Tuesday, July 03, 2018

Chronic Wasting Disease CWD TSE Prion Global Report Update, USA, CANADA, KOREA, NORWAY, FINLAND, Game Farms and Fake news

OIE CWD TSE PRION NORWAY

International reference laboratory for Chronic Wasting Disease 

Publisert 04.04.2018 

The World Organization for Animal Health (OIE) has designated the Norwegian Veterinary Institute as the third reference laboratory for Chronic Wasting Disease (CWD) in the world, and the first one in Europe. Senior researcher Sylvie Benestad has been designated as the expert, responsible for the new reference laboratory. OIE has previously appointed laboratories in Canada and South Korea. 

-Being designated as a reference laboratory for OIE is a major professional recognition. This is the result of 20 years of work on prion diseases, says senior researcher Sylvie Benestad who will be responsible for the new reference laboratory. Photo: Agnete Brun. The Norwegian Veterinary Institute is a national reference laboratory for the Norwegian Food Safety Authority regarding several diseases and infectious agents. As a reference laboratory worldwide, the institute will collaborate with other countries to confirm diagnoses and exchange knowledge within diagnostics, disease and epidemiology. Sharing of material for diagnostics is also an important task. An international reference function will also create opportunities for academic cooperation worldwide.

- Being designated as a reference laboratory for OIE is first and foremost a major professional recognition. This is the result of 20 years of work on prion diseases and shows that Norway has been central in this field, such as in connection to the Nor98 scrapie disease in sheep and goats. I hope that with this we can increase the cooperation with the North America and South Korea and facilitate exchange of material and experience. We will also be able to assist other countries in the world that will detect CWD, such as Finland recently did, says Sylvie Benestad.

As of today, the Norwegian Veterinary Institute has analyzed more than 40 500 CWD samples from cervids. 18 cases of CWD have been detected in wild reindeer, 3 in moose and 1 in red deer.



Department for Environment, Food and Rural Affairs Animal and Plant Health Agency Veterinary & Science Policy Advice Team - International Disease Monitoring 1 

Preliminary Outbreak Assessment Cervid Spongiform Encephalopathy in Norway 

7 th April 2016 Ref: VITT/1200 

Cervid disease in Norway


WEDNESDAY, MARCH 28, 2018 

The executioner in Nordfjella and Chronic Wasting Disease CWD TSE Prion Skrantesjuke


TUESDAY, FEBRUARY 27, 2018 

NORWAY CWD TSE PRION Skrantesjuke Nordfjella zone 1 Complete Eradication Complete


TUESDAY, DECEMBER 05, 2017 

Norway 30,000 deer animals have so far been tested for Skrantesyke chronic wasting disease CWD TSE PRION DISEASE


THURSDAY, NOVEMBER 30, 2017 

Norway Animal welfare surveillance at Nordfjella Skrantesjuke CWD TSE Prion Update


WEDNESDAY, NOVEMBER 29, 2017

 Norway another case of Skrantesjuke CWD TSE Prion Adult Reindeer pitcher field in Nordfjella (preliminary testing) 13th case if confirmed


FRIDAY, NOVEMBER 24, 2017 

Norwegian Food Safety Authority makes changes to measures to limit the spread of disease Skrantesjuke (CWD) in deer wildlife


SATURDAY, NOVEMBER 18, 2017 

Norway detects more Chronic Wasting Disease CWD TSE Prion Skrantesjuke


This is the eighth case of the lethal deer disease in the area since the survey started in 2016.

The reindeer cub was shot by a flock from the Norwegian National Guard, and the infectious agent was detected in the animal's lymph nodes.


WEDNESDAY, NOVEMBER 01, 2017 

Norway detects CWD Skrantesjuke Deer possibly atypical Nor-98-type TSE?

Greetings TSE prion world, 

i am seeing more and more references to the atypical Nor-98-type CWD TSE Prion in Norway as being of the non-infectious or non-infective variant. with science documented to date, i do not believe that any CWD Skrantesjuke TSE Prion typical or atypical in Norway or anywhere else can be classified as ''non-infective variant''. IF, Norway takes the USDA OIE views and makes atypical Nor-98 type CWD in Deer a International trading commodity fueled by junk science, as they did with sheep, i.e. no trade restrictions for Nor-98 in sheep, the world should then weep...terry 

Nor-98 atypical Scrapie Transmission Studies Review

snip...see full text;



FRIDAY, OCTOBER 13, 2017 

Norway, Two More New Cases of Chronic Wasting Disease CWD TSE Prion Skrantesjuke


TUESDAY, OCTOBER 10, 2017

Norway detects another case of CWD TSE PRION Skrantesjuke


SATURDAY, SEPTEMBER 30, 2017 

Norway, CWD TSE Prion, Humans, Zoonosis, Fortsatt lite sannsynlig at mennesker kan smittes av skrantesyke?


MONDAY, AUGUST 14, 2017 

NORWAY CWD, SHEEP GRAZING, and Scrapie, What If?


TUESDAY, JUNE 20, 2017 

Norway Confirms 6th Case of Skrantesjuke CWD TSE Prion Disease


Tuesday, December 13, 2016

Norway Chronic Wasting Disease CWD TSE Prion disease Skrantesjuke December 2016 Update


Thursday, September 22, 2016

NORWAY DETECTS 5TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION Skrantesjuke


Saturday, September 03, 2016

NORWAY Regulation concerning temporary measures to reduce the spread of Chronic Wasting Disease (CWD) as 4th case of skrantesjuke confirmed in Sogn og Fjordane


Wednesday, August 31, 2016

*** NORWAY CONFIRMS 4TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN SECOND CARIBOU


Wednesday, August 31, 2016

NORWAY CONFIRMS 4TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN SECOND CARIBOU


Tuesday, August 02, 2016

Chronic wasting disease of deer – is the battle to keep Europe free already lost?


Tuesday, June 14, 2016

*** Chronic Wasting Disease (CWD) in a moose from Selbu in Sør-Trøndelag Norway ***


Thursday, July 07, 2016

Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd Norwegian moose

14/06/2016 - Norway reports a third case


Tuesday, April 12, 2016

The first detection of Chronic Wasting Disease (CWD) in Europe free-ranging reindeer from the Nordfjella population in South-Norway.


Saturday, April 9, 2016

The Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer (Rangifer tarandus tarandus)

Department for Environment, Food and Rural Affairs


Saturday, July 16, 2016

Chronic wasting Disease in Deer (CWD or Spongiform Encephalopathy) The British Deer Society 07/04/2016

Red Deer Ataxia or Chronic Wasting Disease CWD TSE PRION?

could this have been cwd in the UK back in 1970’S ??? 




Clinical Communication Enzootic ataxia in Red deer 

P.R. Wilson , Marjorie B. Orr & E.L. Key Pages 252-254 | Published online: 23 Feb 2011


SEE FULL TEXT ;


Sunday, February 25, 2018 

PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW


Singeltary Submissions to EU on CWD TSE Prion

Friday, November 22, 2013

Wasting disease is threat to the entire UK deer population CWD TSE PRION disease in cervids

***SINGELTARY SUBMISSION

The Scottish Parliament's Rural Affairs, Climate Change and Environment Committee has been looking into deer management, as you can see from the following press release,

***and your email has been forwarded to the committee for information:



Friday, November 22, 2013

Wasting disease is threat to the entire UK deer population


Sunday, July 21, 2013

Welsh Government and Food Standards Agency Wales Joint Public Consultation on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations 2013

*** Singeltary Submission WG18417


Sunday, June 23, 2013

National Animal Health Laboratory Network Reorganization Concept Paper (Document ID APHIS-2012-0105-0001)

***Terry S. Singeltary Sr. submission


ruminant protein and risk factors there from with TSE Prion disease, but we missed the rest of the feed i.e. FEED GRAINS. YES, science has shown in the past, and now recently, the shedding of the CWD TSE Prion into the environment is indeed a risk factor, and for all the grains and such that goes into feed, even hay, hell, Norway does not require any APHIS-Veterinary Services certification for the import of hay/straw. see for yourself ;

Hay/Straw

Norway does not require any APHIS-Veterinary Services certification for the import of hay/straw.


you add up all the other grains in feed, and then wonder about potential exposure to the CWD TSE PRION from cervid and risk factor from the CWD there from via shedding or right down to the soil these grains were grown in, and you have a world of problems. see ;

Feed Grains Data: Yearbook Tables Created March 10, 2016 Updates of this data, and data covering more years and countries, can be found at http://www.ers.usda.gov/data-products/feed-grains-database/feed-grains-yearbook-tables.aspx U.S. Acreage, Production, Yield, and Farm Price Table 1--Corn, sorghum, barley, and oats: Planted acreage, harvested acreage, production, yield, and farm price World Production, Supply, and Disappearance Table 2--Foreign coarse grains: Supply and disappearance Table 3--Feed grains (corn, sorghum, barley, and oats): Supply and disappearance U.S. Supply and Disappearance Table 4--Corn: Supply and disappearance Table 5--Sorghum: Supply and disappearance Table 6--Barley: Supply and disappearance Table 7--Oats: Supply and disappearance U.S. Production, Yield, and Stocks Table 8--Hay: Production, harvested acreage, yield, and stocks Domestic and International Prices Table 9--Corn and sorghum: Average prices received by farmers, United States Table 10--Barley and oats: Average prices received by farmers, United States Table 11--Hay: Average prices received by farmers, United States Table 12--Corn: Cash prices at principal markets Table 13--Sorghum: Cash prices at principal markets Table 14--Barley and oats: Cash prices at principal markets Table 15--Feed-price ratios for livestock, poultry, and milk Table 16--Byproduct feeds: Average wholesale price, bulk, specified markets Table 17--Processed corn products: Quoted market prices Exports and Imports Table 18--U.S. corn and sorghum exports Table 19--U.S. barley and oats exports Table 20--U.S. corn and sorghum imports Table 21--U.S. barley and oats imports Table 22--U.S. corn and sorghum exports by selected destinations Table 23--U.S. barley and oats exports by selected destinations Table 24--U.S. corn and sorghum imports by selected sources Table 25--U.S. barley and oats imports by selected sources Table 26--U.S. white corn exports by selected destinations Table 27--World coarse grain trade: Selected exporters and importers by commodity Rail rates and shipments Table 28--Rail rates and grain shipments Processed feeds and animal unit indexes Table 29--Processed feeds: Quantities fed and feed per grain-consuming animal unit Table 30--Indexes of feed consuming animal units Feed, seed, and industrial uses Table 31—Corn: Feed, seed, and industrial uses Exports and imports for ethyl alcohol and brewers’ and distillers’ dregs and waste Table 32—U.S. exports of ethyl alcohol by selected destinations Table 33—U.S. imports of ethyl alcohol by selected sources Table 34—U.S. exports of brewers’ and distillers’ dregs and waste by selected commodities Table 35—U.S. imports of brewers’ and distillers’ dregs and waste by selected sources Contact: Thomas Capehart at tcapehart+A25@ers.usda.gov


‘’The statement you were concerned about was corrected to "One sorghum DDGS out of 168 DG samples was contaminated with animal protein prohibited for use in ruminant feed and was channeled to poultry feed."

Subject: Re: TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES

***UDATED CORRECTION BY AUTHOR...SEE EMAIL TO ME...terry

From: Kyung-Min Lee Sent: Thursday, October 01, 2015 1:39 PM To: Terry S. Singeltary Sr. ; BSE-L@LISTS.AEGEE.ORG Cc: CJD-L@LISTS.AEGEE.ORG ; cjdvoice@yahoogroups.com ; bloodcjd@yahoogroups.com ; jcattanach@foodprotection.org ; cnc3@psu.edu ; dloynachan@foodprotection.org ; lhovey@foodprotection.org ; Timothy J. Herrman Subject: RE: TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES

Dear Terry S. Singeltary Sr.

Thank for your interest and concern about our published article entitled “Evaluation of Selected Nutrients and Contaminants in Distillers Grains from Ethanol Production in Texas”. I should apologize you and others that there were some errors and misleading statements in this article due to inappropriate terminology. The statement you were concerned about was corrected to "One sorghum DDGS out of 168 DG samples was contaminated with animal protein prohibited for use in ruminant feed and was channeled to poultry feed." We requested the journal editor to correct some errors and the relevant statements, or to withdraw the article from the journal.

Again I sincerely apologize for any confusion and inconvenience this may cause. Thanks.

best wishes,

Kyung-Min

Kyung-Min Lee, Ph. D. Research Scientist Office of the Texas State Chemist

Texas A&M AgriLife Research P.O. Box 3160, College Station, TX 77841-3160 Phone: 979-845-4113 (ext 132) Email:kml@otsc.tamu.edu Fax: 979-845-1389

snip...end...tss

my link corrected

Sunday, September 27, 2015

TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES


FINLAND MOOSE FOUND DEAD IN FOREST WITH CHRONIC WASTING DISEASE 8.3.2018 12:56 

The chronic wasting disease (CWD) has been found in a moose or European elk (Alces alces) for the first time ever in Finland. The disease was diagnosed in Kuhmo in a 15-year old moose that had died naturally. The results of the analyses carried out by Finnish Food Safety Authority Evira have been verified by a EU reference laboratory. Species of the deer family, known as “cervids”, can suffer from the chronic wasting disease, and it is always fatal. The disease is not known to have been contracted by people.

Norway was before this case the only European country where CWD has been diagnosed. The monitoring of the occurrence of the disease was intensified from the beginning of 2018 in Finland and five other EU Member States.

