Transmissible Spongiform Encephalopathy

SAMPLE COLLECTION FROM CATTLE UNDER THE BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) ONGOING SURVEILLANCE PROGRAM 2/14/12

2012-02-24T10:17:00.000-08:00

UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE WASHINGTON, DC FSIS NOTICE

13-12

2/14/12

DISTRIBUTION: Electronic NOTICE EXPIRES: 3/1/13 OPI: OPPD

SAMPLE COLLECTION FROM CATTLE UNDER THE BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) ONGOING SURVEILLANCE PROGRAM

I. PURPOSE

This notice provides Food Safety and Inspection Service (FSIS) inspection program personnel (IPP) with instructions regarding the collection of brain samples for the Animal and Plant Health Inspection Service’s (APHIS) Bovine Spongiform Encephalopathy (BSE) ongoing surveillance program. The contents in this notice were last issued in FSIS Notice 05-10.

II. DEFINITION OF COLLECTION PROCEDURES

A. At federally-inspected slaughter establishments that have approved alternative off-site sample collection arrangements with APHIS:

1. APHIS will provide for the collection of brain (obex) samples from an allocated number of cattle 30 months and older condemned for any reason on ante-mortem inspection and from cattle of any age displaying Central Nervous System (CNS) symptoms.

2. At such establishments, FSIS IPP will provide the following to plant management, to the APHIS Area Veterinarian in Charge (AVIC), and to sample collecting contractors:

a. Condemn tag (Z-tag) numbers (not the Z-tag itself); and

b. Disposition information (i.e., the reason for condemnation under 9 CFR Part 309), including history, clinical signs and the condemnation code assigned.

B. At federally-inspected establishments that do not have approved alternative off-site sample collection arrangements with APHIS, FSIS Public Health Veterinarians (PHVs) are to:

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1. Notify the APHIS AVIC when an animal has been condemned for CNS reasons and provide the information outlined in II.A.2.

2. If arrangements with the APHIS AVIC cannot be made, collect appropriate BSE samples from cattle of all ages that display CNS symptoms.

NOTE: Certain Alternative Off-Site Agreements that were in place during Enhanced Surveillance may no longer be in effect. Therefore, IPP may need to advise the establishment that they need to establish new agreements with APHIS and potential collectors.

III. FSIS PERSONNEL RESPONSIBILITIES

A. Upon receipt of this notice, the FSIS PHV is to ask establishment management whether:

1. It has an approved alternative off-site sample collection arrangement with APHIS for collecting allocated samples (as per paragraph II. A.); or

2. It is not an establishment that has an alternative off-site sample collection arrangement with APHIS. If the establishment does not have such an arrangement, then FSIS is to follow the directions in paragraph II.B.

B. If during the meeting establishment management states that it has submitted an application to APHIS to begin off-site sampling, until APHIS approves that arrangement, FSIS PHVs are to:

1. Identify all CNS animals condemned on ante-mortem with a "U. S. Condemned” tag;

2. If an animal is condemned for this reason, contact the APHIS AVIC and follow the directions in paragraph II.B.;

3. Ensure that the animals are humanely euthanized, unless APHIS requests that the animal not be euthanized; and

4. Not allow any CNS animal condemned on ante-mortem to move off the premises of the establishment until APHIS collects the sample or APHIS requests otherwise.

C. In a memorandum of interview (MOI), the FSIS PHV is to document who was present at the meeting with establishment management, the date and time of the meeting, how the establishment plans to proceed based on the choices set out in A. above, and any documents shared with management.

D. If the establishment states that it has submitted a request to APHIS to begin off-site sampling, the FSIS PHV is to update the MOI as to whether the establishment reached an agreement, and in general, what the agreement was.

E. The FSIS PHV is to maintain a copy of the MOI in the official government file, provide a copy to the plant management, and e-mail a copy to the APHIS AVIC. Any

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changes in the agreement with APHIS for off-site sample collection are to be reflected in an updated MOI, which is then distributed as above.

IV. FSIS RESPONSIBILITIES RELATED TO APPROVED ALTERNATIVE OFF-SITE SAMPLE COLLECTION

A. The FSIS PHV is to complete the condemnation form, FSIS Form 6000-13 (Certification of Ante-mortem or Post-mortem Disposition of Tagged Animals), and FSIS Form 6150-1 (Identification Tag – Ante-mortem). The FSIS PHV is to pay special attention when providing a full description of the reason for the condemnation on FSIS Form 6000-13 and fill out fully FSIS Form 6150-1.

B. Incoming animal identification, except the Z-tag, is to be left on these animals to provide needed identifying information on collection forms at the approved alternative off-site collection location. IPP are, or someone under their supervision is to remove Z-tags before any carcasses leave the official establishment.

NOTE: Information supplied to plant management to take to the approved alternative off-site collection locations needs to be complete and accurate. FSIS PHVs need to provide a full description of the reason for the condemnation on FSIS Form 6000-13. APHIS will use this information to triage which condemned animals are sampled.

V. FSIS SAMPLE COLLECTION FOR CATTLE DISPLAYING CNS SYMPTOMS

A. If the establishment does not have an arrangement with APHIS for off-site sampling of cattle with CNS symptoms, the FSIS PHV is to follow the directions in paragraph II.B. The FSIS PHV is to make all final disposition decisions regarding whether to condemn cattle in accordance with 9 CFR part 309.

NOTE: FSIS PHVs can find information regarding BSE sampling (e.g., forms, sampling supply information) on the FSIS intranet under Public Folders, OPPD, PDD, BSE, at:

http://collaboration/sites/InfoExch/OPPD/default.aspx?RootFolder=%2fsites%2fInfoExch%2fOPPD%2fOPPD%2fPDD%2fBSE%20Training%20Info&FolderCTID=&View=%7b6F518F12%2d11E4%2d4A8C%2dB891%2dAACB8FDD96BD%7d

Additional BSE sampling information is provided on the APHIS website at:

http://www.aphis.usda.gov/animal_health/lab_info_services/downloads/BSE_Procedures_Manual.pdf

B. If the responsibility to collect the BSE sample falls to the FSIS PHV, the FSIS PHV, or the establishment under the supervision of the FSIS PHV, is to promptly remove the head in order to collect the brain sample. If the establishment does not arrange to remove the head, the FSIS PHV may need to collect the brain sample as a priority over other ante-mortem or post-mortem procedures.

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C. The FSIS PHV, being mindful of other potential CNS disease conditions of public health significance that may be present, is to collect the brain sample either in the inedible area of the establishment or in an isolated area set aside for such collection to prevent human exposure or the creation of insanitary conditions. Establishment personnel and FSIS IPP are to take proper sanitary measures before returning to edible areas of the establishment after brain sample collection, in accordance with 9 CFR 416.5.

D. In situations where the FSIS PHV has missed the last UPS pick-up for the day, or the FSIS PHV collected the sample on a day when UPS does not pick up, the PHV is to refrigerate the samples until the next available UPS pick-up day. Remember, the sample is not to pass through or to be stored in areas of the establishment where the establishment produces edible product. The FSIS PHV is to maintain the sample’s chain-of-custody.

E. The FSIS PHV is to verify the collection, documentation, and control of all animal identification associated with cattle condemned during ante-mortem inspection that are to be sampled by FSIS. The FSIS PHV is to attach the “U. S. Condemned” tag to cattle condemned during ante-mortem inspection in accordance with 9 CFR 309.13. This documentation will facilitate traceback in the event that the sample result is positive for BSE. The FSIS PHV is to include in the documentation all pertinent information to facilitate trace back of the animal in question in accordance with 9 CFR 320.1.

F. The FSIS PHV is to verify that the presence of condemned cattle or parts does not create insanitary conditions (9 CFR Part 416). The establishment is responsible for the disposal of the condemned cattle in accordance with 9 CFR part 314. The FSIS PHV also is to verify that the establishment maintains records regarding the disposal of the condemned cattle in accordance with 9 CFR 320.1.

G. IPP may inform the establishment that it may choose to hold the carcass and parts until testing results are available. If the establishment chooses to dispose of any carcass or parts before it receives test results, IPP are to advise the establishment that it must dispose of the carcass in one of the following ways:

1. Render it at a facility for non-animal feed use (e.g., biofuel or cement);

2. Alkaline digestion;

3. Incineration; or

4. Lined landfills.

H. Documentation for Cattle Showing Signs of CNS Symptoms

1. For locations without high-speed internet connections, the FSIS PHV is to forward the completed BSE Veterinary Services Laboratory Submissions (BSE-VSLS) sample collection sheets to the corresponding APHIS,VS area office by FAX or by e-mail. The following site lists the VS office FAX numbers and e-mail where available:

http://www.aphis.usda.gov/import_export/downloads/vsavic.pdf

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NOTE: The FSIS PHV can get copies of BSE-VSLS forms by contacting the local APHIS office. The APHIS AVIC in each area office may assist with sample delivery verification and troubleshooting.

2. For locations with high-speed connections, the FSIS PHV is to enter the relevant information into the BSE-VSLS.

NOTE: FSIS PHVs can refer to the BSE-VSLS training for assistance getting access to BSE-VSLS and inputting information. The FSIS PHV may contact the District Office (DO) if he or she needs a copy of the training CD.

VI. TEST RESULTS FOR FSIS SAMPLING FROM CATTLE SHOWING CNS SYMPTOMS

A. The FSIS PHV will receive, by e-mail, a report from the AVIC on the BSE test results. The AVIC will also send copies of the results to the DO.

B. If the test on the carcass condemned for CNS conditions is negative (reported as “not detected”), then any carcasses and parts the establishment has held may be released for rendering or other disposal in accordance with 9 CFR 314. C. If the test is inconclusive, the FSIS PHV will receive supervisory instruction on further actions.

D. For any sample confirmed positive for BSE, the FSIS PHV is to verify that the establishment disposes of the carcasses and parts in the proper manner as set out in paragraph V. G.

VII. PHIS PROCEDURES FOR BSE SAMPLING FROM CATTLE SHOWING CNS SIGNS

A. Enter disposition information into PHIS in ADR.

B. Enter BSE sampling information into the ADR APHIS Lab Sampling page in ADR.

VIII. RABIES

A. When an animal is condemned by the FSIS PHV on ante-mortem for rabies, the FSIS PHV is to contact the DO, which will advise APHIS. In these cases, APHIS will see that the animal is tested for rabies. APHIS will work with the laboratory to get appropriate samples forwarded for BSE surveillance from rabies negative animals.

