Thursday, November 12, 2020

Armour hormones, pigs, cows, BSE, CWD, Scrapie, TSE, Prion, from the frying pan and into the skillet

Armour hormones, pigs, cows, BSE, CWD, Scrapie, TSE, Prion, from the frying pan and into the skillet

CJD FOUNDATION VIRTUAL CONFERENCE CJD Foundation Research Grant Recipient Reports Panel 2 Nov 3, 2020

zoonotic potential of PMCA-adapted CWD PrP 96SS inoculum


4 different CWD strains, and these 4 strains have different potential to induce any folding of the human prion protein. 


***> PIGS, WILD BOAR, CWD <***

***> POPULATIONS OF WILD BOARS IN THE UNITED STATES INCREASING SUPSTANTUALLY AND IN MANY AREAS WE CAN SEE  A HIGH DENSITY OF WILD BOARS AND HIGH INCIDENT OF CHRONIC WASTING DISEASE

HYPOTHOSIS AND SPECIFIC AIMS

HYPOTHOSIS 

BSE, SCRAPIE, AND CWD, EXPOSED DOMESTIC PIGS ACCUMULATE DIFFERENT QUANTITIES AND STRAINS OF PRIONS IN PERIPHERAL TISSUES, EACH ONE OF THEM WITH PARTICULAR ZOONOTIC POTENTIALS


Final Report – CJD Foundation Grant Program A. 

Project Title: Systematic evaluation of the zoonotic potential of different CWD isolates. Principal Investigator: Rodrigo Morales, PhD.


Systematic evaluation of the zoonotic potential of different CWD isolates. Rodrigo Morales, PhD Assistant Professor Protein Misfolding Disorders lab Mitchell Center for Alzheimer’s disease and Related Brain Disorders Department of Neurology University of Texas Health Science Center at Houston Washington DC. July 14th, 2018

Conclusions and Future Directions • We have developed a highly sensitive and specific CWD-PMCA platform to be used as a diagnostic tool. • Current PMCA set up allow us to mimic relevant prion inter-species transmission events. • Polymorphic changes at position 96 of the prion protein apparently alter strain properties and, consequently, the zoonotic potential of CWD isolates. • Inter-species and inter-polymorphic PrPC → PrPSc conversions further increase the spectrum of CWD isolates possibly present in nature. • CWD prions generated in 96SS PrPC substrate apparently have greater inter-species transmission potentials. • Future experiments will explore the zoonotic potential of CWD prions along different adaptation scenarios, including inter-species and inter-polymorphic.



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 - Orise Fellow item Kunkle, Robert item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item SMITH, JODI - Iowa State University item KANTHASAMY, ANUMANTHA - Iowa State University item WEST GREENLEE, M - Iowa State University 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 month challenge groups). The remaining pigs (>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 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 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.



Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research

Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP 

Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.

Interpretive Summary:

Technical Abstract: We have previously shown that the chronic wasting disease (CWD) agent from white-tailed deer can be transmitted to domestic pigs via intracranial or oral inoculation although with low attack rates and restricted PrPSc accumulation. The objective of this study was to assess the potential for cross-species transmission of pig-passaged CWD using bioassay in transgenic mice. Transgenic mice expressing human (Tg40), bovine (TgBovXV) or porcine (Tg002) PRNP were inoculated intracranially with 1% brain homogenate from a pig that had been intracranially inoculated with a pool of CWD from white-tailed deer. This pig developed neurological clinical signs, was euthanized at 64 months post-inoculation, and PrPSc was detected in the brain. Mice were monitored daily for clinical signs of disease until the end of the study. Mice were considered positive if PrPSc was detected in the brain using an enzyme immunoassay (EIA). In transgenic mice expressing porcine prion protein the average incubation period was 167 days post-inoculation (dpi) and 3/27 mice were EIA positive (attack rate = 11%). All 3 mice were found dead and clinical signs were not noted prior to death. One transgenic mouse expressing bovine prion protein was euthanized due to excessive scratching at 617 dpi and 2 mice culled at the end of the study at 700 dpi were EIA positive resulting in an overall attack rate of 3/16 (19%). None of the transgenic mice expressing human prion protein that died or were euthanized up to 769 dpi were EIA positive and at study end point at 800 dpi 2 mice had positive EIA results (overall attack rate = 2/20 = 10%). The EIA optical density (OD) readings for all positive mice were at the lower end of the reference range (positive mice range, OD = 0.266-0.438; test positive reference range, OD = 0.250-4.000). To the authors’ knowledge, cervid-derived CWD isolates have not been successfully transmitted to transgenic mice expressing human prion protein. The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.


cwd scrapie pigs oral routes 

***> 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. <*** 

***> 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 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 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. 




Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation 

 S. Jo Moore1,2, M. Heather West Greenlee3, Naveen Kondru3, Sireesha Manne3, Jodi D. Smith1, Robert A. Kunkle1, Anumantha Kanthasamy3 and Justin J. Greenlee1* + Author Affiliations 

 1Virus and Prion Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, Ames, Iowa, United States of America 2Oak Ridge Institute for Science and Education, Oak Ridge, Tennessee, United States of America 3Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, Iowa, United States of America

ABSTRACT

Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting 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. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled (‘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 western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from one or more pigs in each inoculated group. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high. However, 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.

IMPORTANCE We challenged domestic swine with the chronic wasting disease agent by inoculation directly into the brain (intracranially) or by oral gavage (orally). Disease-associated prion protein (PrPSc) was detected in brain and lymphoid tissues from intracranially and orally inoculated pigs as early as 8 months of age (6 months post-inoculation). Only one pig developed clinical neurologic signs suggestive of prion disease. The amount of PrPSc in the brains and lymphoid tissues of positive pigs was small, especially in orally inoculated pigs. Regardless, positive results in orally inoculated pigs suggest that it may be possible for swine to serve as a reservoir for prion disease under natural conditions.

FOOTNOTES

↵*Corresponding author: Email: justin.greenlee@ars.usda.gov This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply.


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.....


SOME HISTORY ON BSE AND PIGS AND PHARMACEUTICALS

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.
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
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...
It was not until . . . August 1990, that the result from the pig persuaded both SEAC and us to change our view and to take out of pig rations any residual infectivity that might have arisen from the SBOs.
4.303 The minutes of the meeting record that:
It was very difficult to draw conclusions from one experimental result for what may happen in the field. However it would be prudent to exclude specified bovine offals from the pig diet. Although any relationship between BSE and the finding of a spongiform encephalopathy in cats had yet to be demonstrated, the fact that this had occurred suggested that a cautious view should be taken of those species which might be susceptible. The 'specified offals' of bovines should therefore be excluded from the feed of all species. 17
IN CONFIENCE
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought igs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. ...see full text ;
IN CONFIDENCE
So it is plausible pigs could be preclinically affected with BSE but since so few are allowed to reach adulthood this has not been recognised through clinical disease. ...
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.
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
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.....
BSE TO PIGS NEWS RELEASE
CONFIDENTIAL
BSE: PRESS PRESENTATION
INDUSTRY RESPONSE TYPICAL
DEFENSIVE BRIEFING
CONFIDENTIAL
pigs & pharmaceuticals
COMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUP
There are only two products using porcine brain and these use corticotrophin BP, made from porcine pituitary, source from outside the UK.............
snip...
7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;
1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,
The neuropathology of experimental bovine spongiform encephalopathy in the pig.
Ryder SJ, Hawkins SA, Dawson M, Wells GA.
Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.
In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.
PMID: 10684682 [PubMed - indexed for MEDLINE]
snip...
In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility.
see full text and more transmission studies here ;
Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie.
Emerg Infect Dis. 2009 Aug; [Epub ahead of print]
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


desiccated bovine thyroid (Armour Thyroid) 

desiccated porcine thyroid (Armour Thyroid) 

tse prion, what if?

ARMOUR THYROID- thyroid, porcine tablet 
PD-Rx Pharmaceuticals, Inc.

snip...

WARNINGS

Drugs with thyroid hormone activity, alone or together with other therapeutic agents, have been used for the treatment of obesity. In euthyroid patients, doses within the range of daily hormonal requirements are ineffective for weight reduction. Larger doses may produce serious or even life-threatening manifestations of toxicity, particularly when given in association with sympathomimetic amines such as those used for their anorectic effects.

The use of thyroid hormones in the therapy of obesity, alone or combined with other drugs, is unjustified and has been shown to be ineffective. Neither is their use justified for the treatment of male or female infertility unless this condition is accompanied by hypothyroidism.

The active ingredient (desiccated natural thyroid) in Armour Thyroid (thyroid tablets, USP) is derived from porcine (pig) thyroid glands of pigs processed for human food consumption and is produced at a facility that also handles bovine (cow) tissues from animals processed for human food consumption.  As a result, a potential risk of product contamination with porcine and bovine viral or other adventitious agents cannot be ruled out. Forest is not aware of any cases of disease transmission associated with the use of Armour ® Thyroid (thyroid tablets, USP).

https://dailymed.nlm.nih.gov/dailymed/fda/fdaDrugXsl.cfm?setid=c815faa3-1d02-4680-96ef-5fad1645e99b&type=display


Import Alert 17-04

(Note: This import alert represents the Agency's current guidance to FDA field personnel regarding the manufacturer(s) and/or products(s) at issue. It does not create or confer any rights for or on any person, and does not operate to bind FDA or the public).

Import Alert # 17-04

Published Date: 03/18/2011

Type: DWPE

Import Alert Name:

"Detention Without Physical Examination Bulk Shipments of High-Risk Bovine Tissue from BSE-Countries--Bovine Spongiform Encephalopathy"

snip...

We strongly recommend that firms manufacturing or importing dietary supplements which contain specific bovine tissues (see appendix A), including extracts or substances derived from such tissues, take whatever steps are necessary to assure themselves and the public that such ingredients do not come from cattle born, raised, or slaughtered in countries where BSE exists.

FDA believes that immediate and concrete steps should be taken by manufacturers to reduce the potential risk of human exposure to the infectious agent which causes BSE in cattle.