In Finland, the occurrence of the disease has been studied already since 2003. None of the ca. 2 500 samples analysed so far had tested positive for the disease. The monitoring of the disease will now be further intensified in the Kuhmo and Kainuu region. Hunters are going to be provided with more instructions before the start of the next hunting season, if appropriate.

The chronic wasting disease is not known to have been contracted by people. Moose meat is safe to eat and no restrictions are imposed on the sales and exportation of meat of animals of the deer family. As a precautionary measure the export of live animals of the deer family to other countries will be discontinued for now.

CWD is a slowly progressing disease of deer, elk, reindeer, and moose which always leads to death. The chronic wasting disease is a prion disease and related to the BSE (bovine spongiform encephalopathy) and other TSE diseases (transmissible spongiform encephalopathy). The disease is common in North America. The moose found in Kuhmo did not suffer from the North American, highly contagious form of the chronic wasting disease. The disease seems to resemble most the form of cervid TSE diagnosed in Norway, which appears to be found incidentally in individual animals of the deer family.

For more information, please contact:

Leena Räsänen, Director, tel. +358 50 388 6518 (Food Safety)

Terhi Laaksonen, Head of Unit, tel. +358 40 159 5812 (Control of Animal Diseases)

Sirkka-Liisa Korpenfelt, Senior Resarcher, tel. + 358 50 351 0308 (Laboratory Analyses)

Antti Oksanen, Research Professor, tel. +358 44 561 6491 (Wild Animal Diseases)

Kajsa Hakulin, Ministerial Advisor, Ministry of Agriculture and Forestry, tel. +358 295 162361 (National and EU Legislation)


SATURDAY, MARCH 10, 2018

Chronic Wasting Disease CWD TSE Prion Goes Global Finland Falls, Behind Norway and S. Korea

FINLAND REPORTS FIRST CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN A moose or European elk (Alces alces)


KOREA CWD TSE Prion

CWD outbreaks in farmed animals were reported in 2001, 2004, 2005, 2010, and *2016 in the Republic of Korea. 

Korean CWD was introduced by elk imported from Canada in 1997. 

CWD outbreaks in farmed animals were reported in 2001, 2004, 2005, 2010, and ***2016 in the Republic of Korea. 

The Korean water deer is the dominant species of wild deer in Korea, with approximately 620 thousand heads (8.0 heads/100 ha) [9].



*2016 in the Republic of Korea. I LACK A REPORT ON THAT~!??? i have asked about it to Korea officials and scientist, with no reply to date...so, total count on CWD in Korea, your guess is good as mine...terry



WS-03 

Epidemiology of Chronic wasting disease in Korea 

Hyun-Joo Sohn, In Soon Roh, Hyo Jin Kim, Tae Young Suh, Kyung Je Park, Hoo Chang Park, Byounghan Kim 

Foreign Animal Disease Division (FADD), Animal and Plant Quarantine Agency (QIA), 

Korea Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrPSc). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrPSc. Based on export information of Chronic wasting disease (CWD) suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture, Food and Rural Affairs (MAFRA) in 2001. CWD control measures included stamping out of all animals in the affected farm, and through cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervid and improved measures to ensure reporting of CWD suspect cases were implemented. 

Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002. Additional CWD cases- 12 elks and 2 elks - were diagnosed in 2004 and 2005. 

On 2010, six elks, seven sika deer, one red deer and five cross-breeds were confirmed as positive. 

Further epidemiological investigations showed that these CWO outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences. 

CWD is the prion disease that is known spread horizontally. 

The experimental studies have shown that PrPCWD is capable of transmitting CWD through saliva and blood. 

We conducted sPMCA and animal biosassy using contaminated soils in the playground of farm 2 which considered horizontal transmission between cervid and have been confirmed infectious PrPCWD. 

This result suggests PrPCWD shedding in the CWD contaminated soil is progressive through the disease course. 

Curriculum Vitae 

Hyun-Joo Sohn 

ACADEMIC EDUCATION: 

 2009 Ph.D. KonKuk University, Seoul, RO Korea 

 1995 MSc KonKuk University, Seoul, RO Korea 

EXPERIENCE: 

 2000 - 2008 Research Scientist, Foreign Animal Disease Division Animal and Plant Quarantine Agency (QIA), Anynag, RO Korea 

2009 - present Senior Research Scientist, Foreign Animal Disease Division Animal and Plant Quarantine Agency (QIA), Anynag, RO Korea 

Peer-reviewed journal publication (CWO and prion disease) 

⦁ Tark DS Kim HJ, Michael H. Neale, Kim MJ, Sohn HJ, Lee YH, Cho IS, Joo YS, Otto Windl Generation of a persistently infected MDBK cell line with natural bovine spongiform encephalopathy (BSE) PLOS ONE 2015 

⦁ Lee YH, Sohn HJ, Kim MJ, Kim HJ, Lee VVY, Yun EI, Tark DS, Choi Yp, Cho IS. Aru Balachandran. Strain characterization of the Korean CWD cases in 2001 and 2004. Journal of Veterinary Medicine Science. 75(1):1377- 1380, 2013. 

⦁ Lee YH, Sohn HJ, Kim MJ, Kim HJ, Park KJ, Lee VVY, Yun EI, Tark DS, Choi Yp, Cho IS. Aru Balachandran Experimental Chronic Wasting Disease in wild type VM mice. Journal of Veterinary Medicine Science. 75(8):1377- 1380, 2013. 

⦁ Kim HJ, Tark DS, Lee YH, Kim MJ, Lee VVY, Cho IS, Sohn HJ, T Yokoyama. Establishment of a cell line persistently infected with chronic wasting disease prions. Journal of Veterinary Medicine Science. 74(10):1377-1380, 2012. 

⦁ Lee YH, Sohn HJ, Kim MJ, Kim HJ, Lee VVY, Choi Yp, Tark DS, Joo IS, Kweon CH, Cho IS. PrPSc detection in affected tissues and blood of mice infected with murine- adapted Bovine Spongiform Encephalopathy strain 301 C. Korean Journal of Veterinary public Health, 36(2):81-88, 2012. ~ 

⦁ HJ, Lee VVY, Kim MJ, Tark DS, Cho IS, Sohn HJ, Lee YH. Sequential study on the first appearance of PrPCWD in TgElk mice model 

⦁ Gene expression profile of a persistently chronic wasting disease (CWD) prion-infected RK13 cell line. Korean Journal of Veterinary public Health, 36(4) :81-88, 2012 

⦁ Lee YH, Kim MJ, Tark DS, Sohn HJ, Yun EI, Cho IS, Choi YP, Kim CL, Kweon CH, Joo IS, Chung GS, Lee JH. Bovine Spongiform Encephalopathy Surveillance in Republic of Korea 31 (3): 2012 

- 76- 


Prion 2016 Conference


Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency's (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.

***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.


KOREA CWD TSE PRION

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea

Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea

Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.

On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea.

These consisted of 23 elk in 1994 originating from the so-called "source farm" in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the "source farm".

Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.

All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify.

CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises.

In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.

*Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.

*Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.

*Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program.

Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).

*In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive.

*Consequently, all cervid - 54 elks, 41 Sika deer and 5 Albino deer - were culled and one elk was found to be positive.

Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.

*Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis.

*Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.

All cervids at Farm 3 and Farm 4 - 15 elks and 47 elks - were culled and confirmed as negative.

Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.

*In December 2010, one elk was confirmed as positive at Farm 5.

*Consequently, all cervid - 3 elks, 11 Manchurian Sika deer and 20 Sika deer - were culled and one Manchurian Sika deer and seven Sika deer were found to be positive.

This is the first report of CWD in these sub-species of deer.

*Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.

*In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo.

All cervid - 19 elks, 15 crossbreed (species unknown) and 64 Sika deer - of Farm 6 were culled, but all confirmed as negative.

: Corresponding author: Dr. Hyun-Joo Sohn (+82-31-467-1867, E-mail: shonhj@korea.kr) 2011 Pre-congress Workshop: TSEs in animals and their environment 5




FULL PAPER 

Additional Cases of Chronic Wasting Disease in Imported Deer in Korea 

Tae-Yung KIM, Hyun-Joo SHON, Yi-Seok JOO, Un-Kyong MUN, Kyung-Sun KANG, Yong-Soon LEE Author information Keywords: Chronic Wasting Disease (CWD), horizontal transmission JOURNALS FREE ACCESS 2005 Volume 67 Issue 8 Pages 753-759


Abstract 

Chronic Wasting Disease (CWD), which had previously occurred only in the U.S.A. and Canada, broke out in a farm at Chungbuk, Korea from imported Canadian deer (Aug. 8, 2001). CWD distribution, through surveillance and epidemiologic investigations, was reported for 93 deer (43 from the CWD originating farm and 50 imported with the CWD originating farm's deer) out of 144 deer (72 from the CWD originating farm and 72 imported with the CWD originating farm's deer) that were breeding at 30 different farms. On Oct. 4 and Oct. 8, 2001, additional cases of CWD were investigated. As a result of slaughtering cohabitating deer, it was verified that other imported deer from Canada were also infected with CWD. Since it was thought that this might cause horizontal transmission, 93 deer imported from Canada in 1997 and 130 cohabitating Korean deer were slaughtered and examined. There were no infected Korean deer, but CWD re-occurred on Nov. 20, 2004 and is still under investigation.

snip... 


DISCUSSION

Fig. 3. Present status of farms that sold or resold imported Canadian elk in 1997.

A total of 129 deer (deer/year: 27/1994, 30/1995, and 72/ 1997) were imported from the CWD originating farm in Canada, None ofthe 57 deer imported in 1994 and 1995 fell dead during the advanced surmise period, 60 months, and were confirmed to have no clinical disorders by Canadian authorities and no clinical matters examined. Korean deer were raised for 3.5 years with 144 deer imported in 1997, during which time only 9 of the imported deer became infected, Five of them were imported from the CWD affected farm in Canada and the other 4 were gathered at the CWD affected farm (SK 3 farm) for quarantine and shipped to Korea on the same boat.

It can be considered that horizontal CWD transmission took place, but it is still unclear whether only 4 of the cohabitating Canadian deer became infected. Therefore, Korean authorities should exchange further information on the number of quarantine certificates and coupons with the Canadian Communicable Disease Control Department in order to re— investigate whether only 5 deer were raised at the CWD affected farm, with the other 4 deer being raised at a CWD free farm, or whether the disease was transmitted during shipping. Furthermore, why cohabitating Korean deer were not infected by CWD is considered to be a subject for further research.

The Korean Communicable Disease Control Department did its best to prevent the spread of CWD, but failed to trace back 43 out of 144 deer imported from Canada in 1997,

CHRONIC WASTING DISEASE CASES IN KOREA 759

Among these, 25 deer were from the CWD affected farm and 18 deer were imported with the deer from the CWD affected farm (Table 5). The department is currently investigating a new case of CWD found on Nov, 20, 2004 to determine whether it is a deer that was missing in 2001, or a vertically or horizontally transmitted deer. 

 ACKNOWLEDGMENTS, This work was supported by the National Veterinary Research & Quarantine Service, Anyang 430-016, Korea. 

REFERENCES 


Strain Characterization of the Korean CWD Cases in 2001 and 2004

Yoon-Hee LEE1), Hyun-Joo SOHN1)*, Min-Jeong KIM1), Hyo-Jin KIM1), Won-Yong LEE1), Eun-Im YUN1), Dong-Seob TARK1), In-Soo CHO1) and Aru BALACHANDRAN2)

1)Animal, Plant and Fisheries Quarantine and Inspection Agency, Ministry for Food, Agriculture, Forestry and Fisheries, Anyang 430–757, Republic of Korea

2)National and OIE Reference Laboratory for Scrapie and CWD, Ottawa Laboratory Fallowfield, Ottawa, Canadian Food Inspection Agency, Ottawa, Ontario K2H 8P9, Canada

(Received 22 February 2012/Accepted 14 August 2012/Published online in J-STAGE 28 August 2012)

ABSTRACT. Chronic wasting disease (CWD) has been recognized as a naturally occurring prion disease in North American deer (Odocoileus species), Rocky Mountain elk (Cervus elaphus nelsoni) and moose (Alces alces). The disease was confirmed only in elk in the Republic of Korea in 2001, 2004 and 2005. Epidemiological investigations showed that CWD was introduced via importation of infected elk from Canada between 1994 and 1997. In spite of the increasing geographic distribution and host range of CWD, little is known about the prion strain (s) responsible for distinct outbreaks of the disease. We carried out strain characterization, using transgenic mice overexpressing elk prion protein, including clinical assessment, pathological examination and biochemical analyses, in brain tissues derived following primary through tertiary transmissions. The final incubation period was shortened to approximately 130 dpi due to adaptation. Biochemical profiles remained identical between passages. Lesion profiling in recipient mice brains showed similar patterns of vacuolation scores and intensity. It is clear that there were no biochemical or histopathological differences in Korean CWD cases in 2001 and 2004, suggesting a single strain was responsible for the outbreaks.

Chronic wasting disease (CWD) has been recognized as an important prion disease in North American deer and Rocky mountain elk [13]. This disease was confirmed only in elk in the Republic of Korea in 2001, 2004 and 2005 [7, 10]. Additional CWD cases were observed in red deer, sika deer, and crossbred sika and red deer in 2010 (unpublished data). However, these cases were not included in the present study, which focuses only on elk CWD. Recently, using a model of transgenic mice overexpressing mule deer prion, the possibility of at least two CWD strains existing in North American cervids was raised [1]. More evidence on the two distinct CWD strains that originated from the mule deer was suggested using the ferret model [9] and from Syrian hamster model studies, and the emergence of a new “wasting strain” (WST) would appear to have occurred in white-tailed deer [2]. Epidemiological investigations showed that CWD was introduced to the Korean peninsula via importation of infected elk from Canada in 1994, 1995 and 1997 [7]. It is possible that more than one strain might have been introduced from Canada, although a Canadian retrospective study underway shows no emergence of other phenotypes so far (Dr. Gordon Mitchell, personal comm.). 