B. Rabies booster vaccination for PHVs collecting BSE samples is still highly recommended. PHVs can be reimbursed for rabies vaccinations or boosters. Rabies vaccinations are voluntary. Only PHVs who are actually involved with BSE sample collection will be eligible for reimbursement on the vaccination series. PHVs are to make

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arrangements for the vaccinations with their private physician. PHVs are to contact their Front-line supervisor for approval on reimbursement prior to beginning the three shot vaccination series. Refer questions regarding this notice to the Policy Development Division through askFSIS at http://askfsis.custhelp.com or by telephone at 1-800-233-3935.

Assistant Administrator

Office of Policy and Program Development

http://www.fsis.usda.gov/OPPDE/rdad/FSISNotices/13-12.pdf

Tuesday, November 02, 2010

IN CONFIDENCE

The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".

BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992

http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html

2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006

http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html

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

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

Owens, Julie From: Terry S. Singeltary Sr. [flounder9@verizon.net]

Sent: Monday, July 24, 2006 1:09 PM

To: FSIS RegulationsComments

Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98

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

FSIS, USDA, REPLY TO SINGELTARY

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

Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

snip...

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip...

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1

http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf

see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html

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

Sunday, November 13, 2011

California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/california-bse-mad-cow-beef-recall-qfc.html

Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis

http://www.youtube.com/watch?v=zf3lfz9NrT4

http://www.youtube.com/watch?v=c0tWkNvhO4g

http://www.youtube.com/watch?v=zf3lfz9NrT4&feature=results_main&playnext=1&list=PL780BE2AF0B62A944

full text with source references ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html

Friday, February 10, 2012

Creutzfeldt-Jakob disease (CJD) biannual update (2012/1) potential iatrogenic (healthcare-acquired) exposure to CJD, and on the National Anonymous Tonsil Archive

http://creutzfeldt-jakob-disease.blogspot.com/2012/02/creutzfeldt-jakob-disease-cjd-biannual.html

Sunday, February 12, 2012

National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html

Saturday, June 25, 2011

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

"BSE-L in North America may have existed for decades"

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

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

Friday, December 23, 2011

Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model

Volume 18, Number 1—January 2012 Dispatch

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/oral-transmission-of-l-type-bovine.html

TSS

Annual reports of Member States on BSE and Scrapie 2010 excluding North America (for obvious reasons i.e. corruption)

2012-02-23T14:11:00.003-08:00

BSE/Scrapie - TSE in Goats

Annual reports of Member States on BSE and Scrapie 2010

http://ec.europa.eu/food/food/biosafety/tse_bse/docs/annual_report_tse2010_en.pdf

Tuesday, February 14, 2012

White House budget proposes cuts to ag programs including TSE PRION disease aka mad cow type disease

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/white-house-budget-proposes-cuts-to-ag.html

Thursday, February 16, 2012

Bovine Spongiform Encephalopathy BSE

31 USA SENATORS ASK PRESIDENT OBAMA TO HELP SPREAD MAD COW DISEASE 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/bovine-spongiform-encephalopathy-bse-31.html

Thursday, February 23, 2012

EIGHT FORMER SECRETARIES OF AGRICULTURE SPEAKING AT USDA'S 2012 AGRICULTURE OUTLOOK FORUM INDUCTED INTO USA MAD COW HALL OF SHAME

http://madcowusda.blogspot.com/2012/02/eight-former-secretaries-of-agriculture.html

Thursday, February 23, 2012

Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012

snip...

RESEARCH

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011

Experimental Oral Transmission of Atypical Scrapie to Sheep

Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos

To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals’ peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specifi c prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These fi ndings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain.

SNIP...

Although we do not have epidemiologic evidence that supports the effi cient spread of disease in the fi eld, these data imply that disease is potentially transmissible under fi eld situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing fi nding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown.

How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantifi ed, although infectivity has been shown unequivocally. No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and confi rmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected.

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011

http://wwwnc.cdc.gov/eid/article/17/5/pdfs/10-1654.pdf

OIE Scrapie Chapter Revision • Current draft recognizes Nor98-like scrapie as a separate disease from classical scrapie • USDA provided comments on the draft to OIE

http://www.animalagriculture.org/Solutions/Proceedings/Annual%20Meeting/2009/Sheep%20&%20Goat/Myers,%20Thomas.pdf

Atypical scrapie/Nor 98 October 2009

Last year, after examining member country submissions and investigating rigorous scientific research, the World Organisation for Animal Health (OIE) decided that Nor 98 should not be listed in its Terrestrial Animal Health Code. The Code sets out trade recommendations or restrictions for listed diseases or conditions, and the OIE determined there was no need for such recommendations around Nor 98.

http://www.nzfsa.govt.nz/publications/ce-column/ce-web-nor98.htm

http://www.biosecurity.govt.nz/files/pests/atypical-scrapie/atypical-scrapie-faq-oct09.pdf

Sutton reported that USDA has urged the World Organization for Animal Health (OIE) to categorize Nor98-like scrapie as a separate disease from classical scrapie. Currently, the OIE has proposed a draft revision of their scrapie chapter that would exclude Nor98-like scrapie from the chapter. USDA will be submitting it's comments on this proposal soon.

http://www.ohiosheep.org/Events/ScrapieNewsletterMarch09.pdf

snip...

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/atypical-scrapie-nor-98-confirmed.html

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

Sunday, February 12, 2012

National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html

TSS

Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012

2012-02-23T13:00:00.001-08:00

Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012

PLEASE NOTE, the _spontaneous_ aspect of the rhetoric that USDA, CFIA, OIE, Australian, and every other Industry/Government is putting out, that atypical scrapie does not transmit to sheep, goat, or any other species, and that atypical Scrapie just happens spontaneously, is totally fabricated, and is not true. THERE IS NO SCIENCE showing this. IN fact, Science has shown that atypical scrapie does transmit, and it is very similar to some cases of sporadic CJD and GSS in humans. FOR the OIE et al to ratify a totally flawed trade policy, that makes legal the trading of atypical scrapie as a global commodity, is insane, and the ramifications of this insanity, will be played out for decades to come on man and animal. ...TSS

Fatal disease confirmed in sheep  

Herd quarantine unlikely

Posted Feb. 23rd, 2012

by Mary MacArthur

A single case of atypical scrapie was confirmed in an Alberta sheep in January.

Dr. Bob Cooper, a veterinary program specialist with the Canadian Food Inspection Agency, said the case was discovered as part of the national surveillance program to eradicate scrapie in Canada.

The surveillance program tests samples of sheep and goats for scrapie in an effort to understand where the disease is found in Canada and how to eliminate it.

Scrapie is a fatal disease that affects the central nervous system of sheep and goats. It is in the same family as BSE in cattle and chronic wasting disease in deer and elk.

It is a reportable disease in Canada.

Unlike classical scrapie, atypical scrapie doesn’t require that sheep farms be quarantined or the flock investigated.

Cooper said there would be some follow up to determine where the sheep lived its life, but there will be no large scale investigation or quarantine.

The atypical scrapie case was posted on the CFIA website’s monthly reportable disease update.

Canada has developed the national voluntary scrapie flock certification program in an attempt to eliminate scrapie from the national flock.

Alberta Lamb Producer chair Phil Kolodychuk was relieved the case was atypical scrapie and not classic scrapie.

“It’s a bad disease. We’d like to get rid of it in our country,” he said.

http://www.producer.com/2012/02/fatal-disease-confirmed%E2%80%A8in-sheep-%E2%80%A9/

Current as of: 2012-01-31

Date confirmed Location Animal type infected
January 26* Alberta Sheep

*Atypical scrapie

http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/2012/flocks-infected-in-2012/eng/1329724998646/1329725166676

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

J Vet Diagn Invest 21:454-463 (2009)

Nor98 scrapie identified in the United States

Christie M. Loiacono,' Bruce V. Thomsen, S. Mark Hall, Matti Kiupe!, Diane Sutton, Katherine O'Rourke, Bradd Barr, Lucy Anthenill, Deiwyn Keane

Abstract.

A distinct strain of scrapic identified in sheep of Norway in 1998 has since been identified in numerous countries throughout Europe. The disease is known as Nor98 or Not-98-like scrapic. among other names. Distinctions between classic scrapie and Nor98 scrapie are made based on histopathologv and immunodiagnostic results. There are also differences in the epidemiology, typical signalment, and likelihood of clinical signs being observed. In addition, sheep that have genotypes associated with resistance to classic scrapie are not spared from Nor98 disease. The various differences between classic and Nor98 scrapie have been consistently reported in the vast majority of cases described across Europe. The current study describes in detail the patholo gic changes and diagnostic results of the first 6 cases of' Nor98 scrapic disease diagnosed in sheep of the United States.

Key words: Hisiopathology: Nor98: PrP imniunolabeling; scrapie: sheep.

snip...

Results

Case I

The first case identified as consistent with Nor98 scrapie had nonclassic PrP distribution in brain tissue, no PrPSC in lymph tissue, and nonclassic migration of protein bands on a Western blot test. The animal was an aged, mottled-faced ewe that was traced back to a commercial flock in Wyoming. ...

Case 2

The second case was a clinically normal 8-year-old Suffolk ewe that had been in a quarantined flock for 5 years at a USDA facility in Iowa.

Case 3

A 16-year-old, white-faced, cross-bred wether was born to a black-faced ewe. He lived his entire life as a pet on a farm in California.

Case 4

The fourth case of Nor98 scrapie was identified in an approximately 8-year-old Dorset ewe that was born into a flock of approximately 20 ewes in Indiana.

Case 5

The fifth case was a clinically normal, approximately 3-year-old, white-faced, cross-bred ewe from an approximately 400 head commercial flock in Minnesota.

Case 6

The sixth case of Nor98 scrapie was identified in a 4-year-old, white-faced ewe that was purchased and added to a commercial flock in Pennsylvania

snip...

see full text ;

http://ddr.nal.usda.gov/bitstream/10113/33943/1/IND44241920.pdf

Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

snip...

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip...

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1

http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf

see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html

Monday, 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

Friday, February 11, 2011

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

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

Sunday, December 12, 2010

EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html

Wednesday, January 18, 2012

Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural Scrapie Isolates Similar to CH1641 Experimental Scrapie

Journal of Neuropathology & Experimental Neurology: February 2012 - Volume 71 - Issue 2 - p 140–147

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html

Thursday, July 14, 2011

Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html

Wednesday, January 18, 2012

BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE

February 1, 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html

Thursday, December 23, 2010

Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002-2009

Volume 17, Number 1 January 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html

Thursday, November 18, 2010

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html

hmmm, no I ponder why some of these sporadic CJD cases, are now being linked to a genetic TSE, that has NO link to the family ?

hmmm, could it be these atypical TSE in animals, that are linked to the human TSE in the USA, and also, these animals have been fed back and forth to each other ?

hmmm, why no link there $$$

P03.141

Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

PR-26

NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS

R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway

Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.