The list of countries where BSE is known to exist is maintained by the U.S. Department of Agriculture (USDA) and codified in Title 9, Code of Federal Regulations, Part 94.18. The following is the current list:

USDA LIST OF COUNTRIES WHERE BSE EXISTS

(Current as of May 1996)

Great Britain (including Northern Ireland and the Falklands)

Switzerland

France

Republic of Ireland

Oman

Portugal

A range of research projects into the exact nature of both the BSE agent and other TSE agents is ongoing. Available scientific information indicates that these agents are extremely resistant to inactivation by normal disinfection or sterilization procedures. A number of dietary supplement products use bovine-derived tissues or extracts of such tissues as ingredients. These ingredients include, for example, specific tissues and organs or their extracts (e.g., liver powder, "orchic" extracts, ovaries, eye tissue, mammary tissue), glandular powders or extracts (e.g., adrenal gland, thyroid gland), or specific substances extracted from glands or tissues (e.g., melatonin extracted from the pineal gland).

At a future date, we will contact you with guidance on how best to provide assurance that your products do not contain potentially BSE-infected materials.

We appreciate your attention to and cooperation in this matter. If you need more information, please contact Dr. Elisa Elliot by telephone at (202)

205-5140.

Sincerely yours,

/s/

Michael A. Friedman, M.D.

Deputy Commissioner for Operations

Enclosure Appendix A

List of Tissues With Suspected Infectivity

snip...


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.....


i have been concerned about this and nutritional supplements and the tse prion for decades...see;

years ago, ARMOUR use to sell a BOVINE based thyroid drug. i don't believe they sell it anymore. i think it was called thylar or something. wonder how many women used that one ??? its documented in the voice archive years back somewhere. ...terry

Q. The Claim: Synthroid is the Best Thyroid Hormone Replacement Drug

If you are hypothyroid, your doctor will probably prescribe Synthroid. This levothyoxine (synthetic thyroxine) drug, made by Abbott Labs, is the top-selling thyroid drug in the U.S., commanding some two-thirds of the market for thyroid replacement. Synthroid is, however, often more costly than its competitors. Some doctors won't hear of prescribing anything but Synthroid however, and claim unequivocally that "Synthroid is the best." Is That So? A. Levothyroxine is the synthetic form of T4, one of the two main hormones the thyroid produces. The most widely prescribed levothyroxine product is the brand name Synthroid. Given that levothyroxine is the conventional medical world's accepted treatment for hypothyroidism, most patients will find themselves prescribed

levothyroxine, and usually Synthroid. Synthroid's manufacturer has at times claimed their drug to be better than its competitors, but research proved Synthroid to be merely bioequivalent -- or equal, in terms of what function they perform in the body -- to their competition, rather than better. This claim of superiority, therefore, actually has no merit. Many doctors, however, still erroneously believe that Synthroid is "better," after being subject to years of this misleading advertising message. All the major brandname levothyroxine products, Synthroid, Unithroid, Levoxyl and Levothroid, have different fillers and binders, so people may have different allergic responses to the different brands.

http://pagead2.googlesyndication.com/


So, if you react to one levothyroxine, your doctor might want to try other brands to see if you react to those brands as well.

Some people who are on levothyroxine also need the addition of the second key hormone, T3. Among that group, some people do best with the T3 drug Cytomel. Anecdotally, however, some patients have reported allergic reactions to Cytomel. The option, compounded or time-released compounded T3, has been used successfully by other patients, but there have been concerns about these products, due to inconsistent production. Other doctors and patients prefer a product known as Thyrolar, a synthetic combination of T4 and T3. Some patients do best on natural desiccated thyroid drugs, such as Armour thyroid, or, in some cases, people find the hypoallergenic formula of natural drug, Nature-throid, works best for them. (Pork allergies, however, may make these products problematic for some patients. There are some patients and practitioners who are also concerned about these products due to fears of prion-related diseases such as Mad Cow Disease, despite manufacturer assurances that these products are safe.) So is Synthroid, or any thyroid drug, better than the others? I think Dr. Richard Shames, a Boca Raton, Florida holistic practitioner and co-author of Thyroid Power and Fat, Fuzzy and Frazzled? -- who has treated thyroid conditions for a quarter century -- has the best advice for patients. "In 25 years of practice, I have found that it doesn't necessarily matter which kind of thyroid hormone you start with so much, as which kind you end up with after trying several different types to see which one works best for you. Initially, I typically recommend whatever type they have either heard about, have a "gut-feeling" about, know family members who have a good response to a particular kind of medicine, or have a philosophical inclination for one kind or another. Sometimes it it the combination of two or three of the above medicines that proves to be the magic solution for a particular person. If the initial item tried does not give 85-95% improvement, I then encourage the person to either add something to their first choice product or discontinue it and start something totally new. It is my firm belief that the state of the art in finding the optimal medicine is still trial and error." The answer is, the best drug is the drug which safely makes you feel your best. And there's no predetermined formula to tell which drug will be the best for you, until you try them, find optimal doses, and see how you do over time.

Mary Shomon, About.com's Thyroid Guide since 1997, is a nationally-known patient advocate and best-selling author of 10 books on health, including "The Thyroid Hormone Breakthrough: Overcoming Sexual and Hormonal Problems at Every Age," "The Thyroid Diet: Manage Your Metabolism for Lasting Weight Loss," "Living Well With Hypothyroidism: What Your Doctor Doesn't Tell You...That You Need to Know," "Living Well With Graves' Disease and Hyperthyroidism," "Living Well With Autoimmune Disease," and "Living Well With Chronic Fatigue Syndrome and Fibromyalgia." Click _here_


(http://thyroid.about.com/mbiopage.htm)


for more information on Mary Shomon.

From: Terry S. Singeltary Sr. (wt-d4-166.wt.net) Subject: Re: THYROID MEDICATION, PIGS , PIG FEED, AND MADCOW Date: August 16, 1998 at 14:14:48 EST

In Reply to: THYROID MEDICATION, PIGS , PIG FEED, AND MADCOW posted by Terry S. Singeltary Sr. on July 28, 1998 at 14:12:38:

I am having a hard time getting information on ingrediants of these drugs. Nobody wants to cooperate. Although I have found the names and ingrediants of some with DESICCATED ANIMAL (T4/T3). ARMOUR Thyroid tablets for oral use are natural preparations derived from porcine (Pork) thyroid glands. From the late 1890's until relatively recently, physicians worldwide have treated hypothroid patients with tablets containing desiccated (dried and powdered) animal thyroid glands. These tablets contained both levothyroxine (T4) and triiodothyronine (T3). In 1958, the first synthetic levothyroxine tablets were marketed in the United States. Because thyroid hormones were on the market before the Food and Drug Admimistration (FDA) laws were in place, manufacturers of these hormones were not required to meet the extensive testing requirements of safety and effectiveness required of all new drugs introduced after 1938. In other words, thyroid hormone replacements, such as synthetic levothyroxine, were "GRANDFATHERED" into the system, consequently, there are no FDA approved procedures or standards for testing these preparations other than specifying that each pill contain betwee 90% to 110% of the standard chemical content. Also Thyrolar contains synthetic T3. There is also Cytomel. I believe all these contain desiccated animal. I am still searching. Maybe the Thyroid Society could find time to list these drugs and their Ingrediants. None of the Drug company's will cooperate. You start talking about dessicated animals in these drugs and asking for ingrediants from people and they lose their tounge./

MADCOWDEADMOMMADSON/TERRY

PLUS, ARMOUR MADE A BOVINE THYROID MEDICATION SOME TIME BACK CALLED "THYRAR" MADE FROM DESSICATED BOVINE THYROID GLAND...

Subject: Mad Cow / Mad Pig and Thyroid Risks Date: November 10, 2000 at 2:24 pm PST Mad Cow / Mad Pig and Thyroid Risks

Could food supplements and medications be inadvertent media for the spread of prion based brain diseases? Multiple sources would suggest this is possible, even likely, due to the use of animal gelatins. This probability goes up even more when the medication itself is a glandular extract.

Importance

BSE / Mad Cow / TSE (Transmissible Spongiform Encephalopathies) are NOT a small topic!

Nobel Prize awarded to Carleton Gajdusek for Kuru/TSE research Nobel Prize awarded to Stanley Prusiner for TSE/Prion research Pulitzer prize winning author Richard Rhodes wrote "Deadly Feasts" on the controversy ISBN 0-684-84425-7 (Mentioned on 259 web pages) Oprah dedicated a show to BSE/Mad Cow, was sued by Texas cattlemen, Courts upheld her 1st Amendment right to Freedom of Speech! Cows, Sheep, Pigs, Mink, Humans have all caught and died of TSE's Prions can not be killed by mere boiling or cooking Over 200,000 deaths/year by 2015 predicted by Prof. Lacey (below) Over 30,700 web pages mention Mad Cow (AltaVista) Web pages on Chaperonins, chemicals possibly preventing the mis-folding of proteins which are the basis for TSE's and Alzheimer's, jumped from 2 to over 6,000 in one year!

Clearly, Transmissible Spongiform Encephalopathies, such as BSE and CJD (one human form,) are a topic of some controversy, one we should all become more aware of.

Mad Cow Censorship

Some questions were raised on the Thyroid mailing list out of StJohns.EDU regarding where the various natural thyroid supplements come from, and how safe they may be with respect to Mad Cow Disease. The basic text of this article was conveniently "discarded" by the moderator, as it seems are a number posts questioning the safety of natural thyroid extracts, or discussing non-prescription alternatives to them. Such pro-prescription medication biases are not new to certain moderated mailing lists... some of which may be rabidly pro something, others against, at the whims of biased or subsidized moderators. (The biases of that list are mild, compared to some other lists, such as an ozone list several years back.) Always look for biases when considering internet, and any other information sources.

