Wednesday, September 5, 2018

APHIS Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0012]

Subject: APHIS Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0012]

[Federal Register Volume 83, Number 170 (Friday, August 31, 2018)] [Notices]

[Page 44562]

From the Federal Register Online via the Government Publishing Office [www.gpo.gov] [FR Doc No: 2018-18962] 

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

Notices Federal Register 

________________________________________________________________________ 

This section of the FEDERAL REGISTER contains documents other than rules or proposed rules that are applicable to the public. Notices of hearings and investigations, committee meetings, agency decisions and rulings, delegations of authority, filing of petitions and applications and agency statements of organization and functions are examples of documents appearing in this section. 

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

Federal Register / Vol. 83, No. 170 / Friday, August 31, 2018 / Notices

[[Page 44562]] 

 DEPARTMENT OF AGRICULTURE

Animal and Plant Health Inspection Service

[Docket No. APHIS-2018-0012] 

Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy

AGENCY: Animal and Plant Health Inspection Service, USDA.

ACTION: Notice.

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

SUMMARY: We are advising the public of our decision to concur with the World Organization for Animal Health's (OIE) bovine spongiform encephalopathy (BSE) risk designations for four regions. The OIE recognizes these regions as being of negligible risk for BSE. We are taking this action based on our review of information supporting the OIE's risk designations for these regions.

FOR FURTHER INFORMATION CONTACT: Dr. Rebecca Gordon, Senior Staff Veterinarian, Regionalization Evaluation Services, National Import Export Services, VS, APHIS, 920 Main Campus Drive, Suite 200, Raleigh, NC 27606; (919) 855-7741.

SUPPLEMENTARY INFORMATION: The regulations in 9 CFR part 92 subpart B, ``Importation of Animals and Animal Products; Procedures for Requesting BSE Risk Status Classification With Regard To Bovines'' (referred to below as the regulations), set forth the process by which the Animal and Plant Health Inspection Service (APHIS) classifies regions for bovine spongiform encephalopathy (BSE) risk. Section 92.5 of the regulations provides that all countries of the world are considered by APHIS to be in one of three BSE risk categories: Negligible risk, controlled risk, or undetermined risk. These risk categories are defined in Sec. 92.1. Any region that is not classified by APHIS as presenting either negligible risk or controlled risk for BSE is considered to present an undetermined risk. The list of those regions classified by APHIS as having either negligible risk or controlled risk can be accessed on the APHIS website at


The list can also be 

obtained by writing to APHIS at National Import Export Services, 4700 River Road Unit 38, Riverdale, MD 20737.

 Under the regulations, APHIS may classify a region for BSE in one of two ways. One way is for regions that have not received a risk classification from the World Organization for Animal Health (OIE) to request classification by APHIS. The other way is for APHIS to concur with the classification given to a country or region by the OIE.

 If the OIE has recognized a country as either BSE negligible risk or BSE controlled risk, APHIS will seek information to support our concurrence with the OIE classification. This information may be publicly available information, or APHIS may request that countries supply the same information given to the OIE. APHIS will announce in the Federal Register, subject to public comment, its intent to concur with an OIE classification.

 In accordance with that process, we published a notice \1\ in the Federal Register on April 24, 2018 (83 FR 17789, Docket No. APHIS-2018- 0012), in which we announced our intent to concur with the OIE recognition of Croatia, Poland, Northern Ireland, and Scotland as being regions of negligible risk for BSE. We solicited comments on the notice for 60 days ending on June 25, 2018. We received one comment by that date, from a private citizen.

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

 \1\ To view the notice and the comment we received, go to 


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

 The commenter voiced doubts about the efficacy of the BSE minimal risk region policy, concerns about other prion diseases such as chronic wasting disease circulating in the United States and the world, and skepticism that the ruminant-to-ruminant feed ban has been effectively enforced. The commenter did not, however, address our preliminary concurrence with the OIE's risk designations for the four regions or the documentation made available to support that action.

 Therefore, in accordance with the regulations in Sec. 92.5, we are announcing our decision to concur with the OIE risk classifications of the following countries:

 Regions of negligible risk for BSE: Croatia, Poland, Northern Ireland (region of United Kingdom), and Scotland (region of United Kingdom). 

 Authority: 7 U.S.C. 1622 and 8301-8317; 21 U.S.C. 136 and 136a; 31 U.S.C. 9701; 7 CFR 2.22, 2.80, and 371.4. 

 Done in Washington, DC, this 27th day of August 2018. Kevin Shea,

Administrator, Animal and Plant Health Inspection Service. [FR Doc. 2018-18962 Filed 8-30-18; 8:45 am] BILLING CODE 3410-34-P


The is a Comment on the Animal and Plant Health Inspection Service (APHIS) Notice: Concurrence with OIE Risk Designations for Bovine Spongiform Encephalopathy

For related information, Open Docket Folder 

 Comment Docket No. APHIS-2018-0012 Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy Singeltary Submission

Greetings again APHIS et al, 

i would kindly like to submit my comments regarding Docket No. APHIS-2018-0012 Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy.

i would kindly like to address several issues regarding BSE and other strains of Transmissible Spongiform Encephalopathy TSE Prion disease, due to the potential ramifications of the new outbreak of Camel TSE Prion disease (Mad Camel Disease) in Algeria, and imports and exports there from, the recent findings that Scrapie of sheep and goats and Chronic Wasting Disease of Cervid will transmit to PIGS by the ORAL route, and the recent findings of the Macaque studies, and oral transmission of CWD and Scrapie TSE Prion transmission to the macaque, one of the closets monkey's to the human species, and remember, transmission studies to humans from TSE Prion are illegal. 

So, there is much new science and must concern here, and in my opinion, the BSE MRR i.e. Minimal Risk Region is a disaster that is waiting to happen, and has already happened, by allowing the legal trading of the TSE Prion across the globe. 

I once again urge strenuously that the BSE MRR policy be withdrawn and abolished, and that the BSE GBR Risk Assessments be implemented once again, to include ALL TSE PRION DISEASE IN EVERY SPECIES. The ruminant and mammalian feed bans have failed us terribly, the BSE surveillance in the USA failed terribly, and the BSE testing program was a failure as well, and all proven to be so by the GAO and the OIG. 

