Protein in Cases of Bovine Spongiform Encephalopathy Detected by Fallen Stock Surveillance in Japan

http://bse-atypical.blogspot.com/2011/07/neuroanatomical-distribution-of-disease.html



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.

http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf


Wednesday, February 24, 2010

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th

ICID International Scientific Exchange Brochure -

http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html


TSE

http://transmissiblespongiformencephalopathy.blogspot.com/


JULY 2011 PRION TSE UPDATE NORTH AMERICA



Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque

"BSE-L IN NORTH AMERICA MAY HAVE EXISTED FOR DECADES"

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html



ya think $$$


Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

snip...

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...

http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf



Sunday, June 26, 2011

Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html



Thursday, June 23, 2011

Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html


Wednesday, June 15, 2011

Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html


Thursday, February 10, 2011

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31

http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html



Friday, March 4, 2011

Alberta dairy cow found with mad cow disease

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html


Monday, June 20, 2011 2011

Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA

http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html


Monday, June 27, 2011

Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease

http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html


[Docket No. APHIS-2011-0042]

Notice of Request for Extension of Approval of an Information Collection; Interstate Movement of Sheep and Goats

Greetings APHIS et al,

I would kindly like to comment on [Docket No. APHIS-2011-0042] Notice of Request for Extension of Approval of an Information Collection; Interstate Movement of Sheep and Goats.

Due to Transmissible Spongiform Encephalopathy Scrapie and atypical Scrapie in sheep and goats. I strenuously urge to prohibit or restrict the interstate movement of animals and animal products to prevent the dissemination within the United States of animal diseases and pests of livestock and to conduct programs to detect, control, and eradicate pests and diseases of livestock. Scrapie and atypical Scrapie (Nor-98) both are spreading in North America. see ;

Increased Atypical Scrapie Detections

Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.

http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf


Thursday, June 2, 2011

USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California

http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html


POSITIVE SCRAPIE CASES

As of April 30, 2011, 14 cases of classical scrapie and 2 cases of Nor98-like scrapie were confirmed by the National Veterinary Services Laboratories (NVSL); 7 of the positive cases were Regulatory Scrapie Slaughter Surveillance (RSSS) cases (collected between October 1, 2010 and April 30, 2011 and confirmed by May 16, 2011) and 9 were field cases including 1 positive goat (Figure 6). With this positive, 22 cases of scrapie in goats have been confirmed by the NVSL since implementation of the regulatory changes in FY 2002 (Figure7).

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.ppsx



National Scrapie Surveillance Plan United States Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Centers for Epidemiology and Animal Health National Surveillance Unit Fort Collins, CO September 2010

snip...

it is believed that eradication of nonclassical scrapie from the United States is neither necessary nor feasible.

snip...

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/national_scrapie_surv_plan.pdf



Monday, November 30, 2009

USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE

http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html


I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. ...TSS


Friday, February 11, 2011

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html


Monday, April 25, 2011

Experimental Oral Transmission of Atypical Scrapie to Sheep

Volume 17, Number 5-May 2011

http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html


EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE

This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. ........

http://web.archive.org/web/20010305222246/www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf



Wednesday, February 16, 2011

IN CONFIDENCE

SCRAPIE TRANSMISSION TO CHIMPANZEES

IN CONFIDENCE

http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html


Sunday, April 18, 2010

SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010

http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html


I also think that the USDA, OIE et al put the cart before the horse on their decission to exempt the atypical scrapie Nor-98. Transmissible Spongiform Encephalopathies typical and atypical continue to emerge, and new science shows that indeed there is a risk factor for humans. I again strenuously urge that that expemption and free trading of the atypical scrapie TSE around the Globe, due to the OIE and the USDA, should be repealed immediately.



Friday, May 13,

2011 EFSA Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/efsa-joint-scientific-opinion-on-any.html


Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html


UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html


Wednesday, July 06, 2011

Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation

http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html


TEST ! TEST ! TEST !


Friday, August 29, 2008

CREEKSTONE VS USDA COURT OF APPEALS, BUSH SAYS, NO WAY, NO HOW

http://madcowtesting.blogspot.com/2008/08/creekstone-vs-usda-court-of-appeals.html


http://transmissiblespongiformencephalopathy.blogspot.com/


Thursday, August 12, 2010

Seven main threats for the future linked to prions

First threat

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

Second threat

snip...

http://www.neuroprion.org/en/np-neuroprion.html


Rural and Regional Affairs and Transport References Committee

The possible impacts and consequences for public health, trade and agriculture of the Government’s decision to relax import restrictions on beef Final report June 2010

2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo—has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50

http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf


Terry S. Singeltary Sr. has added the following comment:


"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.

The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"

http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101



CENTAUR GLOBAL NETWORK INFORMATION

[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals. It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]

http://centaur.vri.cz.web.atin.cz/docs/cnfi/2011-06-16-110.pdf


CANADA CJD UPDATE 2011

CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011

3. Final classification of 49 cases from 2009, 2010, 2011 is pending.

snip...

http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0111-eng.pdf


USA 2011

USA

National Prion Disease Pathology Surveillance Center

Cases Examined1

(November 1, 2010)

Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

1996 ; earlier 51 33 28 5 0 0

1997 114 68 59 9 0 0

1998 87 51 43 7 1 0

1999 121 73 65 8 0 0

2000 146 103 89 14 0 0

2001 209 119 109 10 0 0

2002 248 149 125 22 2 0

2003 274 176 137 39 0 0

2004 325 186 164 21 0 13

2005 344 194 157 36 1 0

2006 383 197 166 29 0 24

2007 377 214 187 27 0 0

2008 394 231 205 25 0 0

2009 425 258 215 43 0 0

2010 333 213 158 33 0 0

TOTAL 38315 22656 1907 328 4 3

1 Listed based on the year of death or, if not available, on year of referral;

2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;

3 Disease acquired in the United Kingdom;

4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;

5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

http://www.cjdsurveillance.com/pdf/case-table.pdf



Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date. sporadic CJD is on a steady rise, and has been since 1996.

I also urge you to again notice these disturbing factors in lines 5 and 6 ;

5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.


========end=====tss=====2011



UPDATE JULY 2011 MORE OF THE "PENDING CLASSIFICATION CREUTZFELDT JAKOB DISEASE'' STEADY INCREASING...TSS



case; 5 Includes 13 cases in which the diagnosis is pending, and 18 inconclusive cases; 6 Includes 18 (15 from 2011) cases with type determination pending in which the diagnosis of vCJD has been excluded.



http://www.cjdsurveillance.com/pdf/case-table.pdf



Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html


Monday, May 23, 2011



Atypical Prion Diseases in Humans and Animals 2011


Top Curr Chem (2011)

DOI: 10.1007/128_2011_161

# Springer-Verlag Berlin Heidelberg 2011

Michael A. Tranulis, Sylvie L. Benestad, Thierry Baron, and Hans Kretzschmar

http://bse-atypical.blogspot.com/2011/05/atypical-prion-diseases-in-humans-and.html



----- Original Message -----

From: Terry S. Singeltary Sr.

To: Debra.Beasley@aphis.usda.gov

Sent: Tuesday, November 24, 2009 11:01 AM

Subject: OIE has recently published its proposed animal welfare guidelines for public comment

Greetings USDA/APHIS et al,

I would kindly like to comment on OIE proposed guidelines.

AS I said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization. THE reason most every country around the globe came down with BSE/TSE in their cattle, were due to the failed and flawed BSE/TSE testing and surveillance policy of the O.I.E. NOW, they don't even acknowledge atypical scrapie it seems, as one for concern $



Monday, November 23, 2009

BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E.

http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html


Tuesday, May 24, 2011 2:24 PM

O.I.E. Terrestrial Animal Health Standards Commission and prion (TSE) disease reporting 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/oie-terrestrial-animal-health-standards.html


[Docket No. FSIS-2006-0011]

FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)

http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf


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:

http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf


Thursday, July 21, 2011

A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology; Experimental Neurology:

August 2011 - Volume 70 - Issue 8 - pp 698-702

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html


feeding those dead stock downer cows to children for over 4 years was something they should never ever be able to forget about. dead stock downer cows are the most high risk animal for mad cow disease, and they knew this when the feeding to our children of this product was taking place. the USDA et al via the NSLP fed our children all across the USA, from state to state, the largest beef recall in history, they fed our children DEAD STOCK DOWNER COWS, the most HIGH RISK CATTLE FOR MAD COW DISEASE, they fed them to our children, and hid the largest beef recall in USA history, hid this recall under the guise of 'animal abuse'. then told the parents not to worry because none of the kids had been sick or died from it to date. CJD can incubate for decades. anyway, just wanted to tell you about this, and thank you for what you are trying to do...

WHO WILL WATCH THE CHILDREN FOR CJD OVER THE NEXT 5 + DECADES ???

Do you actually believe that the USDA et al jumped in on the law suit against Westland/Hallmark, at the time the largest beef recall in USA history, just because a few animals were abused on a video, or to cover their ass, for letting our children, from school district to school district, from state to state, be fed dead stock downer cows.

In the papers, the government alleges the meatpacking plant slaughtered and processed downer cows for nearly four years — from January 2004 to September 2007 — at the average rate of one every six weeks...



http://downercattle.blogspot.com/2009/09/suit-meatpacker-used-downer-cows-for-4.html



Do you actually believe all these schools recalled this meat because of a few cattle being abused, see list ;


FNS All Regions Affected School Food Authorities By State United States Department of Agriculture Food and Nutrition Service National School Lunch Program March 24, 2008 School Food Authorities Affected by Hallmark/Westland Meat Packing Co. Beef Recall February 2006 - February 2008


DID YOUR CHILD CONSUME DEAD STOCK DOWNERS, THE MOST HIGH RISK CATTLE FOR MAD COW DISEASE ???


http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf



PLEASE SEE ALSO ;



Members of The HSUS are also concerned about the meat products provided to their children through the National School Lunch Program. More than 31 million school children receive lunches through the program each school day. To assist states in providing healthful, low-cost or free meals, USDA provides states with various commodities including ground beef. As evidenced by the HallmarkNVestland investigation and recall, the potential for downed animals to make their way into the National School Lunch Program is neither speculative nor hypothetical.


http://biotech.law.lsu.edu/cases/FDA/hsus-v-schafer-usda-complaint.pdf



PLEASE NOTE *


Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

snip...

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...



http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf




PLEASE be aware, for 4 years, the USDA fed our children all across the Nation dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens. who will watch our children for CJD for the next 5+ decades ???


SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE

http://downercattle.blogspot.com/2009/05/who-will-watch-children.html


http://downercattle.blogspot.com/



how can it be, that in the U.K. in 1995, nvCJD was tied to c-BSE by it's similarities in pathology, and with transmission studies. however, in 2011, in the North America, the exact same science exists with a multitude of species and TSE, but yet none of it is related $$$ how can this be? it can't.

either the UKBSEnvCJD was bogus, or North America, you have a TSE prion mad cow problem...

layperson

Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518

flounder9@verizon.net

PRION, TSE, typical, atypical BSE, aka mad cow disease, spray dried blood, feed, and a recipe for disaster

PRION, TSE, typical, atypical BSE, aka mad cow disease, spray dried blood, feed, and a recipe for disaster


1

APC, Inc.

2425 SE Oak Tree Court :: Ankeny, IA 50021

Division of Dockets Management

(HFA-305)

Food and Drug Administration

5630 Fishers Lane, Room 1061

Rockville, MD 20852

Response to Docket No. 2002N-0273, Proposed Rule Substances Prohibited From Use in Animal

Food or Feed

Executive Summary

APC, Inc. agrees with the conclusion of the FDA that there is no scientific evidence to suggest that BSE infectivity is present in bovine blood. Banning the use of bovine blood or blood fractions in ruminant rations will not reduce the risk of exposure of humans or animals to BSE infectivity. Animal health will be compromised if the use of bovine blood or blood proteins in ruminant feeds is restricted.

APC, Inc. is a member of the North American Spray Dried Blood and Plasma Producers Association (NASDBPP) (see Appendix A). The NASDBPP is a group of companies located in North America involved in the production and development of spray dried blood and plasma products. These companies organized a working group within the American Feed Industry Association (AFIA) with the purpose of developing Manufacturing Standards to insure that the safety of blood derived proteins is preserved. In addition, it is the intention of NASDBPP to insure that data supporting the safe nature of these proteins is communicated to industry and government officials. The NASDBPP is committed to producing safe, high quality blood products for use as an ingredient in feeds for commercial livestock and companion animals. BSE infectivity has never been detected in blood or any component of bovine blood. There is no epidemiological evidence that bovine blood or blood component carries BSE infectivity. Spray dried blood and plasma products are consumed orally, which is the least efficient method of transmission (100,000 times less efficient compared to intracranial injection). The NASDBPP developed Manufacturing Standards to insure that our blood products do not become contaminated with high-risk tissues. The Manufacturing Standards have been reviewed by internationally recognized BSE experts. Finally, the NASDBPP have agreed to and completed annual third party inspections to certify compliance to these Manufacturing Standards.

It is critically important that regulatory policy developed to prevent BSE from becoming established in the US cattle population is grounded on sound science. The NASDBPP support APHIS, FSIS and FDA in their efforts to develop policies to mitigate the risk of BSE. The NASDBPP appreciate the opportunity to comment on the questions and issues raised in the Proposed Rule, Docket No. 2002N-0273, Proposed Rule Substances Prohibited From Use in Animal Food or Feed. We will restrict our comments to the request for further comment and scientific information regarding the need to prohibit the use of blood and blood products in ruminant feed.

2

APC, INC. COMMENTS

There is no scientific evidence to show that the use of bovine blood or blood products in feed pose a risk of BSE transmission in cattle and other ruminants...

snip...