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KEY WORDS: CWD, Republic of Korea, strain characterization.

doi: 10.1292/jvms.12-0077; J. Vet. Med. Sci. 75(1): 95–98, 2013

see full text; 


Friday, May 13, 2011 

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea 


A Case of Chronic Wasting Disease in an Elk Imported to Korea from Canada 

Hyun-Joo SOHN, Jae-Hoon KIM, Kang-Seuk CHOI, Jin-Ju NAH, Yi-Seok JOO, Young-Hwa JEAN, Soo-Whan AHN, Ok-Kyung KIM, Dae-Yong KIM, Aru BALACHANDRAN Author information Keywords: chronic wasting disease, elk, immunohistochemistry JOURNALS FREE ACCESS 2002 Volume 64 Issue 9 Pages 855-858

DOI https://doi.org/10.1292/jvms.64.855

Abstract A seven-year-old male elk (Cervus elaphus nelsoni) was euthanized and necropsied after having a 3-week history of body weight loss, emaciation, excessive salivation, teeth grinding, fever, anorexia, and respiratory distress. The elk was imported into Korea from Canada on March 9, 1997. Gross pathologic findings were restricted to a diffuse fibrinous pneumonia. Microscopic lesions included mild neuronal vacuolation and spongiform change in the neuropil of selected brain stem nuclei and generalized astrocytosis. Immunohistochemistry for protease-resistant prion protein (PrPres) was positive in all brain sections but more pronounced in the section of the obex of the medulla. And the PrPres was also detected by western immunoblotting in the brain and spinal cord. All the remaining elk and deer that had been in contact with this elk were destroyed and negative for chronic wasting disease (CWD). To our knowledge, this is the first case of CWD occurring outside of the U.S.A. and Canada.

References (11)

see full text


P-147 Infection and detection of PrPCWD in soil from CWD infected farm in Korea

Hyun Joo Sohn, Kyung Je Park, In Soon Roh, Hyo Jin Kim, Hoo Chang Park, Byounghan Kim

Animal and Plant Quarantine Agency (QIA), Korea

Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrPSc). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrPSc. Chronic wasting disease (CWD) is the prion disease that is known spread horizontally. CWD has confirmed last in Republic of Korea in 2010 since first outbreak of CWD in 2001. The environmental reservoirs mediate the transmission of this disease. The significant levels of infectivity have been detected in the saliva, urine, and feces of TSE-infected animals. Using serial protein misfolding cyclic amplification (sPMCA), we developed a detection method for CWD PrPSc in soil from CWD affected farm in 2010. We found to detect PrPSc in soil from CWD infected farm, but not detect PrPSc in soil of wild cervid habitats and normal cervid farm in Korea. We also tried the bioassay on transgenic mice overexpressing elk prion protein (TgElk mice) to confirm infectivity of CWD-infected farm soil and washing solution of it. As the results, there was the presence of infectious prions in them. The attack rates were each 12.5% (1/8, soil) and 100% (6/6, soil washing solution). Our method appears to be a very useful technique for monitoring PrPSc levels in environmental conditions.

P-153

Experimental oral transmission of chronic wasting disease to sika deer (Cervus nippon)

Gordon Mitchell1, Hyun-Joo Sohn2, Yoon-Hee Lee2, Antanas Staskevicius1, Nishandan Yogasingam1, Ines Walther1, In-Soo Cho2, Aru Balachandran1

1National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada; 2Animal, Plant and Fisheries Quarantine and Inspection Agency, Ministry for Food, Agriculture, Forestry and Fisheries, Anyang, Republic of Korea

Chronic wasting disease (CWD) persists in North American cervids, and epidemiological evidence indicates CWD was introduced into the Republic of Korea approximately twenty years ago through the importation of an infected elk (Cervus elaphus) from Canada. Additional cases of CWD have since been detected in Korean elk, and recently for the first time in their farmed sika deer (Cervus nippon). Sika deer are also found in regions of North America and Europe, although natural transmission to these populations has not been detected. Understanding the pathogenesis of CWD in this species is therefore essential to developing diagnostic and disease control strategies.

Six sika deer were orally inoculated with a brain homogenate prepared from a farmed Canadian elk with clinical CWD. Four deer developed clinical signs consistent with CWD and were euthanized between 21 and 24 months post-inoculation (mpi). Two deer were removed from the study due to intercurrent disease, at 4 and 11 mpi. At necropsy, an array of tissues and bodily fluids were sampled and preliminary testing of brainstem and lymphoid tissue by ELISA, immunohistochemistry and western blot confirmed CWD transmission. Aggregates of pathological prion protein (PrPCWD) were detected in the retropharyngeal lymph nodes, but not brainstem of the deer sampled at 4 mpi. All other deer, including the deer tested at 11 mpi, displayed marked PrPCWD accumulation in brainstem and lymphoid tissues. Further immunohistochemical analysis of tissues from sika deer with clinical disease revealed widespread PrPCWD deposition in Iymphoreticular tissues, central and peripheral nervous systems, the gastrointestinal tract and neuroendocrine tissues. Western blot molecular profiles in sika deer brainstem samples were similar to the original elk inoculum. Ante-mortem biopsy of recto-anal mucosal associated lymphoid tissue, tested using immunohistochemistry, detected infected sika deer prior to the onset of clinical disease. These findings corroborate studies in other cervids, identifying early and widespread PrPCWD accumulation in tissues following oral inoculation. Efficient transmission of CWD to sika deer dictates a precautionary approach when exposing this species to environments or other cervids potentially infected with CWD.

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Prion 2016 Conference Poster Abstracts


Prion 2016 Oral Abstracts


Prion 2016 Prion Diseases in Animals


Prion 2016 Prion Diseases in Humans


Prion 2016 Invited Lecture Abstracts

IL-19: Epidemiological and clinical features of human prion diseases in Japan: Prospective 17-year surveillance
Masahito Yamada
Tsuyoshi Hamaguchi
Kenji Sakai
Ichiro Nozaki
Moeko Noguchi-Shinohara
Nobuo Sanjo
Tadashi Tsukamoto
Ryusuke Ae
Yosikazu Nakamura
Tetsuyuki Kitamoto
Hidehiro Mizusawa
CJD Surveillance Committee, Japan
Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan
Department of Neurology and Neurological Science, Tokyo Medical and Dental University, Graduate School of Medical and Dental Sciences, Tokyo, Japan
Department of Neurology, National Center of Neurology and Psychiatry, Tokyo, Japan
Department of Public Health, Jichi Medical University, Shimotsuke, Japan
Department of Prion Protein Research, Division of CJD Science and Technology, Tohoku University Graduate School of Medicine, Sendai, Japan
We analyzed the epidemiological and clinical features of patients with prion diseases registered by the Creutzfeldt-Jakob Disease (CJD) Surveillance Committee, Japan over the past 17 y since 1999. Until September 2015, we obtained information on 5,041 Japanese patients suspected as having prion diseases, and judged that 2,596 patients had prion diseases. The annual incidence rate/million of prion diseases during 1999-2013 ranged from 0.7 (1999) to 1.8 (2011/2012/2013) with an average 1.3. The 2,596 patients with prion diseases were classified into 1,999 (77.0%) with sporadic CJD (sCJD), 501 (19.3%) with genetic prion diseases, 87 (3.4%) with acquired prion diseases, including 86 cases of dura mater graft-associated CJD (dCJD) and one case of variant CJD, and 7 cases of unclassified CJD (0.3%). In sCJD, MM1 type (Parchi's classification) is most common; among atypical sCJD cases, MM2 type appeared most common, probably related to the fact that methionine homozygosity at codon 129 polymorphism of the prion protein gene (PrP) was very common (93%) in the general Japanese population. As for iatrogenic CJD, only dCJD cases were reported in Japan and, combined with the data from previous surveillance systems, the total number of dura mater graft-associated Creutzfeldt-Jakob disease was 149, comprising the majority of worldwide dCJD patients. Most of the dCJD patients received cadaveric dura mater graft before or in 1987, and we still had onset of dCJD cases in recent years; the incubation period (i.e., duration from implantation of dura mater grafts to dCJD onset) was increasing to 13.2 ± 6.3 (mean ± SD) years (range, 1 to 30 years). Regarding genetic prion diseases, the most common PrP mutation was V180I (46.7%), followed by P102L (16.6%), E200K (14.0%), and M232R (13.6%). The distribution of the mutations was quite different from that in Europe. The V180I and M232R mutations were quite rare worldwide. Interestingly, patients with V180I or M232R rarely had a family history of prion diseases, and our recent study with large population control cohorts indicated that such missense variants have significant effects on lifetime prion disease risk. In conclusion, our data from the prospective 17-year surveillance revealed distinct features of human prion diseases in Japan: frequent and continuous occurrence of dCJD, and unique phenotypes of sCJD and genetic prion diseases related to the characteristic distribution of PrP mutations and polymorphisms in the Japanese population, different from those in western countries.

IL-21: Surveillance of prion diseases in Taiwan
Shun-Sheng Chen
Taiwan C. J. D. Working Group
Department of Neurology, Kaohsiung Chang Gung Memorial Hospital, Taipei, Taiwan
CJD Working Group, Taiwan Neurological Society, Taipei, Taiwan
Objective: To compare the incidence rate from 1993 to 20105 and figure out the incidence increment and characteristics of CJD in Taiwan through Surveillance of prion disease in Taiwan.
Background: In Taiwan, national CJD surveillance unit (CJDSU) was setup in Taiwan Neurological Society since 1997. The incidence rates of CJD were raised up after 2007 in Taiwan and also in other industrial countries. For this reason, we try to figure out the risk factors which might be connected with this phenomenon.
Methods: Registry and Surveillance system in Taiwan: The surveillance system was a nationwide, hospital-based case report system, which was directed by the government organization, Centers for Disease Control of Taiwan, and Taiwan Neurological society since 1997. This CJDSU system performed a national survey to all the hospitals in Taiwan. In 2007, the health government announced CJD is one of the forth statutory epidemical diseases. All suspected cases are requested to registry on epidemical disease system online and notify the CJDSU for detail following and clinical tracing.
When a case is suspected, the infection control unite or neurologist will contact with CJDSU's assistant first and get a preparation note for continue work. The physician has to offer copy discs of EEG examination and MRI imagines and fill out 3 kinds of structured comprehensive questionnaire sheets. The CJD committee formed by experts of neurologists, neurosurgeons, radiologists and neuropathologists, would hold a case-identifying meeting to discuss the reported cases and determine the diagnosis of CJD.
Our criteria are based on the WHO and European CJD case definition criteria form the basis for disease classification, include EEG and MRI examination, while 'probable cases' and 'possible cases' are classified in accordance with recognized and validated clinical criteria. Also, we introduced 14-3-3 protein examination of cerebrospinal fluid as assistant criteria of CJD since 2000.
During period of 1 Jan 1997 to 31 Dec 2015, the CJDSU received more than 500 suspect TSE case notifications from 38 Neurological Training Centers in Taiwan. All cases are requested to registry online and notify the CJDSU for consensus of diagnosis, tracing and assess differences of categorical and continuous variables between 2 period groups (before and after 2007).
Results: There were more than 500 cases prospectively reported to the CJDSU. Among them, 370 cases were diagnosed with CJD; with a sex ration of M/F 1:1.09. All cases were refereed as probable or possible cases except 4 cases of GSS form and 1 probable case of new-variant CJD immigrant from UK. The incidence rates were between 0.30-1.492 per million populations, and case numbers had notified double during 2008 to 2015 with incidence raised up to 1.414, which had been fall after 2014. Between two groups, the clinical features, EEG , MRI, genetic polymorphism, and CSF 14-3-3 protein had no differences, but age-onset is earlier than before.
Conclusion: The incidence rate of CJD in Taiwan after 2007 was extremely higher than before, probably due to the physician´s sensitivity, improved reporting system, people concerning of variant CJD cases, and the high media coverage.
Keywords: CJD, incidence rate, nvCJD, polymorphism, Taiwan 
IL-22: Real-time quaking-induced conversion analysis for the diagnosis of sporadic Creutzfeldt-Jakob disease in
Korea
Yong-Sun Kim
Ilsong Institute of Life Science, Hallym University/Department of Neurodegenerative Diseases, Korea CJD Diagnostic Center, Chuncheon-si, Korea
The 14-3-3 protein is increased in the cerebrospinal fluid (CSF) of Creutzfeldt-Jakob disease (CJD) patients and has been thus used as a clinical biomarker for the pre-mortem diagnosis of human prion diseases. Nonetheless, the specificity of 14-3-3 protein is less reliable for CJD diagnosis. The newly developed assays including real-time quaking-induced conversion (RT-QuIC) made it possible to detect PrPSc-like abnormal prion isoform with a high sensitivity in animal and human specimens that might have a minute amount of PrPSc by in vitro prion replication. In this study, we performed a highly sensitive RT-QuIC assay using recombinant human PrP for the detection of PrPSc in CSF of 100 sporadic CJD (sCJD) patients in Korea. By analyzing CSF samples of 100 patients with sCJD and of 190 non-CJD patients based on the expression levels of 14-3-3, total tau and RT-QuIC assay, the positivity of RT-QuIC analysis was observed in 77 of 100 CSF samples (sensitivity 77%) but no positive in the non-CJD patients. The sensitivity of RT-QuIC in this study was similar to that in some previous reports and the specificity of RT-QuIC was higher than that of 14-3-3 in CSF, suggesting that RT-QuIC analysis can complement the weakness of the specificity of 14-3-3 for the diagnosis of sCJD. These results indicate that RT-QuIC might be of great use for rapid and specific diagnosis of sCJD and suggest a practicable novel method for the ante-mortem diagnosis of human prion diseases.
This research was supported by the National Research Foundation of Korea Grant Funded by the Korean Government (NRF-2011K3A1A1003362) and by Hallym University Specialization Fund (HRF-S-41).
Keywords. Creutzfeldt-Jakob disease, cerebrospinal fluid, RT-QuIC, 14-3-3, total tau
Prion 2015 Conference Poster Abstracts

2017 North American Deer Summit: CWD Is Worse Than We Thought 
2017 North American Deer Summit: CWD Is Worse Than We Thought 
BY JOSH HONEYCUTT AUTHOR OF BROW TINES AND BACKSTRAP
JUNE 9, 2017
The Chronic Wasting Disease Situation Is a Serious Threat
Despite those who foolishly brush CWD under the rug and claim it should be of no concern to you, it is a problem. Above is one of two panels of experts that discussed CWD at the 2017 North American Deer Summit. (Brita Lewis Turbyfill photo) Despite those who foolishly brush CWD under the rug and claim it should be of no concern to you, it is a problem. Above is one of two panels of experts that discussed CWD at the 2017 North American Deer Summit. (Brita Lewis Turbyfill photo) 

Chronic Wasting Disease (CWD) continues to worry deer biologists, managers and hunters across the country. It isn’t going away. It’s only getting worse.