The massive, copious amounts of banned Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200 i.e. mad cow feed, is so great still to this day, some 2 plus decades post Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200 i.e. mad cow feed of August 1997, that there should be an emergency meeting to address the mad cow feed ban immediately, considering the recent findings of cwd and scrapie transmitting to pigs. 

there should also be a DECLARATION OF EMERGENCY DECLARED OF A FOREIGN ANIMAL DISEASE FROM THE USA, i.e. CWD TSE Prion, and this declaration should go out to the world, as there was back On July 14, 2000, USDA issued a declaration of extraordinary emergency to acquire the sheep. but those test were wrong, and a decade later after FOIA request after request, turns out those sheep from Belgium never had any TSE Prion disease. long story, but what is the difference here, especially since we are dealing with Chronic Wasting Disease CWD TSE Prion, and the fact now that not only has CWD been exported from North America to South Korea, and to Norway, but now Finland has confirmed it's first case of Chronic Wasting Disease CWD TSE Prion. So, where does the 'BUCK' stop? 

why has this 'DECLARATION OF EXTRAORDINARY EMERGENCY FOR FOREIGN ANIMAL DISEASE OF THE United States of America USA' due to Chronic Wasting Disease CWD Transmissible Spongiform Encephalopathy TSE Prion disease, not already been declared, and why has not a Intercontinental, International, Interstate movements of cervid BAN not already been put in place, especially since the recent findings of oral transmission studies with the Macaque, in relations with oral transmission of muscle meat with cwd, and oral transmission of cwd to the pig? 

do we just continue to truck, ship, or fly this CWD TSE Prion all around the globe, just to save the industry? 

see; August 15, 2000 OIG case # NY-3399-56 REDACTED, VT ''Enclosed is OIG's notification that they have scheduled an investigation of the following individual. REDACTED is alleged to have provided possibly inaccurate test results involving diseased sheep. However, because the results were determined to be inconclusive, no actual violation was actually committed.''


I believe that before addressing BSE TSE Prion related issues with Croatia, Poland, Northern Ireland, Scotland, that APHIS/USDA/FSIS/FDA et al should clean up there own back yards. Much BSE TSE Risk factor still reside right here in the USA and North America. 

***> ''One way is for regions that have not received a risk classification from the World Organization for Animal Health (OIE) to request classification by APHIS'' <***

IN my honest opinion, this is the same as letting the wolf guard the hen house.

My Submission of Scientific Facts as follows, and why i believe that the BSE MRR is a terribly failed policy, that only allows the continued spread of the TSE Prion agent, and why THE BSE MRR MUST BE REPEALED IMMEDIATELY!

Attachments (1)


SEE FULL TEXT;

APHIS Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy


Docket No. APHIS-2018-0012 Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy Singeltary Submission


WEDNESDAY, APRIL 25, 2018

Docket No. APHIS-2018-0012 Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy Singeltary Submission

Greetings again APHIS et al, i would kindly like to submit my comments regarding Docket No. APHIS-2018-0012 Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy.



POLAND BSE GBR VS BSE MRR, more on non-species coding system and TSEs and potential 'suitcase bombs';

 
To: Bovine Spongiform Encephalopathy

 
Subject: Re: POLAND FINDS 4TH MAD COW CASE/USA IMPORTS FROM POLAND/non-species coding system strikes again

 
References: <3dc198e3 .8090704="" wt.net=""> Content-Type: text/plain; charset=ISO-8859-1; format=flowed Content-Transfer-Encoding: 8bit X-Virus-Scanner: Found to be clean 

Greetings again List Members, let me kick a madcow around here a bit.

 
on the imports from Poland and the infamous USA 'non-species' coding system. the USDA/APHIS states;

 
> During the past four years (1998 - 2001), US imports from

 
> Poland included non-species specific animal products

 
> used in animal feeds and non-species specific sausage and offal

 
> products (Table 3). Given US restrictions on ruminant product

 
> imports, these US imports should not have contained ruminant

 
> material.

 
NOW, if you read Polands GBR risk assessment and opinion on BSE, especially _cross-contamination_, it states;

 
ANNEX 1 Poland - Summary of the GBR-Assessment, February 2001

 
EXTERNAL CHALLENGE STABILITY INTERACTION OF EXTERNAL CHALLENGE AND STABILITY

 
The very high to extremely high external challenge met a very unstable system and could have led to contamination of domestic cattle in Poland from 1987 onwards. This internal challenge again met the still very unstable system and increased over time. The continuing very high external challenge supported this development. Not OK MBM-ban since 1997, but no feed controls. Reasonably OK Heat treatment equivalent to 133°C / 20min / 3 bar standards, but no evidence provided on compliance. Not OK. No SRM-ban, SRM are rendered and included in cattle feed. BSE surveillance: Not sufficient before 2001. Cross-contamination: Lines for ruminant and non-ruminant feed in feed-mills only separated in time and no analytical controls carried out. Likely present since 1987 and growing.

 
see full text and ANNEX 1 at;

 

 

 
Sunday, January 11, 2015

 
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission

 

 

 
Owens, Julie

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

 
Sent: Monday, July 24, 2006 1:09 PM

 
To: FSIS RegulationsComments

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

 

 
FSIS, USDA, REPLY TO SINGELTARY

 

 
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO DOCKET 2003N-0312]

 
From: Terry S. Singeltary Sr. [flounder@wt.net]

 
Sent: Tuesday, July 29, 2003 1:03 PM

 
To: fdadockets@oc.fda.gov

 
Cc: ggraber@cvm.fda.gov; Linda.Grassie@fda.gov; BSE-L

 
Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO DOCKET 2003N-0312]

 
Greetings FDA,

 
my name is Terry S. Singeltary Sr., i lost my mother to hvCJD (Heidenhain Variant Creutzfeldt Jakob Disease).

 
i would kindly like to comment on the proposed HACCP method of detecting and or preventing TSEs in the human/animal feed supply.

 
it seems to me by implementing something that was designed for Astronauts instead of cattle, something that the GAO has already stated is terribly flawed (HACCP), i find it very disturbing to continue to insist on refusing to use rapid TSE TESTING in sufficient numbers to find TSEs, as with other Countries that they too once thought they were BSE free. for example, it took Italy 1 MILLION rapid TSE tests since 2001 to find 102 cases of BSE. THE USA has only tested 48,000 cattle in the 14 years of surveillance. there is documented proof that indeed the USA cattle have been infected with a TSE for decades, but the FDA/USDA and other USA Gov. agencies continue to conveniently ignore these findings. YOU must not ignore what Richard Marsh found. Plus, you must not ignore Asante/Collinge new findings that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD. The USA has been feeding ruminant by-products back to cattle, deer, elk and sheep for decades, and TSEs in these species have been recycled for feed for decades in the USA. The rendering process here in the USA will not kill this agent. to implement any HACCP over massive rapid TSE testing is only prolonging the inevitable, and will only allow the agent to spread further. it is simply a band-aid approach to something that needs a tourniquet...