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC201-Attach-1.pdf



1

North American Spray Dried Blood and Plasma Producers

Division of Dockets Management

(HFA-305)

Food and Drug Administration

5630 Fishers Lane, Room 1061

Rockville, MD 20852

Response to Docket No. 2002N-0273, Proposed Rule Substances Prohibited From Use in Animal

Food or Feed

Executive Summary

The North American Spray Dried Blood and Plasma Producers Association agrees with the conclusion of the FDA that there is no scientific evidence to suggest that BSE infectivity is present in bovine blood. Banning the use of bovine blood or blood fractions in ruminant rations will not reduce the risk of exposure of humans or animals to BSE infectivity. Animal health will be compromised if the use of bovine blood or blood proteins in ruminant feeds is restricted...

snip...

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC202-Attach-1.pdf



September 6,2007 Via Overnight Mail Robert L. Martin, Ph D. Office of Food Additive Safety (HFS-255) Center for Food Safety and Applied Nutrition Food and Drug Administration 4300 River Road College Park, Maryland 20740-3835 Re: GRAS Notification for ImmunoLinO Brand Spray-Dried Bovine Globulin Concentrate Intended for Use as an Ingredient in Food

snip...

Importantly, while these studies indicate that transmission of vCJD to human from BSE infected cattle via blood is a theoretical possibility, the reality is that the potential for transmissibility is substantially reduced by the cross-species barrier.

snip...

http://www.accessdata.fda.gov/scripts/fcn/gras_notices/710670A.PDF



FDA's Comments and Corresponding Changes Made in Response 1. On pg 14, you report a protein digestibility of 93.4% for Bovine Globulin but your notice does not include information about how your calculation was derived. Additionally, the reported 94.4% digestibility value appears to conflict with the statement in Attachment 19 that the IgG in bovine globulin is resistant to digestion. Please explain how you calculated the 94.4% digestibility value and discuss how that value correlates to the high concentration of IgG in your product.

http://www.accessdata.fda.gov/scripts/fcn/gras_notices/808167A.PDF



Wednesday, March 31, 2010

Atypical BSE in Cattle

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE.

When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2



To date, 27 cases of L-BSE and 24 cases of H-BSE have been report­ed worldwide (16), thus meaning that the prevalence of atypical BSE is considerably lower than that of C-BSE. However, recent studies showed that L-BSE is easily transmissible to transgenic mice expressing human (17,18) or bovine (19,20) prion protein, as well as to non-human primates (21), with shorter incubation periods than for the transmission of C-BSE to these animals. The virulent nature of L-BSE has stimulated new concern for human public health since the transmis­sion of C-BSE to humans resulted in variant Creutz­feldt-Jakob disease (vCJD) (4-7), a new emergent prion disease.

see full text ;

http://www.nih.go.jp/JJID/64/81.pdf




Plasma Use in Bovine Animals




In more recent years, APC, Inc. began to explore the benefits of feeding plasma and more specifically, bovine serum globulin, as a colostrum supplement to young bovine animals. The feeding of our serum globulin to newly born bovine animals has been shown to provide an alternative to colostrum and is being suggested by industry and university experts as a possible means to break the Johnes’ cycle of maternal transmission via colostrundmilk (Section 9.0, Tab A).



During the past 10 years, APC, Inc. has experienced only one documented incident in which a calf feeder claimed that the feeding of our product resulted in the death of calves. After a thorough investigation by APC, Inc. and tests results of the APC feed by recognized outside laboratory experts, it was concluded that the animals did not die as a result of consuming our feed (Section 9.0, Tab B). Poor sanitary conditions inlhe environment were more likely to blame.



A newborn calf weighing 75 pounds would be fed one pound of plasma in two liters of water as a colostrum supplement. Using 15% IgG plasma, this would provide 68.1 grams of Immunoglobulin (2 g/kg body weight). It should be emphasized here that newly born calves have an “open gut” that allows the serum globulin to directly enter the blood stream. This results in direct means of correcting the problem of failure of passive immunity when colostrum is insufficient in providing the necessary IgG to the calf. The data provided in this petition clearly demonstrates not only the safety of our product, but also the positive impact of improving the IgG levels in newly born calves (Section 9.0, Tab C).



Previously we have been discussing the extensive experiences and scientific data we have accumulated on the feeding of plasma and serum globulin in young animals. The consumption of blood and blood derivatives also has a long history in man’s diet. Proliant Inc., the edible division of Lauridsen Group, Inc. and sister company to APC, Inc., has manufactured spray-dried bovine plasma for use in human food for over 8 years.



Blood Plasma Use in Humans Biblical references describe the drinking of animal blood. Blood sausage has been consumed by humans for over 2,000 years and is still a common commodity in France and other European countries. Recipes for blood sausage indicate that the sausage consists of 33 to 50% whole blood (Section 9.0, Tab D). If the blood sausage contains 33% blood, the percentage of globulin in the sausage would be 4.18%. The consumption of globulin would be the following per listed serving size: 0 4 ounces of blood sausage = 1.56 grams of globulin per 4 oz. serving 6 ounces of blood sausage = 2.34 grams of globulin per 6 oz. serving Proliant Inc. has sold spray-dried plasma into the surmimi industry for 10 years with a total of 40 to 50 million pounds being consumed in the Asian and European markets. More recently, Proliant Inc. has manufactured bovine serum globulin for use in the neutraceutical industry. The recommended dose is 75mgkg body weight with a range in application of 37.5 to 125 mgkg body weight. Daily dosage for a child would be 1-2 grams; daily dosage for an adult (150 pounds) would be 2-5 grams.



Regulatory Status The USDALFSIS permits animal blood as an ingredient in meat food products as found in Title 9 CFR 3 18.6(b)(7). Further, USDAESIS in their Food Standards and Labeling Policy book lists blood, blood and tongue sausage, blood pudding, and blood sausage specifiing the restrictions and conditions for the product and product labeling (Section 9.0, Tab E). There are no restrictions as to the quantity of blood used in these products other than they would have to contain some of the other ingredients which are listed in the definition.



Human Studies Additionally, several adult studies and child feeding trials have been conducted to research the potential benefits of consuming bovine blood derivatives. In the Lembcke study, up to 50% of the control sample milk protein was replaced with bovine serum concentrate (BSC) (Section 9.0, Tab F). Conclusion of the Lembcke study: “Each of the diets was well accepted by the study children and there was no evidence of any adverse effects of bovine serum concentrate.” In another study, children were fed 3.1 grams of IgG per day for up to 8 months, or up to 8% IgG in their milk and rice diet (Section 9.0, Tab G). This unpublished study provides significant data to support the premise that spray-dried serum consumption by young children is similarly safe as that found in our animal studies.



We are also providing additional unpublished data on human studies supporting the previously mentioned conclusions with regards to human safety (Section 9.0, Tabs H and I).



SNIP...



Bovine Spong- iform Encephalopathy (BSE) Proliant Inc. is not concerned about the transmission of BSE from our blood products because all of the blood is derived from animals slaughtered in U.S. slaughter facilities under the continuous inspection of USDAFSIS. All animals have been passed as fit for human consumption. Both ante- and post-mortem inspections are conducted on each animal at the time of slaughter. The collection of the blood occurs before the head, hide, spinal column, or any other Specified Risk Materials (SRMs) are removed from the carcass.



In addition, international agencies do not consider blood to be a tissue of risk with regard to the transmission of BSE. Even in a country or zone with high BSE-risk, the importation and trade of blood products is not recommended to be restricted (Section 9.0, Tab K).



http://www.accessdata.fda.gov/scripts/fcn/gras_notices/GRN000169.pdf





WHO Guidelines on Transmissible Spongiform Encephalopathies 5



in relation to Biological and Pharmaceutical Products



http://www.who.int/immunization_standards/vaccine_regulation/BLOOD_TSE_2003.pdf





The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.



http://www.oie.int/boutique/extrait/06heim937950.pdf




The BSE MRR policy is nothing more than a legal tool to trade _all_ strains of TSE Globally. The BSE MRR policy must be repelled and the BSE GBR risk assessment must be enhanced to include all TSE, especially the atypical BSE/TSE showing up in cattle, since the USA BSE GBR risk is III and the fact both typical and atypical BSE/TSE has been documented in the bovine in the USA. ...tss



EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA) Last updated: 19 July 2005 Adopted July 2004 (Question N° EFSA-Q-2003-083)



Report Summary Summary of the Scientific Report



The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.



The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.



A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.



EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.



Publication date: 20 August 2004



http://www.efsa.europa.eu/en/science/tse_assessments/gbr_assessments/573.html





Thursday, November 18, 2010



UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS



http://bse-atypical.blogspot.com/2010/11/united-states-of-america-vs-galen-j.html





Wednesday, November 17, 2010



MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE



http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html





Wednesday, November 17, 2010



MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE



http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html





I remember the same _false_ reassuring statements made years ago about the safety of human blood from nvCJD. until the documented the transmission there from. now, who knows how many were exposed, or how many will become clinical and die in the decades to come ;



http://www.guardian.co.uk/society/2006/dec/08/health.bse





Wednesday, March 31, 2010



Atypical BSE in Cattle



To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.



This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.



http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2





Thursday, August 12, 2010



Seven main threats for the future linked to prions



First threat



The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed. ***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.



Second threat



snip...



http://www.neuroprion.org/en/np-neuroprion.html





http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html




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.



http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf




International Society for Infectious Diseases Web: http://www.isid.org/





Tuesday, February 8, 2011



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



http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html





Tuesday, September 14, 2010



Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)



http://tseac.blogspot.com/2010/09/transmissible-spongiform_14.html



Thursday, April 9, 2009




Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed Thursday, April 09, 2009



Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed



mailto:burt.pritchett@fda.hhs.gov



Greetings FDA et al,



I kindly wish to comment on the following ;



[Docket No. FDA-2002-N-0031] (formerly Docket No. 2002N-0273) RIN 0910-AF46



[Federal Register: April 9, 2009 (Volume 74, Number 67)] [Proposed Rules] [Page 16160-16161] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr09ap09-18]



DEPARTMENT OF HEALTH AND HUMAN SERVICES



Food and Drug Administration



21 CFR Part 589



[Docket No. FDA-2002-N-0031] (formerly Docket No. 2002N-0273) RIN 0910-AF46



Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed Delay of Effective Date



AGENCY: Food and Drug Administration, HHS.



ACTION: Notice of proposed delay of effective date.



http://edocket.access.gpo.gov/2009/E9-8127.htm





MY COMMENT AS FOLLOWS ;



I find it deeply disturbing, that with the science to date, especially with the science to date, transmission studies, the more virulent atypical strains of the BSE i.e. h-BSE and l-BSE, both of which have now been documented in North America, that we are even still discussing this most important topic. The industry involved has beat this mad cow feed ban to death, and still refuse to comply. IF they would have adhered to policy, rules and regulations put forth August 4th, 1997, when the partial, and voluntary ruminant to ruminant feed ban was first put in place, they would not still be crying the same tune. WE need not only to enforce the present ban, but strengthen it, especially to include blood in the ban. WE (the consumer), was promised this would happen years ago. For Pete's sake, this will be the third president to have to address these same questions, and I pray that this one has the guts to finally do something. We need NOT discuss this for one more second. We had 8 years that President Bush literally covered up mad cow disease, and let literally millions and millions of pounds of mad cow feed into commerce to be fed out. IN one feed ban recall alone in 2007, 10 MILLION PLUS POUNDS was fed out into commerce. and under this same President, we now millions of kids across our Nation that have been needlessly exposed to the mad cow agent via the infamous USDA CERTIFIED DOWNER COW DEAD STOCK SCHOOL LUNCH PROGRAM. if you think for one moment that the largest meat recall in the history of the USA was because a few animals were filmed being abused, your only kidding yourself. that meat was recalled because dead stock downer cows are at the highest risk to carry mad cow disease, and they had been feeding our children this stuff for years. AND then had the nerve to lie to us about THE GREAT BSE FIREWALL IN THE USA THAT WOULD PROTECT THE CONSUMER I.E. THE BSE FEED BAN, that never was nothing more than ink on paper. who will monitor these children in the years and decades to come for a human form of Transmissible Spongiform Encephalopathy? who can with a CJD/TSE surveillance system and CJD Questionnaire set up the way it is now? you can't.



ENOUGH already $ NO MORE DISCUSSION PLEASE, WE NEED ACTION !



I strenuously urge President Obama to NOT discuss this for one more moment, actions must be put forth now, and enforce such actions.



I strenuously urge President Obama to ENHANCE the feed ban to include blood, and enforce said regulations, based on sound science.



I strenuously urge President Obama to ban the use of "poultry litter" and the use of all mammalian and poultry protein in ruminant feed,as a feed ingredient for ruminant animals, and enforce said regulations, based on sound science.



I strenuously urge President Obama to ban the use of "plate waste" as a feed ingredient for ruminants, and enforce said regulations, based on sound science.



I strenuously urge President Obama to ban from human food (including dietary supplements please see latest May 2009 CDC warning on these type supplements, CWD, and Elk Antler Velvet), and cosmetics a wide range of bovine-derived material so that the same safeguards that protect Americans from exposure to the agent of BSE through meat products regulated by USDA also apply to food products that FDA regulates, and enforce such actions, based on sound science.



I strenuously urge President Obama to further minimize the possibility of cross-contamination of ruminant and non-ruminant animal feed by requiring equipment, facilities or production lines to be dedicated to non-ruminant animal feeds if they use protein that is prohibited in ruminant feed. Currently, some equipment, facilities and production lines process or handle prohibited and non-prohibited materials and make both ruminant and non-ruminant feed -- a practice which could lead to cross-contamination, and enforce said regulations, based on sound science.