Researchers on BSE / TSE say this kind of censorship is not new. Dr. Harash Narang, a British microbiologist and CJD researcher, says he first detected variant CJD in humans back in 1988. He claims that he was ordered to stop work on BSE in 1990, and subsequently "laid off". He believes that British authorities have blocked and undermined such research and detection efforts. (British press articles)

Thyroid Supplements and Mad Cow / BSE

There are natural thyroid extracts, such as Armour Thyroid, and synthetics such as Cytomel and Synthroid. The natural ones are taken from the thyroid glands of animals, such as pigs.

On page 220 of Rhodes' book, Nobel Price winner Dr. Carleton Gajdusek is quoted saying pigs are routinely slaughtered before the disease would become evident in them. Carleton Gajdusek is one of the foremost researchers of Kuru and other "Transmissible Spongiform Encephalopathies", TSE, of which Bovine Spongiform Encephalopathy, Scrapie, CJD, and Kuru are variants.

In the book, Dr. Gajdusek is quoted: "the disease hasn't turned up in pigs only because you don't keep pigs alive for seven or eight years; they're killed after two or three years at the most. When we kept pigs we'd inoculated in our laboratory for eight years, they came down with scrapie. [a TSE variant] Probably all the pigs in England are infected. And that means not only pork, it means your pigskin wallet. It means catgut surgical suture, because that's made of pig tissue. All the chickens fed on meat-and-bone meal; they're probably infected. You put that stuff in a chicken and it goes right through"... And in America, beef cattle are killed at or before age two, before they are likely to show outward symptoms. (Page 228)

Mad Cow in America

In America, chicken excreta is fed to cattle as a good source of nitrogen. (Page 258.) As for the American FDA's ban on feeding meat and animal by-products to cattle, Rhodes writes "That's a ban with exclusions big enough to drive a cortege of hearses through." Their own TSE advisory committee urged the FDA take stronger measures. (Page 257.)

According to the book, Bovine Spongiform Encephalopathy has been detected in America, and not just in cattle; the American form is yet another variant TSE, which does not cause the staggers and other behaviors found in British cattle, but results in a more "sedate" collapse of the victim, referred to as "downer cattle". The nature of the brain damage is also distinct; a spongiform with differently shaped and oriented vacancies. Other forms have been transmitted via eating wild squirrels, and wild bear. Some zoos have lost animals to TSE's.

Human Epidemic

Dr. John Pattison, Chairman of the British government's Spongiform Encephalopathy Advisory Committee (SEAC), Dean of the University College of London Medical School, believes 500,000 people may already be incubating CJD in Britain. [Dr. Alsleben.] Dr. Alsleben, in his excellent Mad Cow web site, states that prions can be found in white blood cells contaminating milk, and even in the animal grease used in lipstick. (URL at end) Professor Richard Lacey of the Microbiology Department of Chapel Allerton Hospital, Leeds, points out on page 222 of the book that "there was no certainty that the source of infection had been cut off."... "'If it seems that the incubation-period average for CJD in humans begins to be about twenty five years, maybe thirty years,' he told me grimly, 'then the peak human epidemic will come around the year 2015. If the current numbers of variant CJD cases [the main human TSE,] increases by fifty percent per year compound, as they well might, that would take it to about two hundred thousand cases a year by then'. Human cases, that is 200,000 deaths per year" (In Britain.)

Others suggest that 5% OR MORE of the Alzheimer's cases in America may be due to CJD and other TSE variants. If so, are we already seeing the beginning of a growing tide of TSE related deaths?

Limiting Factors

It is noted that amongst the Fore, the cannibals who got kuru, another TSE variant similar to CJD, only some one percent of the population seemed affected.

This one percent figure suggests a genetic bias, and some genetic biases have been detected. This may serve as a model for predicting human death rates. Evidence suggest a one in a million rate of spontaneous occurrence among susceptible species. Once inserted into a food chain that recycles animal protein, one in a hundred may get it.

In America, that one percent would translate to well over two and a half million slow, expensive deaths, a far worse epidemic

than AIDS! But... not the end of civilization as we know it.

One is reminded that there have been many plagues in human history; plagues like the Black Plague, the Justinian Plague, and many others. Humanity has thus far survived, even if reduced in numbers. No need to panic; just act wisely.

Prions and Counters

Several Prion variants have been found, some of which act quickly, some of which act far more slowly, so the 25 year estimate may be considerably off. There is also recent research on chaperonins, biochemicals that assist in folding proteins, which may be related to resistance to prion diseases. (Prion diseases are believed to involve folding of proteins, and what is similar to crystal growth of the mis-folded proteins.) See http://www.mad-cow.org/ and look up chaperonin at http://www.AltaVista.Digital.com , a term that only had two pages on the web last year, and now has over six thousand!

Will we find a cure for Spongiform Encephalopathy? Unlikely, since the spongiform phase is caused by massive death of neural tissue; tissue which can not regrow. That said, we might yet find ways of preventing the degeneration where it has not already occurred. So caution might be well advised.

Incubation

Twenty five years incubation time is a long time.... If one ends up with thyroid supplements in one's late thirties, it might be age 65 when some of the more noticeable effects begin to become evident. Those with less resistant genetics may display effects much sooner. Others may die of other dis-eases before the effects of TSE would become clearly visible. And most... may even avoid coming down with the disease.

And yet... Science News ran an article on Alzheimer's research in which some researchers claimed they could often detect the condition decades early simply by noting the manner of speech and writing of a person. People with pre-Alzheimer's conditions seem to rely more on lists and relationships, than logic and cause-and-effect reasoning about the world. They also tend to write shorter, simpler sentences long before clinical neurological deficits become evident. (Research was done using nuns, comparing their original statements of intent to become nuns, with their conditions decades later.)

Is Alzheimer's a form of TSE? Some would say yes, others would say no. And still others have suggested many cases of Alzheimer's are really TSE, but not all. The lesions in the brain are similar, but not identical.

Weigh the Risks

We must all weigh risks v.s. benefits ourselves. I am not a doctor, I can not advise you; you have to think for yourself. Like Oprah, I have stopped eating beef; as well as all other animal meats and animal products like gelatin. I dump the contents of all my gelatin capsules into a spoon, and discard the empty capsules. I also avoid "ranched" fish like catfish and salmon. Is that enough? I don't know. With luck, I may never find out.

A one percent rate sounds considerably better than other estimates I have run across. However, the real question I have is, what are the subtle effects long before the final destruction? If these prions are indeed the rod-like structures researcher Patricia Merz describes on page 156, then they would likely impede cellular machinery long before they became long enough to break cell membranes and kill the cells. Thus it is possible that long before that final break, subtle neurological effects could

become evident. Dr. Merz findings of prions in spleen tissue and elsewhere is quite disturbing, as it suggests prions may travel freely in the blood of these animals, and thus would imply that all tissue is likely to harbor some prions, not just brain tissue. Thus, over 25 million of us may be at grave risk to our health; and our relatives, at risk for extreme emotional and financial stresses as they contribute to our care as we slowly go mad and die of CJD.

Your health is your responsibility, not your doctor's. It is you who must decide what behaviors, and risks, are acceptable to you.

Books and Resources

"Deadly Feasts", by Pulitzer prize winner Richard Rhodes. ISBN0-684-84425-7. Worth reading! http://www.mad-cow.org/ Mentioned by Rhodes as a valuable current record on this developing topic. Dr. Harry Alsleben, a preventative medicine researcher, calls this "Our Greatest Biological Catastrophe", His excellent web site is dedicated to warning people about prion diseases; and exposing the policies that warn "officials", while attempting to minimize public concerns and short term financial impact to industry. What is more, he use to sell animal collagen products. He stopped and accepted the financial loss when he learned about BSE. I salute him for his responsible actions. Resources from PBS - Nova The Brain Eaters episode on Mad Cow disease. (Presumably, this site will not be up forever.)

http://www.mall-net.com/mcs/madcow.html

From: Terry S. Singeltary Sr. (wt-d4-166.wt.net) Subject: Re: THYROID MEDICATION, PIGS , PIG FEED, AND MADCOW Date: August 16, 1998 at 14:14:48 EST

In Reply to: THYROID MEDICATION, PIGS , PIG FEED, AND MADCOW posted by Terry S. Singeltary Sr. on July 28, 1998 at 14:12:38:

I am having a hard time getting information on ingrediants of these drugs. Nobody wants to cooperate. Although I have found the names and ingrediants of some with DESICCATED ANIMAL (T4/T3). ARMOUR Thyroid tablets for oral use are natural preparations derived from porcine (Pork) thyroid glands. From the late 1890's until relatively recently, physicians worldwide have treated hypothroid patients with tablets containing desiccated (dried and powdered) animal thyroid glands. These tablets contained both levothyroxine (T4) and triiodothyronine (T3). In 1958, the first synthetic levothyroxine tablets were marketed in the United States. Because thyroid hormones were on the market before the Food and Drug Admimistration (FDA) laws were in place, manufacturers of these hormones were not required to meet the extensive testing requirements of safety and effectiveness required of all new drugs introduced after 1938. In other words, thyroid hormone replacements, such as synthetic levothyroxine, were "GRANDFATHERED" into the system, consequently, there are no FDA approved procedures or standards for testing these preparations other than specifying that each pill contain betwee 90% to 110% of the standard chemical content. Also Thyrolar contains synthetic T3. There is also Cytomel. I believe all these contain desiccated animal. I am still searching. Maybe the Thyroid Society could find time to list these drugs and their Ingrediants. None of the Drug company's will cooperate. You start talking about dessicated animals in these drugs and asking for ingrediants from people and they lose their tounge./MADCOWDEADMOMMADSON/TERRY

PLUS, ARMOUR MADE A BOVINE THYROID MEDICATION SOME TIME BACK CALLED "THYRAR" MADE FROM DESSICATED BOVINE THYROID GLAND...

TSS

WONDER if any of our loved ones had taken "THYRAR" ??? (way back)

don't ask, don't find, cjd questionnaire. .............TSS



Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;

Some unofficial information from a source on the inside looking out -

Confidential!!!!

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

---end personal email---end...tss

5. DESCRIBING APHIS' intent to amend the regulations to define susceptible species based on scientific evidence of natural infection or experimental infections through natural routes and adding the genera Rangifer and Muntiacus to the list of susceptible species...