 
3. Meat and Poultry: Better USDA Oversight and Enforcement of Safety

 
Rules Needed to Reduce Risk of Foodborne Illnesses. GAO-02-902, August 30.

 
FSIS Is Not Ensuring that Plants' HACCP Plans Meet Regulatory Requirements

 
snip...

 
According to FSIS's food safety systems correlation reviews, inspectors are not consistently identifying and documenting failures of plants' HACCP plans to meet regulatory requirements. Furthermore, FSIS does not expect its inspectors to determine whether HACCP plans are based on sound science--the cornerstone of an effective plan. While in-depth verification reviews examine the scientific aspects of HACCP plans, they have been conducted in very few plants, and consumer safety officers hired to review the scientific soundness of HACCP plans may take several years to assess the plans at all plants. Moreover, inspectors in 55 percent of the 5,000 plants nationwide did not document any HACCP violations during fiscal year 2001. When we brought this information to the attention of FSIS officials, they were surprised that so many plants had no HACCP violations for an entire year.

 
snip...

 
2. USDA believes that the title of the report is misleading. We disagree. We believe the title accurately reflects the concerns detailed throughout the body of the report.

 
snip...

 

 

 
FDA acknowledges that it has not yet identified and inspected all firms subject to the ban” pg. 3 ;

 

 
The report concludes that “federal actions do not sufficiently ensure that all BSE-infected animals or products are kept out or that if BSE were found it would be detected promptly and not spread to other cattle through animal feed or enter the human food chain” italics added pg. 3 ;

 


***********2015*********

SNIP...SEE FULL TEXT;

TUESDAY, OCTOBER 20, 2015

FBI: Agroterrorism not likely, but very possible, Dr. Stephen Gold­smith FBI Laboratory Division, here's your sign

CC-Dr. Steve Goldsmith, FBI Laboratory Division

please note, I tried to forward this to the FBI, spoke with several folks at FBI headquarters, and they were not interested...just saying...terry



***> USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS September 4, 2018 <***


TSE PRION UPDATE September 4, 2018

TUESDAY, AUGUST 28, 2018 

USDA finds BSE infection in Florida cow 08/28/18 6:43 PM

http://animalhealthreportpriontse.blogspot.com/2018/08/usda-finds-bse-infection-in-florida-cow.html

WEDNESDAY, AUGUST 29, 2018 

USDA Announces Atypical Bovine Spongiform Encephalopathy Detection USDA 08/29/2018 10:00 AM EDT

http://bse-atypical.blogspot.com/2018/08/usda-announces-atypical-bovine.html

WEDNESDAY, AUGUST 29, 2018 

Transmissible Spongiform Encephalopathy TSE Prion Atypical BSE Confirmed Florida Update USA August 28, 2018

http://transmissiblespongiformencephalopathy.blogspot.com/2018/08/transmissible-spongiform-encephalopathy.html

WEDNESDAY, AUGUST 29, 2018 

OIE Bovine spongiform encephalopathy, United States of America Information received on 29/08/2018 from Dr John Clifford, Official Delegate, Chief Trade Advisor, APHIS USDA

''The event is resolved. No more reports will be submitted.''

well, so much for those herd mates exposed to this atypical BSE cow, and all those trace in and trace outs.

The OIE, USDA, and the BSE MRR policy is a joke, a sad, very sad joke...

http://bovineprp.blogspot.com/2018/08/oie-bovine-spongiform-encephalopathy.html

THURSDAY, AUGUST 30, 2018 

Florida Department of Agriculture and Consumer Services announced it is working closely with U.S. Department of Agriculture regarding an atypical case of Bovine Spongiform Encephalopathy BSE


THURSDAY, AUGUST 30, 2018 

TRACKING HERD MATES USDA MAD COW DISEASE, TRACE FORWARD, TRACE BACK RECORDS, WHO CARES, NOT THE OIE



USDA ONLY TESTING 20k HEAD OF CATTLE A YEAR FOR MAD COW DISEASE ...LOL!

WEDNESDAY, AUGUST 29, 2018 

USDA Announces Atypical Bovine Spongiform Encephalopathy Detection USDA 08/29/2018 10:00 AM EDT






WEDNESDAY, AUGUST 29, 2018 

USDA DROPS MAD COW TESTING FROM 40K A YEAR TO JUST 20K A YEAR, IMPOSSIBLE TO FIND BSE, BUT THEY DID, IN FLORIDA!

http://bovineprp.blogspot.com/2018/08/usda-drops-mad-cow-testing-from-40k.html


''Atypical BSE is different, and it generally occurs in older cattle, usually 8 years of age or greater. It seems to arise rarely and spontaneously in all cattle populations.''

FALSE!

''The primary source of infection for classical BSE is feed contaminated with the infectious prion agent, such as meat-and-bone meal containing protein derived from rendered infected cattle.  Regulations from the Food and Drug Administration (FDA) have prohibited the inclusion of mammalian protein in feed for cattle and other ruminants since 1997 and have also prohibited high risk tissue materials in all animal feed since 2009.''

FALSE!

LET'S REVIEW RECENT AND PAST SCIENCE THAT SHOWS THE ABOVE TWO STATEMENTS ARE FAR FROM TRUE;

PRION 2018 CONFERENCE

P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge 

Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States. 

reading up on this study from Prion 2018 Conference, very important findings ;


***> This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. 


***> These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.


PRION 2018 CONFERENCE ABSTRACT



WEDNESDAY, AUGUST 15, 2018 

***> The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge



TEXAS OFFICIALS DEAD WRONG ON AMOUNT OF INFECTIVITY TO CAUSE A TSE PRION DISEASE ;

"FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams – approximately a quarter ounce — of prohibited material. These animals weigh approximately 600 pounds."