LET's take a look back at past promises and discussions on this issue, and then for a breath of fresh air, let's look at some sound science, and why no further discussion is warranted, and why action is needed ASAP ;



http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html





=================================



Sunday, May 10, 2009

Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)

TO : william.freas@fda.hhs.gov



May 8, 2009



Greetings again Dr. Freas, TSEAC et al,



I would kindly, once again, wish to comment at this meeting about the urgent actions that need to be taken asap, to the Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009.



http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html





----- Original Message -----
From: Freas, William
To: flounder9@verizon.net
Cc: flounder9@verizon.net
Sent: Monday, June 08, 2009 5:32 PM
Subject: Written comments regarding TSEAC



Dear Mr. Singeltary,



Thank you for your written statement regarding the June 12, 2009 TSEAC meeting. Your statement will be copied, given to the committee members, made part of the official meeting record and made available to the public.



Thanks again.



Bill Freas Acting TSEAC Exec. Sec.



From: "Terry S. Singeltary Sr." flounder9@verizon.net
To: william.freas@fda.hhs.gov
Cc: "Dave Cavenaugh" ; "MAD COW DR. LAURA MANUELIDIS" ; ; Subject: Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
Date: Sunday, May 10, 2009 12:55 PM TO: william.freas@fda.hhs.gov May 8, 2009



snip...end...tss



http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html






In response to the Washington State case, we announced in January, 2004 our intention to strengthen the >97 feed ban by banning the use of blood products, poultry litter and plate waste, and this was one of the changes in the plan.



*** ALICE



We did not follow through with this set of measures.



After considering the recommendations of the international review PAPER MILL REPORTING 301 495-5831 263 team we, instead, published an advance notice of proposed rule-making in July, 2004 jointly with USDA. In that proposal we tentatively proposed to ban SRMs from all animal feed. What we actually proposed in October, 2005 was a partial SRM ban, limited to brain and spinal cord tissues. It took us until April 25, 2008 to finalize the proposal because we significantly underestimated the costs associated with the measures. Also, commensurate with USDA’s surveillance results and prevalence estimates, and the high level of compliance with our >97 rule, we modified the rule to apply only to brains and spinal cords from cattle 30 months of age and older, rather than cattle of all ages.



http://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/UCM171810.pdf





(Response) FDA agrees that the prevalence of BSE in the United States is very low, and that compliance with the current feed ban by the U.S. animal feed industry is at a high level...



http://www.fda.gov/OHRMS/DOCKETS/98fr/08-1180.pdf




"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."



10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007



Date: March 21, 2007 at 2:27 pm PST



RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II



___________________________________



PRODUCT



Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007



CODE



Cattle feed delivered between 01/12/2007 and 01/26/2007



RECALLING FIRM/MANUFACTURER



Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.



Firm initiated recall is ongoing.



REASON



Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.



VOLUME OF PRODUCT IN COMMERCE



42,090 lbs.



DISTRIBUTION



WI



___________________________________



PRODUCT



Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007



CODE



The firm does not utilize a code - only shipping documentation with commodity and weights identified.



RECALLING FIRM/MANUFACTURER



Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.



REASON



Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.



VOLUME OF PRODUCT IN COMMERCE



9,997,976 lbs.



DISTRIBUTION



ID and NV



END OF ENFORCEMENT REPORT FOR MARCH 21, 2007



http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm





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



______________________________



http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html





PRODUCT Bulk custom dairy pre-mixes,



Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.



VOLUME OF PRODUCT IN COMMERCE 350 tons



DISTRIBUTION AL and MS



______________________________



PRODUCT



a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;



b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;



c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;



d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;



e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;



f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;



g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6



CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.



REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".



VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags



DISTRIBUTION AL, GA, MS, and TN



END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006



###



http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html





Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006



Date: August 6, 2006 at 6:16 pm PST PRODUCT



a) CO-OP 32% Sinking Catfish, Recall # V-100-6;



b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;



c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;



d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;



e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;



f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;



g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;



h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;



i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;



j) CO-OP LAYING CRUMBLES, Recall # V-109-6;



k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;



l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;



m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE



Product manufactured from 02/01/2005 until 06/06/2006



RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.



REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".



VOLUME OF PRODUCT IN COMMERCE 125 tons



DISTRIBUTION AL and FL



END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006



###



http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html




MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67



RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II



______________________________



PRODUCT



a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;



b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;



c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;



d) Feather Meal, Recall # V-082-6 CODE



a) Bulk



b) None



c) Bulk



d) Bulk



RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.



REASON



Possible contamination of animal feeds with ruminent derived meat and bone meal.



VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons



DISTRIBUTION Nationwide



END OF ENFORCEMENT REPORT FOR July 12, 2006



###



http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html





please see full text ;



http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html





Tuesday, March 2, 2010



Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA



http://madcowfeed.blogspot.com/2010/03/animal-proteins-prohibited-in-ruminant.html





Monday, March 1, 2010



ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010



http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.html





Tuesday, September 14, 2010



Feed Safety and BSE/Ruminant Feed Ban Support Project (U18)



http://madcowfeed.blogspot.com/2010/09/feed-safety-and-bseruminant-feed-ban.html





Friday, October 8, 2010



Scientific reasons for a feed ban of meat-and-bone meal, applicable to all farmed animals including cattle, pigs, poultry, farmed fish and pet food



http://madcowfeed.blogspot.com/2010/10/scientific-reasons-for-feed-ban-of-meat.html





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.



http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf





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



PRION DISEASE UPDATE 2010 (11)



SEE;



TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS



INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation



http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129





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 S wiss Foundation



http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html





http://www.aphis.usda.gov/import_export/plants/manuals/ports/downloads/apm_pdf/03_18petfoodsandfeed.pdf





http://www.dardni.gov.uk/index/animal-health/animal-diseases/bse/bse-feed-ban.htm





Date: June 21, 2007 at 2:49 pm PST



Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program



An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.



4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half



http://www.usda.gov/oig/webdocs/sarc070619.pdf





Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program ­ Phase II and Food Safety and Inspection Service



Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III



Report No. 50601-10-KC January 2006



Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain



http://www.usda.gov/oig/webdocs/50601-10-KC.pdf




"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."



Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.



USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.



"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.



http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r





Tuesday, September 28, 2010



Variant CJD: where has it gone, or has it?



Pract Neurol 2010; 10: 250-251



http://vcjdtransfusion.blogspot.com/2010/09/variant-cjd-where-has-it-gone-or-has-it.html




Ruminant Blood

In contrast with humans, sheep, monkeys, mice and hamsters, including sheep and mice infected with BSE and humans infected with vCJD considered identical to BSE, no infectivity has so far been demonstrated in the blood of BSE infected cattle. However, we consider it unlikely that cattle are the sole outlier to what has been a consistent finding in all other TSE diseases where the measurement has been made with sufficient sensitivity to detect the low levels of infectivity that are present in blood. Rather, this failure is more likely the result of the very small volumes of blood that were used for the inoculations (less than 1 ml), whereas whole transfusions were administered to assay animals in the published sheep scrapie/BSE experiments. If blood is infected then all vascularized tissues can be expected to contain some infectivity in proportion to the content of residual blood.

Micro emboli are a possible source of blood-borne agent that could be at much higher titer than blood itself, in slaughtered cattle carrying BSE infection. Stunning can release micro emboli of brain tissue into the circulatory system from where they can be distributed to other tissues in the few moments before the exsanguination and death. (Anil, et al, 2001a & b; Anil et al, 2002; Love, et al, 2000). This source of infection could extend a higher infectivity risk to tissues that would otherwise be at low risk, thereby allowing exposure of cattle through any of the legal exemptions and potentially producing a feed and food risk. Blood-borne contamination may be a special problem where spray-dried blood is being used as a milk replacer for calves, as it is thought that young animals are especially susceptible to infection.

Certainly, blood and blood proteins should not be used as feed without conclusive evidence that they are safe.

see full text ;

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf



http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf



M. E., Simmons M. M., Austin A. R., & Horigan M. W. (1994)

Infectivity in the ileum of cattle challenged orally with bovine spongiform encephalopathy. Vet. Rec., 135, 40-41.

Wells G.A.H., Hawkins, S.A.C., Green R. B., Austin A. R., Dexter I., Spencer, Y. I., Chaplin, M. J., Stack, M. J., & Dawson, M. (1998) Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update. Vet. Rec., 142, 103-106.

Wyatt. J. M. et al. 1991. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.

--------------------------------------------------------------------------------

[RR1] I am not sure of the point here. If they are going to use dead stock then certainly they should at a minimum remove the CNS tissue but rather I would think the point should be that we don’t want them using dead stock with or without the CNS included.

[RR2]I am not sure that the actual text of the CFR is still required to make the point. However, I am glad I had it to verify the original argument.


THE SEVEN SCIENTIST REPORT ***


http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf



http://www.regulations.gov/fdmspublic/component/main?main=DocketDetail&d=FDA-2002-N-0031



9 December 2005 Division of Dockets Management (RFA-305) Food and Drug Administration 5630 Fishers Lane Room 1061 Rockville, MD 20852

Re: Docket No: 2002N-0273 (formerly Docket No. 02N-0273) Substances Prohibited From Use in Animal Food and Feed

Dear Sir or Madame:

Serologicals Corporation is a global provider of biological products to life science companies. The Company’s products are essential for the research, development and manufacturing of biologically based diagnostic, pharmaceutical and biological products. customers include many of the leading research institutions, diagnostic and pharmaceutical companies throughout the world. The Company’s products and technologies are used in a wide variety of applications within the areas of neurobiology, cell signaling, oncology, angiogenesis, apoptosis, developmental biology, cellular physiology, hematology, immunology, cardiology, infectious diseases and molecular biology. A number of our products are derived from bovine blood or other bovine tissues sourced in the United States, hence the overall health of the national herd is extremely important to our company as well as to our customers and their patients. Some of our bovine based products are used in the manufacture of vaccines and drugs for humans, hence it is critical that all measures are taken to assure these are safe and free from disease especially Bovine Spongiform Encephalopathy (BSE).

The most effective way to insure this is to create a system which processes cattle that are BSE free. As a company there are a number of precautions that we can take by our strict specifications but many of the needed precautions require the force of federal regulation, hence we appreciate the opportunity to submit comments to this very important proposed rule. After the identification of bovine spongiform encephalopathy (BSE) in indigenous North American cattle, the U.S. Department of Agriculture (USDA) responded rapidly to implement measures to protect public health in regard to food. Our company recognizes and supports the importance of the current feed ban which went into effect in August 1997. However, given what is known about the epidemiology and characteristically long incubation period of BSE, we urge

5655 Spalding Drive * Norcross, GA 30092 678-728-2000 * 800-842-9099 * Facsimile 678-728-2299 http://www.serologicais.com Division of Dockets Management (HFA-305) Page 2 9 December 2005

the FDA to act without further delay and implement additional measures which will reduce the risk of BSE recycling in the US cattle herd. We feel that for the FDA to provide a more comprehensive and protective feed ban, specified risk materials (SRMs) and deadstock must be removed from all animal feed and that legal exemptions which allow ruminant protein to be fed back to ruminants (with the exception of milk) should be discontinued. SRMs, as defined by the USDA, are tissues which, in a BSE infected animal, are known to either harbor BSE infectivity or to be closely associated with infectivity. If SRMs are not removed, they may introduce BSE infectivity and continue to provide a source of animal feed contamination. Rendering will reduce infectivity but it will not totally eliminate it. This is significant as research in the United Kingdom has shown that a calf may be infected with BSE by the ingestion of as little as .OOl gram of untreated brain. The current proposed rule falls short of this and would still leave a potential source of infectivity in the system. In fact by the FDA’s own statement the exempted tissues which are known to have infectivity (such as distal ileum, DRGs, etc) would cumulatively amount to 10% of the infectivity in an infected animal, This proposed rule would still allow for the possibility that cattle could be exposed to BSE through:

1. Feeding of materials currently subject to legal exemptions from the ban (e.g., poultry litter, plate waste)

2. Cross feeding (the feeding of non-ruminant rations to ruminants) on farms; and

3. Cross contamination of ruminant and non-ruminant feed

We are most concerned that the FDA ha chosen to include a provision which would allow tissues from deadstock into the feed chain. We do not support the provision to allow the removal of brain and spinal cord from down and deadstock over 30 months of age for several reasons. These are the animals with the highest level of infectivity in tissues which include more than brain and spinal cord. We do not feel that there can be adequate removal and enforcement of this regulation especially during warmer weather. In addition there is emerging information that at end stage disease, infectivity may also be included in additionai tissues such as peripheral nerves (Buschmann and Groschup, 2005). Leaving the tissues from these cattle in the animal feed chain will effectively nullify the intent of this regulation. This point is illustrated by the 2001 Harvard risk assessment model which demonstrated that eliminating dead and downer, 4D cattle, from the feed stream was a disproportionately effective means of reducing the risk of re-infection “The disposition of c&e that die on the farm would also have a substantial influence on the spread of BSE if the disease were in traduced. ” The base case scenario showed that the mean total number ofID.50~ (i.e., dosage sufficient to infect SO percent of exposed cattte) from healthy animals at slaughter presented to the food/feed system was 1500, The mean total number of ID.50.s from adult cattle Division of Dockets Management (HFA-305) Page 3 9 December 2005 deadstockpresented to the feed system was 3 7,000. deadstock). This illustrates the risk of “40 cattle” (i.e., From the Harvard Risk Assessment, 2001, Appendix 3A Base Case and Harvard Risk Assessment, 200 1