*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.

119

http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf

A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes

Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,? +Author Affiliations

*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway

***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)

Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. *** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

http://www.pnas.org/content/102/44/16031.abstract

Monday, December 1, 2008

When Atypical Scrapie cross species barriers

Authors

Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.

Content

Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.

The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.

Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.

Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.

(i) the unsuspected potential abilities of atypical scrapie to cross species barriers

(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier

These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf

Thursday, January 26, 2012

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html

Saturday, February 11, 2012

Prion cross-species transmission efficacy is tissue dependent

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/prion-cross-species-transmission.html

Thursday, January 26, 2012

The Risk of Prion Zoonoses

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html

1: J Infect Dis 1980 Aug;142(2):205-8

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

snip...

The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

PMID: 6997404

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract

12/10/76

AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE

Office Note CHAIRMAN: PROFESSOR PETER WILDY

snip...

A The Present Position with respect to Scrapie A] The Problem Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries. The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep. It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible. Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates.

One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias" Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.

snip...

76/10.12/4.6

http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf

Nature. 1972 Mar 10;236(5341):73-4.

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

Gibbs CJ Jr, Gajdusek DC. Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

C. J. GIBBS jun. ; D. C. GAJDUSEK National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).

http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html

Nature. 1972 Mar 10;236(5341):73-4.

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

Gibbs CJ Jr, Gajdusek DC. Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

C. J. GIBBS jun. &; D. C. GAJDUSEK National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).

http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html

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

why do we not want to do TSE transmission studies on chimpanzees $

snip...

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

snip...

R. BRADLEY

http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf

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

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

Thursday, November 18, 2010

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html

Wednesday, January 19, 2011

EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.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

Archive Number 20100312.0803

Published Date 12-MAR-2010

Subject PRO/AH/EDR; Scrapie, atypical, ovine - Australia: (WA) susp

SCRAPIE, ATYPICAL, OVINE - AUSTRALIA: (WESTERN AUSTRALIA) SUSPECTED

*******************************************************************

A ProMED-mail post

ProMED-mail is a program of the International Society for Infectious Diseases

[1] Date: Fri 12 Mar 2010 Source: The Australian [edited]

A West Australian sheep has been found to have signs characteristic of the fatal brain disease atypical scrapie. It comes as Australia faces growing anger from its trade partners over the Rudd government's surprise decision to extend a ban on the importation of beef from countries exposed to mad cow disease for a further 2 years.

Australia's chief veterinarian, Andy Carroll, told the ABC an indicative case of the atypical scrapie had been confirmed but said it posed no risk to human or animal health or the safety of eating meat and animal products.

Nor does atypical scrapie carry the dire trade consequences associated with classical scrapie.

Classical scrapie is in the same transmissible spongiform encephalopathies (TSE) family as BSE, better known as mad cow disease, from which humans can be fatally infected.

Dr Carroll said samples from the sheep's brain were being sent to the World Reference Laboratory in Britain.

Neither atypical scrapie nor classical scrapie has been seen in Australia before, but a sheep in New Zealand tested positive to the atypical form last year [2009].

Atypical scrapie is a relatively recently discovered disease and the common scientific view is that it occurs spontaneously or naturally in very small numbers of older sheep in countries all over the world.

[Byline: Jodie Minus]

-- Communicated by: Sabine Zentis Castleview Pedigree English Longhorns Gut Laach 52385 Nideggen Germany

****** [2] Date: Wed 10 Mar 2010 Source: ABC News (Australian Broadcasting Corporation) [edited]

Animal health authorities are testing a sheep's brain for what could be Australia's 1st case of the disease atypical scrapie.

Although not confirmed, the sheep is thought to be from Western Australia.

This type of scrapie is described as a sporadic degenerative brain condition affecting older sheep, and is not contagious.

Ed Klim, from national advisory group SafeMeat, says a 2nd round of testing is now taking place. "We've been made aware that the Australian Animal Health Laboratory is conducting further routine testing on a sheep sample," he says.

"The disease isn't considered a health risk nor should have any impact on food safety or export markets for sheep meat of live sheep."

Australia's chief veterinarian and WA's Department of Agriculture of Food are both aware of the testing but will not comment.

-- Communicated by: Terry S Singeltary Sr

[Although atypical scrapie is not yet ruled out, it is important to realize this is a type of scrapie that thus far has only tended to appear as a sporadic condition in older animals. Currently it has not been shown to follow the same genetic tendencies for propagation as the usual scrapie.

However, the atypical phenotypic appearance has been shown to be preserved on experimental passage.

Atypical scrapie was first identified in Norwegian sheep in 1998 and has subsequently been identified in many countries, as Australia may join that list. It is likely that this case will be sent to the UK for definitive conformation.

[Ref: M Simmons, T Konold, L Thurston, et al. BMC Veterinary Research 2010, 6:14 [provisional abstract available at ]

"Background ----------- "Retrospective studies have identified cases predating the initial identification of this form of scrapie, and epidemiological studies have indicated that it does not conform to the behaviour of an infectious disease, giving rise to the hypothesis that it represents spontaneous disease. However, atypical scrapie isolates have been shown to be infectious experimentally, through intracerebral inoculation in transgenic mice and sheep. [Many of the neurological diseases can be transmitted by intracerebral inoculation, which causes this moderator to approach intracerebral studies as a tool for study, but not necessarily as a direct indication of transmissibility of natural diseases. - Mod.TG]

"The 1st successful challenge of a sheep with 'field' atypical scrapie from an homologous donor sheep was reported in 2007.

"Results -------- "This study demonstrates that atypical scrapie has distinct clinical, pathological, and biochemical characteristics which are maintained on transmission and sub-passage, and which are distinct from other strains of transmissible spongiform encephalopathies in the same host genotype.

"Conclusions ------------ Atypical scrapie is consistently transmissible within AHQ homozygous sheep, and the disease phenotype is preserved on sub-passage."

Lastly, this moderator wishes to thank Terry Singletary for some of his behind the scenes work of providing citations and references for this posting. - Mod.TG]

The HealthMap/ProMED-mail interactive map of Australia is available at . - Sr.Tech.Ed.MJ]

http://www.promedmail.org/direct.php?id=20100312.0803

UPDATE ATYPICAL SCRAPIE AUSTRALIA CONFIRMED

First occurrence of atypical scrapie

Australia is free of scrapie, also known as ‘classical’ scrapie, and has been assessed as a ‘negligible bovine spongiform encephalopathy (BSE) risk’ (the lowest risk) by the World Organisation for Animal Health (OIE). Both diseases belong to a group of diseases termed transmissible spongiform encephalopathies (TSEs) or ‘prion diseases’.

Active surveillance occurs to validate Australia’s status for both diseases, through the National Transmissible Spongiform Encephalopathies Surveillance Program (NTSESP), consistent with OIE recommendations. Results are routinely reported in Animal Health Surveillance Quarterly.

The first case of atypical scrapie (another TSE) in Australia has been confirmed in a single sheep, through the NTSESP. This is not a surprising finding. Atypical scrapie is a rare, sporadic, degenerative brain condition that spontaneously occurs in a very small proportion of older sheep and, less commonly, in goats. Most countries that test large numbers of sheep for scrapie have found one or more cases of atypical scrapie.

Testing on samples from the affected sheep at the CSIRO Australian Animal Health Laboratory in March 2010 showed preliminary results consistent with atypical scrapie. The results were confirmed by the Veterinary Laboratory Agencies at Weybridge in the United Kingdom, an OIE reference laboratory.

Atypical scrapie is clinically, pathologically, biochemically and epidemiologically unrelated to classical scrapie, and has been recognised as a distinct disease of sheep and goats for about a decade. During this time, the disease has been diagnosed in more than 20 countries worldwide. It does not pose a risk to human health or to the productivity of the Australian sheep flock. There is evidence that it is not naturally spread to other animals. It is not known to have any causal relationship to other TSEs, including BSE in cattle, chronic wasting disease in deer, or any form of Creutzfeldt–Jakob disease in people.

As atypical scrapie is a different disease to classical scrapie, Australia’s internationally recognised status as free from scrapie will not change as a result of this case. Contributed by Reg Butler, Biosecurity Services Group, Australian Government Department of Agriculture, Fisheries and Forestry

http://www.animalhealthaustralia.com.au/fms/Animal%20Health%20Australia/ADSP/AHSQ/AHSQ%20Q1%202010.pdf

Scrapie

Scrapie has been recognised in sheep for more than 250 years, and occurs at a low annual incidence in many countries, but is not present in Australia or New Zealand.

Atypical scrapie In 2009, atypical/Nor98 scrapie was detected in one sheep brain from a consignment of sheep and goat brains sent from New Zealand to the European Union, for use as negative control materials for evaluating rapid tests for BSE and scrapie.50 In 2010, a case of atypical/Nor98 scrapie was diagnosed in a sheep in Australia.

Australian and New Zealand Standard Diagnostic Procedure, August 2010. Page 7 of 27

http://www.animalhealthaustralia.com.au/wp-content/uploads/2011/03/Australia-and-New-Zealand-Standard-Diagnostic-Protocols-for-TSE.pdf

The first case of atypical scrapie in Australia was recently detected through the active surveillance program for transmissible spongiform encephalopathies (TSEs). Atypical scrapie is a rare, degenerative brain condition that occurs spontaneously in a very small proportion of older sheep and goats. It is a different disease to classical scrapie and other known TSEs. Australia remains free from scrapie.

http://www.animalhealthaustralia.com.au/wp-content/uploads/2011/05/AHSQ-Q1-2010.pdf

http://www.animalhealthaustralia.com.au/

Thursday, October 7, 2010

Australia first documented case of atypical scrapie confirmed First occurrence of atypical scrapie

http://nor-98.blogspot.com/2010/10/australia-first-documented-case-of.html

RESEARCH

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011

Experimental Oral Transmission of Atypical Scrapie to Sheep

Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos

To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals’ peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specifi c prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These fi ndings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain.

SNIP...

Although we do not have epidemiologic evidence that supports the effi cient spread of disease in the fi eld, these data imply that disease is potentially transmissible under fi eld situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing fi nding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown.