5.5 GRAMS OF INFECTIOUS PROHIBITED MAD COW FEED FOR EACH OF THE 1,222 ANIMALS (5.5 GRAMS X 1,222 ANIMALS) IS ENOUGH INFECTIOUS MAD COW FEED TO KILL A SMALL HERD OF COWS...TSS

U.S. Food and Drug Administration FDA News | Today the Food and Drug Administ…U.S. Food and Drug Administration FDA News

Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle — a violation of FDA’s 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams – approximately a quarter ounce — of prohibited material. These animals weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA’s Acting Principal Deputy Commissioner, “The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture’s (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE.”

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

http://www.usmef.org/news-statistics/press-releases/us-food-and-drug-administration-fda-news-today-the-food-and-drug-administ-13375/

FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT

Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

http://www.fda.gov/bbs/topics/news/2001/new00752.html

PRION 2009 CONGRESS BOOK OF ABSTRACTS

O.4.3

Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission

Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany

Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).

Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.

Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.

Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p..i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.

Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.

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

Singeltary comment;

http://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone..0010638

http://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53

***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.

***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.

*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***

Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT

http://www.plosone.org/annotation/listThread.action?root=86610

Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle

CDC Volume 23, Number 2—February 2017

*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.

https://wwwnc.cdc.gov/eid/article/23/2/16-1416_article

Prion 2018 Conference

P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge

This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.

Prion 2018 Conference

https://prion2018.org/wp-content/uploads/2018/05/program.pdf

P04.27

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route

Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany

Background:

In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.

Aims:

The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.

Methods:

Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).

Results:

In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.

Conclusions:

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.

The work referenced was performed in partial fulfillment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).

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

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.

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

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.

snip...

BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula

Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa

Calves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. .........

http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose

It is clear that the designing scientists must also have shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.

http://web.archive.org/web/20061003022720/http://www.bseinquiry.gov.uk/files/ws/s145d.pdf

6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.

http://web.archive.org/web/20061003022724/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf

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


Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
 
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...
 
 
 
 
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
 
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
 
 
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” ...page 26.
 
 
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
 

***>2018<***

SEE FULL REPORT;


TUESDAY, SEPTEMBER 4, 2018 

USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS September 4, 2018

prepare for the storm...



10 years post mad cow feed ban August 1997

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
 

USDA 2004 ENHANCED BSE SURVEILLANCE PROGRAM AND HOW NOT TO FIND BSE CASES (OFFICIAL DRAFT OIG REPORT) 

snip... 


CATTLE With CNS Symptoms Were NOT Always Tested 


snip... 


Between FYs 2002 and 2004, FSIS condemned 680 cattle of all ages due to CNS symptoms. About 357 of these could be classified as adult. We could validate that ONLY 162 were tested for BSE (per APHIS records. ... 

snip... 

WE interviewed officials at five laboratories that test for rabies. Those officials CONFIRMED THEY ARE NOT REQUIRED TO SUBMIT RABIES-NEGATIVE SAMPLES TO APHIS FOR BSE TESTING. A South Dakota laboratory official said they were not aware they could submit rabies-negative samples to APHIS for BSE testing. A laboratory official in another State said all rabies-negative cases were not submitted to APHIS because BSE was ''NOT ON THEIR RADAR SCREEN." Officials from New York, Wisconsin, TEXAS, and Iowa advised they would NOT submit samples from animals they consider too young. Four of the five States contacted defined this age as 24 months; Wisconsin defined it as 30 months. TEXAS officials also advised that they do not always have sufficient tissue remaining to submit a BSE sample. ... 

snip... 


FULL TEXT 54 PAGES OF HOW NOT TO FIND BSE IN USA ; 


http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_july_13_ig_rep.pdf 


USDA/FDA MAD COW PROTEIN IN COMMERCE 2006


MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL,
TN, AND WV

Date: September 6, 2006 at 7:58 am PST

PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE
None


RECALLING FIRM/MANUFACTURER


Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone
on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is
complete.


REASON


Dairy and poultry feeds were possibly contaminated with ruminant based
protein.


VOLUME OF PRODUCT IN COMMERCE


477.72 tons


DISTRIBUTION


AL


______________________________


PRODUCT
a) Dairy feed, custom, Recall # V-134-6;
b) Custom Dairy Feed with Monensin, Recall # V-135-6.
CODE
None. Bulk product


RECALLING FIRM/MANUFACTURER


Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on
June 28, 2006.


Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated
recall is complete.


REASON


Possible contamination of dairy feeds with ruminant derived meat and bone
meal.


VOLUME OF PRODUCT IN COMMERCE


1,484 tons


DISTRIBUTION


TN and WV


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




Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA,
MS, AL, GA, AND TN 11,000+ TONS
Date: August 16, 2006 at 9:19 am PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II
______________________________

PRODUCT
Bulk custom made dairy feed, Recall # V-115-6
CODE
None


RECALLING FIRM/MANUFACTURER
Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or
about July 14, 2006. FDA initiated recall is ongoing.


REASON


Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.


VOLUME OF PRODUCT IN COMMERCE


Approximately 2,223 tons


DISTRIBUTION


KY

______________________________


PRODUCT
Bulk custom made dairy feed, Recall # V-116-6
CODE
None


RECALLING FIRM/MANUFACTURER


Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006.


FDA initiated recall is ongoing.


REASON


Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.


VOLUME OF PRODUCT IN COMMERCE


1,220 tons


DISTRIBUTION


KY

______________________________


PRODUCT


Bulk custom made dairy feed, Recall # V-117-6
CODE
None


RECALLING FIRM/MANUFACTURER


Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated
recall is completed.


REASON


Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
meal.


VOLUME OF PRODUCT IN COMMERCE


40 tons


DISTRIBUTION


LA and MS

______________________________

PRODUCT
Bulk Dairy Feed, Recall V-118-6
CODE
None


RECALLING FIRM/MANUFACTURER


Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA
initiated recall is complete.


REASON


Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
meal.


VOLUME OF PRODUCT IN COMMERCE


7,150 tons


DISTRIBUTION


MS

______________________________

PRODUCT
Bulk custom dairy pre-mixes, Recall # V-119-6
CODE
None


RECALLING FIRM/MANUFACTURER


Walthall County Co-op, Tylertown, MS, by telephone on June 26, 2006. Firm
initiated recall is complete.


REASON


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


VOLUME OF PRODUCT IN COMMERCE


87 tons


DISTRIBUTION


MS

______________________________

PRODUCT
Bulk custom dairy pre-mixes, Recall # V-120-6
CODE
None


RECALLING FIRM/MANUFACTURER


Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm
initiated recall is complete.