Executive Summary

Serologicals and companies like ours which supply components of drugs and biologicals have a responsibility to the manufacturers of these products, the medical community and their patients as well as regulatory agencies throughout the world to provide the safest products as possible. Since there is no test for BSE in live cattle or for product, the regulatory agencies throughout the world expect us to reduce or eliminate risk via suurcing criteria, These parameters may include but not be limited to country of origin, herd of origin, age of the animal, etc. The United States is no longer a country with negligible risk, hence individual animal criteria has become more important. In fact other Centers of the FDA have stated that more attention should be given to sourcing from herds likely to be a source of BSE free animals. The exemptions in the current ban as well as in the newly proposed rule make this difficult if not impossible as there are still legal avenues for ruminants to consume potentially contaminated ruminant protein. In addition, the USDA still has not implemented a system of identification and traceability. Serologicals urges agencies of the US government to work with academia and industry on research in the following areas: e Methods to inactivate TSEs agents which then may allow a product to be used and even fed to animals without risk l Alternative uses for animal byproducts which would maintain value Serologicals will continue to work with the FDA and other government agencies to implement a strong BSE risk control program, Serologicals would like to reiterate our opinion that for the FDA to provide a more comprehensive and protective feed ban, specified risk materials (SRMs) and deadstock must be removed from all animal feed and that legal exemptions which allow ruminant protein to be fed back to ruminants (with the exception of milk) should be discontinued. Thank you for the opportunity to submit these comments to the public record. Respectfully, SEROLOGICALS CORPORATION James J. Kramer, Ph.D. Vice President, Corporate Operations

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000435-01-vol36.pdf



03-025IFA 03-025IFA-2 Terry S. Singeltary

From: Terry S. Singeltary Sr. [flounder9@verizon.net] Sent: Thursday, September 08, 2005 6:17 PM To: fsis.regulationscomments@fsis.usda.gov Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf



see Dr. Paul Brown and Seven Scientists comments here ;


Signatories:

Paul W. Brown, M.D. Medical Director, USPHS, and Senior Investigator, NIH (retired) Consultant, TSE Risk Management 7815 Exeter Rd. Bethesda, MD 20814 Fax 301-652-4312 Email: paulwbrown@comcast.net

Neil R. Cashman MD Professor, Department of Medicine (Neurology) Diener Chair of Neurodegenerative Diseases Centre for Research in Neurodegenerative Diseases 6 Queen's Park Crescent West Toronto Ontario M5S3H2 Ph: 416-978-1875 Fax: 416-978-1878 e-mail: neil.cashman@utoronto.ca

Linda A. Detwiler, DVM Consultant, TSE Risk Management 225 Hwy 35 Red Bank, NJ 07701 Ph 732-741- 2290 Fax 732-741-7751 Email: LAVet22@aol.com

Laura Manuelidis, MD Professor and Head of Neuropathology, Department of Surgery and Faculty of Neurosciences Yale Medical School 333 Cedar St. New Haven, CT 06510 email: laura.manuelidis@yale.edu Tel: 203-785-4442 Deleted: p Deleted: 14 Formatted FDA Proposed Rule December 20, 2005

Jason C. Bartz, Ph.D. Assistant Professor Department of Medical Microbiology and Immunology Creighton University 2500 California Plaza Omaha, NE 68178 (402) 280-1811 voice (402) 280- 1875 fax jbartz@creighton.edu

Robert B. Petersen, Ph.D. Associate Professor of Pathology and Neuroscience Case Western Reserve University 5-123 Wolstein Building 2103 Cornell Road Cleveland, OH 44106-2622 Phone 216-368-6709 FAX 360-838-9226 Email rbp@cwru.edu

Robert G. Rohwer, Ph.D. Director, Molecular Neurovirology Laboratory Veterans Affairs Medical Center Medical Research Service 151 Assoc. Professor of Neurology School of Medicine University of Maryland at Baltimore 10 N. Greene St. Baltimore, MD 21201 ph. 410-605-7000 x6462 Fax 410-605-7959 email: rrohwer@umaryland.edu

FDA-2002-N-0031-0131 Paul W. Brown, et al - Comment 02/23/2009 PUBLIC SUBMISSIONS FDA-2002-N-0031-0131.1 Paul W. Brown, et al - Comment 02/23/2009


PUBLIC SUBMISSIONS


http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064808b3843&disposition=attachment&contentType=pdf



http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/docketDetail.jsp#



December 19, 2005 Division of Dockets Management (HFA-305) Food and Drug Administration 5630 Fishers Lane Room 1061 Rockville, MD 20852 Re: Docket No: 2002N-0273 (formerly Docket No. 02N-0273) Substances Prohibited From Use in Animal Food and Feed Dear Sir or Madame: The McDonald's Corporation buys more beef than any other restaurant in the United States.

snip...

SRMs, as defined by the USDA, are tissues which, in a BSE infected animal, are known to either harbor BSE infectivity or to be closely associated with infectivity. If SRMs are not removed, they may introduce BSE infectivity and continue to provide a source of animal feed contamination. Rendering will reduce infectivity but it will not totally eliminate it. This is significant, as research in the United Kingdom has shown that a calf may be infected with BSE by the ingestion of as little as .001 gram of untreated brain. The current proposed rule falls short of this and would still leave a potential source of infectivity in the system. In fact by the FDA's own statement the exempted tissues which are known to have infectivity (such as distal ileum, DRGs, etc) would cumulatively amount to approximately 10% of the infectivity in an infected animal. Leaving approximately 10% of the infectious tissues in the system is not good enough.

snip...

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273_emc-000134-02.pdf



9 December 2005 Division of Dockets Management (RFA-305) Food and Drug Administration 5630 Fishers Lane Room 1061 Rockville, MD 20852 Re: Docket No: 2002N-0273 (formerly Docket No. 02N-0273) Substances Prohibited From Use in Animal Food and Feed Dear Sir or Madame: Serologicals Corporation is a global provider of biological products to life science companies.

We feel that for the FDA to provide a more comprehensive and protective feed ban, specified risk materials (SRMs) and deadstock must be removed from all animal feed and that legal exemptions which allow ruminant protein to be fed back to ruminants (with the exception of milk) should be discontinued. SRMs, as defined by the USDA, are tissues which, in a BSE infected animal, are known to either harbor BSE infectivity or to be closely associated with infectivity. If SRMs are not removed, they may introduce BSE infectivity and continue to provide a source of animal feed contamination. Rendering will reduce infectivity but it will not totally eliminate it. This is significant as research in the United Kingdom has shown that a calf may be infected with BSE by the ingestion of as little as .OOl gram of untreated brain. The current proposed rule falls short of this and would still leave a potential source of infectivity in the system. In fact by the FDA's own statement the exempted tissues which are known to have infectivity (such as distal ileum, DRGs, etc) would cumulatively amount to 10% of the infectivity in an infected animal, This proposed rule would still allow for the possibility that cattle could be exposed to BSE through:


snip...see full text ;


http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf



2002N-0273 Animal Proteins Prohibited in Ruminant Feed

FDA Comment Number : EC240

Submitter : Mr. Masahiro Mori Date & Time: 01/04/2006 05:01:26

Organization : Embassy of Japan

Category : International Government

Issue Areas/Comments

GENERAL

GENERAL

Comments of Japan on the United States? WTO/SPS Notification (G/SPS/N/USA/1141)

The Government of Japan welcomes the opportunity to comment on the United States? notification (G/SPS/N/USA/1141) on substances prohibited from use in Animal food or feed.

The Food safety risk assessment related to the import of beef and beef offal from the U.S.A. and Canada by the Food Safety Commission of Japan (FSC) was completed on December 8, 2005. Regarding the feed ban, the following was noted as an addendum to the conclusion on the risk assessment report of FSC:

To prevent BSE exposure and amplification in U.S.A and Canada, the use of SRM must be prohibited completely. The ban must be applied not only to cattle feed but also to all other animal food/feed that may cause cross-contamination.

To accomplish the effectively enforced feed ban requested in the OIE Terrestrial Animal Health Code (CHAPTER 2.3.13, Bovine Spongiform Encephalopathy), whole SRM should be excluded as high risk material from animal feed chain as the above-mentioned addendum points out. The U.S. Government should also carry out continuous BSE surveillance sufficient to verify the efficacy of U.S. feed ban and make necessary revision of its feed regulations on a basis of its results.

The Government of Japan would like to request that the U.S. Government take account of the above comments in implementing its animal food and feed regulations.

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC240.htm



Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed Delay of Effective Date - Notice of Final Rule Send a Comment or Submission Notification Comments Due: Apr 16, 2009 11:59:59 PM EDT Docket ID: FDA-2002-N-0031

Document ID: FDA- 2002-N-0031-0132 Date Posted: Apr 9, 2009 View this Document:

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648094bc24&disposition=attachment&contentType=pdf



http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648094bc24&disposition=attachment&contentType=html



http://www.regulations.gov/search/search_results.jsp?css=0&&Ntk=All&Ntx=mode+matchall&Ne=2+8+11+8053+8054+8098+8074+8066+8084+8055&N=0&Ntt=Substances%20Prohibited%20From%20Use%20in%20Animal%20Food%20or%20Feed%3B%20Final%20Rule%3A%20Proposed&sid=1208CC5B88DF



submit here ;

http://www.regulations.gov/fdmspublic/component/main?main=SubmitComment&o=090000648094bc24



THE SEVEN SCIENTIST REPORT ***



http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf



http://www.regulations.gov/fdmspublic/component/main?main=DocketDetail&d=FDA-2002-N-0031




NATIONAL RENDERERS ASSOCIATION,

Inc. 801 N. Fairfax Street Suite 205 Alexandria, Virginia 22314 Tel: (703) 683-0155 Fax: (703) 683-2626

March 12, 2007 Docket No. 050-15-1 Regulatory Analysis and Development, PPD, APHIS Station 3A-03.8 4700 River Road Unit 118 Riverdale, Maryland 20737-1238 Re: Docket No. APHIS-2006-0041, Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines.

To Whom It May Concern: The National Renderers Association (NRA) references APHIS’s Docket No. APHIS-2006-0041, the agency’s proposed rule to import cattle and products. NRA is the international trade association for the industry that safely and efficiently recycles animal agriculture by-products into valuable ingredients for the livestock, pet food, chemical and consumer product industries. NRA represents its members’ interests to Congress, regulatory and other government agencies, promotes greater use of rendered products, and fosters the opening and expansion of trade between North American exporters and foreign buyers. NRA’s membership represents more than 98% of the rendering capacity in both the U.S. and Canada. In the proposed rule the USDA details the criterion necessary for the importation of bovine blood products. Specifically the USDA explain: “For all the above three manners of collection, we would require that the blood be collected in a closed system or in an otherwise hygienic manner that prevents contamination of the blood with SRMs.” 1

With current line speeds in U.S. beef slaughter facilities a closed collection system (as described by the USDA in the proposed rule) is not practical and would be cost prohibitive for production of the feed ingredients spray dried bovine plasma or blood meal. Requiring such a collection system would effectively eliminate the supply of feed grade bovine plasma and blood meal. Restricting these products by requiring blood to be collected by a closed system would result in significant damage to the livestock industry both domestically and around the world. Traditional closed collection systems as suggested in the Proposed Rule may be appropriate for the collection of Fetal Calf Serum and other specialized blood products but are impractical for collection of blood used for feed application. The infective agent responsible for BSE has not been identified in bovine blood (USDA’s reference, OIE 2005). However, the North American Spray Dried Blood and Plasma Producers and the NRA recognized the potential for contamination of raw materials with SRM during collection and subsequent processing and have developed a series of Manufacturing Guidelines and a Code of Practice designed to minimize the risk of contamination. These programs include third party audits by the Facilities Certification Institute to ensure compliance with the manufacturing guidelines. These Manufacturing Guidelines have been successfully implemented at the spray dried blood facilities (including Canada) and the Code of Practice has been certified at more than 35 high volume rendering plants in the U.S. so far with many more underway. Many Canadian rendering plants operate under equally effective HACCP programs. Spray dried plasma is a unique feed ingredient. There are no effective substitutes for spray dried plasma. It is important that animal agriculture industry continues to have an adequate supply of this critical feed ingredient. A number of recognized academic and industry organizations agree that continued access to adequate supplies of spray dried bovine blood products is critical. Bovine blood meal represents a very valuable feed ingredient especially for the rations of the lactating dairy cow. It provides high levels of lysine that does not degrade in the rumen. High levels of lysine are necessary to maintain optimum levels of milk production. If bovine blood meal were removed from use in rations, the price of porcine blood meal will continue to increase, placing an additional financial burden on the dairy industry among others. In 2001, the Sparks Company evaluated the impact of prohibiting cattle derived blood meal in ruminant diets on behalf of the NRA. In 2000, 1.48 billion pounds of blood were generated from the slaughter of cattle. A resulting 121.9 million pounds of cattle blood meal and 49.8 million pounds of mixed species blood meal were manufactured. Total ruminant containing blood meal produced was 171.7 million pounds, 70% of which was utilized in ruminant diets. The study determined if the use of blood meal were prohibited in cattle diets, a product loss of $45.3 million would be realized by the cattle sector. Additional indirect losses from reduced animal productivity at the farm level were not considered by the report and are estimated below. [http://www.renderers.org/economic_impact/index.htm] 2