How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantifi ed, although infectivity has been shown unequivocally. No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and confi rmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected.

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011

http://wwwnc.cdc.gov/eid/article/17/5/pdfs/10-1654.pdf

OIE Scrapie Chapter Revision • Current draft recognizes Nor98-like scrapie as a separate disease from classical scrapie • USDA provided comments on the draft to OIE

http://www.animalagriculture.org/Solutions/Proceedings/Annual%20Meeting/2009/Sheep%20&%20Goat/Myers,%20Thomas.pdf

Atypical scrapie/Nor 98 October 2009

Last year, after examining member country submissions and investigating rigorous scientific research, the World Organisation for Animal Health (OIE) decided that Nor 98 should not be listed in its Terrestrial Animal Health Code. The Code sets out trade recommendations or restrictions for listed diseases or conditions, and the OIE determined there was no need for such recommendations around Nor 98.

http://www.nzfsa.govt.nz/publications/ce-column/ce-web-nor98.htm

http://www.biosecurity.govt.nz/files/pests/atypical-scrapie/atypical-scrapie-faq-oct09.pdf

Sutton reported that USDA has urged the World Organization for Animal Health (OIE) to categorize Nor98-like scrapie as a separate disease from classical scrapie. Currently, the OIE has proposed a draft revision of their scrapie chapter that would exclude Nor98-like scrapie from the chapter. USDA will be submitting it's comments on this proposal soon.

http://www.ohiosheep.org/Events/ScrapieNewsletterMarch09.pdf

SCRAPIE

The United States is unable to support the proposed new draft Code Chapter on Scrapie. The draft chapter, as written, departs significantly from the existing chapter, is confusing and is difficult to understand. This version of the scrapie chapter uses much of the same wording as the BSE chapter and is written as if the predominance of evidence revealed that scrapie was a food-borne disease similar to BSE in cattle which is inappropriate. Moreover, several of the new changes are not supported by current scientific evidence. As a result, detailed comments on individual articles would not meaningful at this time.

The United States is not supportive of the proposed draft chapter for the following reasons: 1. Inclusion of “atypical” scrapie: The scientific evidence indicates that “atypical” scrapie, also referred to as Nor-98, Nor-98-like, or non-classical scrapie, is not the same disease as classical scrapie. Further, “atypical” scrapie does not meet the criteria for listing diseases of trade concern by the OIE, as described in Chapter 2.1.1 of the Code. The United States recommends that the scope of this chapter be limited to classical scrapie in sheep and goats. Further, the United States recommends that OIE clearly adopt the position that “atypical” scrapie represents a distinct disease entity from classical scrapie and that it not be a listed disease.

• There is no evidence that “atypical” scrapie is a contagious disease. If it is contagious, available evidence suggests that it has a much lower transmission efficiency. (Hopp, et al, 2006; Green, et al, 2007; Benestad, et al 2008; McIntyre, et al, 2008)

• The disease appears to be ubiquitous in that it has been found wherever sufficient surveillance has been conducted. (Buschmann et al, 2004; De Bosschere et al, 2004; Orge, et al, 2004; Everest et al, 2006; Arsac, 2007; Benestad, et al 2008; Fediaevsky, et al, 2008)

• The disease does not appear to be economically significant in that the prevalence of clinical disease is low and it typically occurs in older animals. (Luhken, et al., 2007; Benestad, et al 2008).

• The disease is as likely as not to be the result of a spontaneous conversion of normal prion protein. (Benestad, et al 2008, De Bosschere et al 2007)

• Removal of exposed sheep is unlikely to reduce the prevalence of “atypical” scrapie infection and removing only those exposed sheep that are phenylalanine (F) at codon 141 is scientifically unsound since the disease is known to affect sheep of most other genotypes. Further, sheep with AHQ alleles have a similar risk of infection with “atypical” strains as sheep with F at codon 141. (Luhken, et al., 2007).

• If “atypical” scrapie is included as a listed disease, the surveillance and diagnostic requirements which are needed to identify these cases should be described in detail in both this Chapter and the Manual of Diagnostic Tests and Vaccines for Terrestrial

2

Animals. Data from Europe illustrates that using the proper test(s) is essential for the identification of atypical scrapie (Fediaevsky et al., 2008).

SNIP...

6. Overemphasis on importation and use of bovine meat and bone meal as a route of scrapie transmission: Given that the draft Chapter is not intended to address risk mitigation for BSE in small ruminants, we believe there is an over-emphasis on this potential route of transmission in the current draft.

The United States recommends that the requirements in this chapter be limited to the inclusion of products from sheep and goats (instead of from all ruminants) in feed or feed ingredients intended for consumption by animals.

• The use of products from sheep and goats as feed or feed ingredients for ruminant or non-ruminant animals represent one possible route of transmission (Philippe, et al, 2005) and a source of environmental contamination with the classical scrapie agent. However, this is not the primary route of transmission for the scrapie agent.

• The need for the exclusion of cattle-derived protein or other animal protein to mitigate BSE risk should be based on a country’s BSE risk status and should be addressed in Chapter 2.3.13 of the Code.

SNIP...

14. Failure to provide scientific justification for the list of permitted commodities in Item 1 of Article 2.4.8.1. .

We recommend that the list be re-evaluated and those items that have not been substantiated as presenting no risk be excluded or those with some risk but where the intended use mitigates the risk the use be specified.

• There is no known human health risk associated with scrapie. As such, if meat and meat products for human consumption are included in this list, sheep and/or goat milk intended for human consumption should also be added to the list of permitted commodities in Item 1 of Article 2.4.8.1.

• In the vast majority of sheep infected with classical scrapie, actual infectivity or PrPres has been identified in most tissues including the lymphoreticular system (tonsils, spleen, lymph nodes), the gastrointestinal tract, brain, and spinal cord (Hadlow et. al. 1979; Hadlow et al., 1980; van Kuelen et al., 1996; van Kuelen et al., 1999, Andreoletti et al., 2000; Heggebø et al., 2002; Caplazi et al., 2004). Infectivity and/or PrPres has also been identified in the placenta (see Hourrigan et al., 1979; Onodera et al., 1993; Pattison et al., 1972; Pattison et al., 1974; Race et al., 1998), blood (Hunter et al., 2002; Houston et al. 2008); peripheral nerves (Groschup et al., 1996), muscle (Pattison and Millson, 1962; Andreoletti et al., 2004; Casalone et al., 2005), salivary gland (Hadlow et al., 1980; Vascellari et al., 2007), kidney (Siso et al., 2006), and skin ( Thomzig et al., 2007). In addition, recent work has shown milk and/or colostrum from scrapie infected ewes transmitted the disease to 17 of 18 lambs (Konold et al., 2008).

• The data on the risk of low protein tallow made from scrapie infected tissues particularly for use in milk replacer is limited and some epidemiologic studies suggest an association of milk replacer use with scrapie risk. Taylor et al., 1997 examined the inactivation capacity of different rendering system in regards to scrapie. The presence of infectivity was determined by bioassay into mice. From the onset of this study, it was assumed that tallow was not the vehicle for the transmission of TSE. Hence only 2 tallow samples were examined.

http://www.aphis.usda.gov/import_export/animals/oie/downloads/tahc_mar-sep08/tahc-scrapie-77-mar08_cmt.pdf

• Most critical is that atypical scrapie shows higher prevalence in so-called resistant ARR homozygote and heterozygote genotypes, compared with classical scrapie. • Atypical scrapie has not been found naturally in VRQ/VRQ sheep, although such sheep can be infected artificially. VRQ sheep are, in contrast, highly susceptible to classical scrapie. In the UK, one case of atypical scrapie has been found in VRQ heterozygote (AF141RQ/VRQ) sheep. It is important to ascertain whether or not VRQ-carrying sheep are significantly resistant to infection with atypical scrapie or whether the data might result from a failure to detect PrPres in atypical scrapie due to a different pattern of PrP distribution in tissues. • Increased incidence of atypical scrapie in sheep with PrP alleles carrying the variant phenylalanine (F) at position 141 (leucine(L)/phenylalanine) has also been observed compared with classical scrapie. • It will be important to clarify the genotype effect, particularly in relation to ARR and L141F in transmission studies. • In classical scrapie, there is clear evidence for a PrP genotype effect on tissue distribution patterns of PrPres. This might also be true for atypical scrapie although the data are less complete. 4. Transmission of atypical scrapie It has recently18 been demonstrated that atypical scrapie is experimentally transmissible to mice and sheep, primarily through intracerebral injection. There are some data suggesting that it may also be transmissible orally to sheep of different genotypes. The subgroup noted that challenge experiments with atypical scrapie in sheep were underway in the UK, with one successful intracerebral challenge to date. The subgroup was informed that positive transmission of infectivity from atypical scrapie isolated from sheep with a range of genotypes had been observed in mice. This included ovinised transgenic mice overexpressing the VRQ allele. Nor98 atypical scrapie had also transmitted to ARR ovinised mice, with transmission experiments in AF141RQ ovinised mice planned. Biochemical features of the isolates were maintained after transmission, and were distinct from BSE and classical scrapie. High infectivity titres were observed in brain tissue from atypical scrapie, including from ARR/ARR sheep. Brain transmission experiments in mice carrying the human PrP gene were at an early stage. 18 Le Dur A., Béringue V., Andréoletti O., Reine F., Laï T.H., Baron T., Bratberg B., Vilotte J.- L., Sarradin P., Benestad S.L. and Laude H.(2005) A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes. PNAS 102, 16031-16036

http://www.seac.gov.uk/pdf/positionstatement-sheep-subgroup.pdf

BSE: TIME TO TAKE H.B. PARRY SERIOUSLY

If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ...

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf

Tuesday, February 14, 2012

White House budget proposes cuts to ag programs including TSE PRION disease aka mad cow type disease

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/white-house-budget-proposes-cuts-to-ag.html

Thursday, February 16, 2012

Bovine Spongiform Encephalopathy BSE

31 USA SENATORS ASK PRESIDENT OBAMA TO HELP SPREAD MAD COW DISEASE 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/bovine-spongiform-encephalopathy-bse-31.html

Thursday, February 23, 2012

EIGHT FORMER SECRETARIES OF AGRICULTURE SPEAKING AT USDA'S 2012 AGRICULTURE OUTLOOK FORUM INDUCTED INTO USA MAD COW HALL OF SHAME

http://madcowusda.blogspot.com/2012/02/eight-former-secretaries-of-agriculture.html

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

TSS

CDC REPORT ON Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease CWD North America

2012-02-19T19:47:00.000-08:00

***CDC REPORT ON CWD***

Saturday, February 18, 2012

Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease

CDC Volume 18, Number 3—March 2012

http://chronic-wasting-disease.blogspot.com/2012/02/occurrence-transmission-and-zoonotic.html

50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE CWD

2012

Tuesday, December 20, 2011

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

>>> The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years.