Many people aren’t aware of CWD, or simply don’t understand the full breadth of the threat it poses. CWD is caused by an abnormal protein referred to as a prion. Prions are neither alive nor dead. You can’t kill it with heat or chemicals.

Once contracted, it is an always-fatal disease that thrives in the nervous system of cervids (deer, elk, reindeer and moose). It can be passed on through saliva, urine, feces, spinal and brain fluids, etc. Similar diseases affect other animals such as Bovine Spongiform Encephalopathy (BSE) which is also referred to as Mad Cow Disease. It’s also found in sheep, known as Scrapie. Interestingly enough, we already know that Creutzfeldt-Jakob Disease (CJD) — a sister disease to BSE and CWD — is capable of infecting humans.

The Issues We Face Several challenges arise with the big issue of CWD. First, we’re met with the challenge of detecting it. We don’t fully understand how it mutates (and science has proven that it can mutate). We have no cure. It’s killing deer throughout half the country and rapidly spreading. Managing it has been near to impossible. Too many people are brushing it under the rug. And funding we currently have for research, testing and management are pennies in comparison to what’s needed to defeat this disease.

“There are lots of hypotheses but very few facts we know about CWD,” said Dr. Grant Woods of Growing Deer TV. “There are some seemingly wild stories being spread such as ‘CWD is not a disease.’ It is a disease that as far as researchers know is 100 percent fatal to members of the deer family. There certainly seems to be a link between transporting deer and the spread of CWD. There are cases that have documented CWD-positive deer being moved and then new cases of CWD being detected at the destination. My message is that CWD is a very legitimate concern and that researchers, agencies, and sportsmen need valid information. Detailed research is needed hence funding is needed to protect deer species. They are certainly a national treasure.”

It’s Spreading to Places It’s Never Been

Ralph Meeker of the Arkansas Game and Fish Commission is on the front lines of the CWD battle. And Arkansas — a once declared CWD-free state little more than a year ago — is a prime example of just how fast things can change. According to Meeker, CWD was first detected there last February in a hunter-harvested elk. He said it was detected in a whitetail two weeks later. It’s already up to a 23 percent prevalence rate in the focal area. Approximately 20 percent of females and 32 percent of males have the disease where it’s prevailing most.

“I think Arkansas’s approach to managing CWD has been viewed by some people and organizations as being aggressive,” said Meeker. “However, our agency has spent a great deal of time with several different researchers, managers, and veterinarians from around the nation who are very familiar with CWD. And, I think that our agency has done a great job to ensure that we are asking the right questions in order to figure out what has and what hasn’t worked. Managing CWD is an example of adaptive management, adjusting deer management efforts on the ground to our every-changing knowledge of CWD.”

False Information Spread by the Captive Cervid Industry According to Lou Cornicelli of the Minnesota DNR and Clayton Wolf of the Texas Parks and Wildlife Department, many of those who have stock in the captive cervid industry will tell you high-fenced animals pose no threat to wild deer. They’ll say that CWD isn’t a serious disease and that it isn’t a significant threat to whitetails. Instead, they’ll claim it’s a political disease dreamed up to end high-fenced hunting. Some are even brave enough to say that EHD (a disease that is not always-fatal and entire populations of deer have grown resistant to) is more of a threat. So let’s put ethics and perceptions (of both hunters and non-hunters) of the high-fenced industry aside for a moment and only look at the health risks they pose to wild deer.

“Misinformation campaigns [spread] belief that CWD won’t impact hunting,” said Cornicelli. “First, the attempt by the farmed cervid industry to cast significant doubt about CWD, including bringing in paid consultants to cast that doubt. Second, some hunters are repeating much of the same information, I think to the detriment of long-term deer health. In some respects, there is a lack of desire to look past the immediate. Given deer are a public resource and agencies are charged with managing populations for the benefit of future generations, I think this is a real problem. A good discussion of how wildlife fits into the concept of Public Trust is important.”

It’s becoming a problem in states that allows captive breeding and hunting operations. This issue is especially growing in the likes of Texas and other key deer hunting states.

“While the disease appears to be off the radars of most hunters in Texas, except in areas where we have mandatory check stations, the majority of those who have been impacted have been cooperative and receptive to information that helps them make educated decisions regarding CWD,” said Wolf. “One of our greatest challenges, and an area we continue to struggle, is trying to debunk and correct the misinformation that’s out there about CWD. The majority of resistance and misinformation has originated from within the captive deer breeding community and its supporters. These folks are convinced the disease is political in nature, blown out of proportion by the government and those who are opposed to captive deer, and that CWD poses no real risk to the resource. Also, because 95 percent of Texas land falls under private ownership, we face an additional challenge from ranchers who fear the detection of CWD on their ranch could result in negative impacts to property values and revenue streams associated with hunting access.”

Is It True Humans Can’t Get It? 

It’s always been assumed that CWD cannot be transferred to humans. They also thought the same thing about Mad Cow Disease, until it happened, as well as hundreds of other diseases that can infect the human body. Interestingly enough, 70 percent of all human diseases originated from animals. At some point in history, each of those diseases — including some of the largest epidemics and pandemics — jumped the barrier and began to infect the human species. Can and/or will CWD do the same? We don’t yet know. But the latest research suggests it is much more likely than originally thought...

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TEXAS SUMMARY MINUTES OF THE 400th COMMISSION MEETING CWD TSE PRION TAHC April 17, 2018

V. SHEEP AND GOATS

A. Scrapie: The first positive scrapie case in Texas since 2008 was identified in the Panhandle in April 2016 and the flock and premises remains under quarantine.

Chronic Wasting Disease – NOT Approved – denied waiver to allow twin moose calves to enter Texas from a non-CWD monitored herd. According to Texas Administrative Code Title 4, Part 2, Chapter 51.10 all CWD susceptible species must meet federal requirements for interstate movements. Additionally, observation of an animal does not provide sufficient evidence of disease freedom, especially when applied to CWD.

VI. CERVIDS

A. Chronic Wasting Disease (CWD) in white-tailed deer (WTD): There are 5 positive WTD breeding facilities in Texas. The total number of positive WTD and current status of each facility is listed below:

Facility Current Status Number Positive

1 Depopulated in 2015 4

2 Depopulated in early 2016 5

3 Quarantined January 2016, managed on herd plan 28, 12 suspects, 2 elk

4 Quarantined March 2016, recently depopulated ~100 does and managed on a herd plan, 25

5 Quarantined May 2017, depopulated herd October 2017 2

In late FY 2017, USDA informed TAHC that some end of year CWD indemnity funds were designated to Texas for the current positive herds. USDA required complete depopulation of the newest facility (Facility #5) based on the smaller size. The herd was depopulated in October and one additional positive doe was disclosed. The remaining available funds were allocated to use on facility 4 to remove deer in high risk pens. Of the 100 deer depopulated in facility #4, 9 were positive and all 9 were in pens in the same section as the index pen. In addition, a hunter harvested buck at facility #4 was positive that was harvested in November 2017.

In facility #3, since January 2016, there are a total of 28 positives and 12 suspects (tonsil biopsy confirmed positive only at this time) WTD. Of those, 31 are from the breeder pens or grower pens (17 bucks and 14 does). In addition, there were 9 positives disclosed from hunter harvested samples from 4 different pastures (6 bucks, 3 does). And there were 2 positive elk cows disclosed from 117 samples in 1 pasture. Both cows were natural additions to the elk herd.

The free ranging summary for the 2017-2018 hunting season include 2 positive mule deer from Hudspeth County, 2 mule deer from Hartley County, and 1 WTD from Hartley County. The WTD was on the Containment Zone border and a slight adjustment to that zone will be addressed before the next hunting season.

8

Summary Minutes of the 400th Commission Meeting – 4/17/2018

9

Statewide exotic CWD susceptible species surveillance monitoring in ongoing. General surveillance includes any facility that is testing CWD susceptible species for their annual premise requirement. Hunter harvest samples include samples collected at check stations in one of the 3 zones (the Panhandle, West Texas, or Medina area). Samples collected on positive premises include testing to meet requirements for a positive premise herd plan.

CWD Susceptible Species Surveillance 2017-18

Exotic Species General Statewide Surveillance Positive PremiseContainment Zone* Hunter Harvest in Zones for ’17-18

Positive Negative Positive Negative Positive Negative

Red Deer 0 70 0 14 0 8

Elk 0 30 2 (cows) 115 0 19

Sika 26 0 1 0 4

Total 0 126 2 130 0 31



SUNDAY, JUNE 17, 2018 

Houston Chronicle Texas deer population would welcome good soaking, deer herd, the largest in the nation, will remain stunningly healthy, what about CWD TSE Prion?


SUNDAY, JUNE 10, 2018 

TEXAS SUMMARY MINUTES OF THE 400th COMMISSION MEETING CWD TSE PRION TAHC April 17, 2018


THURSDAY, MAY 17, 2018 

Texas TAHC CWD TSE Prion Pay to Play Federal Indemnity Program, or what i call, ENTITLEMENT PROGRAM for Game Farm Industry


SATURDAY, MARCH 31, 2018

TEXAS DETECTS IT'S 101 CASE of CWD TSE PRION Breeder White-tailed Deer with no end in sight

2018 03/27/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5


THURSDAY, MARCH 22, 2018 

TEXAS CWD TSE PRION JUMP TO 100 POSITIVE, NEW CASES 17 BREEDER, 1 BREEDER RELEASE, AND 1 WILD SINCE JAN 31, 2018


WEDNESDAY, FEBRUARY 21, 2018 

TEXAS TPWD CWD TSE PRION 2 MORE FROM BREEDER RELEASE SITE TOTALS 81 CASES TO DATE


WEDNESDAY, JANUARY 24, 2018

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING, JUMPS TO 79 CASES TO DATE


FRIDAY, FEBRUARY 16, 2018 

***> Texas Deer Breeders Continue fight against the state’s wildlife agency and its regulations trying to contain CWD TSE Prion


Saturday, April 02, 2016

*** TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE


SUNDAY, MAY 22, 2016 

***> TEXAS CWD DEER BREEDERS PLEA TO GOVERNOR ABBOTT TO CIRCUMVENT TPWD SOUND SCIENCE TO LET DISEASE SPREAD


SATURDAY, JULY 09, 2016

Texas Intrastate – within state movement of all Cervid or Trucking Chronic Wasting Disease CWD TSE Prion Moratorium


Monday, July 18, 2016

Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster


TUESDAY, AUGUST 02, 2016

TEXAS TPWD Sets Public Hearings on Deer Movement Rule Proposals in Areas with CWD Rule Terry S. Singeltary Sr. comment submission


Wednesday, September 28, 2016

TPWD CWD Sample Collector Trainings in the Trans Pecos and Panhandle


Wednesday, November 09, 2016

Chronic Wasting Disease (CWD) Program Standards - Review and Comment By Terry S Singeltary Sr. November 9, 2016


Friday, November 18, 2016

IMPORTANT: SAWCorp CWD Test is NOT APHIS Approved


Thursday, December 08, 2016

TEXAS TAHC confirmed Chronic Wasting Disease (CWD) in a free-ranging elk Dallam County


Saturday, December 03, 2016

*** TEXAS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE 35 CASES TO DATE


FRIDAY, JANUARY 20, 2017 TEXAS TAHC

The Chronic Wasting Disease Rule Proposal Republished for Comment January 20, 2017


SUNDAY, JANUARY 22, 2017

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


WEDNESDAY, JANUARY 25, 2017

Texas First Case of CWD Detected in Free-Ranging Texas Whitetail Surveillance Zone 3 in Medina County


THURSDAY, JANUARY 26, 2017

Texas CWD Discovered Free-Ranging Whitetail DEER Houston Chronicle Shannon Tompkins PLEASE, CAN YOU HEAR ME NOW?