REASON


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


VOLUME OF PRODUCT IN COMMERCE


350 tons


DISTRIBUTION


AL and MS

______________________________

PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet,
50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet,
50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower,
50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD
Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags,
Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags,
Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher,
50 lb bags, Recall # V-127-6
CODE
All products manufactured from 02/01/2005 until 06/20/2006


RECALLING FIRM/MANUFACTURER


Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit
on June 20, 2006, and by letter on June 23, 2006.


Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated
recall is ongoing.


REASON


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


VOLUME OF PRODUCT IN COMMERCE


7,541-50 lb bags


DISTRIBUTION


AL, GA, MS, and TN

END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006

###


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


Subject: MAD COW FEED RECALL MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN
COMMERCE 27,694,240 lbs
Date: August 6, 2006 at 6:14 pm PST
PRODUCT
Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6
CODE
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J.
Baker recalled feed products.


RECALLING FIRM/MANUFACTURER


Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm
initiated recall is complete.


REASON


The feed was manufactured from materials that may have been contaminated
with mammalian protein.


VOLUME OF PRODUCT IN COMMERCE


27,694,240 lbs


DISTRIBUTION


MI

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###

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

Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated,
net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete
Feed for Chickens from Hatch to 20 Weeks, Medicated,
Bacitracin Methylene Disalicylate, 25 and 50 Lbs,
Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED,
net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,
Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,
Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006



RECALLING FIRM/MANUFACTURER



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



REASON



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



VOLUME OF PRODUCT IN COMMERCE



125 tons



DISTRIBUTION



AL and FL


END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###

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

Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ?????
Date: August 6, 2006 at 6:19 pm PST
PRODUCT
Bulk custom made dairy feed, Recall # V-114-6
CODE
None



RECALLING FIRM/MANUFACTURER



Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated
recall is ongoing.



REASON



Custom made feeds contain ingredient called Pro-Lak, which may contain
ruminant derived meat and bone meal.



VOLUME OF PRODUCT IN COMMERCE



?????



DISTRIBUTION



KY



END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###


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

CJD WATCH MESSAGE BOARD
TSS
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE
Sun Jul 16, 2006 09:22
71.248.128.67


RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________

PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals,
Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg),
Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL
FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6
CODE
a) Bulk
b) None
c) Bulk
d) Bulk



RECALLING FIRM/MANUFACTURER



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



REASON



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



VOLUME OF PRODUCT IN COMMERCE



10,878.06 tons



DISTRIBUTION



Nationwide

END OF ENFORCEMENT REPORT FOR July 12, 2006

###


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

***> IMPORTS AND EXPORTS <***

***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***

http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html

http://madcowusda.blogspot.com/2015/10/former-ag-secretary-ann-veneman-talks.html

http://madcowtesting.blogspot.com/

Friday, December 14, 2012

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

snip...

In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

Animals considered at high risk for CWD include:

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

snip...

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).

The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).

Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

snip...

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

snip...

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

snip...

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

snip...

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

snip...


what is Michigan feeding their cervid ??? 

2017 Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed

Subject: MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017

MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017

FDA BSE/Ruminant Feed Inspections Firms Inventory 

11998 DET-DO MI 48846-847 OPR 4/4/2017 OAI 


NAI = NO ACTION INDICATED

OAI = OFFICIAL ACTION INDICATED

VAI = VOLUNTARY ACTION INDICATED

RTS = REFERRED TO STATE

OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions...end...TSS

WEDNESDAY, JULY 11, 2018

CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000


16 years post mad cow feed ban August 1997
 
2013
 
Sunday, December 15, 2013
 
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
 
 
17 years post mad cow feed ban August 1997
 
Tuesday, December 23, 2014
 
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
 
 
Sunday, June 14, 2015
 
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain Specified Risk Materials BSE TSE Prion
 
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
***>>> THIS LOOPHOLE MUST BE CLOSE TO STOP TSE PRION DISEASE IN USA and AROUND THE GLOBE ASAP !

FDA recommends that materials from deer and elk considered at high risk for CWD no longer be entered into the animal feed system. Under present circumstances, FDA is not recommending that feed made from deer and elk from a non-endemic area be recalled if a State later declares the area endemic for CWD or a CWD eradication zone. In addition, at this time, FDA is not recommending that feed made from deer and elk believed to be from a captive herd that contained no CWD-positive animals be recalled if that herd is subsequently found to contain a CWD-positive animal.

 
I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...
 
======
 
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.
 
***However, this recommendation is guidance and not a requirement by law.
 
======
 
31 Jan 2015 at 20:14 GMT
 
*** Ruminant feed ban for cervids in the United States? ***
 
Singeltary et al
 
31 Jan 2015 at 20:14 GMT
 


Singeltary previous submission to DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Fri, 16 May 2003 11:47:37 0500 EMC 1 Terry S. Singeltary Sr. Vol #: 1

Date: Fri, 16 May 2003 11:47:37 0500 EMC 1 Terry S. Singeltary Sr. Vol #: 1



PLEASE SEE FULL TEXT SUBMISSION ;


*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
 
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. *** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *** It also suggests a similar cause or source for atypical BSE in these countries. ***
 
see page 176 of 201 pages...tss
 
 
Thursday, July 24, 2014
 
*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations
 
 
Saturday, August 4, 2012
 
Final Feed Investigation Summary - California BSE Case - July 2012
 
 
THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$

TUESDAY, APRIL 18, 2017 

EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP



***>2018<***


TUESDAY, AUGUST 7, 2018 

Unexpected prion phenotypes in experimentally transfused animals: predictive models for humans?

http://transmissiblespongiformencephalopathy.blogspot.com/2018/08/unexpected-prion-phenotypes-in.html


TUESDAY, AUGUST 07, 2018 

Passage of scrapie to deer results in a new phenotype upon return passage to sheep



new outbreak of TSE Prion in NEW LIVESTOCK SPECIES

mad camel disease



***> IMPORTS AND EXPORTS <***

***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***

http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html

http://madcowusda.blogspot.com/2015/10/former-ag-secretary-ann-veneman-talks.html

http://madcowtesting.blogspot.com/


----Original Message-----
From: Terry Singeltary <flounder9@verizon.net>
To: bse-l l@lists.aegee.org
>
Cc: cjdvoice <cjdvoice@yahoogroups.com>; bloodcjd <bloodcjd@yahoogroups.com>
Sent: Fri, Apr 20, 2018 3:54 pm
Subject: Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?

Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies 2017 Annual Report

1a. Objectives (from AD-416): 
Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.