WELL, THAT WOULD BE A START, especially with Norway CWD and Reindeer there naturally in the field, and muntiacus reefesi in the lab, ORALLY, BUT, WHAT ABOUT HUMANS AND PIGS ??? cwd transmits to the macaque in the lab, orally, by muscle meat, infected with cwd, and CWD HAS TRANSMITTED TO PIGS, orally, in the lab. so, do we continue to roll the dice there with human life? if so, why? and what about feed? pigs are still allowed in the feed, along with cwd risk deer. absolutely crazy imo. let's see what DEFRA/MAFF have to say about this;

SNIP...SEE SINGELTARY FULL TEXT SUBMISSION HERE;



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..... 


***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; 

BSE TESTING (failed terribly and proven to be a sham) 

BSE SURVEILLANCE (failed terribly and proven to be a sham) 

BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) 

these are facts folks. trump et al just admitted it with the feed ban. 

see; 

FDA Reports on VFD Compliance 

John Maday 

August 30, 2019 09:46 AM VFD-Form 007 (640x427) 

Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.


SUNDAY, SEPTEMBER 1, 2019 

***> FDA Reports on VFD Compliance 


 ***> cattle, pigs, sheep, cwd, tse, prion, oh my! 

***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). 

Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable. 


Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY 

Date: Fri, 18 Oct 2002 23:12:22 +0100 

From: Steve Dealler 

Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member 

To: BSE-L@ References: <3daf5023 .4080804="" wt.net="">

Dear Terry,

An excellent piece of review as this literature is desparately difficult to get back from Government sites.

What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!

Steve Dealler 

=============== 


Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk 

BSE Inquiry Steve Dealler

Management In Confidence

BSE: Private Submission of Bovine Brain Dealler

snip...see full text;

MONDAY, FEBRUARY 25, 2019

***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019


WEDNESDAY, AUGUST 5, 2020 

1996-12-04: BBC - Horizon BSE1 - BSE2 The Invisible Enemy, The British Disease, CWD, sporadic CJD


Cervid to human prion transmission

Kong, Qingzhong 

Case Western Reserve University, Cleveland, OH, United States

Abstract

Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that: (1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; (2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; (3) Reliable essays can be established to detect CWD infection in humans; and (4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.

Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of humanized Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental human CWD samples will also be generated for Aim 3.

Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.

Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental human CWD samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.

Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.

Public Health Relevance

There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.

 Funding Agency

Agency

National Institute of Health (NIH)

Institute

National Institute of Neurological Disorders and Stroke (NINDS)

Type Research Project (R01)

Project # 5R01NS088604-04

Application # 9517118

Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)

Program Officer Wong, May

Project Start 2015-09-30

Project End 2019-07-31

Budget Start 2018-08-01

Budget End 2019-07-31 Support Year 4

Fiscal Year 2018

Total Cost Indirect Cost Institution Name Case Western Reserve University Department Pathology Type Schools of Medicine DUNS # 077758407 City Cleveland State OH Country United States Zip Code 44106

 Related projects

NIH 2018

R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University 

NIH 2017

R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University 

NIH 2016

R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University 

NIH 2015 R01 NS Cervid to human prion transmission

Kong, Qingzhong / Case Western Reserve University $337,507

 Publications

Ashok, Ajay; Karmakar, Shilpita; Chandel, Rajeev et al. (2018) Prion protein modulates iron transport in the anterior segment: Implications for ocular iron homeostasis and prion transmission. Exp Eye Res 175:1-13

Kim, Chae; Xiao, Xiangzhu; Chen, Shugui et al. (2018) Artificial strain of human prions created in vitro. Nat Commun 9:2166 Asthana, Abhishek; Baksi, Shounak; Ashok, Ajay et al. (2017) Prion protein facilitates retinal iron uptake and is cleaved at the ?-site: Implications for retinal iron homeostasis in prion disorders. Sci Rep 7:9600

Orrú, Christina D; Yuan, Jue; Appleby, Brian S et al. (2017) Prion seeding activity and infectivity in skin samples from patients with sporadic Creutzfeldt-Jakob disease. Sci Transl Med 9:

Elezgarai, Saioa R; Fernández-Borges, Natalia; Eraña, Hasier et al. (2017) Generation of a new infectious recombinant prion: a model to understand Gerstmann-Sträussler-Scheinker syndrome. Sci Rep 7:9584

Choi, Jin-Kyu; Cali, Ignazio; Surewicz, Krystyna et al. (2016) Amyloid fibrils from the N-terminal prion protein fragment are infectious. Proc Natl Acad Sci U S A 113:13851-13856

Zhan, Yi-An; Abskharon, Romany; Li, Yu et al. (2016) Quiescin-sulfhydryl oxidase inhibits prion formation in vitro. Aging (Albany NY) 8:3419-3429 Nichols, Tracy A; Spraker, Terry R; Gidlewski, Thomas et al. (2016) Dietary magnesium and copper affect survival time and neuroinflammation in chronic wasting disease. Prion 10:228-50


Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Prion 2017 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 
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 2019 ABSTRACTS 

1. Interspecies transmission of the chronic wasting disease agent

Justin Greenlee

Virus and Prion Research Unit, National Animal Disease Center, USDA Agriculture Research Service

ABSTRACT

The presentation will summarize the results of various studies conducted at our research center that assess the transmissibility of the chronic wasting disease (CWD) agent to cattle, pigs, raccoons, goats, and sheep. This will include specifics of the relative attack rates, clinical signs, and microscopic lesions with emphasis on how to differentiate cross-species transmission of the CWD agent from the prion diseases that naturally occur in hosts such as cattle or sheep. Briefly, the relative difficulty of transmitting the CWD agent to sheep and goats will be contrasted with the relative ease of transmitting the scrapie agent to white-tailed deer.

53. Evaluation of the inter-species transmission potential of different CWD isolates

Rodrigo Moralesa, Carlos Kramma,b, Paulina Sotoa, Adam Lyona, Sandra Pritzkowa, Claudio Sotoa

aMitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept. of Neurology, McGovern School of Medicine University of Texas Health Science Center at Houston, TX, USA; bFacultad de Medicina, Universidad de los Andes, Santiago, Chile

ABSTRACT

Chronic Wasting Disease (CWD) has reached epidemic proportions in North America and has been identified in South Korea and Northern Europe. CWD-susceptible cervid species are known to share habitats with humans and other animals entering the human food chain. At present, the potential of CWD to infect humans and other animal species is not completely clear. The exploration of this issue acquires further complexity considering the differences in the prion protein sequence due to species-specific variations and polymorphic changes within species. While several species of cervids are naturally affected by CWD, white-tailed deer (WTD) is perhaps the most relevant due to its extensive use in hunting and as a source of food. Evaluation of inter-species prion infections using animals or mouse models is costly and time consuming. We and others have shown that the Protein Misfolding Cyclic Amplification (PMCA) technology reproduces, in an accelerated and inexpensive manner, the inter-species transmission of prions while preserving the strain features of the input PrPSc. In this work, we tested the potential of different WTD-derived CWD isolates to transmit to humans and other animal species relevant for human consumption using PMCA. For these experiments, CWD isolates homozygous for the most common WTD-PrP polymorphic changes (G96S) were used (96SS variant obtained from a pre-symptomatic prion infected WTD). Briefly, 96GG and 96SS CWD prions were adapted in homologous or heterologous substrate by PMCA through several (15) rounds. End products, as well as intermediates across the process, were tested for their inter-species transmission potentials. A similar process was followed to assess seed-templated misfolding of ovine, porcine, and bovine PrPC. Our results show differences on the inter-species transmission potentials of the four adapted materials generated (PrPC/PrPSc polymorphic combinations), being the homologous combinations of seed/substrate the ones with the greater apparent zoonotic potential. Surprisingly, 96SS prions adapted in homologous substrate were the ones showing the easiest potential to template PrPC misfolding from other animal species. In summary, our results show that a plethora of different CWD isolates, each comprising different potentials for inter-species transmission, may exist in the environment. These experiments may help to clarify an uncertain and potentially worrisome public health issue. Additional research in this area may be useful to advise on the design of regulations intended to stop the spread of CWD and predict unwanted zoonotic events.

56. Understanding chronic wasting disease spread potential for at-risk species

Catherine I. Cullingham, Anh Dao, Debbie McKenzie and David W. Coltman

Department of Biological Sciences, University of Alberta, Edmonton AB, Canada

CONTACT Catherine I. Cullingham cathy.cullingham@ualberta.ca

ABSTRACT

Genetic variation can be linked to susceptibility or resistance to a disease, and this information can help to better understand spread-risk in a population. Wildlife disease incidence is increasing, and this is resulting in negative impacts on the economy, biodiversity, and in some instances, human health. If we can find genetic variation that helps to inform which individuals are susceptible, then we can use this information on at-risk populations to better manage negative consequences. Chronic wasting disease, a fatal, transmissible spongiform encephalopathy of cervids (both wild and captive), continues to spread geographically, which has resulted in an increasing host-range. The disease agent (PrPCWD) is a misfolded conformer of native cellular protein (PrPC). In Canada, the disease is endemic in Alberta and Saskatchewan, infecting primarily mule deer and white-tail deer, with a smaller impact on elk and moose populations. As the extent of the endemic area continues to expand, additional species will be exposed to this disease, including bison, bighorn sheep, mountain goat, and pronghorn antelope. To better understand the potential spread-risk among these species, we reviewed the current literature on species that have been orally exposed to CWD to identify susceptible and resistant species. We then compared the amino acid polymorphisms of PrPC among these species to determine whether any sites were linked to susceptibility or resistance to CWD infection. We sequenced the entire PrP coding region in 578 individuals across at-risk populations to evaluate their potential susceptibility. Three amino acid sites (97, 170, and 174; human numbering) were significantly associated with susceptibility, but these were not fully discriminating. All but one species among the resistant group shared the same haplotype, and the same for the susceptible species. For the at-risk species, bison had the resistant haplotype, while bighorn sheep and mountain goats were closely associated with the resistant type. Pronghorn antelope and a newly identified haplotype in moose differed from the susceptible haplotype, but were still closely associated with it. These data suggest pronghorn antelope will be susceptible to CWD while bison are likely to be resistant. Based on this data, recommendations can be made regarding species to be monitored for possible CWD infection.