TEXAS HISTORY OF CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD COW TYPE DISEASE




SEE OIE CWD


CANADA CWD TSE PRION

Canada Chronic Wasting Disease Voluntary Herd Certification Program Updated

April 03, 2018

Please be advised that the Canadian Food Inspection Agency has updated the following module of the Accredited Veterinarian’s Manual:

Module 13––Chronic Wasting Disease Voluntary Herd Certification Program


The transition period for implementation of the updated National Standards has ended. The 2017 National Standards are in effect for all regional VHCPs in Canada. As a result, the Accredited Veterinarian’s Manual has been updated to remove the 2003 National Standards. All veterinarians accredited for this function must ensure that their knowledge is up-to-date in accordance with the 2017 National Standards and updated Module 13.

There has been a further change in Appendix 4: Program Administration and Status Assessment by Region to update the contact information for Quebec.

Please be advised that the previously announced updates to the national chronic wasting disease (CWD) disease response program came into effect on April 1, 2018. 

Key changes to the CWD disease response include:

• CFIA's response for CWD is moving from an eradication to a control program. • CFIA will only offer full disease response to CWD infected cervid herds enrolled in the voluntary herd certification program (VHCP). Of those herds eligible for CFIA implemented disease control measures, the producer or operator will be able to opt out of a full CFIA implemented disease response (destruction, disposal and associated decontamination). • Any herd infected with CWD and not enrolled in the VHCP will be subject to limited disease control measures.

Accordingly, updates have been made to the CWD fact sheet and the “What to Expect if Your Animals May Be Infected” page on the CFIA’s website. These updated pages may be accessed via the following link: http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/cwd/eng/1330143462380/1330143991594

A transition period is being provided throughout 2018 to give producers time to enroll in and complete 12 months in a VHCP. Starting April 1, 2019, the CFIA will only offer a full disease response to and compensate affected producers who have been enrolled in and compliant with a VHCP for at least 12 months.

To enroll in a VHCP, please contact the appropriate regional administrator in your region of Canada: http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/accredited-veterinarian-s-manual/chapter-13/eng/1502219878461/1502219878904?chap=11

Please be advised that the previously announced updates to the national chronic wasting disease (CWD) disease response program came into effect on April 1, 2018. 

Key changes to the CWD disease response include:

• CFIA's response for CWD is moving from an eradication to a control program.

• CFIA will only offer full disease response to CWD infected cervid herds enrolled in the voluntary herd certification program (VHCP). Of those herds eligible for CFIA implemented disease control measures, the producer or operator will be able to opt out of a full CFIA implemented disease response (destruction, disposal and associated decontamination). 

• Any herd infected with CWD and not enrolled in the VHCP will be subject to limited disease control measures.

Accordingly, updates have been made to the CWD fact sheet and the “What to Expect if Your Animals May Be Infected” page on the CFIA’s website. These updated pages may be accessed via the following link: 


A transition period is being provided throughout 2018 to give producers time to enroll in and complete 12 months in a VHCP. Starting April 1, 2019, the CFIA will only offer a full disease response to and compensate affected producers who have been enrolled in and compliant with a VHCP for at least 12 months.

To enroll in a VHCP, please contact the appropriate regional administrator in your region of Canada: http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/accredited-veterinarian-s-manual/chapter-13/eng/1502219878461/1502219878904?chap=11

''Caribou concerns Alberta’s threatened woodland caribou could also be at risk, said University of Alberta researcher Debbie McKenzie, who is among a group of scientists funded by the Alberta Prion Research Institute. “That’s one thing that we’re very concerned about,” she said, adding at least four CWD strains have been confirmed.''

*** AT LEAST FOUR STRAINS OF CHRONIC WASTING DISEASE CWD TSE PRION HAS BEEN CONFIRMED! 

Province of Alberta 

The 29th Legislature Fourth Session Alberta Hansard 

Thursday afternoon, March 15, 2018 Day 5 The Honourable Robert E. Wanner, Speaker 

 Chronic Wasting Disease 

 Dr. Swann: Mr. Speaker, we learned nothing from the BSE crisis. Mad cow disease, an incurable and rapidly fatal infectious prion disease of the brain, devastated our cattle industry 15 years ago at roughly a cost of $10 billion in lost markets. Conventional wisdom at the time assured us that this could not be transmitted to humans. This proved wrong, and variant CJD cost over 200 human lives. 

 CWD, chronic wasting disease, is a similar, decades-old prion disease which began in deer and elk farms and is now growing across western Canada in the wild. It is spread easily from body fluids, not only from eating the meat, across the deer family, with weak and inconsistent provincial and federal control measures. Both game farming and wildlife management are provincial issues, but the federal food inspection agency, CFIA, sets the standards for meat safety and just last year relaxed the regulations for controlling this disease. 

 Paul Glover, the CFIA director, wrote the following: since 2010 CWD has spread and become firmly established in wild cervids in Saskatchewan and Alberta and cannot be eradicated with the tools currently available. End quote. This highlights the failure of cooperation between federal and provincial governments in control measures. 

 Recent U of C studies on CWD showed that it can be transmitted to experimental monkeys after they eat the flesh of infected deer. This is mobilizing the wildlife and hunting community, especially indigenous communities who depend on wild game. It’s also the agricultural community’s worst nightmare. We know that a significant number of infected deer and elk are consumed without being properly tested. 

 Dr. Neil Cashman, a noted neurobiologist and prion scientist from UBC, recently said, quote, we appear to be waiting till CWD is found in humans, end quote, before taking serious action on control and elimination of the disease. 

 This provincial government is negligent. We have learned nothing from . . . 

 The Speaker: Thank you, hon. member 


 FRIDAY, DECEMBER 15, 2017

Canada CFIA updating its national CWD TSE PRION efforts to eradicate disease farmed cervid NOT successful December 14, 2017


SUNDAY, JULY 02, 2017 

CFIA Notice to Industry – Updates to the federal management of chronic wasting disease in farmed cervids


FRIDAY, JUNE 02, 2017

Alberta Canada Chronic Wasting Disease (CWD) Surveillance Update: 2016/17 Final


MONDAY, MARCH 13, 2017

Herds infected with Chronic Wasting Disease in Canada – 2017


SUNDAY, SEPTEMBER 04, 2016 

Stakeholder Perspectives on Chronic Wasting Disease Risk and Management on the Canadian Prairies 


WEDNESDAY, APRIL 04, 2018 

Canada Chronic Wasting Disease Voluntary Herd Certification Program Updated


MONDAY, JUNE 12, 2017

Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?


WEDNESDAY, MAY 17, 2017

*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***


IOWA CWD TSE Prion


Chronic wasting disease found for the first time in deer outside of northeast Iowa 

FEBRUARY 8, 2018 BY DAR DANIELSON

The Iowa Department of Natural Resources reports the first confirmed case of chronic wasting disease (CWD) in a county outside of northeast Iowa.

Widlife biologist Terry Haindfield says a doe taken in the first shotgun season tested positive for the disease. “In the southeast corner of Wayne County, Iowa. It’s about five miles from the Missouri border,” Haindfield says. He says Missouri has had positive tests for CWD that were about 50 miles from where the deer tested positive in Wayne County.

Haindfield says it is a little disappointing to find CWD in a new county. “It is somewhat inevitable, but we were hoping to have that delayed as long as possible,” he says. The DNR plans to set up a meeting in Wayne County to discuss what this means for local hunters and landowners and listen to their concerns on the disease.

The tests from the 2017 season also found more positives in the northeast Iowa counties that had previously been the only areas to show the disease in wild deer. “We are at eight more in Allamakee County and one in Clayton County,” Haindfield says. “We do have some tests results that we are waiting for on the special test we did not long ago.”

Those special tests were in Allamakee and Clayton counties in January as a follow up to the positive tests there from the 2016 hunting season. There is a possibility that the deer in northeast Iowa could have come from across the border in other states that have had positive tests.

The DNR collected extra samples from deer taken in western Iowa this year after 5 deer harvested in southeast Nebraska in 2016 tested positive. Haindfield says with almost all of those tests back there hasn’t been any positive tests reported there. Haindfield says Iowa is still overall in a lot better shape than many other states.

“You look at adjacent states where they are having 200 or 300 positives that are coming back from their hunter-harvest collections and we’re still on really early onset of this disease. And although we are seeing some movement there — I actually was pleased that we didn’t go more exponential with positives in northeast Iowa,” Haindfield says. “And right now all we know of this in Wayne is that it is one positive.”

He says they contact hunters when a deer tissue test comes back positive. He says they find out if they have shared the meat with others and offer to help dispose of the meat. “That would be of their choosing. This is not a health test that we do, but it is additional information that they can use to make those decisions,” according to Haindfield. The DNR says chronic wasting disease is a neurologic disease apparently affecting only deer, moose and elk. It is always fatal.

The disease first appeared in the wild deer herd in 2013 and each year since, the Iowa DNR has placed extra emphasis on tracking the movement and attempting to stop or slow the disease with the cooperation of hunters.


THURSDAY, FEBRUARY 08, 2018 

Iowa DNR Wayne County Confirms CWD with 7 additional CWD positive tests so far from deer in northeast from 2017 season


IOWA CWD CAPTIVE

i remember an old thread on a game farms forum long time ago, when all that was going on with the Brakkes, before the beginning of the depopulation, i have the complete thread downloaded somewhere, but its not on the web anymore. i think they had forgot i was on the board at the time. but it was when cwd was first confirmed, before the eradication and testing, during litigation, when the Brakkes were rounding up support, and there was a thread where they all were talking of going and cutting the fences and let all those cwd exposed deer were penned in at, this was because the Brakkes posted a photo of all those healthy looking deer, yet she did not know at the time most had cwd, and in the end, the count was around 80% positive in the end, but how many more and of what, were exposed, during that time period of litigation??? the whole situation really sad. here is a small portion of that thread...

=====

#10 This is What CWD Looks Like on Our Farm: 

post #10 G O Whitetails G O Whitetails Senior Member

Posted August 03 2014 - 02:51 PM

I think we should do what they did at Wind Cave. Let's just take the fence down and let them loose. Gary

Whitetail Sanctuary, IowaMike, sdbigbucks and 2 others like this

#11 This is What CWD Looks Like on Our Farm: post #11 Bell Bell Senior Member

Posted August 03 2014 - 03:04 PM Gary

That would bring the news. If 100 deer farmers showed up and started taking the fence down. I think another great idea would be to take all the staples out but one then as soon as they fired the first killing shot with all the media present let it go. They will knock that last staple out. 

Rhonda Brakke and Deer MGR 200 like this

Jonathan Bell & Jerry Bell Hurricane Creek Whitetails Greensburg, Indiana 

http://www.deerforums.org/

http://www.deerforums.org/index.php?/topic/9659-this-is-what-cwd-looks-like-on-our-farm/

http://www.deerforums.org/index.php?/topic/9659-this-is-what-cwd-looks-like-on-our-farm/page-2

 >>> Let's just take the fence down and let them loose.

 I THOUGHT that had already been done on the Brakkes farm ???

=====see;





B. September 7, 2012 Agreement. On September 7, the Brakkes and the DNR signed an “Agreement for Chronic Wasting Disease Recovery Plan at Pine Ridge Hunting Lodge” (Agreement). Under the Agreement, the Brakkes were allowed to carry out planned hunts at Pine Ridge scheduled between September 8, 2012, and December 25, 2012. The Brakkes, however, were required to install jointly with the DNR an electronic fence inside the perimeter of the existing fence surrounding Pine Ridge, with the costs split evenly between the DNR and Pine Ridge. After construction of the electric fence, the Brakkes were solely responsible for fence repair and maintenance. DNR staff was to conduct weekly perimeter and fence inspections, with all repairs identified by DNR staff to be submitted to the Brakkes in writing and completed by the Brakkes within twenty-four hours.

snip...

By June 5, the DNR discovered the gates at Pine Ridge were standing open and that portions of the fence were damaged or had been removed. D. The Emergency Order. On June 6, the DNR issued an emergency order to require the Brakkes to stop their deconstruction of the fence surrounding Pine Ridge and to immediately restore the portions of the fence that were damaged. The emergency order also required the Brakkes to close and keep closed all of the gates and to authorize the DNR to access Pine Ridge for a limited duration in order to kill any deer that may be present on the property. Finally, the emergency order required the Brakkes submit and agree to execute a plan designed to ensure that CWD be quarantined within, and not spread beyond, Pine Ridge. On June 7, the Brakkes closed the gates at Pine Ridge and repaired the fence. On June 11, however, wild deer were seen inside the fence.



IOWA, AS of Spring of 2018, 28 deer have tested positive for CWD...