1b. Approach (from AD-416): 
The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.

3. Progress Report: 
All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.

4. Accomplishments 
1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.
Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.
Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016. A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation. Frontiers in Veterinary Science. 3:78.
Greenlee, J.J., Kunkle, R.A., Smith, J.D., West Greenlee, M.H. 2016. Scrapie in swine: a diagnostic challenge. Food Safety. 4(4):110-114.
Kondru, N., Manne, S., Greenlee, J., West Greenlee, H., Anantharam, V., Halbur, P., Kanthasamy, A., Kanthasamy, A. 2017. Integrated organotypic slice cultures and RT-QuIC (OSCAR) assay: implications for translational discovery in protein misfolding diseases. Scientific Reports. 7:43155. doi:10.1038/srep43155.
Mammadova, N., Ghaisas, S., Zenitsky, G., Sakaguchi, D.S., Kanthasamy, A.G., Greenlee, J.J., West Greenlee, M.H. 2017. Lasting retinal injury in a mouse model of blast-induced trauma. American Journal of Pathology. 187(7):1459-1472. doi:10.1016/j.ajpath.2017.03.005.




***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***



>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***


THE Aug. 1997 mad cow feed ban was/is a joke, BSE surveillance also was proven to be terribly flawed, along with BSE testing, shown to be flawed as well. 

ALSO, WHAT ABOUT CWD TRANSMITTING TO PIGS AS WELL, AND MAD CAMEL DISEASE NOW, BIG OUTBREAK, NOT SPONTANEOUS, WHAT ABOUT THAT, and the feed ban concern there as well? AND what about Scrapie transmission to the Macaque recently. seems the tse prion poker continue to goes up. very worrying...terry

please see these facts below...thank you///


***> CWD TO PIGS <***

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

Location: Virus and Prion Research

Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease

Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin

Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:

Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.

Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.

Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:

This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.

CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.

Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.


CONFIDENTIAL

EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY

While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...


we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.

 
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....


snip...see much more here ;

WEDNESDAY, APRIL 05, 2017

Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease


WEDNESDAY, APRIL 05, 2017

*** Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease ***


WEDNESDAY, JULY 11, 2018 

CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000

http://transmissiblespongiformencephalopathy.blogspot.com/2018/07/confidential-in-confidence-spongiform.html

TUESDAY, JULY 10, 2018
 
CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS
 
*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''
 
CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS
 
http://madporcinedisease.blogspot.com/2018/07/confidential-in-confidence-spongiform.html

THURSDAY, JULY 20, 2017 

USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200



TUESDAY, AUGUST 28, 2018 

Wyoming WGFD confirmed bull elk harvested hunter tested positive chronic wasting disease CWD Elk Hunt Area 66

http://chronic-wasting-disease.blogspot.com/2018/08/wyoming-wgfd-confirmed-bull-elk.html

SATURDAY, FEBRUARY 03, 2018 

Arkansas Reports 346 Positive CWD TSE Prion cases found as of January 8, 2018

http://chronic-wasting-disease.blogspot.com/2018/02/arkansas-reports-346-positive-cwd-tse.html

MONDAY, AUGUST 27, 2018 
 Michigan Adds Another CWD TSE Prion Case Total Increases To 61 to date
 
 
WEDNESDAY, AUGUST 22, 2018 
 
***> TEXAS CWD TSE PRION 16 MORE CASES DETECTED TOTAL TO DATE 117 CONFIRMED NEW 14 BREEDERS 2 FREE RANGE
 
http://chronic-wasting-disease.blogspot.com/2018/08/texas-cwd-tse-prion-16-more-cases.html

August 27, 2018

CHRONIC WASTING DISEASE CWD TSE PRION UPDATE FDA LEGISLATIVE REPLY TO SINGELTARY and THE TEXAS TWO STEP

http://fdafailedus.blogspot.com/2018/08/chronic-wasting-disease-cwd-tse-prion.html
 
MONDAY, MAY 21, 2018 

Colorado Chronic Wasting disease CWD TSE Prion hits 16 percent of male deer, elk, moose tested in some parts of state
http://chronic-wasting-disease.blogspot.com/2018/05/colorado-chronic-wasting-disease-cwd.html
 
SATURDAY, MARCH 03, 2018 

WISCONSIN CHRONIC WASTING DISEASE TSE Prion DNR Study Finds CWD-Infected Deer Die At 3 Times Rate Of Healthy Animals
http://chronic-wasting-disease.blogspot.com/2018/03/wisconsin-chronic-wasting-disease-tse.html
 
TUESDAY, AUGUST 07, 2018 
 
Cervid Health Operational Plan Fiscal Year 2018 Animal and Plant Health Inspection Services Veterinary Services
 
 
TUESDAY, JULY 03, 2018 
 
Chronic Wasting Disease CWD TSE Prion Global Report Update, USA, CANADA, KOREA, NORWAY, FINLAND, Game Farms and Fake news 
 
 
SUNDAY, APRIL 8, 2018 
 
Transmissible Spongiform Encephalopathy TSE Prion Disease Global Pandemic Urgent Update April 9, 2018
 

THURSDAY, AUGUST 17, 2017 

*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017 Singeltary et al

http://creutzfeldt-jakob-disease.blogspot.com/2017/08/monitoring-occurrence-of-emerging-forms.html


WEDNESDAY, JULY 04, 2018 

CREUTZFELDT-JAKOB DISEASE: GUIDELINES FOR SOCIAL WORKERS IN ENGLAND June 2018

http://creutzfeldt-jakob-disease.blogspot.com/2018/07/creutzfeldt-jakob-disease-guidelines.html


SUNDAY, JUNE 24, 2018 

Validation and utilization of amended diagnostic criteria in Creutzfeldt-Jakob disease surveillance

http://creutzfeldt-jakob-disease.blogspot.com/2018/06/validation-and-utilization-of-amended.html


SATURDAY, JUNE 23, 2018 

Diagnosis of Methionine/Valine Variant Creutzfeldt-Jakob Disease by Protein Misfolding Cyclic Amplification 

Volume 24, Number 7—July 2018 Dispatch

https://wwwnc.cdc.gov/eid/article/24/7/17-2105_article

http://vcjd.blogspot.com/2018/06/diagnosis-of-methioninevaline-variant.html


TUESDAY, JULY 31, 2018 

USA CJD TSE Tables of Cases Examined National Prion Disease Pathology Surveillance Center Cases Examined May 1, 2018

http://prionunitusaupdate.blogspot.com/2018/07/usa-cjd-tse-tables-of-cases-examined.html


USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS 2017 

TUESDAY, DECEMBER 12, 2017 

Bovine Spongiform Encephalopathy BSE TSE Prion (aka mad cow disease) Report December 14, 2017 2017


TUESDAY, DECEMBER 12, 2017 

SCRAPIE TSE PRION UPDATE USA DECEMBER 14, 2017


TUESDAY, DECEMBER 12, 2017 

Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017


TUESDAY, DECEMBER 12, 2017 

Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017


Tuesday, December 12, 2017 

Neuropathology of iatrogenic Creutzfeldt–Jakob disease and immunoassay of French cadaver-sourced growth hormone batches suggest possible transmission of tauopathy and long incubation periods for the transmission of Abeta pathology



Friday, January 10, 2014 

vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ??? 