KEYWORDS: Chronic wasting disease; Prnp; wildlife disease; population genetics; ungulates

Thursday, May 23, 2019 

Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts


see full Prion 2019 Conference Abstracts


SATURDAY, FEBRUARY 09, 2019
Experts: Yes, chronic wasting disease in deer is a public health issue — for people
SATURDAY, FEBRUARY 23, 2019 

Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019


TUESDAY, NOVEMBER 04, 2014 

Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011

Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "


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.... 


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. 


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. 


*** 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 

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


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 ; 


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

sporadic, spontaneous CJD, 85%+ of all human TSE, just not just happen. never in scientific literature has this been proven.

if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;



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).*** 



FRIDAY, JULY 26, 2019 

Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species


TUESDAY, JANUARY 21, 2020 

***> 2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020


***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***

***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<*** 

***> 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. <***

***> 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.<*** 

***> 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) <***


MONDAY, OCTOBER 05, 2020 

USA, UK, JAPAN, CJD TSE PRION STATISTICS UPDATE OCTOBER 2020


MONDAY, JANUARY 20, 2020

sporadic CJD one in a million, FAKE NEWS PEOPLE!

this myth has been incorrect for decades, and had been stated as such by a few, but again, the media is too lazy to do it's job and print the facts.

human tse prion, including 85%+ of all human tse i.e. sporadic cjd, is now one in 5,000!


ZOONOSIS OF SCRAPIE TSE PRION

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. 

============== 


***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. 

 
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. 

 
***> 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


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. 


***> 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.


Like lambs to the slaughter 

* 31 March 2001 * 

Debora MacKenzie * 

Magazine issue 2284 

Suspect symptoms 

What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie? 

Exclusive from New Scientist magazine 

Four years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. 

The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease. 

Photo: Murdo McLeod 

Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. 

He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. 

Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America. 

Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. 

To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD. 

"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. 

Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb. 

Brain damage Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. 

But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE. 

Deslys and colleagues were originally studying vCJD, not sCJD. 

They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. 

Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms. 

As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. 

As expected, they all affected the brain in a different way from BSE and vCJD. 

But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology. Multiple strains "The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. 

"You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie," she says. 

In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar. But there are more than 20 strains of scrapie, and six of sCJD. 

"You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. 

Bruce is cautious about the mouse results, but agrees they require further investigation. 

Other trials of scrapie and sCJD in mice, she says, are in progress. 

Deformed proteins People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. 

Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD. But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. 

"If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection." 

There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. 

Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. 

Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted. 

Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. 

And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments. 

More at: Proceedings of the National Academy of Sciences (vol 98, p 4142) 

http://www.pnas.org/cgi/content/full/041490898v1

Correspondence about this story should be directed to letters@newscientist.com 1900 GMT, 28 March 2001 

* New Scientist 

http://www.newscientist.com/dailynews/news.jsp?id=ns9999560

http://www.newscientist.com/article.ns?id=mg16922840.300

https://www.newscientist.com/article/mg16922840-300-like-lambs-to-the-slaughter/

http://nor-98.blogspot.com/

2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains

PLEASE NOTE;

2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains

Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).

In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.


FRIDAY, OCTOBER 23, 2020 

Scrapie TSE Prion Zoonosis Zoonotic, what if?


SATURDAY, SEPTEMBER 26, 2020 

A nationwide trend analysis in the incidence and mortality of Creutzfeldt–Jakob disease in Japan between 2005 and 2014 with increasing trends of incidence and mortality

snip...

Overall, the AAPCs of age-adjusted CJD-associated mortality rates rose significantly over the study period (3.2%; 95% confidence interval [CI] 1.4–5.1%). The AAPC of the age-adjusted incidence rates also increased (overall 6.4%; 95% CI 4.7–8.1%). The CJD-associated increases in the mortality and incidence rates were especially prominent among adults over the age of 70 years. Given this trend in aging of population, the disease burden of CJD will continue to increase in severity. Our findings thus recommend that policymakers be aware of the importance of CJD and focus on preparing to address the increasing prevalence of dementia.

snip...


Volume 26, Number 8—August 2020 

Sporadic Creutzfeldt-Jakob Disease among Physicians, Germany, 1993–2018 high proportion of physicians with sCJD were surgeons


THURSDAY, JULY 02, 2020 

Variant Creutzfeldt–Jakob Disease Diagnosed 7.5 Years after Occupational Exposure


Diagnosis and Reporting of Creutzfeldt-Jakob Disease 

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease 

To the Editor: 

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

Terry S. Singeltary, Sr Bacliff, Tex 

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


doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk

Tracking spongiform encephalopathies in North America

Xavier Bosch

Available online 29 July 2003. 

Volume 3, Issue 8, August 2003, Page 463 

“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem..” ...


January 28, 2003; 60 (2) VIEWS & REVIEWS

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States

Ermias D. Belay, Ryan A. Maddox, Pierluigi Gambetti, Lawrence B. Schonberger

First published January 28, 2003, DOI: https://doi.org/10.1212/01.WNL.0000036913.87823.D6

Abstract

Transmissible spongiform encephalopathies (TSEs) attracted increased attention in the mid-1980s because of the emergence among UK cattle of bovine spongiform encephalopathy (BSE), which has been shown to be transmitted to humans, causing a variant form of Creutzfeldt-Jakob disease (vCJD). The BSE outbreak has been reported in 19 European countries, Israel, and Japan, and human cases have so far been identified in four European countries, and more recently in a Canadian resident and a US resident who each lived in Britain during the BSE outbreak. To monitor the occurrence of emerging forms of CJD, such as vCJD, in the United States, the Centers for Disease Control and Prevention has been conducting surveillance for human TSEs through several mechanisms, including the establishment of the National Prion Disease Pathology Surveillance Center. Physicians are encouraged to maintain a high index of suspicion for vCJD and use the free services of the pathology center to assess the neuropathology of clinically diagnosed and suspected cases of CJD or other TSEs.

Received May 7, 2002. Accepted August 28, 2002.


RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 

Terry S. Singeltary, retired (medically) 

Published March 26, 2003

26 March 2003

Terry S. Singeltary, retired (medically) CJD WATCH

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


Reply to Singletary Ryan A. Maddox, MPH Other Contributors: Published March 26, 2003 

Mr. Singletary raises several issues related to current Creutzfeldt- Jakob disease (CJD) surveillance activities. Although CJD is not a notifiable disease in most states, its unique characteristics, particularly its invariably fatal outcome within usually a year of onset, make routine mortality surveillance a useful surrogate for ongoing CJD surveillance.[1] In addition, because CJD is least accurately diagnosed early in the course of illness, notifiable-disease surveillance could be less accurate than, if not duplicative of, current mortality surveillance.[1] However, in states where making CJD officially notifiable would meaningfully facilitate the collection of data to monitor for variant CJD (vCJD) or other emerging prion diseases, CDC encourages the designation of CJD as a notifiable disease.[1] Moreover, CDC encourages physicians to report any diagnosed or suspected CJD cases that may be of special public health importance (e.g...., vCJD, iatrogenic CJD, unusual CJD clusters).

As noted in our article, strong evidence is lacking for a causal link between chronic wasting disease (CWD) of deer and elk and human disease,[2] but only limited data seeking such evidence exist. Overall, the previously published case-control studies that have evaluated environmental sources of infection for sporadic CJD have not consistently identified strong evidence for a common risk factor.[3] However, the power of a case-control study to detect a rare cause of CJD is limited, particularly given the relatively small number of subjects generally involved and its long incubation period, which may last for decades. Because only a very small proportion of the US population has been exposed to CWD, a targeted surveillance and investigation of unusual cases or case clusters of prion diseases among persons at increased risk of exposure to CWD is a more efficient approach to detecting the possible transmission of CWD to humans. In collaboration with appropriate local and state health departments and the National Prion Disease Pathology Surveillance Center, CDC is facilitating or conducting such surveillance and case- investigations, including related laboratory studies to characterize CJD and CWD prions.

Mr. Singletary also expresses concern over a recent publication by Asante and colleagues indicating the possibility that some sporadic CJD cases may be attributable to bovine spongiform encephalopathy (BSE).[4] The authors reported that transgenic mice expressing human prion protein homozygous for methionine at codon 129, when inoculated with BSE prions, developed a molecular phenotype consistent with a subtype of sporadic CJD. Although the authors implied that BSE might cause a sporadic CJD-like illness among persons homozygous for methionine, the results of their research with mice do not necessarily directly apply to the transmission of BSE to humans. If BSE causes a sporadic CJD-like illness in humans, an increase in sporadic CJD cases would be expected to first occur in the United Kingdom, where the vast majority of vCJD cases have been reported. In the United Kingdom during 1997 through 2002, however, the overall average annual mortality rate for sporadic CJD was not elevated; it was about 1 case per million population per year. In addition, during this most recent 6-year period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of UK sporadic CJD deaths.[3, 5] Furthermore, surveillance in the UK has shown no increase in the proportion of sporadic CJD cases that are homozygous for methionine (Will RG, National CJD Surveillance Unit, United Kingdom, 2003; personal communication)..

References

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Diagnosis and reporting of Creutzfeldt-Jakob disease. JAMA 2001;285:733-734.

2. Belay ED, Maddox RA, Gambetti P, Schonberger LB. Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States. Neurology 2003;60:176-181.

3. Belay ED. Transmissible spongiform encephalopathies in humans. Annu Rev Microbiol 1999;53:283-314.

4. Asante EA, Linehan JM, Desbruslais M, et al. BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J 2002;21:6358-6366.