However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil.

Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. <<<

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

SNIP...SEE FULL TEXT ;

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

Thursday, February 09, 2012

50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE

http://chronic-wasting-disease.blogspot.com/2012/02/50-game-farms-to-date-in-usa-infected.html

Friday, February 03, 2012

Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-farm-raised-deer-farms-and.html

Saturday, February 04, 2012

Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-16-age-limit-on-testing-dead.html

Thursday, February 09, 2012

Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/colorado-farm-raised-deer-farms-and-cwd.html

Tuesday, February 14, 2012

Oppose Indiana House Bill 1265 game farming cervids

http://chronic-wasting-disease.blogspot.com/2012/02/oppose-indiana-house-bill-1265-game.html

Monday, February 13, 2012

Stop White-tailed Deer Farming from Destroying Tennessee's Priceless Wild Deer Herd oppose HB3164

http://chronic-wasting-disease.blogspot.com/2012/02/stop-white-tailed-deer-farming-from.html

Wednesday, February 15, 2012

West Virginia Deer Farming Bill backed by deer farmers advances, why ? BE WARNED CWD

http://chronic-wasting-disease.blogspot.com/2012/02/west-virginia-deer-farming-bill-backed.html

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html

Tuesday, February 14, 2012

White House budget proposes cuts to ag programs including TSE PRION disease aka mad cow type disease

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/white-house-budget-proposes-cuts-to-ag.html

Thursday, February 16, 2012

Bovine Spongiform Encephalopathy BSE

31 USA SENATORS ASK PRESIDENT OBAMA TO HELP SPREAD MAD COW DISEASE 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/bovine-spongiform-encephalopathy-bse-31.html

Africa in Texas

January 29, 2012 7:09 PM

Can hunting endangered animals save the species?

http://www.cbsnews.com/video/watch/?id=7396832n&tag=contentMain;contentBody

Lunacy is a kind word. conservation, sustaining a species is one thing, saving a species, to hunt it as high dollar exotics, that’s not conservation. if it makes you fell good, call it what you want. I weep. I’m sure God did not want man to muck up the world so bad, calling it progress, while bringing species after species to extinction, then pooling what’s left over in game farms and calling it ‘exotic hunting’ for high dollar price $$$, and then calling it conservation. call me stupid, I call it the end as we once knew it. I weep.

with kind regards,

I am sincerely,

Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518

flounder9@verizon.net

Bovine Spongiform Encephalopathy BSE 31 USA SENATORS ASK PRESIDENT OBAMA TO HELP SPREAD MAD COW DISEASE 2012

2012-02-16T09:31:00.000-08:00

Bovine Spongiform Encephalopathy BSE 31 USA SENATORS ASK PRESIDENT OBAMA TO HELP SPREAD MAD COW DISEASE 2012

A bipartisan group of 31 senators are asking the Obama administration to move along with a comprehensive rule that would loosen restrictions on imported beef and, they contend, facilitate better trade opportunities...

USDA OIE GBR MRR $$$

Sens. Charles Grassley (R-Iowa) and Ben Nelson (D-Neb.) et al ;

UNITED STATES SENATE

WASHINGTON, DC 20510

February 13,2012

The Honorable Jeffrey Zients

Acting Director

Office of Management and Budget

725 1 ill Street, NW

Washington, D.C. 20503

Dr. Gregory Parham

Administrator

Animal Plant Health and Inspection Services

U.S. Department of Agriculture

1400 Independence Ave., SW

Washington, D.C. 20250

Dear Acting Director Zients and Administrator Parham:

On behalf of America's beef producers, we urge you to move forward and publish the comprehensive rule for BSE (bovine spongiform encephalopathy). Non-tariff trade barriers limit our ability to sell U.S. beef to consumers in other countries. Beef producers need our trade negotiators to significantly reduce or eliminate non-tariff trade barriers by requiring our trading partners to make science-based decisions regarding U.S. beef. By the same logic, it is also important for our government to take the necessary steps to properly address risks related to BSE by adopting a comprehensive rule. For the benefit of U.S. beef producers, APHIS and OMB must issue a comprehensive BSE rule as soon as possible.

A prime example of where non-science based standards have significantly limited our ability to sell U.S. beef is in the country of Mexico. Since 2004, Mexico has not allowed the importation of U.S. cattle that are over 30 months of age. Mexico has traditionally been one of the top export markets for U.S. beef; however due to the 30 month age restriction, it is estimated U.S. beef producers are losing $100 million annually.

The World Organization for Animal Health (OIE) has formally classified the United States and Mexico as controlled risk countries. According to the OIE's guidelines on BSE, this common classification reflects the fact that both countries have effective BSE risk mitigation measures in place. Moreover, the OIE guidelines establish that beef and beef products from cattle of all ages in either country can be safely traded and consumed once specified risk materials have been properly removed.

The failure of Mexico to abide by the international guidelines on BSE represents a lost opportunity on at least two levels. First, it unduly restricts U.S. beef exports and results in ongoing financial losses for U.S. beef producers. Beyond its immediate commercial impact, Mexico's treatment of U.S. beef also has implications on our ability to negotiate beef market access agreements with other nations.

By having a comprehensive BSE rule in place, the U.S. will show leadership on the global scale and will give USTR and USDA a stronger position to press other nations to follow the OIE's guidelines and adopt science-based BSE policies. As a result, when nations base their decisions on sound science, we are confident more markets will be expanded or opened to U.S. beef.

In 2004, USDA announced its plans for developing a comprehensive BSE rule, a comprehensive rule the U.S. beef industry has requested for many years. Earlier this year, APHIS submitted a proposed comprehensive BSE rule to OMB, but it has yet to be printed in the "Federal Register" asking for public comment. During a June 23,2011 hearing on livestock before the Senate Committee on Agriculture, Nutrition, and Forestry, Administrator Parham stated he expected the comprehensive BSE rule to be released sometime in FY2012.

We appreciate Administrator Parham's commitment; however, there is a lot of time left in fiscal year 2012. We urge you to release the rule as soon as possible. The sooner the rule is allowed to move through the required rule-making process, the sooner we will be able to give our international negotiators this important tool for pushing our trading partners to adopt similar science-based approaches.

We appreciate your attention to this important matter.

Sincerely,

Sens. Charles Grassley (R-Iowa) and Ben Nelson (D-Neb.

and

A bipartisan group of 31 senators are asking the Obama administration to move along with a comprehensive rule that would loosen restrictions on imported beef and, they contend, facilitate better trade opportunities...

http://www.grassley.senate.gov/news/upload/Agriculture-Trade-02-14-12-BSE-Letter-with-Nelson.pdf

McCaskill: Lift Limits on U.S. Beef Exports

USAgNet - 02/15/2012

U.S. Senator Claire McCaskill is urging the U.S. Department of Agriculture (USDA) to finally move forward and establish a rule that will pave the way for increased exports of U.S. beef products.

In a letter on behalf of America's beef producers, McCaskill--along with Senators Chuck Grassley (R-Ia.) and Ben Nelson (D-Neb.)--asked the USDA to move forward and publish the long-awaited comprehensive rule for Bovine Spongiform Encephalopathy (BSE), commonly referred to as "Mad-Cow Disease." The rule is expected to enhance the ability of U.S. beef producers to access foreign export markets for their products.

In current trade negotiations, beef producers have urged compliance with the science-based International Organization for Animal Health guidelines on BSE. However, the U.S. has yet to adopt a comprehensive rule that would allow producers to look for opportunities to expand overseas, and also allow the government to take necessary steps to properly address risks related to BSE.

The Senators also reiterated that by adding a science-based comprehensive BSE rule, the U.S. would show leadership and put the USDA in a stronger position to press other nations to follow the guidelines from the International Organization for Animal Health and adopt similar policies. When other countries make science-based decisions, they are far more likely to expand or open their markets to U.S. beef, enhancing the industry's competitive position in global markets.

In 2004, the USDA announced its plans to develop a comprehensive BSE rule at the request of the U.S. beef industry. Despite promises from the USDA that the rule would be released for FY2012, no rule has yet been released.

http://www.usagnet.com/story-national.php?Id=360&yr=2012

WHAT a bunch of hipocrits i.e. Washington. for almost 25 years, the USDA, OIE, et al, went by the OIE guidelines like they were something Biblical, wrote on stone tablets, even though every country that went by these terribly flawed BSE TSE Prion OIE USDA et al industry friendly regulations, every country that went by these flawed OIE USDA guidelines all went down with BSE TSE prion disease. these Biblical tablets that the OIE and USDA went by, the mad cow surveillance tablets claim that testing 400 animals out of about 1,000,000 animals, is good enough for them to find said disease i.e. TSE PRION mad cow type disease. really ? it does not get any better than this when it comes to a totally flawed and corrupt system. has been for decades. red, white, right, left, republican, or democrat, they all have a hand in this corporate corruption, i.e. BSe, bull sh!t encephalopathy, i.e. corporate and political science $$$ just because the incubation period is long, not enough _DOCUMENTED_ body bags, sporadic CJD, TSE, Prion disease victims are expendable, for trade. now if it were a fast acting disease like e-coli, listeria or any other fast acting fatal disease, things would be different. but our best bet now, is to die from something else before the TSE prion disease get’s us. because if your not a teenager, and a TSE prion disease kills you, even though now science has linked up sporadic CJD with atypical BSE and atypical Scrapie, both of which are here in the USA, it just not matter, politics and industry have made you expendable, and even all those that are exposed and die from friendly fire there from i.e. iatrogenic CJD. because all that is is sporadic CJD, until source is proven. there ya go. keep it all sporadic CJD. problem solved. we have all been exposed one way or the other. only by Gods grace have we not all gone clinical. continue to roll the dice, as these TSE prion disease mutates, they become more virulent, continue to roll the dice, it might not be so pretty. times catching up, the TSE prion disease have mutating. the cover up continues i.e. sporadic FFI and sporadic GSS, and VPSPr type BSe. continue to ignore the science, continue to roll the dice, just for trade, God will make the ultimate decision, and God, or whom ever you worship, are neither red nor blue.