Greetings Friends, Neighbors, and Colleagues, 

http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/vpspr-sgss-sffi-tse-iatrogenic-by.html


Sunday, June 17, 2018 

Reviews Prion-like Propagation of α-synuclein, Parkinson, and tse prion

http://alpha-synuclein.blogspot.com/2018/06/reviews-prion-like-propagation-of.html


DECEMBER 14, 2017, 20 YEARS POST DOD MOM HEIDENHAIN VARIANT CREUTZFELDT JAKOB DISEASE HVCJD DECEMBER 14, 1997, JUST MADE A PROMISE TO MOM, AND YOU DON'T BREAK PROMISES WITH YOUR MOM, NEVER FORGET, AND NEVER LET THEM FORGET...TERRY S. SINGELTARY SR.

2018

ZOONOSIS UPDATE ON THE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE aka mad cow type disease


During the course of the investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE. 

200 adult animals of interest were determined to have left the index farm. 

Of these 200, APHIS officials determined that 143 had gone to slaughter, two were found alive (one was determined not to be of interest because of its age and the other tested negative), 34 are presumed dead, one is known dead and 20 have been classified as untraceable. 

In addition to the adult animals, APHIS was looking for two calves born to the index animal. 

Due to record keeping and identification issues, APHIS had to trace 213 calves. 

Of these 213 calves, 208 entered feeding and slaughter channels, four are presumed to have entered feeding and slaughter channels and one calf was untraceable.



***> The majority of these animals entered rendering and/or slaughter channels well before the investigation began.

THE USA IS DOING JUST WHAT THE U.K. DID, WHEN THEY EXPORTED THEIR MAD COW DISEASE ALL AROUND THE GLOBE, EXCEPT NOW, THE USDA KNOWS AND HAVE KNOWN WHAT THEY ARE DOING, AND THE OIE IS HAPPY WITH IT...



 O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations 

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). 

Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), 

***is the third potentially zoonotic PD (with BSE and L-type BSE), 

***thus questioning the origin of human sporadic cases. 

We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. 

=============== 

***thus questioning the origin of human sporadic cases*** 

=============== 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. 

============== 
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf 

***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20 


PRION 2016 TOKYO

Saturday, April 23, 2016

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

Taylor & Francis

Prion 2016 Animal Prion Disease Workshop Abstracts

WS-01: Prion diseases in animals and zoonotic potential

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion.. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20


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

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
https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf


Title: Transmission of scrapie prions to primate after an extended silent incubation period) 

*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. 

*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. 

*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. 
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160


***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***

Transmission of scrapie prions to primate after an extended silent incubation period 

Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation

Abstract 

Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.

SNIP...

Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.

The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.

We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.

Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.

The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.

Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.

Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.

Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.

Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.

In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free.. Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.


Singeltary on Scrapie and human transmission way back, see;


ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE

 here is the latest;

 
PRION 2018 CONFERENCE
 
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice 
 
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge). 
 
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. 
 
Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. 
 
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.
 
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
 

 
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
 
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States 
 
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA. 
 
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states.
 
AND ANOTHER STUDY;
 
P172 Peripheral Neuropathy in Patients with Prion Disease 
 
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.
 
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017, AND included 104 patients.
 
SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%), AND THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
 
snip...see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry
 
 

 
Prion 2017 
 
Conference Abstracts CWD 2017 PRION CONFERENCE 
 
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 
 
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 
 
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen 
 
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. 
 
PRION 2017 
 
DECIPHERING NEURODEGENERATIVE DISORDERS 
 
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO 
 
PRION 2017 
 
CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS 
 
*** PRION 2017 CONFERENCE VIDEO 
 
 

 
TUESDAY, JUNE 13, 2017 
 
PRION 2017 CONFERENCE ABSTRACT 
 
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 
 
 
 
SATURDAY, JULY 29, 2017 
 
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC 
 
 
just out CDC...see;

 
Research
 
Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions
 
Marcelo A. BarriaComments to Author , Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell)
 
M. A. Barria et al.
 
ABSTRACT
 
Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form. We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted. 
 

 
Molecular Barriers to Zoonotic Transmission of Prions 
 
Marcelo A. Barria, Aru Balachandran, Masanori Morita, Tetsuyuki Kitamoto, Rona Barron, Jean Manson, Richard Knight, James W. Ironside, and Mark W. Headcorresponding author 
 
snip... 
 
The conversion of human PrPC by CWD brain homogenate in PMCA reactions was less efficient when the amino acid at position 129 was valine rather than methionine. 
 
***Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype. 
 
snip... 
 
However, we can say with confidence that under the conditions used here, none of the animal isolates tested were as efficient as C-type BSE in converting human PrPC, which is reassuring. 
 
***Less reassuring is the finding that there is no absolute barrier to the conversion of human PrPC by CWD prions in a protocol using a single round of PMCA and an entirely human substrate prepared from the target organ of prion diseases, the brain. 
 
 
ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION 

10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question... 

''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II)

EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors 

First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132 ;

also, see; 

8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available. 

snip... 

The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure. 
https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132


zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm 

***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116*** 
https://www.tandfonline.com/doi/pdf/10.4161/pri.29237
 

To date there is no direct evidence that CWD has been or can be transmitted from animals to humans. 

However, initial findings from a laboratory research project funded by the Alberta Prion Research Institute (APRI) and Alberta Livestock Meat Agency (ALMA), and led by a Canadian Food Inspection Agency (CFIA) scientist indicate that CWD has been transmitted to cynomolgus macaques (the non-human primate species most closely related to humans that may be used in research), through both the intracranial and oral routes of exposure. 