The unique nutritional properties of blood meal, primarily a high level of non-degradable lysine, provide a high return when used by dairy producers. Lysine is considered the first limiting amino acid vital to high milk production. Unlike poultry and swine, high producing dairy cows can’t utilize synthetic lysine, thus milk production will drop if this ingredient is removed. Typically 0.5 pounds/day of dried blood meal is fed to a dairy cow. A reduction of 4 pounds of milk/cow/day would be expected if blood meal were no longer utilized in these diets. Using the figure from the Sparks report that 70% of ruminant blood meal was utilized in dairy rations, an overall drop in milk production of 9.6 million hundredweight would occur. At $12/cwt this loss in milk production would reduce dairy farm income by $115.4 million. Thus, combined losses to the U.S. beef cattle and dairy sectors would total $160.7 million. It is critical the dairy industry continues to have access to bovine blood and bovine blood fractions. Over 41% of the heifer calves raised in the U.S. suffer from failure of passive transfer due to inadequate colostral Ig intake. Approximately 11% of heifer calves died before weaning, and half of this mortality can be attributed to inadequate supply of quality colostrum (NAHMS, 1992, 1996). Colostrum is also recognized as a vector for transmission of a number of disease-causing organisms, including Mycobacterium paratuberculosis (Johne’s disease). Published studies indicate bovine serum and fractions thereof are the only effective alternatives for colostrum (Arthington, et al., 2000 a,b; Quigley et al., 1998, 2000, 2001; McCoy et al, 1997; Holloway et al, 2002; Poulsen et al, 2003). If access to these proteins is restricted, there is no effective alternative to reduce calf mortality or to break these disease cycles. For a more complete review see the review of Quigley et al. (2004). Many studies from the involved sectors have been shared with FDA on the economic and environmental impacts of banning the use of bovine blood meal in feed, especially representatives from blood processors and the poultry industry. Collectively, the dual impacts (economic and environmental) could be very great on the industries. If these products are prohibited from animal feed, there is reduced market for such products and their disposal costs increase. This could lead to improper disposal, disposal in landfills, or by land application on farms. If feeding of blood meal were prohibited for cows, farmers would either feed higher protein levels and/or milk additional cows to maintain milk production. Either course of action would result in increased nitrogen and methane release into the environment. There is no need to stop the feeding of ruminant blood products to ruminants or any other animals because there is no science to support such a restriction. There is no scientific or peer reviewed literature linking the feeding of bovine blood in the form of blood meal or other blood products in feed to any risk of BSE transmission in cattle and other ruminants. Bovine blood has never been implicated in bovine-to-bovine transmission of either natural or experimental BSE. If there are concerns that some collection methods could allow small amounts of neural tissue to be collected with the blood, technology can be employed to remove neural tissue 3 from blood without requiring the closed system or sterile procedures. The possibility was considered in the Harvard Risk Analysis and not deemed a significant risk to spread BSE. Products resulting from processes such as filtering or centrifuging should be allowed to be imported because these steps would remove any particles or tissue residue. Any unnecessarily restrictive regulation imposed on minimum risk regions by the U.S. could easily be applied to U.S. products globally and cause severe problems with the marketing of blood products which are safe and extremely valuable to livestock and aquaculture production. The NRA urges the USDA to resume the import of blood products from minimal risk regions fo feed applications when those products are produced in a manner consistent with the current manufacturing guidelines. Sincerely, David L. Meeker, Ph.D., MBA Vice President, Scientific Services National Renderers Association 4

http://www.animalprotein.org/news_articles/NRA_Comments_APHIS_Minmal_Risk_Rule_3-07.pdf





"Bovine blood has never been implicated in bovine-to-bovine transmission of either natural or experimental BSE"



yep, that's what they use to say about the blood from the nvCJD victims too, however they were wrong about that too. so to wait until bovine blood has been implicated, by then, it's too late. ...TSS



Fourth case of transfusion-associated vCJD infection in the United Kingdom

Editorial team (eurosurveillance.weekly@hpa.org.uk), Eurosurveillance editorial office

A case of variant Creutzfeldt-Jakob disease (vCJD) has recently been diagnosed in a patient in the United Kingdom (UK), who received a blood transfusion from a donor who later developed vCJD [1]. This is the fourth case of probable transfusion transmission of vCJD infection in the UK. Three of the four recipients developed symptoms of vCJD. The first symptomatic case of vCJD associated with blood transfusion was identified in December 2003. This individual developed vCJD six and a half years after transfusion of red cells donated by an individual who developed symptoms of vCJD three and a half years after donation.

A second case of vCJD 'infection' was identified a few months later in a person who had received red cells from a donor who developed symptoms of vCJD 18 months after donation. This patient (the second case) died from causes unrelated to vCJD five years after transfusion. Post-mortem investigations found abnormal prion protein in the spleen and a cervical lymph node., However, prion protein was not found in the brain, and no pathological features of vCJD were found.

A third case developed symptoms of vCJD six years after receiving a transfusion of red blood cells, and died two years and eight months later. The donor of the blood involved developed vCJD about 20 months after donating it.

These three cases have been published as case reports and in the findings of the ongoing collaborative study between the National Blood Services, the National CJD Surveillance Unit, and the Office for National Statistics. This study aims to collect evidence about transmission of CJD or vCJD via the blood supply [2,3,4,5].

The new, fourth case is in a patient who developed symptoms of vCJD eight and a half years after receiving a transfusion of red blood cells from a donor who developed vCJD about 17 months after this blood was donated [1]. The donor to this case also donated the vCJD-implicated blood transfused to the third case. As for all other reported clinical vCJD cases that have been tested for genotype, this patient is a methionine homozygote at codon 129 of the prion protein gene. The patient is currently alive.

All four cases had received transfusions of non-leucodepleted red blood cells between 1996 and 1999. Since October 1999, leucocytes have been removed from all blood used for transfusion in the UK. The effect of leucodepletion on the reduction of the risk of transmission of vCJD from an infective donation is uncertain.

This fourth case of vCJD infection associated with blood transfusion further increases the level of concern about the risk of vCJD transmission between humans by blood transfusion, although much remains unknown. This reinforces the importance of the existing precautions that have been introduced to reduce the risk of transmission of vCJD infection by blood and blood products [6]. No cases of vCJD have been associated with fractionated plasma products. The small group of living recipients of vCJD-implicated blood transfusion in the UK have been informed of their potential exposure to vCJD by blood transfusion, asked to take certain precautions to reduce the risk of onward person-to-person transmission of vCJD during health care, and offered specialist neurological evaluation and advice.

This article has been adapted from reference 1

References: Health Protection Agency. Fourth case of variant CJD associated with blood transfusion (press release). Press release, 18 January 2007. (http://www.hpa.org.uk/hpa/news/articles/press_releases/2007/070118_vCJD.htm) Llewelyn CA, Hewitt PE, Knight RSG, Amar K, Cousens S, Mackenzie J, et al. Possible transmission of variant CJD disease by blood transfusion. Lancet 2004; 363:417-21. Peden AH, Head MW, Ritchie DL, Bell JE, Ironside JW. Preclinical vCJD after blood transfusion in a PRNP codon 129 heterozygous patient. Lancet 2004 ; 364: 527-9. Wroe SJ, Pal S, Siddique D, Hyare H, Macfarlane R, et al Clinical presentation and pre-mortem diagnosis of blood transfusion-associated variant CJD. Lancet 2006;368:2061-67. Hewitt PE, Llewelyn CA, Mackenzie J, Will RG. Creutzfeldt-Jakob disease and blood transfusion: results of the UK Transfusion Medicine Epidemiology review study. Vox Sang. 2006;91(3):221-230. Department of Health [London]. Further precautions to protect blood supply. Press release 2004/0104, 16 March 2004.


(http://www.dh.gov.uk/PublicationsAndStatistics/PressReleases/PressReleasesNotices/fs/en?CONTENT_ID=4076608&chk=MTwE%2Bl)



http://www.eurosurveillance.org/ew/2007/070118.asp



http://bloodindex.org/view_news_zone.php?id=206





HARVARD BSE risk assessment was a joke as well, bought and paid for by your local cattle dealer i.e. USDA et al



*** Suppressed peer review of Harvard study October 31, 2002 ***


http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf




[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) [TSS] Date: August 26, 2006 at 12:09 pm PST

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

8/3/2006

Greetings FSIS,

snip... see full text ;


http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf




Response to Public Commentson theHarvard Risk Assessment of Bovine SpongiformEncephalopathy Update,October 31, 2005

snip...

RESPONSE TO COMMENTS FROM TERRY S. SINGELTARY SR.

Comment #1: SINCE the first Harvard BSE Risk Assessment was so flawed and fraught with error after the PEER REVIEW assessment assessed this fact, how do you plan on stopping this from happening again, will there be another peer review with top TSE Scientists, an impartial jury so-to-speak, to assess this new and updated Harvard BSE/TSE risk assessment and will this assessment include the Atypical TSE and SRM issues?

Response: The original (October 2003) and the revised (October 2005) Harvard BSE risk assessments underwent external peer review. Subsequently, revisions were made to the analysis. In the most recent review, the most significant revisions have been:

1) theaddition of explicit modeling of the poultry litter pathway for the potential recycling ofbovine protein into cattle feed; and

2) a decrease in the assumed effectiveness of antemortem inspection in the identification of animals with BSE.

Comment #2: WITH A RECENT NATION WIDE MAD COW FEED BAN RECALL in the past few months that consisted of some 10,878.06 TONS, then another Mad Cow feed ban warning letter in May, IT should seem prudent to ask why our feed bans continue to fail in 2006, and continue to fail today?

Response: This question about feed bans is a matter for policy. As such, it is not addressed in this response.

Comment #3: WHY still now only partial ruminant feed ban, with the fact that now we seem to have 3 cases of nvCJD to humans i.e. human bovine TSE that were responsible from blood, and the fact the last 2 mad cows documented in the USA were that of an Atypical strain, would it not seem prudent to remove blood as well from ruminant feed?WOULD it not seem prudent to improve and expand the SRM list now? as per your ownthinking; If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM)removal.

Response: This comment pertains to policy. As such, it is not addressed here.

Comment #4: WHAT does USDA/FDA ET AL intend to do about the risks of atypical BSE/TSE in cattle now that infectivity shows in tissue samples other than CNS in Japan, the fact now that the last Texas mad cow and that last mad cow in Alabama were indeed of the atypical strain, the fact that the studies long ago in Mission, Texas of USA sheep scrapie transmission to the USA bovine, which proved an 'atypical tse' in the USA bovine, the fact also that USDA/FDA are still floundering on the last SRM regulations, but with the BASE strain now in cattle that is not similar to nvCJD, but very similar to the sporadic CJD, and sporadic CJD has tripled in the last few years in the USA. WHAT do you plan to do to protect human health from these atypical strains of TSE, in relations to SRMs ?

- 19 -

----------------------------------------------------------

Page 20

Response: The BSE risk assessment simulation model characterizes the disease history of BSE, including the agent's spread within the body of the animal over time. It also quantifies the agent's persistence during the feed manufacture process, and ultimately the agent's ability to cause disease in other exposed animals. There is no definitive evidence that these properties differ substantially for atypical BSE strains, compared to the typical BSE agent.

Comment #5: THE 2004 Enhanced BSE surveillance program, that tested all those cows, but then we found just how terribly flawed the program was, from testing protocols, to testing the most likely to have BSE i.e. high risk, to the geographical distribution of the testing and high risk areas, to letting the tissue samples of one mad cow sit on a shelf for 7+ months and then having to have an act of Congress to ever get that cow finally confirmed, to that other Texas mad cow they decided to not even bother testing at all, just rendered that very suspect cow, too suspect to test evidently, back to that Alabama madcow that they could only give a guess as to age with dentition where we all know that the age of that cow was so close to 10 years it could have been 9 years 7 months to 10 years 3 months, thus possibly being an BAPB i.e. USA 'born after partial ban', to all those rabies suspect cows that did not have rabies, and DID NOT get tested for BSE/TSE in that June 2004 enhanced surveillance program, even though the common lay person knows the suspect rabies negative cows are suppose to be BSE/TSE tested, how does one correct all these blatant failures and will they be corrected?

Response: This comment pertains to policy. As such, it is not addressed here.

Comment #6: WHAT happened to the test results and MOUSE BIO-ASSAYS of those imported sheep from Belgium that were confiscated and slaughtered from the Faillace's, what sort of TSE did these animals have?

Response: It is not clear how the test results referred to in this comment are relevant to the Harvard BSE Risk Assessment Update. Sheep were not considered in the risk assessment.

Comment #7: WHY is it that the Farm of the Mad Sheep of Mad River Valley were quarantined for 5 years, but none of these farms from Texas and Alabama with Atypical TSE in the Bovine, they have not been quarantined for 5 years, why not, with the real risk of BSE to sheep, whom is to say this was not BSE ?

Response: This comment pertains to policy. As such, it is not addressed here.

- 20 -

snip...END

FULL TEXT ;


http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf




and just recently, private email from abroad, you can take this with how ever many grains of salt you wish ;



snip...

we had four cases of 'typical' BSE over a four year period. Herd size around 120. Two of these were half sisters, born a year apart. Their mother stayed in the herd until she died at a good age of other reasons. Friends and neighbours were hit much harder. We had four young cows 'taken' for slaughter as 'cohorts' at a later date.

We had close links with a farm advisor and nutritionist working for a local feed compounder, and a few years later were made aware that the feed company had been given notice that blood meal inclusion would be banned in a couple of months time. As they had 200 tonnes in stock, the inclusion rate was dramatically raised (farmers later were asking for the dark brown cake that the heifers grew so well on) to use the stocks up. Two of our clinical cases were fed this cake before we knew better. Ingredient declaration was not made, only nutritional analysis. The timing also co-incided with permission being given to the big rendering companies to be allowed to lower the processing temperatures (first fuel crisis, and Mrs Thatcher's husband was on the board of the largest processor)...snip...end...TSS



Schweiz Arch Tierheilkd. 2009 Sep;151(9):433-6.

[Protease-resistant prion protein (PrPres) in the blood of offspring of cows that developed BSE].