Sadly, once again, sound science will NOT play a part in any sound policy decision making in matters relating to Bovine Spongiform Encephalopathy BSE either typical or atypical. YOU can thank the OIE and the USDA for doing away with sound science long ago, with the BSE MRR policy, when they bypassed the BSE GBR for each country. It was a legal tool to make TSE prion disease a legal trading commodity, and they did just that with atypical TSE, which is now a legal trading commodity thanks to the OIE USDA BSE MRR i.e. minimal risk region. the USDA, FSIS, APHIS, FDA, have all failed terribly with the surveillance and eradication efforts of all strains of the TSE Prion disease in livestock and wild animals. BSE mad cow type disease and countries there from were all banned from the USA, until the USA accidently ran across and had to document 3 cases of mad cow disease. Texas successfully covered up one case of mad cow disease, and almost cover-up a second case, if not for the OIG and the Honorable Phyllis Fong. That Texas mad cow sat on a shelf and not tested for 7 months, so the BSE MRR policy could get set in place and ratified. it’s all about money folks, human and animal health went out the door long ago $$$

science has now linked atypical BSE and atypical Scrapie to some cases of sporadic CJD in humans, also, TSE Prion scientist around the globe are very concerned about the potential for CWD in deer and elk to be a zoonosis disease, especially now since mutating into a second strain, documented, to date, i.e. the Wisconsin CWD strain. All of these TSEs have been documented in North America, traded between Mexico, USA, and Canada, like two lovers swapping spit. all these TSE prion disease in different species have been rendered up and fed to food producing animals for humans and livestock for over a decade (please see 2012 BSE mad cow feed ban report below), the August 4, 1997 partial and voluntary mad cow feed ban was nothing but ink on paper, where some 10,000,000 MILLION POUNDS OF BLOOD LACED MEAD AND BONE MEAL went out into commerce, to be fed out, as late as one decade, post partial and voluntary mad cow feed ban, as late as 2007.

ALL the USA has done, with this BSE MRR minimal risk region was what the U.K. did when they poisoned the globe, except now it’s been made legal with the BSE MRR policy.

WHAT these senators are asking, is to just throw in the towel, the TSE Prion disease have one, let’s just trade them now around the globe.

THAT SHOULD NOT BE ACCEPTABLE, under any circumstances $$$

Geographical BSE risk assessment and its impact on disease detection and dissemination

Original Research Article

Preventive Veterinary Medicine, Available online 1 February 2012,

Mo Salman, Vittorio Silano, Dagmar Heim, Joachim Kreysa

Preventive Veterinary Medicine

1 February 2012

Geographical BSE risk assessment and its impact on disease detection and dissemination

Salman M, Silano V, Heim D, Kreysa J.

Source

Campus Stop 1644, Animal Population Health Institute, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523-1644, USA.

Abstract

Bovine Spongiform Encephalopathy (BSE) rapidly evolved into an issue of major public concern particularly when, in 1996, evidence was provided that this disease had crossed the species barrier and infected humans in the UK with what has become known as "variant Creutzfeldt Jakob Disease" (vCJD). The aim of this paper is to describe the European Geographical BSE risk assessment (GBR) that was successfully used for assessing the qualitative likelihood that BSE could be present in a country where it was not yet officially recognized. It also discusses how this can lead to risk-based and therefore preventive management of BSE at national and international levels. The basic assumption of the GBR method is that the BSE agent is initially introduced into a country's domestic cattle production system through the importation of contaminated feedstuffs or live cattle. This is referred to as an "external challenge". The ability of the system to cope with such a challenge is, in turn, referred to as its "stability": a stable system will not allow the BSE agent to propagate and amplify following its introduction, while an unstable system will. The BSE-status of a country assessed by this system was used by the European Commission as the basis for trade legislation rules for cattle and their products. The GBR was an invaluable tool in evaluating the potential global spread of BSE as it demonstrated how a disease could be transferred through international trade. This was shown to be a critical factor to address in reducing the spread and amplification of BSE throughout the world. Furthermore, GBR resulted in the implementation of additional measures and management activities both to improve surveillance and to prevent transmission within the cattle population.

Copyright © 2012 Elsevier B.V. All rights reserved.

http://www.sciencedirect.com/science/article/pii/S0167587712000244

Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

snip...

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip...

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1

http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf

see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html

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

2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49

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

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

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

The conclusions state that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Active screening has allowed the identification of 3 new forms of animal TSEs (H-type atypical BSE, L-type atypical BSE, and atypical scrapie), but the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs. There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential. Transmission experiments to human PrP transgenic mice or primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential and indicate that that of the L-type atypical BSE agent appears similar or even higher than that of the classical BSE agent. A single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.

http://www.promedmail.org/direct.php?id=20110607.1736

Wednesday, January 18, 2012

BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE

February 1, 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html

Owens, Julie

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

Sent: Monday, July 24, 2006 1:09 PM

To: FSIS RegulationsComments

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

Page 1 of 98

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

FSIS RFEPLY TO TSS ;

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

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

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

Wednesday, February 08, 2012

Scrapie, Israel via OIE 02/02/2012

From: Terry S. Singeltary Sr.

Sent: Wednesday, February 08, 2012 10:28 AM

To: BSE-L BSE-L

Cc: hmb-central@icba.org.il ; delegation-israel@eeas.europa.eu ; Cvo_vsah@moag.gov.il ; galonn@moag.gov.il ; CJDVOICE CJDVOICE ; bloodcjd bloodcjd

Subject: Scrapie, Israel via OIE 02/02/2012

http://scrapie-usa.blogspot.com/2012/02/scrapie-israel-via-oie-02022012.html

Wednesday, May 25, 2011

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

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

From: Terry S. Singeltary Sr.

To: BSE-L@LISTS.AEGEE.ORG

Cc: trade@oie.int ; oie@oie.int ; f.diaz@oie.int ; scientific.dept@oie.int ; cjdvoice@yahoogroups.com ; BLOODCJD@YAHOOGROUPS.COM

Sent: Tuesday, May 24, 2011 2:24 PM

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

http://ec.europa.eu/food/international/organisations/docs/eu_position_oie_tahsc_en.pdf

Greetings OIE et al,

I think that the OIE et al, should explain to the lay public, as to why the OIE post TSE prion disease reports and incidence there from different species on their disease reporting reports via email and or on their news feed web site, daily and or weekly, for just a chosen few Countries, yet other Countries seem to be exempt from this reporting to the public. WHY is this ?

For instance, Japan just reported another incidence of scrapie, this time in goat.

http://web.oie.int/wahis/public.php?page=single_report&pop=1&reportid=10624

however, the USA (Michigan), is awash in scrapie in goat cases, to a point of epidemic, however, the OIE does not report this, WHY is this ?

the USA and Canada Nor-98 scrapie cases are mounting. NO reports from the OIE. WHY is this ?

we the lay public deserve an answer. i have ask this question before. i have ask it about CWD to the OIE a decade ago.

WHY do some Countries get their TSE prion reports posted, and the USA does not, the USA is exempt from this Global embarrassment?

i am confused.

IF the OIE is going to be a reputable global disease control reporting agency, then the OIE needs to be honest and trust worthy and equal reporting for all Countries, not just a chosen few, while others are exempt. This weakens the animal disease reporting system, and really in all reality, seems to enhance fraud, and undermines reporting of actual disease, thus, defeats the very purpose of the O.I.E., thus undermines the very reason the OIE was suppose to be set up for.

If countries can choose and pick whether or not their different animal disease are reported, and or NOT reported, then what's the point of the O.I.E. $$$

MY personal opinion, if a country is going to belong to the OIE, and or boast about OIE regulations they go by, then they should be made to report animal disease just as any other country does to the OIE, or they should not be a part of this OIE, and should not be allowed to be boasting that they go by OIE guidelines. ...

with sincere regards, terry

snip...see full text ;

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

IN SHORT, AND IN A NUT SHELL ;

(Adopted by the International Committee of the OIE on 23 May 2006)

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,

http://www.oie.int/eng/Session2007/RF2006.pdf

Saturday, December 18, 2010

OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html

I see again that the OIE has done little to help eradicate all animal TSE from the globe, and in fact in my opinion, have help enhance the spread of BSE and other animal TSE globally by their industry friendly regulations. I tried to warn the OIE in 2002 about CWD and the potential, but very real threat of CWD to humans. I was told that they were seriously considering this. what happened ? NOW, the OIE and the USDA collaborate to make legal the trading of all strains of atypical BSE legal, and in fact have done so with the atypical scrapie, when science has made perfectly clear the risk factors to humans and other species. I have said it once (see below), and i will say again ;

"THE OIE has now shown they are nothing more than a National Trading Brokerage for all strains of animal TSE. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization."

NOW, some history on the failed OIE BSE/TSE policy, and why the OIE allowed BSE and other TSE to spread around the globe $$$

snip...see full text ;

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html

Docket APHIS-2006-0026 Docket Title Bovine Spongiform Encephalopathy; Animal Identification and Importation of Commodities Docket Type Rulemaking Document APHIS-2006-0026-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions, Identification of Ruminants and Processing and Importation of Commodities Public Submission APHIS-2006-0026-0012 Public Submission Title Comment from Terry S Singletary

http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801e47e1

Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028 Public Submission Title Comment from Terry S Singletary

Comment 2006-2007 USA AND OIE POISONING GLOBE WITH BSE MRR POLICY

THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted products from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone. These are the facts as I have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species.

MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did...

http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8151

Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028.1 Public Submission Title Attachment to Singletary comment

January 28, 2007

Greetings APHIS,

I would kindly like to submit the following to ;

BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f8152&disposition=attachment&contentType=msw8

Saturday, April 10, 2010

TOYOTA VS MAD COW DISEASE USA OIE BSE MRR IMPORT AND EXPORT TRADE WARS

http://usdameatexport.blogspot.com/2010/04/toyota-vs-mad-cow-disease-usa-oie-bse.html

Friday, December 23, 2011

Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model

Volume 18, Number 1—January 2012 Dispatch

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/oral-transmission-of-l-type-bovine.html

Saturday, June 25, 2011

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

"BSE-L in North America may have existed for decades"

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

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

snip...