Both infected brain and muscle tissues were found to transmit disease. 

Health Canada’s Health Products and Food Branch (HPFB) was asked to consider the impact of these findings on the Branch’s current position on CWD in health products and foods. 

Summary and Recommendation: 

snip...

Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle. 

These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle. 
https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf


*** WDA 2016 NEW YORK *** 

We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. 

In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. 

***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. 

Student Presentations Session 2 

The species barriers and public health threat of CWD and BSE prions 

Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University 

Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. 

These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. 

The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. 

We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. 

We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. 

***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf
 

CDC CWD 2018 TRANSMISSION
https://www.cdc.gov/prions/cwd/transmission.html


TUESDAY, SEPTEMBER 12, 2017 

CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat 
http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html


SATURDAY, JANUARY 27, 2018 

CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html


Subject: CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018

CHRONIC WASTING DISEASE CWD TSE PRION IS THE USA AND NORTH AMERICA'S MAD COW DISEASE. 

THE USDA INC ET AL WORKED VERY HARD CONCEALING BSE TSE PRION IN CATTLE. they almost succeeded $$$

BUT CWD TSE PRION IN CERVIDS IS A DIFFERENT BEAST, THE COVER UP THERE, USDA INC COULD NOT CONTAIN.

SPORADIC CJD IS 85%+ OF ALL HUMAN TSE PRION DISEASE.

SPORADIC CJD HAS NOW BEEN LINKED TO TYPICAL AND ATYPICAL BSE, SCRAPIE, AND CWD.

SPORADIC/SPONTANEOUS TSE HAS NEVER BEEN PROVEN.

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
https://www.nature.com/articles/srep11573 


CDC CWD TSE PRION UPDATE USA JANUARY 2018

As of January 2018, CWD in free-ranging deer, elk and/or moose has been reported in at least 22 states in the continental United States, as well as two provinces in Canada. In addition, CWD has been reported in reindeer and moose in Norway, and a small number of imported cases have been reported in South Korea. The disease has also been found in farmed deer and elk. CWD was first identified in captive deer in the late 1960s in Colorado and in wild deer in 1981. By the 1990s, it had been reported in surrounding areas in northern Colorado and southern Wyoming. Since 2000, the area known to be affected by CWD in free-ranging animals has increased to at least 22 states, including states in the Midwest, Southwest, and limited areas on the East Coast.. It is possible that CWD may also occur in other states without strong animal surveillance systems, but that cases haven’t been detected yet. Once CWD is established in an area, the risk can remain for a long time in the environment. The affected areas are likely to continue to expand. Nationwide, the overall occurrence of CWD in free-ranging deer and elk is relatively low. However, in several locations where the disease is established, infection rates may exceed 10 percent (1 in 10), and localized infection rates of more than 25 percent (1 in 4) have been reported. The infection rates among some captive deer can be much higher, with a rate of 79% (nearly 4 in 5) reported from at least one captive herd. As of January 2018, there were 186 counties in 22 states with reported CWD in free-ranging cervids.. 

Chronic Wasting Disease Among Free-Ranging Cervids by County, United States, January 2018 

snip.... 
https://www.cdc.gov/prions/cwd/occurrence.html


*** 2017-2018 CWD TSE Prion UPDATE
https://www.cdc.gov/prions/cwd/occurrence.html


*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. 
http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf


Transmission Studies

Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}...TSS

resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.

snip...
https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf


Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ 

Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations

In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
http://jvi.asm.org/content/83/18/9608.full


Prions in Skeletal Muscles of Deer with Chronic Wasting Disease 

Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
http://science.sciencemag.org/content/311/5764/1117.long


*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.

see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”

From: TSS (216-119-163-189.ipset45.wt.net)

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

Date: September 30, 2002 at 7:06 am PST

From: "Belay, Ermias"

To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

Sent: Monday, September 30, 2002 9:22 AM

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Dear Sir/Madam,

In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

Ermias Belay, M.D. Centers for Disease Control and Prevention

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

From: Sent: Sunday, September 29, 2002 10:15 AM

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.

snip...

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

snip... full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html

> However, to date, no CWD infections have been reported in people. 

key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry 

*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** 
http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys
http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true
https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article


SEE; Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Monday, May 23, 2011

CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning

Public release date: 23-May-2011

Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier Health Sciences

CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or “Mad Cow Disease”), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.

“While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases,” commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta.”But it’s also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents.”

Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.

CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.

Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.

The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.

The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.

According to Abrams, “The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health.”

###

The article is “Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey” by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.

In an accompanying podcast CDC’s Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast.
http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php


Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD

Accepted 15 November 2010. Abstract Full Text PDF References .

Abstract

The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.
http://www.adajournal.org/article/S0002-8223(11)00278-1/abstract


PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ; 

Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html


NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;

Wednesday, March 18, 2009

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html

 
Transmissible Spongiform Encephalopathies

Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY
https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf


BSE INQUIRY

CJD9/10022

October 1994

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane 

BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf


*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***

*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***

*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

snip...

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

snip...

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

snip...

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

snip...see full report ;
https://web.archive.org/web/20170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf

 
TUESDAY, JULY 31, 2018 

USA CJD TSE Tables of Cases Examined National Prion Disease Pathology Surveillance Center Cases Examined May 1, 2018

http://prionunitusaupdate.blogspot.com/2018/07/usa-cjd-tse-tables-of-cases-examined.html


HUMAN MAD COW DISEASE nvCJD TEXAS CASE NOT LINKED TO EUROPEAN TRAVEL CDC
Sunday, November 23, 2014

Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas

Updated: October 7, 2014

CDC and the Texas Department of State Health Services (DSHS) have completed the investigation of the recently reported fourth vCJD case in the United States. It confirmed that the case was in a US citizen born outside the Americas and indicated that the patient's exposure to the BSE/vCJD agent most likely occurred before he moved to the United States; the patient had resided in Kuwait, Russia and Lebanon. The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.

https://www.cdc.gov/ncidod/dvrd/vcjd/other/confirmed-case-in-texas.htm

https://vcjd.blogspot.com/2014/11/confirmed-variant-creutzfeldt-jakob.html
TUESDAY, SEPTEMBER 4, 2018 

USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS September 4, 2018



Terry S. Singeltary Sr.
Posted by at

No comments:

Post a Comment

Subscribe to: Post Comments (Atom)