Iowa Chronic Wasting Disease May 23, 2018 | 6 min


MICHIGAN CWD TSE PRION

Michigan CWD TSE reaches 58 cases to date;


THURSDAY, JUNE 21, 2018 

Michigan First case of chronic wasting disease suspected in Jackson County


THURSDAY, JUNE 07, 2018 

Michigan DNR to present chronic wasting disease recommendations to Natural Resources Commission Singeltary submission


WEDNESDAY, MARCH 07, 2018 

***> Michigan DNR CWD National Perspective: Captive Herd Certification Program - Dr. Tracy Nichols


***> CURRENT STATUS OF CWD IN CAPTIVE CERVID HERDS IN 16 STATES AS OF MAY 2017

43 ELK HERDS

37 WTD HERDS

1 RED DEER HERD

6 MIX SPECIES HERDS

85 CWD-POSITIVE CAPTIVE HERDS 

snip...see


THURSDAY, JUNE 21, 2018 

Michigan First case of chronic wasting disease suspected in Jackson County


WEDNESDAY, MARCH 07, 2018 

***> Michigan DNR CWD National Perspective: Captive Herd Certification Program - Dr. Tracy Nichols


***> CURRENT STATUS OF CWD IN CAPTIVE CERVID HERDS IN 16 STATES AS OF MAY 2017

43 ELK HERDS

37 WTD HERDS

1 RED DEER HERD

6 MIX SPECIES HERDS

85 CWD-POSITIVE CAPTIVE HERDS 

snip...see


THURSDAY, JUNE 07, 2018 

Michigan DNR to present chronic wasting disease recommendations to Natural Resources Commission Singeltary submission

FRIDAY, MARCH 30, 2018 

PLEASE WATCH THIS VIDEO, AND BE SURE TO SEE AROUND THE 8 MINUTE MARK, VERY, VERY, DISTURBING...terry



WISCONSIN CWD TSE PRION


LISTEN TO THIS NICE LITTLE CWD BLUES DIDDY BY TAMI ABOUT WISCONSIN CWD TSE PRION. WOW, ANNUAL UPDATES NOW, FROM HERE ON OUT, ABOUT CWD...200,000 CWD TESTS, WITH OVER 3500 CWD POSITIVE CASES, SEEING INCREASING TRENDS IN PREVALENCE AND DISTRIBUTION...CARCASS DISPOSAL SIGNIFICANT CHALLENGE...CWD SAMPLING EFFORTS GONE DONE, WHILE CWD POSITIVES HAVE GONE UP...ALSO, 40 SELF SERVING KIOSKS ACROSS STATE AND FREE HUNTER SERVICE CWD TESTING AND SICK DEER POLICY REPORTING AND TESTING ACROSS STATE!



MONDAY, JUNE 18, 2018 

Wisconsin DATCP Confirms CWD-Positive Deer in Marinette County farm has been quarantined


WEDNESDAY, JUNE 13, 2018 

Wisconsin DATCP NVSL confirmed 21 WTD from a deer farm Iowa County tested positive for chronic wasting disease (CWD)



FRIDAY, FEBRUARY 16, 2018 

Wisconsin Deer from Now-Quarantined PA Lancaster County Farm Tests Positive for Chronic Wasting Disease CWD TSE Prion


FRIDAY, JANUARY 26, 2018 

WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE


Feb. 16, 2018

Durkin: Stop private deer industry from trucking CWD across state 

Patrick Durkin, For USA TODAY NETWORK-Wisconsin Published 10:13 a.m. CT Feb. 16, 2018 

A Waupaca County captive-deer shooting preserve that discovered its first two cases of chronic wasting disease in October found 10 more CWD cases last fall, with 11 of the deer coming from a breeding facility in Iowa County — Wisconsin’s most infected county.

Hunt’s End Deer Ranch near Ogdensburg is one of 376 fenced deer farms in Wisconsin, according to the Department of Agriculture, Trade and Consumer Protection. Hunt’s End bought the diseased deer from Windy Ridge Whitetails, a 15-acre, 110-deer breeding facility south of Mineral Point in Iowa County. Of Wisconsin’s 4,175 CWD cases in wild deer, 2,261 (54 percent) are in Iowa County.

Since CWD’s discovery in three wild deer shot during the November 2001 gun season, CWD has been detected on 18 Wisconsin deer farms, of which 11 were “depopulated.” DATCP has identified 242 CWD cases in captive facilities the past 16 years.

The state’s worst site remains the former Buckhorn Flats Game Farm near Almond in Portage County, where 80 deer tested positive for this always-fatal disease from 2002 to 2006. When the U.S. Department of Agriculture shot out the 70-acre pen in January 2006, 60 of the remaining 76 deer carried CWD, a nearly 80 percent infection rate. 

The Department of Natural Resources bought the heavily contaminated site for $465,000 in 2011 and has kept it fenced and deer-free since.

The last time DATCP exterminated a captive herd was November 2015, when it killed 228 deer at Fairchild Whitetails, a 10-acre breeding facility in Eau Claire County, and paid its owner, Richard Vojtik, $298,770 in compensation. Tests revealed 34 of those deer carried CWD (15 percent), but two bucks had escaped earlier. Those bucks roamed five months before being shot and tested. They, too, had CWD.

Both operations were outside the endemic CWD region in southern Wisconsin; Buckhorn Flats by about 60 miles and Fairchild Whitetails by about 120. Wisconsin’s four most active CWD outbreaks on deer farms are north of U.S. 10, and farther away from the endemic region — basically the DNR’s Southern Farmlands district — which had 584 CWD cases 2017-18 and 4,148 since 2001.

Those businesses are:

• Wilderness Whitetails, near Eland in Marathon County: 68 CWD cases, including 43 in 2017-18. DATCP first reported CWD there in December 2013 in a 5-year-old buck shot by a facility client. The operation also found three cases in 2014, nine in 2015 and 12 in 2016. 

The preserve held about 310 deer in its 351-acre pen last summer. Since beginning tests in 2002, the facility tested 373 deer before finding its first case 11 years later.

• Hunt’s End, Waupaca County: 12 cases, all in 2017-18. The owners, Dusty and Mandy Reid, didn’t detect CWD on the 84-acre shooting facility until two 4-year-old bucks tested positive last fall. DATCP announced those cases Oct. 20, and disclosed 10 additional cases in response to my open-records request in January.

Both Oct. 20 bucks originated from Windy Ridge Whitetails. Nine other bucks from Windy Ridge, owned by Steven and Marsh Bertram, tested positive for CWD after being shot by Hunt’s End clients.

Now DATCP records covering the past five years showed Hunt’s End acquired 31 deer from Windy Ridge, which also sent a combined 67 whitetails to nine other Wisconsin deer farms during that period.

Paul McGraw, DATCP’s state veterinarian and administrator in animal health, quarantined three Hunt’s End properties Oct. 20, but let its owners, continue selling hunts because “properly handled dead animals leaving the premises do not pose a disease risk.”

McGraw also quarantined Windy Ridge, but the specifications let the business move more deer to the Waupaca shooting facility. It made two more shipments to Hunt’s End, the last occurring Nov. 13.

• Apple Creek Whitetails, Oconto County: 11 cases. Since discovering CWD in September 2016 in an 18-month-old doe killed inside the facility near Gillett, DATCP has identified 10 more cases, including three in 2017-18. The preserve held about 1,850 deer on 1,363 acres, and tested 466 in 2016. After first testing for CWD in 2009, the business processed 1,192 deer before finding its first case 18 months ago.

• Three Lakes Trophy Ranch, Oneida County: Nine cases. Since discovering CWD in December 2015 in a 3-year-old buck at Three Lakes, DATCP has identified eight more cases, including two in 2017-18. The preserve held about 545 whitetails on 570 acres.

Although the Hunt’s End outbreak traces to Iowa County deer, Windy Ridge Whitetails sent even more deer, 42, to Vojtik’s American Adventures Ranch near Fairchild with no documented problems. DATCP reports no CWD cases there, and Vojtik, who also owned the 10-acre Fairchild Whitetails breeding facility, said he hasn’t bought Windy Ridge deer the past two years.

Vojtik said Wednesday that he and his clients shoot out his enclosure’s herd of about 200 deer each year to reduce CWD risks. And because he’s not in DATCP’s herd-status program, he must only test 50 percent of deer dying there.

Meanwhile, Wilderness Whitetails tests all of its dead deer. It leads the state with 68 CWD cases, even though it has maintained a “closed herd” since opening its Eland facility in 2004, said its owner, Greg Flees, when reached Wednesday. Flees said all deer in the 351-acre facility were born there or came from his family’s Portage County breeding pen, which began in the 1970s and has never had CWD.

Flees said the jump from 12 CWD cases in 2016 to 43 in 2017 is no mystery or surprise. “We shot more deer to lower our densities, so we found more CWD,” he said. He thinks CWD was in the facility’s soils when they enclosed it with an 8-foot-high fence 14 years ago, or it arrived in alfalfa bales brought in for feed.

Perhaps the bigger mystery is why DATCP allows any deer from Iowa County to be shipped anywhere. Windy Ridge Whitetails is one of eight captive-deer facilities in CWD-infected counties — Sauk, Dane, Iowa, Rock, Walworth and Richland — enrolled in DATCP’s herd-status program, which allows deer transfers if facilities follow specified guidelines.

That won’t change soon, either. In a letter Jan. 30 responding to my open records request, Paul Dedinsky, DATCP’s chief legal counsel, wrote, “The Department is not proposing any rule changes to prohibit movement from CWD endemic areas.”

No doubt Wisconsin’s wild deer provide a vast, mostly undocumented pool for spreading CWD, but sick deer can only carry disease as far as they walk. With DATCP’s approval, privately owned deer could spread CWD wherever they’re trucked.

Patrick Durkin is a freelance writer who covers outdoors for USA TODAY NETWORK-Wisconsin.. Email him at patrickdurkin56@gmail.com.


FRIDAY, FEBRUARY 16, 2018 

Wisconsin Stop private deer industry from trucking CWD across state


captive deer farmers breeders entitlement program, i.e. indemnity program, why?

how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms, and why do tax payers have to pay for it ???

WEDNESDAY, FEBRUARY 10, 2016 

Wisconsin Two deer that escaped farm had chronic wasting disease CWD



FRIDAY, FEBRUARY 03, 2012 

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


Tuesday, December 20, 2011

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

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.

SUMMARY:



PENNSYLVANIA CWD TSE PRION


FRIDAY, JUNE 15, 2018 

Pennsylvania CWD Cases Triple in One Year



MONDAY, FEBRUARY 12, 2018 

Pennsylvania CWD TSE Prion has been found in captive deer in Huntingdon and Lancaster counties



SATURDAY, JANUARY 20, 2018

Pennsylvania CWD TSE Prion Cases Explodes 51 deer from the 2017-18 hunting seasons have 
tested positive for CWD majority of samples collected still are being analyzed

http://chronic-wasting-disease.blogspot.com/2018/01/pennsylvania-cwd-tse-prion-cases.html


U.S. Attorneys » 

District of Kansas » 

News SHARE Department of Justice U.S. Attorney’s Office District of Kansas 

FOR IMMEDIATE RELEASE 

Monday, February 5, 2018 

Pennsylvania Outfitter Pleads Guilty To Violating the Lacey Act in Kansas 

WICHITA, KAN. – A Pennsylvania man who owns a company called Horseshoe Hill Outfitters pleaded guilty Monday in federal court in Kansas to violating the Lacey Act, U.S. Attorney Stephen McAllister said.

Robert P. McConnell, 48, Slippery Rock, Penn., pleaded guilty to four counts of importing deer into Kansas in violation of the Lacey Act, which regulates the trade in wildlife, fish and plants that has been illegally taken, possessed, transported or sold. Horseshoe Hill Outfitters advertises what it calls “trophy North American big game hunting adventures” in Kansas, Pennsylvania, New Mexico and Ontario.

In two counts, McConnell admitted importing deer that were not from an accredited heard, were not officially identified and did not have a certificate of veterinary inspection. In two other counts, he admitted importing domesticated deer.

Sentencing is set for May 21. Both parties have agreed to recommend a sentence of five years on probation during which McConnell is prohibited from doing business in Kansas, and a fine of not less than $10,000.

McAllister commended the U.S. Fish and Wildlife Service and Assistant U.S. Attorney Greg Hough for their work on the case.

Topic(s): Wildlife Component(s): USAO - Kansas Updated February 5, 2018



MISSOURI CWD TSE PRION


THURSDAY, JUNE 28, 2018 

Missouri Hunters For Fair Chase Docket No. APHIS-2018-0011 (APHIS) Notice: Chronic Wasting Disease Herd Certification Program Standards


TUESDAY, JUNE 19, 2018 

Missouri MDC sets CWD sampling efforts for upcoming deer season with 75 free ranging deer confirmed positive to date



January 14, 2018

Missouri MDC REPORTS 15 NEW CASES OF CWD TSE Prion in Deer

http://chronic-wasting-disease.blogspot.com/2018/01/missouri-mdc-reports-15-new-cases-of.html


COLORADO CWD TSE PRION


MONDAY, MAY 21, 2018 

Colorado Chronic Wasting disease CWD TSE Prion hits 16 percent of male deer, elk, moose tested in some parts of state



TUESDAY, JANUARY 30, 2018 

Colorado Chronic Wasting Disease CWD TSE Prion 7/2015-6/2016 Results (2017?)

http://chronic-wasting-disease.blogspot.com/2018/01/colorado-chronic-wasting-disease-cwd.html


MINNESOTA CWD TSE PRION



SATURDAY, APRIL 21, 2018 

MINNESOTA STATE AUDITORS Board of Animal Health has failed to enforce some laws relating to deer and elk farms A CWD TSE PRION GLOBAL UPDATE


FRIDAY, NOVEMBER 24, 2017 

Todd Robbins-Miller President of Minnesota Deer Farmers Association is oblivious to Chronic Wasting 
CWD TSE PRION DISEASE risk factors

http://chronic-wasting-disease.blogspot.com/2017/11/todd-robbins-miller-president-of.html

WEDNESDAY, NOVEMBER 22, 2017 

Minnesota Chronic Wasting Disease discovered in Winona County farm

http://chronic-wasting-disease.blogspot.com/2017/11/minnesota-chronic-wasting-disease.html


MONTANA CWD TSE PRION


CURRENT CWD POSITIVES SHOW 10 CASES



Montana Fish, Wildlife, and Parks’ 2017 

Chronic Wasting Disease Surveillance and Special Hunt Report

Discussion 

In the fall of 2017, Montana unfortunately joined the ranks of the now 23 states and 2 provinces that have detected CWD within their wild cervid populations in North America. Between general surveillance efforts and the ensuing Special CWD Hunts that were called to measure prevalence and distribution, we identified CWD-positive areas in south-central and north-central Montana. We found no additional positives during the Sage Creek Hunt on our northern border, suggesting that that local mule deer prevalence there is quite low (<1 div="" nbsp="">

***However, we did identify a larger CWD endemic area in south-central Montana with prevalences of 2% in mule deer and 1% in white-tailed deer. 