5. The UK Creutzfeldt-Jakob Disease Surveillance Unit. CJD statistics. Available at: http://www.cjd.ed.ac.uk/figures.htm. Accessed February 18, 2003.

Competing Interests: None declared.


Diagnosis and Reporting of Creutzfeldt-Jakob Disease

2 January 2000 British Medical Journal U.S. 

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


15 November 1999 British Medical Journal hvCJD in the USA * BSE in U.S. 


Volume 2: Science 

4. The link between BSE and vCJD 

Summary 4.29 The evidence discussed above that vCJD is caused by BSE seems overwhelming. Uncertainties exist about the cause of CJD in farmers, their wives and in several abattoir workers. It seems that farmers at least might be at higher risk than others in the general population. 1 Increased ascertainment (ie, increased identification of cases as a result of greater awareness of the condition) seems unlikely, as other groups exposed to risk, such as butchers and veterinarians, do not appear to have been affected. The CJD in farmers seems to be similar to other sporadic CJD in age of onset, in respect to glycosylation patterns, and in strain-typing in experimental mice. Some farmers are heterozygous for the methionine/valine variant at codon 129, and their lymphoreticular system (LRS) does not contain the high levels of PrPSc found in vCJD. 

***>It remains a remote possibility that when older people contract CJD from BSE the resulting phenotype is like sporadic CJD and is distinct from the vCJD phenotype in younger people...end

BSE INQUIRY


SATURDAY, JUNE 23, 2018

CDC 

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

Volume 24, Number 7—July 2018 Dispatch 



WEDNESDAY, OCTOBER 21, 2020 

Human Prion Disease Surveillance in Washington State, 2006-2017


WEDNESDAY, NOVEMBER 4, 2020 

CWD TSE PRION, SCRAPIE, BSE, AND PORCINE, PIGS, WILD BOAR, ZOONOTIC ZOONOSIS RISK FACTORS AND POTENTIALS


SATURDAY, OCTOBER 24, 2020 

Texas Kimble County Farm Chronic Wasting Disease CWD TSE Prion Approximate Herd Prevalence 12%


TUESDAY, OCTOBER 20, 2020 

Public ownership of Texas’ white-tailed deer re-affirmed


SUNDAY, AUGUST 30, 2020 

Texas CWD TSE Prion 3 More Documented, 185 Cases To Date 


FRIDAY, OCTOBER 16, 2020 

TAHC Rules and Resources for Harvesting Exotic CWD Susceptible Species this 2020-21 Hunting Season


WEDNESDAY, SEPTEMBER 09, 2020 

TEXAS TAHC CWD TSE Prion SUMMARY MINUTES OF THE 406th COMMISSION MEETING


FRIDAY, DECEMBER 20, 2019

TEXAS ANIMAL HEALTH COMMISSION EXECUTIVE DIRECTOR ORDER DECLARING A CHRONIC WASTING DISEASE HIGH RISK AREA CONTAINMENT ZONE FOR PORTIONS OF VAL VERDE COUNTY


TUESDAY, DECEMBER 31, 2019 

In Vitro detection of Chronic Wasting Disease (CWD) prions in semen and reproductive tissues of white tailed deer bucks (Odocoileus virginianus 

SUNDAY, AUGUST 02, 2015  

TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if? 


SUNDAY, FEBRUARY 16, 2020
***> Jerking for Dollars, Are Texas Politicians and Legislators Masturbating Deer For Money, and likely spreading CWD TSE Prion?
https://chronic-wasting-disease.blogspot.com/2020/02/jerking-for-dollars-are-texas.html

TUESDAY, FEBRUARY 04, 2020 

TEXAS REPORTS 20 NEW CWD TSE PRION CASES 3 WILD 17 BREEDER 166 POSITIVE TO DATE


FRIDAY, MAY 22, 2020 

TPW Commission has adopted rules establishing Chronic Wasting Disease (CWD) management zones to further detection and response efforts among WTD


SUNDAY, MARCH 01, 2020 

Texas As one CWD investigation continues, another launches...THE FULL MONTY!


SATURDAY, DECEMBER 02, 2017 

TEXAS TAHC CWD TSE PRION Trace Herds INs and OUTs Summary Minutes of the 399th and 398th Commission Meeting – 8/22/2017 5/9/2017 


SUNDAY, MAY 14, 2017 

85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play 


SUNDAY, JANUARY 22, 2017 

Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry 


*** TEXAS TAHC OLD STATISTICS BELOW FOR PAST CWD TESTING ***

CWD TEXAS TAHC OLD FILE HISTORY

updated from some of my old files, some of the links will not work.

*** Subject: CWD testing in Texas ***

Date: Sun, 25 Aug 2002 19:45:14 –0500

From: Kenneth Waldrup


snip...see ;


MONDAY, AUGUST 14, 2017

*** Texas Chronic Wasting Disease CWD TSE Prion History ***


SATURDAY, OCTOBER 10, 2020 

Utah As of October 7, 2020, 118 mule deer and two elk have tested positive for CWD TSE Prion


FRIDAY, OCTOBER 09, 2020 

Maryland detects additional 28 positives from last year's CWD TSE Prion sampling, total stands at 80 confirmed cases to date


THURSDAY, SEPTEMBER 24, 2020 

ARKANSAS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE 845 Cases Positive To Date


FRIDAY, JANUARY 24, 2020 

Arkansas Chronic Wasting Disease CWD TSE Prion FY2020 211 Positive Cases as of January 17, 2020


SUNDAY, JANUARY 05, 2020 

Arkansas Chronic Wasting Disease CWD TSE Prion 2019 to 2020 Totals As Of December 3, 2019 399 Confirmed with more pending results


SUNDAY, SEPTEMBER 20, 2020 

Wisconsin Sinks Further Into the Abyss With CWD TSE Prion 2020


THURSDAY, OCTOBER 08, 2020 

Wyoming Chronic wasting disease 2020 surveillance and monitoring 


FRIDAY, SEPTEMBER 18, 2020 

CWD found in new deer and elk hunt areas in northeast Wyoming


TUESDAY, SEPTEMBER 22, 2020 

Michigan CWD TSE Prion 189 Positive To Date UPDATE September 2020


SATURDAY, JANUARY 04, 2020 

Mississippi CWD TOTALS JUST ABOUT DOUBLE Since October 1, 2019 To Date Statewide Total is 37 Confirmed


WEDNESDAY, OCTOBER 28, 2020 

Missouri MDC FINDS FIRST CASE OF CWD IN PULASKI COUNTY


WEDNESDAY, MAY 06, 2020 

Missouri 46 new cases Chronic Wasting Disease found, total to date at 162 documented CWD


SUNDAY, JANUARY 19, 2020 

Missouri CWD TSE Prion 2019-2020 SAMPLING RESULTS TO DATE 25 Positive


THURSDAY, JANUARY 02, 2020 

Missouri MDC officially reports more than 20 new cases of Chronic Wasting Disease CWD TSE Prion


WEDNESDAY, OCTOBER 21, 2020 

Montana 18 deer test positive for chronic wasting disease CWD TSE Prion 

CWD positives from across the state, no new areas


TUESDAY, MAY 19, 2020 

Montana White-tailed deer in Gallatin County suspected positive for CWD


FRIDAY, FEBRUARY 07, 2020 

Montana 142 animals tested positive for CWD thus far during 2019/20 sampling


FRIDAY, JANUARY 17, 2020

Montana Moose Tests Positive for Chronic Wasting Disease CWD TSE PRION in Libby Area

Montana Fish, Wildlife & Parks 2019 CWD Surveillance Hunter Test Results CWD TSE PRION LOOKS LIKE 136 POSITIVE SO FAR, count them up...


WEDNESDAY, DECEMBER 25, 2019 

Montana 16 more deer positive for CWD first time positive hunting district 705 in southeast


WEDNESDAY, MARCH 25, 2020 

Michigan CWD TSE Prion Total Suspect Positive Deer Moves Up To 188 with total deer tested 80,687 to date



THURSDAY, JANUARY 30, 2020 

Michigan CWD TSE Prion Total Suspect Positive Deer Jumps To 181 to date


MONDAY, JANUARY 27, 2020 

updated

Michigan CWD TSE Prion MDARD 3 positive white-tailed deer from a Newaygo County deer farm depopulation and quarantine efforts update?


THURSDAY, OCTOBER 29, 2020 

Spatial analysis of chronic wasting disease in free-ranging white-tailed deer (Odocoileus virginianus) in Illinois, 2008-2019


SUNDAY, DECEMBER 22, 2019 

Illinois CWD TSE Prion 90 CWD-positive deer with 826 confirmed positive Total positives through June 30, 2019


TUESDAY, FEBRUARY 11, 2020 

Missouri MDC 2019-2020 SAMPLING RESULTS CWD TSE PRION TO DATE 28 Positive


SUNDAY, APRIL 12, 2020 

PENNSYLVANIA REVISED CWD RESPONSE PLAN DRAFT AVAILABLE FOR REVIEW

https://chronic-wasting-disease.blogspot.com/2020/04/pennsylvania-revised-cwd-response-plan.html

WEDNESDAY, MARCH 04, 2020 

Politicians State Rep. David Maloney, R-Berks Helping to Spread Chronic Wasting Disease CWD TSE Prion

https://chronic-wasting-disease.blogspot.com/2020/03/politicians-state-rep-david-maloney-r.html

FRIDAY, OCTOBER 16, 2020 

Minnesota CWD TSE Prion confirmed in Houston County farmed deer herd


SATURDAY, MARCH 14, 2020 

Minnesota 4 More Farmed Deer and 1 wild positive for CWD TSE Prion


FRIDAY, FEBRUARY 28, 2020 
Virginia DGIF say 21 new cases of CWD TSE Prion confirmed in white-tailed deer in northwest Virginia throughout 2019
TUESDAY, MARCH 03, 2020 

North Dakota Eight deer taken during the 2019 deer gun season tested positive for chronic wasting disease CWD TSE Prion

https://chronic-wasting-disease.blogspot.com/2020/03/north-dakota-eight-deer-taken-during.html