[Article in German] Braun U, Tschuor A, Hässig M, Franitza S, Berli E, El Gedaily A, Franscini N, Matthey U, Zahn R. SourceDepartement für Nutztiere der Universität Zürich. ubraun@vetclinics.uzh.ch

Abstract


The goal of the present study was to investigate whether protease-resistant prion protein (PrPres) occurs in plasma samples of offspring of cows that developed bovine spongiform encephalopathy (BSE; group A) and to compare the prevalence with that of a healthy control group in 2006 (Group B). Group A consisted of 181 offspring of cows that developed BSE and group B consisted of 240 healthy animals from a region in Switzerland where no cases of BSE occurred from 2001 to the end of 2006. All plasma samples were evaluated using Alicon PrioTrap, an antemortem test for PrPres. The time between birth of the offspring and onset of BSE in the dam was calculated to determine its relationship with the presence of PrPres in the plasma of the offspring. From 181 offspring, 29 (16.1%) had PrPres-positive plasma samples. Offspring that were born within one year of the onset of BSE in the dam had a significantly higher prevalence of PrPres-positive plasma samples than those born more than one year before the onset of BSE in the dam. Ten (4.2%) of 240 control cattle had PrPres-positive plasma samples. Thus, PrPres can be detected in bovine blood and occurs more frequently in the offspring of cows that develop BSE than in cattle of a healthy control population.

PMID:19722131[PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/pubmed/19722131




http://www.cabdirect.org/abstracts/20093248407.html;jsessionid=24FBC2B634B62B6FDE444A591296B3AF




http://agris.fao.org/agris-search/search/display.do?f=2010/CH/CH1001.xml;CH2010000047





I suppose my next concern besides the potential for transmission of TSE PrP via blood in feed, my next concern from spreading blood on the ground would be TSE infection to the soil, thus contaminating pasture land for years, and years. ...TSS



COMERCIAL IN CONFIDENCE


SPREADING OF UNPROCESSED BLOOD ON LAND


http://web.archive.org/web/20040315202749/www.bseinquiry.gov.uk/files/yb/1991/02/15003001.pdf






Saturday, January 24, 2009

Research Project: Detection of TSE Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: 2008 Annual Report


http://bse-atypical.blogspot.com/2009/01/research-project-detection-of-tse.html





PPo4-4:

Survival and Limited Spread of TSE Infectivity after Burial

Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK

Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.

The authors gratefully acknowledge funding from DEFRA.


PPo8-13:

Degradation of Pathogenic Prion Protein and Prion Infectivity by Lichens

Christopher J. Johnson,1 James P. Bennett,1 Steven M. Biro,1,2 Cynthia M. Rodriguez,1,2 Richard A. Bessen3 and Tonie E. Rocke1

1USGS National Wildlife Health Center; 2Department of Bacteriology; University of Wisconsin, Madison; 3Department of Veterinary Molecular Biology; Montana State University; Bozeman, MT USA

Key words: prion, lichen, bioassay, protease, degradation

Few biological systems have been identified that degrade the transmissible spongiform encephalopathy (TSE)-associated form of the prion protein (PrPTSE) and TSE infectivity. Stability of the TSE agent allows scrapie and chronic wasting disease agents to persist in the environment and cause disease for years. Naturally-occurring or engineered processes that reduce infectivity in the environment could aid in limiting environmental TSE transmission. We have previously identified that species of at least three lichens, unusual, symbiotic organisms formed from a fungus and photosynthetic partner, contain a serine protease capable of degrading PrPTSE under gentle conditions. We tested the hypothesis that lichen extracts from these three species reduce TSE infectivity by treating infected brain homogenate with extracts and examining infectivity in mice. We found lichen extracts diminished TSE infectious titer by factors of 100 to 1,000 and that reductions in infectivity were not well-correlated with the extent of PrPTSE degradation observed by immunoblotting. For example, treatment of brain homogenate with Cladonia rangiferina extract caused <100-fold reduction in PrP immunoreactivity but ~1,000-fold decrease in infectivity, suggesting that some PrPTSE remaining after extract treatment was rendered uninfectious or that the lichen protease favors more infectious forms of PrPTSE. Our data also indicate that lichen species closely related to those with prion-degrading protease activity do not necessarily degrade PrPTSE. Characterization of the lichen species-specificity of PrPTSE degradation within the genera Cladonia and Usnea and comparison with known lichen phylogeny has yielded clusters of species on which to focus searches for anti-prion agents.


http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html



TSEs And The Environment


The LANCET Volume 351, Number 9110 18 April 1998

BSE: the final resting place


How to dispose of dangerous waste is a question that has vexed the human race for hundreds of years. The answer has usually been to get it out of sight--burn it or bury it. In Periclean Athens, victims of the plague were incinerated in funeral pyres; in 14th century Venice, a law stipulated that Black Death corpses should be buried to a minimum depth of 5 feet; and now, as the 20th century draws to a close, we are challenged by everything from industrial mercury to the smouldering reactors of decommissioned atomic submarines. The Irish Department of Agriculture will convene an expert panel on April 27-29 to discuss the disposal of tissues from animals with bovine spongiform encephalopathy (BSE). Proper disposal of tissues from infected cattle has implications for both human and animal safety. Safety for human beings is an issue because there is now unassailable if still indirect evidence that BSE causes infections in man in the form of "new variant" Creutzfeld-Jakob disease (nvCJD).1-3 Safety for animals is also an issue because BSE-affected cattle could possibly transmit disease to species other than cattle, including sheep, the species that was almost surely the unwitting source of the BSE epidemic. 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. A second consideration relates to the routes by which TSE infection can occur. Decades of accumulated data, both natural and experimental, have shown clearly that the most efficient method of infection is by direct penetration of the central nervous system; penetration of peripheral sites is less likely to transmit disease. Infection can also occur by the oral route, and the ingestion of as little as 1 g of BSE brain tissue can transmit disease to other cattle.5 Infection by the respiratory route does not occur (an important consideration with respect to incineration), and venereal infection either does not occur or is too rare to be detected. How can tissue infectivity be destroyed before disposal? The agents that cause TSE have been known almost since their discovery to have awesome resistance to methods that quickly and easily inactivate most other pathogens. Irradiation, chemicals, and heat are the three commonest inactivating techniques. Irradiation has proved entirely ineffective, and only a handful of a long catalogue of chemicals have produced more than modest reduction in infectivity. The most active of these are concentrated solutions of sodium hypochlorite (bleach) or sodium hydroxide (lye). As for heat, even though the agent shares with most other pathogens the feature of being more effectively damaged by wet heat than by dry heat, boiling has little effect, and steam heat under pressure (autoclaving) at temperatures of 121ºC is not always sterilising. To date, the most effective heat kill requires exposure of infectious material to steam heat at 134ºC for 1 h in a porous-load autoclave.6 Exposure to dry heat even at temperatures of up to 360ºC for 1 h may leave a small amount of residual infectivity.7 The standard method of incineration, heating to about 1000ºC for at least several seconds, has been assumed to achieve total sterilisation, but needs experimental verification in the light of suggestions that rendered tissue waste might find some useful purpose as a source of heating fuel. Thus, TSE agents are very resistant to virtually every imaginable method of inactivation, and those methods found to be most effective may, in one test or another, fail to sterilise. It seems that even when most infectious particles succumb to an inactivating process, there may remain a small subpopulation of particles that exhibit an extraordinary capacity to withstand inactivation, and that, with appropriate testing, will be found to retain the ability to transmit disease. Also, almost all available inactivation data have come from research studies done under carefully controlled laboratory conditions, and it is always difficult to translate these conditions to the world of commerce. Even when the data are applied in the commercial process, the repetitive nature of the process requires vigilance in quality control and inspection to ensure adherence to its regulations. The final issue that must be addressed is the "lifespan" of the infectious agent after disposal if it has been only incompletely inactivated beforehand. Given the extraordinary resistance of the agent to decontamination measures, the epidemiological and experimental evidence indicating that TSE agents may endure in nature for a long time should come as no surprise. The first real clue to this possibility came from the Icelandic observation that healthy sheep contracted scrapie when they grazed on pastures that had lain unused for 3 years after having been grazed by scrapie-infected sheep.8 Support for this observation was obtained from an experiment in which scrapie-infected brain material was mixed with soil, placed in a container, and then allowed to "weather" in a semi-interred state for 3 years.9 A small amount of residual infectivity was detected in the contaminated soil, and most of the infectivity remained in the topmost layers of soil, where the tissue had originally been placed--in other words, there had been no significant leaching of infectivity to deeper soil layers. It is therefore plausible for surface or subsurface disposal of TSE-contaminated tissue or carcasses to result in long-lasting soil infectivity. Uncovered landfills are a favourite feeding site for seagulls, which could disperse the infectivity.10 Other animals might do likewise, and if the landfill site were later used for herbivore grazing, or tilled as arable land, the potential for disease transmission might remain. A further question concerns the risk of contamination of the surrounding water table, or even surface waste-water channels, by effluents and discarded solid waste from treatment plants. A reasonable conclusion from existing data is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge number of uncertainties and assumptions that attend each stage of the disposal process. On the positive side, spongiform encephalopathy can be said to be not easily transmissible. Although the level of infectivity to which creatures are exposed is not known, it is probably very low, since sheep that die from scrapie, cattle that die from BSE, and human beings who die from nvCJD represent only a small proportion of their respective exposed populations. Whatever risk exists is therefore extremely small, but not zero, hence all practical steps that might reduce the risk to the smallest acceptable level must be considered. What is practical and what is acceptable are concepts that will be hammered out on the anvil of politics: scientific input, such as it is, already waits in the forge. A fairly obvious recommendation, based on the science, would be that all material that is actually or potentially contaminated by BSE, whether whole carcasses, rendered solids, or waste effluents, should be exposed to lye and thoroughly incinerated under strictly inspected conditions. Another is that the residue is buried in landfills to a depth that would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source. Certainly, it has been, and will continue to be, necessary in many instances to accept less than the ideal.



Paul Brown Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892, USA 1 Will RG, Ironside JW, Zeidler M, et al. A new variant of Creutzfeldt-Jakob disease in the UK. Lancet 1996; 347: 921-25 [PubMed]. 2 Bruce M, Will RG, Ironside JW, et al. Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature 1997: 389: 498-501. 3 Collinge J, Sidle KCL, Heads J, Ironside J, Hill AF. Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature 1996; 383: 685-90 [PubMed]. 4 Wells GAH, Hawkins SAC, Green RB, et al. Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update. Vet Rec 1998; 142: 103-06 [PubMed]. 5 Collee JG, Bradley R. BSE: a decade on--part 2. Lancet 1997; 349: 715-21 [PubMed]. 6 Taylor DM. Exposure to, and inactivation of, the unconventional agents that cause transmissible degenerative encephalopathies. In: Baker HF, Ridley RM, eds. Methods in molecular medicine: prion diseases. Totawa NJ: Humana Press, 1996: 105-18. 7 Brown P, Liberski PP, Wolff A, Gajdusek DC. Resistance of scrapie infectivity to steam autoclaving after formaldehyde fixation and limited survival after ashing at 360°C: practical and theoretical implications, J Infect Dis 1990; 161: 467-72 [PubMed]. 8 Palsson PA. Rida (scrapie) in Iceland and its epidemiology. In: Prusiner SB, Hadlow WJ, eds. Slow transmissible diseases of the nervous system, vol I. New York: Academic Press, 1979: 357-66. 9 Brown P, Gajdusek DC. Survival of scrapie virus after 3 years' interment. Lancet 1991; 337; 269-70. 10 Scrimgoeur EM, Brown P, Monaghan P. Disposal of rendered specified offal. Vet Rec 1996; 139: 219-20 [PubMed].


http://www.thelancet.com/newlancet/sub/issues/vol351no9110/body.commentary1146.html



snip...


88. Natural decay: Infectivity persists for a long time in the environment. A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep, after they had grazed on land which had previously been grazed by scrapie-infected sheep, even though the land had lain fallow for three years before the healthy sheep were introduced. Brown also quoted an early experiment of his own (1991), where he had buried scrapie-infected hamster brain and found that he could still detect substantial infectivity three years later near where the material had been placed.


89. Potential environmental routes of infection: Brown discusses the various possible scenarios, including surface or subsurface deposits of TSE-contaminated material, which would lead to a build-up of long-lasting infectivity. Birds feeding on animal remains (such as gulls visiting landfill sites) could disperse infectivity. Other animals could become vectors if they later grazed on contaminated land. "A further question concerns the risk of contamination of the surrounding water table or even surface water channels, by effluents and discarded solid wastes from treatment plants. A reasonable conclusion is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge numbers of uncertainties and assumptions that attend each stage of the disposal process". These comments, from a long established authority on TSEs, closely echo my own statements which were based on a recent examination of all the evidence.


90. Susceptibility: It is likely that transmissibility of the disease to humans in vivo is probably low, because sheep that die from scrapie and cattle that die from BSE are probably a small fraction of the exposed population. However, no definitive data are available.


91. Recommendations for disposal procedures: Brown recommends that material which is actually or potentially contaminated by BSE should be: 1) exposed to caustic soda; 2) thoroughly incinerated under carefully inspected conditions; and 3) that any residue should be buried in landfill, to a depth which would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source.


92. This review and recommendations from Brown have particular importance. Brown is one of the world's foremost authorities on TSEs and is a senior researcher in the US National Institutes of Health (NIH). It is notable that such a respected authority is forthright in acknowledging the existence of potential risks, and in identifying the appropriate measures necessary to safeguard public health.


Paper by SM Cousens, L Linsell, PG Smith, Dr M Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will, "Geographical distribution of variant CJD in the UK (excluding Northern Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41 (02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD (variant CJD) might live closer to rendering factories than would be expected by chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were studied. The incubation period of vCJD is not known but by analogy with other human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure to rendering products, such exposure might plausibly have occurred 8-10 years before the onset of symptoms. The authors were able to obtain the addresses of all rendering plants in the UK which were in production in 1988. For each case of vCJD, the distance from the place of residence on 1st January 1998 to the nearest rendering plant was calculated...


snip...


http://web.archive.org/web/20030326042814/http://www.bseinquiry.gov.uk/files/ws/s019b.pdf


Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).


http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf



PAUL BROWN SCRAPIE SOIL TEST

http://collections.europarchive.org/tna/20080102120203/http://www.bseinquiry.gov.uk/files/sc/seac07/tab03.pdf



Some unofficial information from a source on the inside looking out - Confidential!!!! As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!