***Within the southern-most hunt district in the Bridger Special Hunt Area, where positive CWD cases were clustered, we estimated prevalences as high as 8% in mule deer. 


Montana Fish, Wildlife and Parks CWD Action Team April 19, 2018


CWD and human health

To date, several lines of evidence suggest that humans are at low risk of contracting CWD. There have been no documented cases of CWD causing disease in humans, despite epidemiological investigations of known or suspected exposures (Belay et al. 2004, MaWhinney et al. 2006). Several studies have demonstrated that normal prion proteins in humans, either in cell-free culture (Raymond et al. 2000) or as expressed in transgenic mice (Kong et al. 2005, Tamgüney et al. 2006, Sandberg et al. 2010, Wilson et al. 2012), do not readily convert to the diseased form when challenged with CWD prions. Furthermore, studies published to date suggest that exposure experiments in cynomolgus macaques, a primate considered a close experimental model for humans, do not result in disease expression (Race et al. 2009, Race et al. 2014); 

***however, a recent preliminary, non-peer reviewed Canadian study (Czub et al. 2017) suggests that macaques can be infected by oral administration of CWD-infected meat.

Scientists and human health officials agree that it is prudent to minimize human exposure to CWD. The Centers for Disease Control (CDC) and the World Health Organization (WHO) advise against consuming any animal known to be infected with CWD. Furthermore, the CDC recommends that hunters strongly consider having their animals tested before eating the meat when hunting in areas where CWD is known to be present. 


SATURDAY, FEBRUARY 17, 2018 

Montana Special Hunts 9 more cases CWD TSE Prion to date, more samples still pending

http://chronic-wasting-disease.blogspot.com/2018/02/montana-special-hunts-9-more-cases-cwd.html

WEDNESDAY, NOVEMBER 08, 2017 
Montana Chronic Wasting Disease CWD TSE Prion Response Plan Singeltary Submission
TUESDAY, JULY 19, 2016
MONTANA CHRONIC WASTING DISEASE CWD TSE PRION UPDATE STILL SHOWS ONLY 9 CAPTIVE CASES CONFIRMED FROM Philipsburg Kesler Game game since 1999

MISSISSIPPI CWD TSE PRION

FRIDAY, FEBRUARY 09, 2018 

Mississippi Chronic Wasting Disease confirmed in a White-tailed Deer

http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-chronic-wasting-disease.html


TUESDAY, FEBRUARY 13, 2018 

*** MISSISSIPPI STATE DEPARTMENT OF HEALTH Chronic Wasting Disease: Public Health Recommendations ***

http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-state-department-of-health.html


NEW MEXICO CWD TSE PRION

NEW MEXICO CWD TSE PRION TOTAL COUNT TO DATE? 

SOME ANIMALS IN THESE UNITS (how many the public does not know due to lack of effort by the state of New Mexico to relay that information to the public on it's website with updated information, tracking of cwd positive cases in the wild and captive, and updating all it's old out of date data. New Mexico needs updated MAPS, regions of where these cwd positive cases are at, and how close to neighboring states cwd is moving) but some animals in these UNIT HAVE TESTED POSITIVE IN THE STATE OF NEW MEXICO;

New Mexico Department of Game and Fish 2017 - 2018 New Mexico HUNTING 

snip...

Unit 28 (Some animals in this unit have tested positive for CWD) 

28 McGregor Range Nov. 18–19 . . DER–1–256 . . S . . . . 20 . .FAD 

28 McGregor Range, Military Only . .Nov. 18–19 . . DER–1–257 . . HD . . . 20 . .FAD

Unit 34 (Some animals in this unit have tested positive for CWD) 

34 - Youth Only . . . . . . . .Oct. 21–25 . . DER–1–286 . . S . . . . 45 . .FAD 

34 - Mobility Impaired Only . . . . Oct. 21–25 . . DER–1–287 . . S . . . . 50 . .FAD 

34 . . . . . . . . . . . . Oct. 28–Nov. 1 DER–1–284 . . S . . . . 735 . .FAD 

34 . . . . . . . . . . . . Nov. 11–15 . . DER–1–285 . . S . . . . 735 . .FAD

Unit 19 (Animals in this unit have tested positive for CWD) 

 (Excluding White Sands Missile Range) 

19 . . . . . . . . . . . . Jan. 1–15, '18 . DER–2–195 . . S . . . . 10 . .FAD

Unit 34 (Some animals in this unit have tested positive for CWD)

34 . . . . . . . . . . . . Sept. 1–24 . . DER–2–288 . . S . . . . 780 . .FAD Jan. 1–15, '18

Unit 19 (Animals in this unit have tested positive for CWD.) 

(Excluding White Sands Missile Range.) 

19 . . . . . . . . . . . . Oct. 28–Nov. 1 DER–3–196 . . S . . . . 10 . .FAD

Unit 34 (Some animals in this unit have tested positive for CWD.) 

34 Sept. 30–Oct. 4 DER–3–289 S 340 FAD

Unit 28 (Some animals in this unit have tested positive for CWD) 

28 - McGregor Range, Military Only . Dec. 9–13 . . ELK–1–357 . . HD . . . 10 . .ES 

28 - McGregor Range . . . . . . Dec. 9–13 . . ELK–1–358 . . S . . . . 10 . .ES

Unit 34 (Some animals in this unit have tested positive for CWD) 

34 - Youth Only . . . . . . . .Oct. 7–11 . . .ELK–1–305 . . S . . . . 75 . .ES 

34 - Youth Only, NM Residents Only . Oct. 7–11 . . .ELK–1–306 . . S . . . . 120 . .A 

34 - Mobility Impaired Only . . . . Oct. 7–11 . . .ELK–1–307 . . S . . . . 50 . .ES 

34 . . . . . . . . . . . . Oct. 21–25 . . ELK–1–309 . . S . . . . 150 . .MB 

34 - NM Residents Only . . . . . Nov. 25–29 . . ELK–1–310 . . S . . . 300 . .A 

34 - NM Residents Only . . . . . Dec. 2–6 . . . ELK–1–311 . . S . . . 300 . .A 

34 - NM Residents Only . . . . . Dec. 9–13 . . ELK–1–312 . . S . . . 300 . .A

Unit 34 (Some animals in this unit have tested positive for CWD) 

34 . . . . . . . . . . . . Sept. 1–14 . . ELK–2–303 . . HD . . 200 . .ES 

34 . . . . . . . . . . . . Sept. 15–24 . . ELK–2–304 . . HD . . 200 . .ES

Unit 34 (Some animals in this unit have tested positive for CWD)

34 . . . . . . . . . . . . Oct. 14–18 . . ELK–3–308 . . HD . . . 250 . .MB

Unit 34 (Some animals in this unit have tested positive for CWD) 

Unit 34 Dec. 16–20 . . ELK–2–534 . . S . . . 200 . .APRE/6

Unit 34 . . . . . . . . . . Dec. 26–30 . . ELK–1–523 . . S . . . . 80 . .A  (Some animals in this unit have tested positive for CWD) 

Chronic Wasting Disease Rules Apply to Units 19, 28 and 34 It is unlawful to transport dead deer or elk or their parts taken from any chronic wasting disease (CWD) control area designated by the director of the New Mexico Department of Game and Fish. The exceptions are: 

• Meat that is cut and wrapped either privately or commercially. 

• Quarters or other portions of meat with no part of the head or spinal column attached. 

• Meat that has been boned out. 

• Hides with no heads attached. 

• Clean skull plates with antlers attached. 

• Antlers with no meat or tissue attached. 

• Upper canine teeth, also known as ivories. 

• Finished heads mounted by a taxidermist. 

You may not remove the whole head and spinal column. 

You must keep proof of sex with all game species until you get the game to the place where it will be consumed or placed in cold storage.

Chronic Wasting Disease Rules Apply to Units 19, 28 and 34 

It is unlawful to transport dead deer or elk or their parts taken from any chronic wasting disease (CWD) control area designated by the director of the New Mexico Department of Game and Fish. The exceptions are: 

• Meat that is cut and wrapped either privately or commercially. 

• Quarters or other portions of meat with no part of the head or spinal column attached. 

• Meat that has been boned out. 

• Hides with no heads attached. 

• Clean skull plates with antlers attached. 

• Antlers with no meat or tissue attached. 

• Upper canine teeth, also known as ivories. 

• Finished heads mounted by a taxidermist. 

You may not remove the whole head and spinal column. 

You must keep proof of sex with all game species until you get the game to the place where it will be consumed or placed in cold storage.

Chronic Wasting Disease Rules Apply to Units 19, 28 and 34 It is unlawful to transport dead deer or elk or their parts taken from any chronic wasting disease (CWD) control area designated by the director of the New Mexico Department of Game and Fish. The exceptions are: 

• Meat that is cut and wrapped either privately or commercially. 

• Quarters or other portions of meat with no part of the head or spinal column attached. 

• Meat that has been boned out. 

• Hides with no heads attached. 

• Clean skull plates with antlers attached. 

• Antlers with no meat or tissue attached. 

• Upper canine teeth, also known as ivories. 

• Finished heads mounted by a taxidermist. 

You may not remove the whole head and spinal column. 

You must keep proof of sex with all game species until you get the game to the place where it will be consumed or placed in cold storage.

Chronic Wasting Disease Rules Apply to Units 19, 28 and 34 

It is unlawful to transport dead deer or elk or their parts taken from any chronic wasting disease (CWD) control area designated by the director of the New Mexico Department of Game and Fish. The exceptions are: 

• Meat that is cut and wrapped either privately or commercially. 

• Quarters or other portions of meat with no part of the head or spinal column attached. 

• Meat that has been boned out. 

• Hides with no heads attached. 

• Clean skull plates with antlers attached. 

• Antlers with no meat or tissue attached. 

• Upper canine teeth, also known as ivories. 

• Finished heads mounted by a taxidermist. 

You may not remove the whole head and spinal column. 

You must keep proof of sex with all game species until you get the game to the place where it will be consumed or placed in cold storage.

Transportation of Game Game accompanied with a properly recorded license or by a written statement may be transported within and outside the state. However, bighorn sheep ram heads must have a seal. Bear, cougar and bobcat hides must have a pelt tag. It is unlawful to transport portions of deer or elk taken in areas where chronic wasting disease (CWD) has been confirmed (see page 46).


THURSDAY, APRIL 12, 2018 

New Mexico Chronic Wasting Disease CWD TSE Prion 2017 2018 Sample Survey Update


WEDNESDAY, FEBRUARY 07, 2018 

New Mexico Bans All Live Cervid Importation Due To CWD TSE Prion still NO Final 2017 Positives Update for N.M.

http://chronic-wasting-disease.blogspot.com/2018/02/new-mexico-bans-all-live-cervid.html

THURSDAY, APRIL 19, 2018

Theodore Roosevelt Conservation Partnership Chronic Wasting Disease CWD What You Can Do!


THURSDAY, APRIL 05, 2018 

Boone and Crocket Club B&C News Release CHRONIC WASTING DISEASE TSE Prion



VIRGINIA CWD TSE PRION


FRIDAY, FEBRUARY 09, 2018 

Virginia 2017 Hunt Confirms 16 Cases Chronic Wasting Disease CWD TSE Prion

http://chronic-wasting-disease.blogspot.com/2018/02/virginia-2017-hunt-confirms-16-cases.html


NEBRASKA CWD TSE PRION


MONDAY, FEBRUARY 05, 2018 

Nebraska Chronic Wasting Disease CWD TSE Prion 2017 Survey Confirms 203 Positives From 1,807 
Deer Sampled

http://chronic-wasting-disease.blogspot.com/2018/02/nebraska-chronic-wasting-disease-cwd.html


ARKANSAS CWD TSE PRION


SATURDAY, FEBRUARY 03, 2018 

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

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


UTAH CWD TSE PRION


THURSDAY, FEBRUARY 08, 2018 

Utah Chronic Wasting Disease CWD TSE Prion Update to date from 2017 Hunting Season

http://chronic-wasting-disease.blogspot.com/2018/02/utah-chronic-wasting-disease-cwd-tse.html


OHIO CWD TSE PRION


OHIO Chronic Wasting Disease CWD TSE Prion

OHIO CWD to date holding at 19 cases to date, all captive, NO CWD found in the wild to date...see;

Since 2002 the ODNR Division of Wildlife has conducted statewide CWD surveillance, testing 17,493 deer. To date, there has yet to be a wild, free-ranging deer test positive for the disease in Ohio. In 2017, a total of 1,512 deer were submitted for CWD testing. ODNR Division of Wildlife staff collected 779 road-killed deer from 57 counties and hunters submitted 661 deer (16 of which were escaped captive deer) for CWD testing. An additional 15 escaped or confiscated captive cervids, deer displaying abnormal behavior and/or poor physical condition (n=55), a euthanized research animal, and one deer found dead under suspicious circumstances were also tested for CWD in 2017. CWD was not detected in any of these samples.