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

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

Sunday, February 5, 2012

February 2012 Update on Feed Enforcement Activities to Limit the Spread of BSE

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/february-2012-update-on-feed.html

EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA)

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.

http://www.efsa.europa.eu/en/efsajournal/pub/3r.htm

see full text ;

http://www.efsa.europa.eu/en/efsajournal/doc/3r.pdf

Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the United States of America (USA) Question number: EFSA-Q-2003-083 Adopted date: 1 July 2004 Summary (0.1Mb)

Document (0.2Mb)

Summary

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

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

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

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

http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1178620779461.htm

http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_annex_en1.pdf?ssbinary=true

http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_v2_en1.pdf?ssbinary=true

http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_summary_en1.pdf?ssbinary=true

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/bbs/topics/enforce/2007/ENF00996.html

Thursday, March 19, 2009

MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS ANYMORE $$$

http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html

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

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

snip...

Topics that will be covered in ongoing or planned reviews under Goal 1 include:

soundness of BSE maintenance sampling (APHIS),

implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),

snip...

The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.

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

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

-MORE Office of the United States Attorney District of Arizona FOR IMMEDIATE RELEASE For Information Contact Public Affairs February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625 Cell: (602) 525-2681

CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT'S MAD COW DISEASE SURVEILLANCE PROGRAM

PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel Knauss stated, "The integrity of the system that tests for mad cow disease relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without that honest cooperation, consumers both in the U.S. and internationally are at risk. We want to thank the USDA's Office of Inspector General for their continuing efforts to safeguard the public health and enforce the law." Farm Fresh Meats and Farabee were charged by Information with theft of government funds, mail fraud and wire fraud. According to the Information, on June 7, 2004, Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S. Department of Agriculture (the "USDA Agreement") to collect obex samples from cattle at high risk of mad cow disease (the "Targeted Cattle Population"). The Targeted Cattle Population consisted of the following cattle: cattle over thirty months of age; nonambulatory cattle; cattle exhibiting signs of central nervous system disorders; cattle exhibiting signs of mad cow disease; and dead cattle. Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per obex sample for collecting obex samples from cattle within the Targeted Cattle Population, and submitting the obex samples to a USDA laboratory for mad cow disease testing. Farm Fresh Meats further agreed to maintain in cold storage the sampled cattle carcasses and heads until the test results were received by Farm Fresh Meats.

Evidence uncovered during the government's investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or caused to be submitted, obex samples from healthy, USDA inspected cattle, in order to steal government moneys.

Evidence collected also demonstrated that Farm Fresh Meats and Farabee failed to maintain cattle carcasses and heads pending test results and falsified corporate books and records to conceal their malfeasance. Such actions, to the extent an obex sample tested positive (fortunately, none did), could have jeopardized the USDA's ability to identify the diseased animal and pinpoint its place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee pleaded guilty to stealing government funds and using the mails and wires to effect the scheme. According to their guilty pleas:

(a) Farm Fresh Meats collected, and Farabee directed others to collect, obex samples from cattle outside the Targeted Cattle Population, which were not subject to payment by the USDA;

(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests to the USDA knowing that the requests were based on obex samples that were not subject to payment under the USDA Agreement;

(c) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Data Collection Forms to the USDA's testing laboratory that were false and misleading;

(d) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Submission Forms filed with the USDA that were false and misleading;

(e) Farm Fresh Meats falsified, and Farabee directed others to falsify, internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats was seeking and obtaining payment from the USDA for obex samples obtained from cattle outside the Targeted Cattle Population; and

(f) Farm Fresh Meats failed to comply with, and Farabee directed others to fail to comply with, the USDA Agreement by discarding cattle carcasses and heads prior to receiving BSE test results. A conviction for theft of government funds carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud convictions carry a maximum penalty of 20 years imprisonment. Convictions for the above referenced violations also carry a maximum fine of $250,000 for individuals and $500,000 for organizations. In determining an actual sentence, Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide appropriate sentencing ranges. The judge, however, is not bound by those guidelines in determining a sentence.

Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The investigation in this case was conducted by Assistant Special Agent in Charge Alejandro Quintero, United States Department of Agriculture, Office of Inspector General. The prosecution is being handled by Robert Long, Assistant U.S. Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE NUMBER: 2007-051(Farabee) # # #

http://www.usdoj.gov/usao/az/press_releases/2007/2007-051(Farabee).pdf

IN my opinion, the OIE lost all it's credibility when they went with the Bush administration on the BSE MRR policy. Science was not involved in that policy, only trade. IT did nothing but make legal, the trading of all strains of TSE globally, and set back the eradication of mad cow disease, to the beginning of the epidemic. with the atypical mad cow cases showing up, it will be interesting how this plays out in the years, and decades to come.

IN my opinion, the USA should be classified as undetermined risk, because these are the hard cold facts, they have absolutely no idea, and neither does anyone else. ...

TSS

Friday, March 6, 2009

Risk of Introduction of BSE into Japan by the Historical Importation of Live Cattle from the United Kingdom

http://bseusa.blogspot.com/2009/03/risk-of-introduction-of-bse-into-japan.html

Sunday, May 10, 2009

Identification and characterization of bovine spongiform encephalopathy cases diagnosed and not diagnosed in the United States

http://bse-atypical.blogspot.com/2009/05/identification-and-characterization-of.html

Saturday, November 19, 2011

Novel Prion Protein in BSE-affected Cattle, Switzerland

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/novel-prion-protein-in-bse-affected.html

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

J Vet Diagn Invest 21:454-463 (2009)

Nor98 scrapie identified in the United States

Christie M. Loiacono,' Bruce V. Thomsen, S. Mark Hall, Matti Kiupe!, Diane Sutton, Katherine O'Rourke, Bradd Barr, Lucy Anthenill, Deiwyn Keane

Abstract.

A distinct strain of scrapic identified in sheep of Norway in 1998 has since been identified in numerous countries throughout Europe. The disease is known as Nor98 or Not-98-like scrapic. among other names. Distinctions between classic scrapie and Nor98 scrapie are made based on histopathologv and immunodiagnostic results. There are also differences in the epidemiology, typical signalment, and likelihood of clinical signs being observed. In addition, sheep that have genotypes associated with resistance to classic scrapie are not spared from Nor98 disease. The various differences between classic and Nor98 scrapie have been consistently reported in the vast majority of cases described across Europe. The current study describes in detail the patholo gic changes and diagnostic results of the first 6 cases of' Nor98 scrapic disease diagnosed in sheep of the United States.

Key words: Hisiopathology: Nor98: PrP imniunolabeling; scrapie: sheep.

snip...

Results

Case I

The first case identified as consistent with Nor98 scrapie had nonclassic PrP distribution in brain tissue, no PrPSC in lymph tissue, and nonclassic migration of protein bands on a Western blot test. The animal was an aged, mottled-faced ewe that was traced back to a commercial flock in Wyoming. ...

Case 2

The second case was a clinically normal 8-year-old Suffolk ewe that had been in a quarantined flock for 5 years at a USDA facility in Iowa.

Case 3

A 16-year-old, white-faced, cross-bred wether was born to a black-faced ewe. He lived his entire life as a pet on a farm in California.

Case 4

The fourth case of Nor98 scrapie was identified in an approximately 8-year-old Dorset ewe that was born into a flock of approximately 20 ewes in Indiana.

Case 5

The fifth case was a clinically normal, approximately 3-year-old, white-faced, cross-bred ewe from an approximately 400 head commercial flock in Minnesota.

Case 6

The sixth case of Nor98 scrapie was identified in a 4-year-old, white-faced ewe that was purchased and added to a commercial flock in Pennsylvania

snip...

see full text ;

http://ddr.nal.usda.gov/bitstream/10113/33943/1/IND44241920.pdf

http://scrapie-usa.blogspot.com/

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

Friday, February 11, 2011

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

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

Sunday, December 12, 2010

EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html

Wednesday, January 18, 2012

Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural Scrapie Isolates Similar to CH1641 Experimental Scrapie

Journal of Neuropathology & Experimental Neurology: February 2012 - Volume 71 - Issue 2 - p 140–147

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html

Thursday, July 14, 2011

Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html

Thursday, December 23, 2010

Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002-2009

Volume 17, Number 1 January 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html

Thursday, November 18, 2010

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html

hmmm, no I ponder why some of these sporadic CJD cases, are now being linked to a genetic TSE, that has NO link to the family ?

hmmm, could it be these atypical TSE in animals, that are linked to the human TSE in the USA, and also, these animals have been fed back and forth to each other ?

hmmm, why no link there $$$

P03.141

Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

PR-26

NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS

R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway

Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.

*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.

119

http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf

A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes

Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,? +Author Affiliations

*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway

***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)

Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. *** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

http://www.pnas.org/content/102/44/16031.abstract

Monday, December 1, 2008

When Atypical Scrapie cross species barriers

Authors

Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.

Content

Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.

The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.

Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.

Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.

(i) the unsuspected potential abilities of atypical scrapie to cross species barriers

(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier

These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf

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

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

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

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

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

2012

Tuesday, December 20, 2011

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

> The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years.

However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil.

Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. < < <

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

SNIP...SEE FULL TEXT ;

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

Thursday, February 09, 2012

50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE

http://chronic-wasting-disease.blogspot.com/2012/02/50-game-farms-to-date-in-usa-infected.html

Friday, February 03, 2012

Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-farm-raised-deer-farms-and.html

Saturday, February 04, 2012

Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-16-age-limit-on-testing-dead.html

Thursday, February 09, 2012

Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/colorado-farm-raised-deer-farms-and-cwd.html

Tuesday, February 14, 2012

Oppose Indiana House Bill 1265 game farming cervids

http://chronic-wasting-disease.blogspot.com/2012/02/oppose-indiana-house-bill-1265-game.html

Monday, February 13, 2012

Stop White-tailed Deer Farming from Destroying Tennessee’s Priceless Wild Deer Herd oppose HB3164

http://chronic-wasting-disease.blogspot.com/2012/02/stop-white-tailed-deer-farming-from.html

Wednesday, February 15, 2012

West Virginia Deer Farming Bill backed by deer farmers advances, why ? BE WARNED CWD

http://chronic-wasting-disease.blogspot.com/2012/02/west-virginia-deer-farming-bill-backed.html

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html

Thursday, January 26, 2012

The Risk of Prion Zoonoses

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html

Thursday, January 26, 2012

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html

Saturday, February 11, 2012

Prion cross-species transmission efficacy is tissue dependent

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/prion-cross-species-transmission.html

PIG IN A POKE !!!