----------



You can also take that with however many grains of salt you wish, and we can debate these issues all day long, but the bottom line, this is not rocket-science, all one has to do is some experiments and case studies. But for the life of me, I don't know what they are waiting on?


Einstein once said, 'The definition of insanity is doing the same thing over and over again and expecting different results.' re-transmission studies on TSE's...TSS



and as late as 2007, 10 MILLION POUNDS of blood laced MBM went into commerce in the USA ;


"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."



WHAT about that partial and voluntary ruminant to ruminant mad cow feed ban of August 4, 1997 ?


lets take a look at progress 10 years later, fast forward 2007 ;



10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007 Date: March 21, 2007 at 2:27 pm PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

___________________________________


PRODUCT

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007


RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007. Firm initiated recall is ongoing.


REASON


Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.


VOLUME OF PRODUCT IN COMMERCE 42,090 lbs.


DISTRIBUTION WI

___________________________________


PRODUCT


Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007


CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified.


RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.


REASON


Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.


VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs.


DISTRIBUTION ID and NV


END OF ENFORCEMENT REPORT FOR MARCH 21, 2007


http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm



Subject: Calf Claimer Powder with prohibited bovine blood meal which did not bear the cautionary BSE statement


DISTRIBUTION NATIONWIDE


Date: June 13, 2007 at 10:59 am PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II


___________________________________


PRODUCT O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged in 11-oz. bottles, For Animal Use Only. Recall # V-043-2007 CODE A06


RECALLING FIRM/MANUFACTURER Springer Magrath Co., Mc Cook, NE, by telephone on January 2, 2007, fax dated January 9, 2007, by letters on February 22, 2007, March 12, March 14 and March 21, 2007. Firm initiated recall is ongoing.


REASON


The finished product was manufactured with prohibited bovine blood meal and did not bear the cautionary BSE statement that the product should not be fed to ruminants.


VOLUME OF PRODUCT IN COMMERCE


Approximately 13,255 bottles


DISTRIBUTION Nationwide


END OF ENFORCEMENT REPORT FOR JUNE 13, 2007


###


http://www.fda.gov/bbs/topics/enforce/2007/ENF01008.html




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

PRION DISEASE UPDATE 2010 (11)

SEE;

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation


http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129





Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation


http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html




http://www.aphis.usda.gov/import_export/plants/manuals/ports/downloads/apm_pdf/03_18petfoodsandfeed.pdf




http://www.dardni.gov.uk/index/animal-health/animal-diseases/bse/bse-feed-ban.htm





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)


http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html





NOW, back to August 1995 ;

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 ;


http://collections.europarchive.org/tna/20080102153800/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf





PPo4-15:

A Surprisingly High Number of the Plaque-Like VV sCJD Subtype Among the Polish sCJD—is There a Connection with BASE?

Beata Sikorska and Pawel P. Liberski Department of Molecular Pathology and Neuropathology; Medical University of Lodz; Lodz, Poland

Recently described bovine amyloidotic spongiform encephalopathy (BASE) or L type BSE—was is overrepresented in Poland (15% of all cases of BSE). Moreover, the number of BASE cases in Poland per million bovines is the highest in Europe. A potential human risk from BASE is evident from experimental transmission to “humanized” transgenic animals and primates. Taking into consideration that non-human primate inoculated with BASE had a shorter incubation period than monkeys infected with classical BSE, and that humanized Tg mice have been found to be highly susceptible to infection with atypical form of BSE, it seems probable that BASE may be more pathogenic for humans than BSE, but the transmitted disease may differ from BSE-derived vCJD. Among 47 cases which have been diagnosed as definite in our laboratory, in 19 cases complete histopathological examination and codon 129 status were available. On the basis of the histological pattern and codon 129 status the cases of sCJD were divided into subtypes according to the Parchi&Gambetti classification. The results are as follows: type 1 (MMorMV)- 42%, type 2 (VV)-32%, type 3 (MV)-10.5%, type 4c (MM)- 10.5% and type 5 (VV)-5 %. Although the number of cases is too low to conclude a significantly different distribution of sCJD subtypes in Polish population those data show surprisingly high number of the plaque-like VV sCJD subtype. Interestingly, it was shown before that Tg mice inoculated with BASE showed granular and plaque-like aggregates or PrPSc in brains resembling those observed in VV2 subtype of sCJD.


PPo2-26:

Transmission of Classical and Atypical (L-type) Bovine Spongiform Encephalopathy (BSE) Prions to Cynomolgus macaques

Fumiko Ono,1 Yoshio Yamakawa,2 Minoru Tobiume,3 Yuko Sato,3 Harutaka Katano,3 Kenichi Hagiwara,2 Iori Itagaki,1 Akio Hiyaoka,1 Katuhiko Komatuzaki,1 Yasunori Emoto,1 Hiroaki Shibata,4 Yuichi Murayama,5 Keiji Terao,4 Yasuhiro Yasutomi4 and Tetsutaro Sata3

1The Corporation for Production and Research of Laboratory Primates; Tsukuba City, Japan; 2Departments of Cell Biology and Biochemistry; and 3Pathology; National Institute of Infectious Diseases; Tokyo, Japan; 4Tsukuba Primate Research Center; National Institute of Biomedical Innovation; Tsukuba City, Japan; 5Prion Disease Research Team; National Institute of Animal Health; Tsukuba City, Japan

Key words: L-type BSE, cBSE, cynomolgus macaques, transmission

BSE prion derived from classical BSE (cBSE) or L-type BSE was characterized by inoculation into the brain of cynomolgus macaques. The neurologic manifestation was developed in all cynomolgus macaques at 27–43 months after intracerebral inoculation of brain homogenate from cBSE-affected cattle (BSE JP/6). Second transmission of cBSE from macaque to macaque shortened incubation period to 13–18 months. cBSE-affected macaques showed the similar clinical signs including hyperekplexia, tremor and paralysis in both primary and second transmission.

Two macaques were intracerebrally inoculated brain homogenate from the L-type BSE-affected cattle (BSE JP/24). The incubation periods were 19–20 months in primary transmission.

The clinical course of the L-type BSE-affected macaques differed from that in cBSE-affected macaques in the points of severe myoclonus without hyperekplexia. The glycoform profile of PrPSc detected in macaque CNS was consistent with original pattern of either cBSE or L-typeBSE PrPSc, respectively. Although severe spongiform change in the brain was remarkable in all BSE-affected macaques, severe spongiform spread widely in cerebral cortex in L-type BSE-affected macaques. Heavy accumulation of PrPSc surrounded by vacuola formed florid plaques in cerebral cortex of cBSE-affected macaques. Deposit of PrPSc in L-type BSE-affected macaque was weak and diffuse synaptic pattern in cerebrum, but large PrPSc plaques were evident at cerebellum. MRI analysis, T2, T1, DW and flair sequences, at the time of autopsy revealed that brain atrophy and dilatation of cerebral ventricles were significantly severe in L-type BSE-affected macaques. These results suggest that L-type BSE is more virulent strain to primates comparing to cBSE.


SP1-4:

Evidence from Molecular Strain Typing

Gianluigi Zanusso Department of Neurological and Visual Sciences; Section of Clinical Neurology; University of Verona; Verona, Italy

Key words: molecular analysis, strain typing, atypical BSE, CJD

In 2001, active surveillance for bovine spongiform encephalopathy (BSE) led to the discovery of atypical BSE phenotypes in aged cattle distinct from classical BSE (C-type). These atypical BSE cases had been classified as low L-type (BASE) or high H-type BSE based on the molecular mass and the degree of glycosylation of of the pathological prion protein (PrPSc). Transmission studies in TgBov mice showed that H-type BSE, C-type BSE and BASE behave as distinct prion strains with different incubation periods, PrPSc molecular patterns and pathological phenotypes. A still unclear issue concerns the potential transmissibility and phenotypes of atypical BSEs in humans. We previously indicated that BASE was similar to a distinct subgroup of sporadic form of Creutzfeldt-Jakob disease (sCJD) MV2, based on molecular similarities and on neuropathological pattern of PrP deposition. To investigate a possible link between BASE and sCJD, Kong et al. and Comoy et al. experimentally inoculated TgHu mice (129MM) and a non-human primate respectively, showing in both models that BASE was more virulent compare to BSE. Further, non-human primate reproduced a clinical phenotype resembling to that of sCJD subtype MM2. Here, we presented a comparative analysis of the biochemical fingerprints of PrPSc between the different sCJD subtypes and animal TSEs and after experimental transmission to animals.



http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099




Opinion of the Scientific Steering Committee on the GEOGRAPHICAL RISK OF BOVINE SPONGIFORM ENCEPHALOPATHY (GBR) in POLAND Adopted on 30/03/2001

It is concluded that it is likely but not confirmed that one or several cattle that are (pre-clinically or clinically) infected with the BSE agent are currently present in the domestic herd of Poland (GBR III).


http://ec.europa.eu/food/fs/sc/ssc/out185_en.pdf




http://bse-atypical.blogspot.com/2010/09/atypical-bse-strains-and-sporadic-cjd.html





Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate

Emmanuel E. Comoy1*, Cristina Casalone2, Nathalie Lescoutra-Etchegaray1, Gianluigi Zanusso3, Sophie Freire1, Dominique Marcé1, Frédéric Auvré1, Marie-Magdeleine Ruchoux1, Sergio Ferrari3, Salvatore Monaco3, Nicole Salès4, Maria Caramelli2, Philippe Leboulch1,5, Paul Brown1, Corinne I. Lasmézas4, Jean-Philippe Deslys1

1 Institute of Emerging Diseases and Innovative Therapies, CEA, Fontenay-aux-Roses, France, 2 Istituto Zooprofilattico Sperimentale del Piemonte, Turin, Italy, 3 Policlinico G.B. Rossi, Verona, Italy, 4 Scripps Florida, Jupiter, Florida, United States of America, 5 Genetics Division, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America

Abstract Top Background Human variant Creutzfeldt-Jakob Disease (vCJD) results from foodborne transmission of prions from slaughtered cattle with classical Bovine Spongiform Encephalopathy (cBSE). Atypical forms of BSE, which remain mostly asymptomatic in aging cattle, were recently identified at slaughterhouses throughout Europe and North America, raising a question about human susceptibility to these new prion strains.

Methodology/Principal Findings Brain homogenates from cattle with classical BSE and atypical (BASE) infections were inoculated intracerebrally into cynomolgus monkeys (Macacca fascicularis), a non-human primate model previously demonstrated to be susceptible to the original strain of cBSE. The resulting diseases were compared in terms of clinical signs, histology and biochemistry of the abnormal prion protein (PrPres). The single monkey infected with BASE had a shorter survival, and a different clinical evolution, histopathology, and prion protein (PrPres) pattern than was observed for either classical BSE or vCJD-inoculated animals. Also, the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine.

Conclusion/Significance Our results point to a possibly higher degree of pathogenicity of BASE than classical BSE in primates and also raise a question about a possible link to one uncommon subset of cases of apparently sporadic CJD. Thus, despite the waning epidemic of classical BSE, the occurrence of atypical strains should temper the urge to relax measures currently in place to protect public health from accidental contamination by BSE-contaminated products.

Citation: Comoy EE, Casalone C, Lescoutra-Etchegaray N, Zanusso G, Freire S, et al. (2008) Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate. PLoS ONE 3(8): e3017. doi:10.1371/journal.pone.0003017

Editor: Neil Mabbott, University of Edinburgh, United Kingdom

Received: April 24, 2008; Accepted: August 1, 2008; Published: August 20, 2008

Copyright: © 2008 Comoy et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This work has been supported by the Network of Excellence NeuroPrion.

Competing interests: CEA owns a patent covering the BSE diagnostic tests commercialized by the company Bio-Rad.

* E-mail: emmanuel.comoy@cea.fr


http://www.plosone.org/article/info:doi/10.1371/journal.pone.0003017





Session I - Prions: Structure, Strain and Detection (II)

Searching for BASE Strain Signature in Sporadic Creutzfedlt-Jakob Disease

Gianluigi Zanusso

Department of Neurological and Visual Sciences, Section of Clinical Neurology University of Verona, Verona, Italy.

Bovine amyloidotic spongiform encephalopathy (BASE) is a newly recognized form of bovine prion disease, which was originally detected in Italy in 2004 as an effect of active surveillance. BASE or BSE L-type (L is referred to the lower electrophoretic PrPSc migration than classical BSE) has now been reported in several countries, including Japan. All field cases of BASE were older than 8 years and neurologically normal at the time of slaughtered. By experimental transmission, we defined the disease phenotype of cattle BASE, which is quite distinct from that seen in typical BSE and characterized by mental dullness and amyotrophy. Surprisingly, following intraspecies and interspecies transmission the incubation period of BASE was shorter than BSE. The relatively easy transmission of BASE isolate as well as the molecular similarity with sporadic Creutzfeldt-Jakob disease (sCJD) have raised concern regarding its potential passage to humans. Tg humanized mice Met/Met at codon 129 challenged with both BSE and BASE isolates, showed a resistance to BSE but a susceptibility to BASE at a 60% rate; in addition, BASE-inoculated Cynomolgus (129 Met/Met) had shorter incubation periods than BSE-inoculated primates. In this study we compared the biochemical properties of PrPSc in Cynomolgus and in TgHu Met/Met mice challenged with BSE and BASE strains, by conventional SDS-PAGE analysis and 2D separation. The results obtained disclose distinct conformational changes in PrPSc, which are dependent on the inoculated host but not on the codon 129 genotype.