TUESDAY, FEBRUARY 11, 2020 

South Dakota Chronic Wasting Disease CWD TSE Prion Detected in New Areas 

https://chronic-wasting-disease.blogspot.com/2020/02/south-dakota-chronic-wasting-disease.html

MONDAY, FEBRUARY 10, 2020 

Iowa CWD TSE Prion 2019/20 (confirmed or suspect) 43 cases to date Wild Cervid


SATURDAY, FEBRUARY 01, 2020 

Colorado confirmed CWD TSE Prion in 24 game management units in the state where it previously hadn’t been found


WEDNESDAY, JANUARY 29, 2020 

Utah CWD TSE Prion Since July 1, 2019, the DWR confirmed 16 positive deer statewide Six of those, including Coal, were in the La Sal Unit, 59 test pending


TUESDAY, JANUARY 28, 2020 

Mississippi MDWFP North MS CWD Management Zone Since October 2019, 25 CWD-positive deer have been detected from this zone


SATURDAY, JANUARY 25, 2020 

Tennessee 2019-20 deer season 462 CWD TSE Prion Confirmed To Date


WEDNESDAY, OCTOBER 28, 2020 

Wyoming Hunter-submitted CWD samples identify three new positive deer hunt areas


Fri, Jan 24, 2020 2:29 pm

Wyoming Game & Fish Discovers CWD-Positive Mule Deer in Pinedale, Discourages Feeding of Wildlife

''As of September 2019, CWD has been identified in 31 of 37 (84%) Wyoming mule deer herds, nine of 36 (25%) elk herds, and generally wherever white-tailed deer occur. Increasing prevalence and distribution of CWD has the potential to cause widespread and long-term negative impacts to Wyoming’s cervid populations. Prevalence of this disease in chronically infected Wyoming deer herds has exceeded 40%, with one elk herd exhibiting nearly 15% prevalence.''

''for the first time, there is clear evidence that CWD is adversely affecting the overall health and viability of some herds.''


MONDAY, FEBRUARY 03, 2020 

Montana Chronic Wasting Disease CWD TSE Prion in Eastern Part of State Game Farm Elk


TUESDAY, JANUARY 07, 2020 

Oklahoma Farmed Elk Lincoln County CWD Depopulation 3 Positive Elk with 1 Additional Dead Trace Out Confirmed Positive


THURSDAY, JULY 30, 2020 
Ohio Deer Summary 2019 - 2020 CWD TSE Prion 24 Confirmed To Date All Captive Cervid
WEDNESDAY, JANUARY 29, 2020 

Pennsylvania CWD TSE Prion 2019-20 hunting seasons as of January 14, 148 of the samples had tested positive for CWD in Wild Deer

WEDNESDAY, JANUARY 29, 2020 

Pennsylvania CWD TSE Prion 2019-20 hunting seasons as of January 14, 148 of the samples had tested positive for CWD in Wild Deer


SUNDAY, DECEMBER 22, 2019 

Pennsylvania Steady Climb of CWD TSE Prion Confirms 250 Positive To Date In Wild Cervid As At September 12, 2019 

Pennsylvania Captive Cervid Industry Total CWD TSE Prion ??? anyone's guess...


SUNDAY, OCTOBER 11, 2020 

Michigan Chronic Wasting Disease CWD TSE Prion increases to 191 positive to date


TUESDAY, SEPTEMBER 22, 2020 

Michigan CWD TSE Prion 189 Positive To Date UPDATE September 2020


MONDAY, JANUARY 27, 2020 

Michigan CWD TSE Prion MDARD 3 positive white-tailed deer from a Newaygo County deer farm depopulation and quarantine efforts update?


TUESDAY, JANUARY 07, 2020 

Michigan Total CWD TSE Prion Positive Suspect-Positive Deer Jump To 174 confirmed to date

TUESDAY, JANUARY 14, 2020 

Michigan MDARD has confirmed chronic wasting disease (CWD) in 3 white-tailed deer from a Newaygo County deer farm


SATURDAY, JANUARY 25, 2020 

Tennessee 2019-20 deer season 462 CWD TSE Prion Confirmed To Date


FRIDAY, JANUARY 24, 2020

Wyoming Game & Fish Discovers CWD-Positive Mule Deer in Pinedale, Discourages Feeding of Wildlife

''As of September 2019, CWD has been identified in 31 of 37 (84%) Wyoming mule deer herds, nine of 36 (25%) elk herds, and generally wherever white-tailed deer occur. Increasing prevalence and distribution of CWD has the potential to cause widespread and long-term negative impacts to Wyoming’s cervid populations. Prevalence of this disease in chronically infected Wyoming deer herds has exceeded 40%, with one elk herd exhibiting nearly 15% prevalence.''

''for the first time, there is clear evidence that CWD is adversely affecting the overall health and viability of some herds.''


THURSDAY, SEPTEMBER 24, 2020 

ARKANSAS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE 845 Cases Positive To Date


FRIDAY, JANUARY 24, 2020 

Arkansas Chronic Wasting Disease CWD TSE Prion FY2020 211 Positive Cases as of January 17, 2020


SUNDAY, JANUARY 05, 2020 

Arkansas Chronic Wasting Disease CWD TSE Prion 2019 to 2020 Totals As Of December 3, 2019 399 Confirmed with more pending results


WEDNESDAY, JANUARY 29, 2020 

Utah CWD TSE Prion Since July 1, 2019, the DWR confirmed 16 positive deer statewide Six of those, including Coal, were in the La Sal Unit, 59 test pending


FRIDAY, JANUARY 17, 2020 

North Dakota 11 Positive Chronic Wasting Disease CWD TSE Prion detected since Sept 1, 2019

TUESDAY, JANUARY 21, 2020 

Minnesota CWD update test results from deer harvested in the 2019 hunting season and the special hunts have returned 27 wild deer tested positive for CWD all from the southeast DMZ


FRIDAY, JANUARY 10, 2020 

Minnesota Investigation leads to additional CWD positive deer on Pine County farm


THURSDAY, NOVEMBER 05, 2020 

Nebraska Chronic wasting disease testing paused, will resume in 2021


THURSDAY, JANUARY 23, 2020 

Canadian Food Inspection Agency (CFIA) has updated the following chapter of the Accredited Veterinarian's Manual: Chapter 13 Chronic Wasting Disease Herd Certification Programs


TUESDAY, JANUARY 21, 2020 

2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020


SUNDAY, FEBRUARY 09, 2020 

Management of chronic wasting disease in ranched elk: conclusions from a longitudinal three-year study

Although the herd owners were presented with additional management directives, including culling of CWD positive bulls and those animals positive by an amplification assay (RT-QuIC), they were not implemented due to concern regarding its potential impact on hunting revenue. 


FRIDAY, DECEMBER 06, 2019 

Estimating relative CWD susceptibility and disease progression in farmed white-tailed deer with rare PRNP alleles


THURSDAY, DECEMBER 19, 2019

TSE surveillance statistics exotic species and domestic cats Update December 2019


FRIDAY, NOVEMBER 15, 2019 

Southwest Wisconsin CWD, Deer and Predator Study


FRIDAY, NOVEMBER 08, 2019 

EFSA Panel on Biological Hazards (BIOHAZ) Update on chronic wasting disease (CWD) III

PRICE OF TSE PRION POKER GOES UP!
MONDAY, NOVEMBER 02, 2020 

***> Successful transmission of the chronic wasting disease (CWD) agent to white-tailed deer by intravenous blood transfusion


Monday, September 14, 2020 

Assessing the aggregated probability of entry of a novel prion disease agent into the United Kingdom


Tuesday, September 15, 2020 

Mad Camel Disease CPD TSE Prion dromedary camels (Camelus dromedarius) is spreading


MONDAY, AUGUST 24, 2020 

Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease


SUNDAY, OCTOBER 4, 2020 

Cattle Meat and Offal Imported from the United States of America, Canada and Ireland to Japan (Prions) Food Safety Commission of Japan


TUESDAY, MARCH 12, 2019 

Early preclinical detection of prions in the skin of prion-infected animals


SUNDAY, OCTOBER 11, 2020 

Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ 


THURSDAY, SEPTEMBER 24, 2020 

The emergence of classical BSE from atypical/ Nor98 scrapie


TUESDAY, SEPTEMBER 22, 2020 

APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020


WEDNESDAY, MAY 29, 2019 

Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!


THURSDAY, AUGUST 20, 2020 

Why is USDA "only" BSE TSE Prion testing 25,000 samples a year?


TUESDAY, SEPTEMBER 29, 2020 

ISO's Updated 22442 Animal Tissue Standards — What Changed? TSE Prion!


FRIDAY, OCTOBER 2, 2020 

H.R.925 America's Conservation Enhancement Act 116th Congress 2019-2020 SEC 104 CHRONIC WASTING DISEASE TASK FORCE


TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE AND FRIENDLY FIRE, IATROGENIC SPREAD

WEDNESDAY, OCTOBER 31, 2018 

***> PIG HEART VALVES and Potential Iatrogenic Transmissible Spongiform Encephalopathy TSE Prion Disease in Humans, what if?


MONDAY, OCTOBER 05, 2020 

USA, UK, JAPAN, CJD TSE PRION STATISTICS UPDATE OCTOBER 2020


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


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

Date: Tue, 9 Jan 2001 16:49:00 -0800

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de

######### Bovine Spongiform Encephalopathy #########


Greetings List Members,

I was lucky enough to sit in on this BSE conference call today and even managed to ask a question. that is when the trouble started.

I submitted a version of my notes to Sandra Blakeslee of the New York Times, whom seemed very upset, and rightly so.

"They tell me it is a closed meeting and they will release whatever information they deem fit. Rather infuriating."

and i would have been doing just fine, until i asked my question. i was surprised my time to ask a question so quick.

(understand, these are taken from my notes for now. the spelling of names and such could be off.)

[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.

[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?

[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]

[host Richard] could you repeat the question?

[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?

[not sure whom ask this] what group are you with?

[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.

[not sure who is speaking] could you please disconnect Mr. Singeltary

[TSS] you are not going to answer my question?