Sunday, January 29, 2012

Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Dr. Detwiler

Dr. Detwiler published Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Forum\Presentations TSE\ Page 33 and 34 of 44 ;

http://www.pda.org/

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/prion-disease-risks-in-21st-century.html

Sunday, February 12, 2012

National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html

Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis

http://www.youtube.com/watch?v=zf3lfz9NrT4

http://www.youtube.com/watch?v=c0tWkNvhO4g

http://www.youtube.com/watch?v=zf3lfz9NrT4&feature=results_main&playnext=1&list=PL780BE2AF0B62A944

full text with source references ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html

THESE CUTS BY THE WHITE HOUSE TO TSE PRION FUNDING COULD NOT HAVE COME AT A WORSE TIME !!!

Tuesday, February 14, 2012

White House budget proposes cuts to ag programs including TSE PRION disease aka mad cow type disease

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/white-house-budget-proposes-cuts-to-ag.html

layperson

Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518

flounder9@verizon.net

White House budget proposes cuts to ag programs including TSE PRION disease aka mad cow type disease

2012-02-14T09:57:00.000-08:00

White House budget proposes cuts to ag programs including TSE PRION disease aka mad cow type disease

page 91 or 213

Justification

The purpose of APHIS is to prevent the introduction and spread of pests and diseases that could affect agriculture and other resources. The Budget proposes to reduce or eliminate Federal support in programs that are no longer needed or may have limited impact in responding to an infestation (e.g., the infestation may no longer be able to be controlled). Examples of programs that are being reduced or eliminated are: Johne's Disease; Cotton Pest; and Chronic Wasting Disease programs. These reductions will allow the Department of Agriculture (USDA) to focus on areas where it can achieve success. In some cases, reductions assume additional support from State and local cooperators. Total reductions of $65 million in lower-priority pest and disease programs are partially offset by increases in higher-priority programs for a net reduction of $54 million.

http://www.whitehouse.gov/sites/default/files/omb/budget/fy2013/assets/ccs.pdf

Thursday, October 27, 2011

CHRONIC WASTING DISEASE (CWD) funds disappearing

http://chronic-wasting-disease.blogspot.com/2011/10/chronic-wasting-disease-cwd-funds.html

PRION TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY RESEARCH FUNDING U.S.A.

COMPARE TO USA PRION FUNDING 2011

"which includes the ___elimination___ of Prion activities ($5,473,000),"

All Other Emerging and Zoonotic Infectious Diseases CDC‘s FY 2012 request of $52,658,000 for all other emerging and zoonotic infectious disease activities is a decrease of $13,607,000 below the FY 2010 level, which includes the elimination of Prion activities ($5,473,000), a reduction for other cross-cutting infectious disease activities, and administrative savings. These funds support a range of critical emerging and zoonotic infectious disease programs such Lyme Disease, Chronic Fatigue Syndrome, and Special Pathogens, as well as other activities described below.

http://www.cdc.gov/fmo/topic/Budget%20Information/appropriations_budget_form_pdf/FY2012_CDC_CJ_Final.pdf

Friday, April 15, 2011

PRION TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PROJECTS, RESEARCH FUNDING, BSE VOLUNTARY TESTING UPDATE IN NORTH AMERICA 2011

http://prionunitusaupdate2008.blogspot.com/2011/04/prion-transmissible-spongiform.html

Greetings mad cow TSE Prion community et al ;

this does NOT surprise me. the USDA, FSIS, APHIS, CDC, FDA, NIH et al gave up a long time ago on human and animal TSE prion disease aka mad cow type disease. they failed terribly on the surveillance, testing and eradication of the mad cow type agent in all species, and just gave up$ these TSE prion disease are mutating and spreading, espeically the CWD in deer, elk, who knows what other species. yep, they cannot stop it now. so they just throw in the towel. sporadic CJD has now been linked to atypical BSE, atypical Scrapie, and scientist around the globe are very concerned about the zoonosis of CWD. however, the feds know they have lost the fight, so why waste the money on it $$$

STOP HOUSE BILLS Tennessee’s HB3164 and Indiana House Bill 1265 game farming cervids

Monday, February 13, 2012

Stop White-tailed Deer Farming from Destroying Tennessee’s Priceless Wild Deer Herd oppose HB3164

http://chronic-wasting-disease.blogspot.com/2012/02/stop-white-tailed-deer-farming-from.html

Tuesday, February 14, 2012

Oppose Indiana House Bill 1265 game farming cervids

http://chronic-wasting-disease.blogspot.com/2012/02/oppose-indiana-house-bill-1265-game.html

Thursday, February 09, 2012

50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE

http://chronic-wasting-disease.blogspot.com/2012/02/50-game-farms-to-date-in-usa-infected.html

Friday, February 03, 2012

Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-farm-raised-deer-farms-and.html

Saturday, February 04, 2012

Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-16-age-limit-on-testing-dead.html

Thursday, February 09, 2012

Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/colorado-farm-raised-deer-farms-and-cwd.html

Comment from Terry Singeltary

Document ID: APHIS-2011-0032-0002Document Type: Public Submission

This is comment on Notice: Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program

Docket ID: APHIS-2011-0032RIN:

Topics: No Topics associated with this document

View Document:

Show Details

Document Subtype: Public Comment

Status: Posted

Received Date: January 24 2012, at 12:00 AM Eastern Standard Time

Date Posted: January 25 2012, at 12:00 AM Eastern Standard Time

Comment Start Date: January 24 2012, at 12:00 AM Eastern Standard Time

Comment Due Date: March 26 2012, at 11:59 PM Eastern Daylight Time

Tracking Number: xxxxxxx
First Name: Terry
Middle Name: S.
Last Name: Singeltary
City: Bacliff
Country: United States
State or Province: TX
Organization Name: LAYPERSON
Submitter's Representative: CJD TSE PRION VICTIMS

Comment:

Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001) I believe that any voluntary program for CWD free herd certification from game farms will be futile, as was the partial and voluntary mad cow feed ban of August 4, 1997. That failed terribly, with some 10,000,000 of banned blood laced MBM being fed out in 2007, a decade post August 4, 1997 partial and voluntary ban. Game farms are a petri dish for CWD TSE Prion disease, with Wisconsin having documented 9 CWD infected game farms, with one having the highest CWD infection rate in the world, 80% CWD infection rate. I believe that all game farms should be SHUT DOWN PERMANENTLY. CWD TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. you cannot cook the CWD TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. the TSE prion agent also survives Simulated Wastewater Treatment Processes. IN fact, you should also know that the CWD TSE Prion agent will survive in the environment for years, if not decades. you can bury it and it will not go away. CWD TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

Tuesday, December 20, 2011 CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer

(Buckhorn Flats) Farm Update DECEMBER 2011

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

http://chronic-wasting-disease.blogspot.com/

additional data submission ;

Name: Terry S. Singeltary

Address:
Bacliff, TX,

Submitter's Representative: CJD TSE PRION VICTIMS

Organization: LAYPERSON

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

General Comment
Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001)

I believe that any voluntary program for CWD free herd certification from game farms will be futile, as was the partial and voluntary mad cow feed ban of August 4, 1997. That failed terribly, with some 10,000,000 of banned blood laced MBM being fed out in 2007, a decade post August 4, 1997 partial and voluntary ban.

Game farms are a petri dish for CWD TSE Prion disease, with Wisconsin having documented 9 CWD infected game farms, with one having the highest CWD infection rate in the world, 80% CWD infection rate.

I believe that all game farms should be SHUT DOWN PERMANENTLY.

CWD TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.

you cannot cook the CWD TSE prion disease out of meat.

you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.

the TSE prion agent also survives Simulated Wastewater Treatment Processes.

IN fact, you should also know that the CWD TSE Prion agent will survive in the environment for years, if not decades.

you can bury it and it will not go away.

CWD TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.

it’s not your ordinary pathogen you can just cook it out and be done with.

that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

Tuesday, December 20, 2011

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

http://chronic-wasting-disease.blogspot.com/

http://www.regulations.gov/#!documentDetail;D=APHIS-2011-0032-0002

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html

Thursday, January 26, 2012

The Risk of Prion Zoonoses

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html

Thursday, January 26, 2012

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html

Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

snip...

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip...

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1

http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf

see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html

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

2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49

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

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

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

The conclusions state that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Active screening has allowed the identification of 3 new forms of animal TSEs (H-type atypical BSE, L-type atypical BSE, and atypical scrapie), but the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs. There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential. Transmission experiments to human PrP transgenic mice or primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential and indicate that that of the L-type atypical BSE agent appears similar or even higher than that of the classical BSE agent. A single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.

http://www.promedmail.org/direct.php?id=20110607.1736

Wednesday, January 18, 2012

BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE

February 1, 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html

Owens, Julie

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

Sent: Monday, July 24, 2006 1:09 PM

To: FSIS RegulationsComments

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

Page 1 of 98

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

FSIS RFEPLY TO TSS ;

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

THE steady rise of sporadic CJD cases in Canada AND USA, with many unusual cases of ''PENDING CLASSIFICATIONS" which have been pending now FOR 3 YEARS. HOW long can this cover-up continue $$$

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

SEE FULL TEXT AND MORE HERE ;

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

PIG AND A POKE !!!

pharmaceuticals and porcine and TSE prion

old concerns made new again. they had the science and risk factor there from 2 decades ago, political science won out $$$ i.e. TRADE $$$ thanks to the OIE and the USDA et al. ...TSS

Sunday, January 29, 2012

Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Dr. Detwiler

Dr. Detwiler published Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Forum\Presentations TSE\ Page 33 and 34 of 44 ;

http://www.pda.org/

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/prion-disease-risks-in-21st-century.html

Wednesday, February 1, 2012

CJD and PLASMA / URINE PRODUCTS EMA Position Statements Alberto Ganan Jimenez, European Medicines Agency PDA TSE Safety Forum, 30 June 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/cjd-and-plasma-urine-products-ema.html

Wednesday, February 1, 2012

Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Update on CJD and VCJD Transmission RG Will

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/prion-disease-risks-in-21st-century.html

WHAT ABOUT THAT partial and voluntary mad cow feed ban of August 4, 1997, you know the one, the one that was NOTHING BUT INK ON PAPER $$$

Sunday, February 5, 2012

February 2012 Update on Feed Enforcement Activities to Limit the Spread of BSE

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/february-2012-update-on-feed.html

Friday, February 10, 2012

Creutzfeldt-Jakob disease (CJD) biannual update (2012/1) potential iatrogenic (healthcare-acquired) exposure to CJD, and on the National Anonymous Tonsil Archive

http://creutzfeldt-jakob-disease.blogspot.com/2012/02/creutzfeldt-jakob-disease-cjd-biannual.html

Sunday, February 12, 2012

National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html

layperson

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518