This work was supported by Neuroprion contract n. FOOD CT 2004 -506579 (NOE)


http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf





P02.35

Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE

Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden

Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK-resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.


http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf





Thursday, October 07, 2010

Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice

Thursday, October 07, 2010 Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice

Vet Pathol 0300985810382672, first published on October 4, 2010

Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice

H. Okada okadahi@affrc.go.jp Prion Disease Research Center, National Institute of Animal Health, Tsukuba, K. Masujin Prion Disease Research Center, National Institute of Animal Health, Tsukuba, Y. Imamaru Prion Disease Research Center, National Institute of Animal Health, Tsukuba, M. Imamura Prion Disease Research Center, National Institute of Animal Health, Tsukuba, Y. Matsuura Prion Disease Research Center, National Institute of Animal Health, Tsukuba, S. Mohri Prion Disease Research Center, National Institute of Animal Health, Tsukuba, S. Czub Animal Disease Research Institute, Canadian Food Inspection Agency, T. Yokoyama Prion Disease Research Center, National Institute of Animal Health, Tsukuba,

Abstract

To characterize the biological and biochemical properties of H-type bovine spongiform encephalopathy (BSE), a transmission study with a Canadian H-type isolate was performed with bovinized transgenic mice (TgBoPrP), which were inoculated intracerebrally with brain homogenate from cattle with H-type BSE. All mice exhibited characteristic neurologic signs, and the subsequent passage showed a shortened incubation period. The distribution of disease-associated prion protein (PrPSc) was determined by immunohistochemistry, Western blot, and paraffin-embedded tissue (PET) blot. Biochemical properties and higher molecular weight of the glycoform pattern were well conserved within mice. Immunolabeled granular PrPSc, aggregates, and/or plaque-like deposits were mainly detected in the following brain locations: septal nuclei, subcallosal regions, hypothalamus, paraventricular nucleus of the thalamus, interstitial nucleus of the stria terminalis, and the reticular formation of the midbrain. Weak reactivity was detected by immunohistochemistry and PET blot in the cerebral cortex, most thalamic nuclei, the hippocampus, medulla oblongata, and cerebellum. These findings indicate that the H-type BSE prion has biological and biochemical properties distinct from those of C-type and L-type BSE in TgBoPrP mice, which suggests that TgBoPrP mice constitute a useful animal model to distinguish isolates from BSE-infected cattle.

© 2010 Sage Publications, Inc.


http://vet.sagepub.com/content/early/2010/10/02/0300985810382672.abstract





let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.

This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$

ALABAMA MAD COW g-h-BSEalabama

In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.


http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156




http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF




her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).

This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine–human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks.

Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA

NATURE|Vol 457|26 February 2009


http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html




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)


http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html





Sunday, May 01, 2011

STUDY OF ATYPICAL BSE 2010 Annual Report May 2011


http://bse-atypical.blogspot.com/2011/05/study-of-atypical-bse-2010-annual.html




Sunday, January 30, 2011

Vaccines and Transmissible Spongiform Encephalopathy the Prion Disease, what if ?

COMMERCIAL IN CONFIDENCE


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/vaccines-and-transmissible-spongiform.html




Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA


http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html





Blood products and related biologicals

Transmissible spongiform encephalopathies (TSE) The appearance of a variant form of human Creutzfeldt-Jakob Disease (CJD) in the mid-1990s, as a result of the Bovine Spongiform Encephalopathy (BSE) epidemic in the United Kingdom, has increased the profile of transmissible spongiform encephalopathies as a risk to human health and has already affected public health policy worldwide. It is assumed that the variant CJD (vCJD) results from the consumption of meat products from cattle infected with BSE and that there is a relation of the incidence of vCJD to the incidence of BSE in the countries where the disease has occurred. Since 1996, over 140 cases of vCJD have occurred in UK, seven in France and one each in Ireland, Italy, USA and Canada.

Policies related to vCJD and the potential risk of human to human transmission are based on three main factors:

an unknown number of individuals who might be infected with the BSE agent;

presence of the pathological prion protein in many peripheral tissues from vCJD terminal patients and

evidence of experimental transmission in animals from blood of rodents and sheep infected with vCJD and BSE respectively.

There is increasing concern about the troubling possibility that blood or blood products, vaccines and other pharmaceutical products could spread the agent of variant CJD (vCJD) worldwide, especially in countries where BSE has not yet been reported. Bovine derived materials involved in the production of vaccines and other pharmaceutical products could represent a way of potential transmission of the disease. Moreover, the possibility that human blood and plasma could be a vehicle for the transmission and spread of the disease have led to a number of donor deferral policies aimed at minimizing the risk of accepting a blood donor who might be incubating the human form of BSE. In addition, blood fractionated products such as albumin are used as stabilizers in the production of vaccines and recombinant pharmaceutical products. There is, therefore, a need to ensure that regulatory authorities with limited resources can have reliable information when making their risk assessment and evaluation of product safety to prevent the transmission of TSE to human via biological and pharmaceutical products.

A WHO Consultation was held in February 2003 to update the WHO Recommendations on Medicinal Products in relation to Human TSEs which were prepared in 1997, following a WHO Consultation on the same subject.

This Consultation complemented other important efforts of WHO in the follow up of the scientific and epidemiological developments in TSEs such as the Joint WHO/FAO/OIE Technical Consultation on BSE organized by the WHO Department of Communicable Disease Surveillance and Response (CSR) and the activities of the "Working Group on International Reference Materials for Diagnosis and Study of TSEs", established in 1999 as a scientific forum to advance development of diagnostic tests based on available research methods and their application in health technology and pharmaceuticals.

The primary aim of this Consultation was to provide evidence-based information to medicines regulatory authorities of Member States, specially to those where BSE has not yet been reported, with regard to risk assessment, precautionary and control measures of medicinal products.

The Recommendations of the Consultation form the basis of the WHO Guidance Document to support regulatory decisions by National Regulatory Authorities in developing countries. Based on scientific information available, a tissue infectivity category was developed for the first time, that serves as a global basis for the development of risk assessment models for biological and pharmaceutical products derived from human or animal tissues or body fluids in relation to the transmission of TSE agents.

Creutzfeldt-Jakob Disease reagents

WHO Reference Reagents for In Vitro Assays of CJD Specimens. ECBS 2003. WHO/BS/03.1965 Rev.1 pdf, 127kb Catalogue of WHO International Reference Materials (for CJD specimens see Miscellaneous) Distribution of WHO International Reference Materials The characteristics of all reference preparations as well as the information regarding establishment can be found in the WHO Reference Material section.

Related documents WHO Guidelines on Tissue Infectivity Distribution in TSEs 2006 pdf, 638kb Report on International Reference Materials for Diagnosis and Study of Transmissible Spongiform Encephalopathies (TSEs). Working group fourth meeting, Geneva, Switzerland (April 2002) pdf, 99kb Report on International Reference Materials for Diagnosis and Study of Transmissible Spongiform Encephalopathies (TSEs). Working group third meeting, Geneva, Switzerland (March 2001) pdf, 81kb Report on International Reference Materials for Diagnosis and Study of Transmissible Spongiform Encephalopathies (TSEs). Working group second meeting, Geneva, Switzerland (May 2000) pdf, 86kb Report on International Reference Materials for Diagnosis and Study of Transmissible Spongiform Encephalopathies (TSEs). Working group first meeting, Geneva, Switzerland (Sep 1999) pdf, 62kb Report on WHO Consultation on Diagnostic Procedures for Transmissible Spongiform Encephalopathies (TSEs): Need for Reference Reagents and Reference Panels. Geneva, Switzerland (March 1999) pdf, 77kb Related links


http://www.who.int/bloodproducts/tse/en/




Sunday, May 1, 2011

W.H.O. T.S.E. PRION Blood products and related biologicals May 2011


http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/who-tse-prion-blood-products-and.html




The documents below were provided by Terry S. Singeltary Sr on 8 May 2000.

They are optically character read (scanned into computer) and so may contain typos and unreadable parts.

TIP740203/l 0424 CONFIDENTIAL

snip...

The responses by the companies were presented by Ms Turner and were categorised by MCA standards, the products that were discussed were all low volume usage products eg sutures, heart valves.

8. As the responses included some materials of human origin it was decided that more information should be sought about CJD. There had been 2 recent deaths reported associated with human growth hormone. These were being investigated.

snip...


http://www.mad-cow.org/00/may00_news.html#aaa




5.3.3 The greatest risk, in theory, would be from parenteral injection of material derived from bovine brain or lymphoid tissue. Medicinal products for injection or surgical implantation which are prepared from bovine tissues, or which utilise bovine serum albumin or similar agents in their manufacture, might also be capable of transmitting infectious agents. All medicinal products are licensed under the Medicines Act by the Licensing Authority following guidance, for example from the Committee on Safety of Medicines (CSM), the Committee on Dental and Surgical Materials (CDSM) and their subcommittees. The Licensing Authority have been alerted to potential concern about BSE in medicinal products and will ensure that scrutiny of source materials and manufacturing processes now takes account of BSE agent.

see all 76 pages ;


http://collections.europarchive.org/tna/20080102132706/http://www.bseinquiry.gov.uk/files/ib/ibd1/tab02.pdf





EXPORT OF BRITISH BIOLOGICAL PHARMACEUTICALS...

snip...please see full text ;

Sunday, January 30, 2011

Vaccines and Transmissible Spongiform Encephalopathy the Prion Disease, what if ?

COMMERCIAL IN CONFIDENCE


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/vaccines-and-transmissible-spongiform.html




Saturday, February 26, 2011

Supreme Court Protects Vaccine Manufacturers, Not Injured Children there from Bruesewitz vs Wyeth


http://vcjdtransfusion.blogspot.com/2011/02/supreme-court-protects-vaccine.html




Sunday, May 18, 2008


MAD COW DISEASE BSE CJD CHILDREN VACCINES Sunday, May 18, 2008

MAD COW DISEASE BSE CJD CHILDREN VACCINES

TIP740203/l 0424 CONFIDENTIAL


http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html





Saturday, April 30, 2011

Blood product, collected from a donor who was at risk for variant Creutzfeldt-Jakob disease (vCJD), was distributed APRIL 27, 2011


http://vcjdtransfusion.blogspot.com/2011/04/blood-product-collected-from-donor-who.html





Sunday, January 30, 2011

Vaccines and Transmissible Spongiform Encephalopathy the Prion Disease, what if ?

COMMERCIAL IN CONFIDENCE


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/vaccines-and-transmissible-spongiform.html




Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA


http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html




WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies Updated 2010

snip...

Finally, it is critically important to understand that categories of infectivity are not the same as categories of risk, which require consideration not only of the level of infectivity in tissue, but also of the amount of tissue to which a person or animal is exposed, and the route by which infection is transmitted. For example, although the level of tissue infectivity is the most important factor in estimating the risk of transmission by instrument crosscontamination during surgical procedures (e.g., neurosurgery versus general surgery), it will be only one determinant of the risk of transmission by blood transfusions, in which a large amount of low-infectivity blood is administered intravenously, or the risk of transmission by foodstuffs that, irrespective of high or low infectivity, involve a comparatively inefficient oral route of infection.

snip...

17. A wealth of data from studies of blood infectivity in experimental rodent models of TSE have been extended by recent studies documenting infectivity in the blood of sheep with naturally occurring scrapie and in sheep transfused with blood from BSEinfected cattle [Houston et al., 2008]; of deer with naturally occurring CWD [Mathiason et al., 2006]; and (from epidemiological observations) in the red cell fraction (which includes significant amounts of both plasma and leukocytes) of four blood donors in the pre-clinical phase of vCJD infections [reviewed in Brown, 2006;

Hewitt et al., 2006]. Plasma Factor VIII administration has also been potentially implicated in a subclinical case of vCJD in a hemophilia patient [Peden et al., 2010]. Blood has not been shown to transmit disease from humans with any form of ‘classical’ TSE [Dorsey et al., 2009], or from cattle with BSE (including fetal calf blood). A WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies

11

number of laboratories using new, highly sensitive methods to detect PrPTSE are reporting success in a variety of animal and human TSEs. However, several have experienced difficulty obtaining reproducible results in plasma, and it is not yet clear that positive results imply a potential for disease transmissibility, either because of false positives, or of ‘true’ positives that are due to sub-transmissible concentrations of PrPTSE. Because of these considerations (and the fact that no data are yet available on blinded testing of specimens from naturally infected humans or animals) the expert group felt that it was still too early to evaluate the validity of these tests with sufficient confidence to permit either a negative or positive conclusion.

18. Evidence that infectivity is not present in milk from BSE-infected bovines includes temporo-spatial epidemiologic observations failing to detect maternal transmission to calves suckled for long periods; clinical observations of over a hundred calves suckled by infected cows that have not developed BSE; and experimental observations that milk from infected cows reared to an age exceeding the minimum incubation period has not transmitted disease when administered intracerebrally or orally to mice [Middleton and Barlow, 1993; Taylor et al., 1995]. Also, PrPTSE has not been detected in milk from cattle incubating BSE following experimental oral challenge [SEAC, 2005]. However, low levels (µg to ng/L) of normal PrP have been detected in milk from both animals and humans [Franscini et al., 2006]. PrPTSE has been detected in the mammary glands of scrapie-infected sheep with chronic mastitis [Ligios et al., 2005], and very recently it has been reported that milk (which in some cases also contained colostrum) from scrapie-infected sheep transmitted disease to healthy animals [Konold et al., 2008; Lacroux et al., 2008].

snip...

please see tables and full text here ;


http://www.who.int/bloodproducts/tablestissueinfectivity.pdf




WITH the confirmed transmission of nvCJD to humans via blood, the ever so emerging strains of TSE called atypical, some much more virulent than that of the typical c-BSE, to continue the practice of feeding animals blood and the spreading of blood on land, in my opinion is a recipe for disaster. ...


layperson


Kind regards,

Terry S. Singeltary Sr. Bacliff, Texas USA