[not sure whom speaking] NO

from this point, i was still connected, got to listen and tape the whole conference. at one point someone came on, a woman, and ask again;

[unknown woman] what group are you with?

[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD and other human TSE's world wide. i was invited to sit in on this from someone inside the USDA/APHIS and that is why i am here. do you intend on banning me from this conference now?

at this point the conference was turned back up, and i got to finish listening. They never answered or even addressed my one question, or even addressed the issue. BUT, i will try and give you a run-down for now, of the conference.

IF i were another Country, I would take heed to my notes, BUT PLEASE do not depend on them. ask for transcript from;

RBARNS@ORA.FDA.GOV 301-827-6906

he would be glad to give you one ;-)

Rockville Maryland, Richard Barns Host

BSE issues in the U.S., How they were labelling ruminant feed? Revising issues.

The conference opened up with the explaining of the U.K. BSE epidemic winding down with about 30 cases a week.

although new cases in other countries were now appearing.

Look at Germany whom said NO BSE and now have BSE.

BSE increasing across Europe.

Because of Temporary Ban on certain rendered product, heightened interest in U.S.

A recent statement in Washington Post, said the New Administration (old GW) has a list of issues. BSE is one of the issues.

BSE Risk is still low, minimal in U.S. with a greater interest in MBM not to enter U.S.

HOWEVER, if BSE were to enter the U.S. it would be economically disastrous to the render, feed, cattle, industries, and for human health.

(human health-they just threw that in cause i was listening. I will now jot down some figures in which they told you, 'no need to write them down'. just hope i have them correct. hmmm, maybe i hope i don't ???)

80% inspection of rendering

*Problem-Complete coverage of rendering HAS NOT occurred.

sizeable number of 1st time FAILED INITIAL INSPECTION, have not been reinspected (70% to 80%).

Compliance critical, Compliance poor in U.K. and other European Firms.

Gloria Dunason Major Assignment 1998 goal TOTAL compliance. This _did not_ occur. Mixed level of compliance, depending on firm.

Rendering FDA license and NON FDA license

system in place for home rendering & feed 76% in compliance 79% cross contamination 21% DID NOT have system 92% record keeping less than 60% total compliance

279 inspectors 185 handling prohibited materials

Renderer at top of pyramid, significant part of compliance. 84% compliance

failed to have caution statement render 72% compliance & cross contamination caution statement on feed, 'DO NOT FEED TO CATTLE'

56 FIRMS NEVER INSPECTED

1240 FDA license feed mills 846 inspected

"close to 400 feed mills have not been inspected"

80% compliance for feed.

10% don't have system.

NON-FDA licensed mills There is NO inventory on non licensed mills. approximately 6000 to 8000 Firms ??? 4,344 ever inspected. "FDA does not have a lot of experience with"

40% do NOT have caution statement 'DO NOT FEED'.

74% Commingling compliance

"This industry needs a lot of work and only half gotten to"

"700 Firms that were falitive, and need to be re-inspected, in addition to the 8,000 Firms."

Quote to do BSE inspection in 19 states by end of January or 30 days, and other states 60 days. to change feed status??? Contract check and ask questions and pass info.

At this time, we will take questions.

[I was about the third or fourth to ask question. then all B.S.eee broke loose, and i lost my train of thought for a few minutes. picked back up here]

someone asking about nutritional supplements and sourcing, did not get name. something about inspectors not knowing of BSE risk??? the conference person assuring that Steve Follum? and the TSE advisory Committee were handling that.

Some other Dr. Vet, whom were asking questions that did not know what to do???

[Dennis Wilson] California Food Agr. Imports, are they looking at imports?

[Conference person] they are looking at imports, FDA issued imports Bulletin.

[Linda Singeltary ??? this was a another phone in question, not related i don't think] Why do we have non-licensed facilities?

(conference person) other feed mills do not handle as potent drugs???

Dennis Blank, Ken Jackson licensed 400 non FDA 4400 inspected of a total of 6000 to 8000,

(they really don't know how many non licensed Firms in U.S. they guess 6000 to 8000??? TSS)

Linda Detwiler asking everyone (me) not to use emergency BSE number, unless last resort. (i thought of calling them today, and reporting the whole damn U.S. cattle herd ;-) 'not'

Warren-Maryland Dept. Agr. Prudent to re-inspect after 3 years. concerned of Firms that have changed owners.

THE END

TSS

############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

FROM New York TIMES

Subject: Re: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA Posting of cut version...

Date: Thu, 11 Jan 2001 22:02:47 -0700

From: "Sandy Blakeslee"

To: "Terry S. Singeltary Sr." References: 1

Hi terry -- thanks for all your help. I know it made a difference with the FDA getting out that release.

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

From: "Terry S. Singeltary Sr."

To: Sent: Thursday, January 11, 2001 2:06 PM

Subject: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA Posting of cut version...

hi sandy,

From the New York Times NYTimes.com, January 11, 2001

Many Makers of Feed Fail to Heed Rules on Mad Cow Disease By SANDRA BLAKESLEE

Large numbers of companies involved in manufacturing animal feed are not complying with regulations meant to prevent the emergence and spread of mad cow disease in the United States, the Food and Drug Administration said yesterday.

The widespread failure of companies to follow the regulations, adopted in August 1997, does not mean that the American food supply is unsafe, Dr. Stephen Sundlof, director of the Center for Veterinary Medicine at the F.D.A., said in an interview.

But much more needs to be done to ensure that mad cow disease does not arise in this country, Dr. Sundlof said.

The regulations state that feed manufacturers and companies that render slaughtered animals into useful products generally may not feed mammals to cud-chewing animals, or ruminants, which can carry mad cow disease.

All products that contain rendered cattle or sheep must have a label that says, "Do not feed to ruminants," Dr. Sundlof said. Manufacturers must also have a system to prevent ruminant products from being commingled with other rendered material like that from chicken, fish or pork. Finally, all companies must keep records of where their products originated and where they were sold.

Under the regulations, F.D.A. district offices and state veterinary offices were required to inspect all rendering plants and feed mills to make sure companies complied. But results issued yesterday demonstrate that more than three years later, different segments of the feed industry show varying levels of compliance.

Among 180 large companies that render cattle and another ruminant, sheep, nearly a quarter were not properly labeling their products and did not have a system to prevent commingling, the F.D.A. said. And among 347 F.D.A.-licensed feed mills that handle ruminant materials - these tend to be large operators that mix drugs into their products - 20 percent were not using labels with the required caution statement, and 25 percent did not have a system to prevent commingling.

Then there are some 6,000 to 8,000 feed mills so small they do not require F.D.A. licenses. They are nonetheless subject to the regulations, and of 1,593 small feed producers that handle ruminant material and have been inspected, 40 percent were not using approved labels and 25 percent had no system in place to prevent commingling.

On the other hand, fewer than 10 percent of companies, big and small, were failing to comply with the record-keeping regulations.

The American Feed Industry Association in Arlington, Va., did not return phone calls seeking comment.

http://www.nytimes.com/2001/01/11/science/11COW.html

Subject: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001

Date: Wed, 10 Jan 2001 14:04:21 -0500

From: "Gomez, Thomas M."

Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de

######### Bovine Spongiform Encephalopathy #########

USDA/APHIS would like to provide clarification on the following point from Mr. Singeltary's 9 Jan posting regarding the 50 state conference call.

[Linda Detwiler asking everyone (me) not to use emergency BSE number, unless last resort. (i thought of calling them today, and reporting the whole damn U.S. cattle herd ;-) 'not']

Dr. Detwiler was responding to an announcement made during the call to use the FDA emergency number if anyone wanted to report a cow with signs suspect for BSE. Mr. Singeltary is correct that Dr. Detwiler asked participants to use the FDA emergency number as a last resort to report cattle suspect for BSE. What Mr. Singeltary failed to do was provide the List with Dr. Detwiler's entire statement. Surveillance for BSE in the United States is a cooperative effort between states, producers, private veterinarians, veterinary hospitals and the USDA. The system has been in place for over 10 years. Each state has a system in place wherein cases are reported to either the State Veterinarian, the federal Veterinarian in Charge or through the veterinary diagnostic laboratory system. The states also have provisions with emergency numbers. Dr. Detwiler asked participants to use the systems currently in place to avoid the possibility of a BSE-suspect report falling through the cracks. Use of the FDA emergency number has not been established as a means to report diseased cattle of any nature.

############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

Subject: Re: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL Jan.9, 2001

Date: Wed, 10 Jan 2001 13:44:49 -0800

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de References: 1

######### Bovine Spongiform Encephalopathy #########

snip...

[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.

[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?

[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]

[host Richard] could you repeat the question?

[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?

[not sure whom ask this] what group are you with?

[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.

[not sure who is speaking] could you please disconnect Mr. Singeltary

[TSS] you are not going to answer my question?

[not sure whom speaking] NO

snip...see full transcript here;

U.S. 50 STATE CONFERENCE CALL Jan.9, 2001

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

TUESDAY, SEPTEMBER 29, 2020 

ISO's Updated 22442 Animal Tissue Standards — What Changed? TSE Prion!


FSIS [Docket No. FSIS–2019–0021] Notice of Request To Renew an Approved Information Collection: Specified Risk Materials Singeltary Submission 

Food Safety and Inspection Service [Docket No. FSIS–2019–0021] Notice of Request To Renew an Approved Information Collection: Specified Risk Materials 

Greetings FSIS et al, I would kindly like to comment on the following docket; 

[Docket No. FSIS–2019–0021] Notice of Request To Renew an Approved Information Collection: Specified Risk Materials Federal Docket SRM TSE Prion DEPARTMENT OF AGRICULTURE Food Safety and Inspection Service [Docket No. FSIS–2019–0021] Notice of Request To Renew an Approved Information Collection: Specified Risk Materials AGENCY: Food Safety and Inspection Service, USDA. ACTION: Notice and request for comments.


MY FULL TEXT SUBMISSION FILE;


Terry S. Singeltary Sr.
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