Holmes County Disease Surveillance Area

In October 2014, a mature buck from a shooting preserve in Holmes County tested positive for CWD, becoming the first-ever CWD-positive deer in Ohio. The shooting preserve was depopulated in April 2015, and testing revealed no additional CWD-positive animals. Subsequent testing of nearly 300 free-ranging deer in an eight-township area around the shooting preserve failed to detect any CWD-positive deer as well. However, in spring of 2015, two more CWD-positive deer were reported from a captive white-tailed deer breeding pen in Holmes County. This herd was depopulated in June 2015, and 16 additional deer tested positive for the disease, bringing the total of CWD-positive animals found in Ohio to 19 (all in captive herds). In response to these findings, the ODNR Division of Wildlife conducted targeted surveillance in the immediate vicinity of the infected facility during the summer of 2015. Staff collected 18 deer, including two that had escaped from captive facilities, with none testing positive for CWD.

Additionally, the focus area in 2015 was expanded to include two townships in southern Wayne County, and the 10-township focus area was declared a Disease Surveillance Area (DSA, Figure 12). This DSA designation will remain in effect for a minimum of three years and the following regulations apply: 1) required submission of deer harvested within the DSA to ODNR Division of Wildlife inspection stations for sampling during the gun and muzzleloader seasons, 2) prohibit the placement of or use of salt, mineral supplement, grain, fruit, vegetables or other feed to attract or feed deer within the DSA boundaries, 3) prohibit the hunting of deer by the aid of salt, mineral supplement, grain, fruit, vegetables or other feed within the DSA boundaries, and 4) prohibit the removal of a deer carcass killed by motor vehicle within the DSA boundaries unless the carcass complies with the cervidae carcass regulations (see wildohio.gov for additional information on carcass regulations). During the 2017-18 season, the third year under DSA rules, 657 deer from the DSA were tested for CWD. Most samples (n=506) were collected from hunter-harvested deer at inspection stations during Ohio’s three firearms seasons (n=13 days). An additional 127 hunter-harvested samples were obtained from processors, taxidermists, and other modes of collection. In addition to these 633 hunter-harvested deer, 20 road-killed, 2 suspect (poor condition and/or displaying odd behavior), and 2 escaped captive deer were tested for CWD. Again, CWD was not detected in any of the deer tested.


THURSDAY, JANUARY 25, 2018 

Ohio Chronic Wasting Disease CWD TSE Prioin aka mad deer update 2016-2017 SEASON SUMMARY

http://chronic-wasting-disease.blogspot.com/2018/01/ohio-chronic-wasting-disease-cwd-tse.html

January 14, 2018

Ohio ODA confirms CWD TSE Prion in more captive deer




2018 updates for trace in's and out's from this Ohio positive cwd captive? any positives there from? just wondering....terry

WEDNESDAY, AUGUST 16, 2017 

OHIO Chronic Wasting Disease CWD TSE Prion UPDATE?


Monday, June 11, 2012

*** OHIO Captive deer escapees and non-reporting ***



ILLINOIS CWD TSE PRION


WEDNESDAY, JANUARY 24, 2018 

Illinois Chronic Wasting Disease CWD TSE Prion cases mounting with 75 confirmed 2017 and 685 total to date

http://chronic-wasting-disease.blogspot.com/2018/01/illinois-chronic-wasting-disease-cwd.html

THURSDAY, APRIL 12, 2018 

Illinois Legislation and SB-2493 set to help spread chronic wasting disease cwd tse prion, please vote NO!



MARYLAND CWD TSE PRION


WEDNESDAY, FEBRUARY 21, 2018 

Maryland Chronic Wasting Disease CWD TSE Prion Found In Ten Deer Allegany and Washington Counties




NORTH DAKOTA CWD TSE PRION


MONDAY, JANUARY 29, 2018 

North Dakota CWD Confirmed whitetail buck and a mule deer doe 2017 deer gun season from unit 3F2



NEW YORK CWD TSE PRION


NEW YORK STATE CWD TSE PRION

New York State Chronic Wasting Disease CWD TSE Prion History in Wild and Capitve Herds 

SATURDAY, MARCH 24, 2018 

New York Status Chronic Wasting Disease CWD TSE Prion History To Date


SATURDAY, AUGUST 05, 2017 

CWD PLAN Singeltary Submission Comment New York State DEC


Subject: POSITIVE CASE OF CWD FOUND IN ONEIDA COUNTY NY DEER 

From: "Terry S. Singeltary Sr."  

Reply-To: Bovine Spongiform Encephalopathy L@KALIV.UNI -KARLSRUHE.DE> 

Date: Thu, 31 Mar 2005 13:50:50 -0600 Content-Type: text/plain Parts/Attachments: Parts/Attachments text/plain (107 lines) Reply Reply 

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

Department of Agriculture & Markets News Thursday, March 31, 2005 Contact: Jessica A. Chittenden 518-457-3136 jessica.chittenden@agmkt.state.ny.us 

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

POSITIVE CASE OF CWD FOUND IN ONEIDA COUNTY DEER Mandatory Testing Protocols Find CWD in a Captive White-Tailed Doe

The first positive case of chronic wasting disease (CWD) in New York State has been confirmed in a white-tailed doe from a captive herd in Oneida County. CWD is a transmissible disease that affects the brain and central nervous system of deer and elk.

There is no evidence that CWD is linked to disease in humans or domestic livestock other than deer and elk.

The animal that tested positive for CWD was a six-year old white-tailed doe that was slaughtered from a captive herd in Oneida County as part of the State s mandatory CWD surveillance and testing protocols. Preliminary tests performed at the New York State Veterinary Diagnostic Laboratory at Cornell University determined the presumptive positive, which was confirmed late yesterday by the National Veterinary Services Laboratory in Ames, Iowa.

The New York State Department of Agriculture and Markets has officially quarantined the index herd in which the positive deer was found, and will depopulate and test all deer on the premises. Other herds associated with the index herd have also been quarantined and an investigation has been initiated to find and test any susceptible deer that came into contact with the index herd and to assess the health and environmental risks associated with such establishments. The Department of Environmental Conservation (DEC) will conduct intensive monitoring of the wild deer population surrounding the index herd to ensure CWD has not spread to wild deer.

CWD is a transmissible spongiform encephalopathy (TSE) of deer and elk. Scientific and epidemiological research into CWD is ongoing. To date, research shows that the disease is typified by chronic weight loss, is always fatal, and is transmissible between susceptible species. CWD has only been found in members of the deer family in North America, which include white-tailed deer, mule deer, elk and moose.

CWD has been detected in both wild and captive deer and elk populations in isolated regions of North America. To date, CWD has been found in Colorado, Illinois, Kansas, Minnesota, Montana, Nebraska, New Mexico, Oklahoma, South Dakota, Utah, Wisconsin and Wyoming in the United States, and in Saskatchewan and Alberta in Canada.

Establishing the known CWD health status of captive and wild cervid populations is a critical component for controlling CWD. In New York, the responsibility for controlling CWD is shared between the State Department of Agriculture and Markets, DEC, and the U.S. Department of Agriculture s (USDA) Animal and Plant Health Inspection Service (APHIS). New York s cooperative, active surveillance program serves as a model for the nation in CWD control.

The State Department of Agriculture and Markets monitors the health and movement of all captive deer and elk for the presence of common livestock diseases, including CWD. In July 2004, the Department initiated the CWD Enhanced Surveillance and Monitoring Program, which requires captive deer and elk herd owners to take various actions, including routine sampling and testing, animal identification and an annual herd inventory. Since the inception of testing for CWD in 2000, 681 captive deer and elk have been tested and found negative for CWD.

DEC issues licenses to individuals who possess, import or sell white-tailed deer. DEC also routinely tests New York s wild deer population. Following the discovery of CWD in Wisconsin, DEC implemented a statewide surveillance program in April 2002 to test wild white-tailed deer for the presence of CWD. Samples are collected and sent to an approved USDA laboratory for analysis. To date, DEC has taken samples from 3,457 wild white-tailed deer, including 40 from the county where the positive deer was found. All samples from wild white-tailed deer have tested to date have been negative for CWD.

DEC will also implement precautionary regulations limiting transportation and possession of whole carcasses and some parts of wild deer taken near the location of the captive herd. These regulations will be similar to those currently in place for importation of carcasses and parts of deer into New York.

DEC has also implemented regulations restricting various activities to help control CWD within the State, including restrictions on the importation of live deer and elk, deer feeding, importation and possession of certain deer parts and carcasses, and transportation of deer and elk carcasses through New York State.

USDA APHIS supports individual State programs by providing funding for CWD prevention and surveillance. USDA APHIS reimburses states conducting CWD testing on their wild and captive cervid population and also provides indemnification dollars for captive herds that must be destroyed due to the presence of CWD.

New York State has 433 establishments raising 9,600 deer and elk in captivity. In the wild, DEC estimates there are approximately one million deer statewide.

###

http://www.agmkt.state.ny.us/AD/release.asp?ReleaseID=1420

TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########

Re: CHRONIC WASTING DISEASE FOUND IN ONEIDA COUNTY WILD DEER 
Terry S. Singeltary Sr.  
Thu, 28 Apr 2005 20:49:23 -0500 429 lines 

CHRONIC WASTING DISEASE FOUND IN ONEIDA COUNTY WILD DEER The New York State Department of Environmental Conservation (DEC) today announced it has received a preliminary positive result for chronic wasting disease (CWD) in a wild deer sampled in Oneida County. If confirmed, this will be the first known occurrence of CWD in the wild in New York State.Terry S. Singeltary Sr. Thu, 28 Apr 2005 09:13:20 -0500 145 lines 

DEC TO TEST FOR CHRONIC WASTING DISEASE IN HAMILTON COUNTY Terry S. Singeltary Sr. Thu, 14 Apr 2005 16:26:38 -0500 95 lines 

CWD NY CONSUMPTION AND CONTACT 'DON'T TOUCH THAT ANIMAL' or 'don't worry, be happy' Terry S. Singeltary Sr. Sat, 9 Apr 2005 11:30:23 -0500 111 lines New Thread 

CWD NY DEPT OF HEALTH FACTS AND FICTION CWD NY DEPT OF HEALTH FACTS AND FICTION Terry S. Singeltary Sr. Sun, 10 Apr 2005 14:44:06 -0500 1827 lines

CWD UPDATE, TEST RESULTS REVEAL ***THREE ADDITIONAL POSITIVES FROM INDEX HERD Terry S. Singeltary Sr. Fri, 8 Apr 2005 17:07:46 -0500 97 lines 

DEC RELEASES RESULTS OF TESTS FOR CHRONIC WASTING DISEASE Oneida County to Date Shows No Signs of CWD in Wild Herd 

DEC has implemented intensive monitoring efforts after CWD was found in two captive white-tailed deer herds in Oneida County – the first incidents of CWD in New York State. 

***Earlier this month, the State Department of Agriculture and Markets (DAM) completed testing of the captive deer and found a total of ***five positive results for CWD in the two captive herds. 

Terry S. Singeltary Sr.  

CHRONIC WASTING DISEASE UPDATE NEW YORK Herds Depopulated, Public Meeting Scheduled for Friday Terry S. Singeltary Sr. Wed, 6 Apr 2005 15:59:50 -0500 115 lines 

you can see a run down on cwd in NY state here;




TUESDAY, DECEMBER 12, 2017 

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

(zoonosis and environmental risk factors towards the bottom, after state by state reports)



MONDAY, MARCH 13, 2017 

CHRONIC WASTING DISEASE CWD TSE PRION UDATE March 13, 2017



SATURDAY, JANUARY 14, 2017 

CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017



Date: May 4, 2018 at 12:39:00 PM EDT

To: Terry Singeltary <flounder9@verizon.net>

Subject: Mineral licks as environmental reservoirs of chronic wasting disease prions

Mineral licks as environmental reservoirs of chronic wasting disease prions

Ian H. Plummer,Chad J. Johnson,Alexandra R. Chesney,Joel A. Pedersen,Michael D. Samuel 



FRIDAY, JUNE 08, 2018 

Chronic wasting disease management in ranched elk using rectal biopsy testing URGENT UPDATE!




SUNDAY, DECEMBER 10, 2017 

***Detection of Prions in Blood of Cervids at the Asymptomatic Stage of Chronic Wasting Disease



TUESDAY, JULY 04, 2017

*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***



TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD



Wednesday, May 24, 2017 

PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1 



MAD COW FEED, WHAT ABOUT MAD DEER AND ELK AND PIG AND SHEEP FEED ??? scrapie and cwd transmits to pigs orally...terry


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

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


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


FDA BSE/Ruminant Feed Inspections Firms Inventory 


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


http://www.accessdata.fda.gov/scripts/BSEInspect/bseinspections.csv 


NAI = NO ACTION INDICATED


OAI = OFFICIAL ACTION INDICATED


VAI = VOLUNTARY ACTION INDICATED


RTS = REFERRED TO STATE


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


V. Use in animal feed of material from deer and elk NOT considered at high risk for CWD 

FDA continues to consider materials from deer and elk NOT considered at high risk for CWD to be acceptable for use in NON-RUMINANT animal feeds in accordance with current agency regulations, 21 CFR 589.2000. 

Deer and elk not considered at high risk include: 

(1) deer and elk from areas not declared by State officials to be endemic for CWD and/or to be CWD eradication zones; and 

(2) deer and elk that were not at some time during the 60-month period immediately before the time of slaughter in a captive herd that contained a CWD-positive animal.




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...



TUESDAY, APRIL 18, 2017 

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



TUESDAY, JANUARY 17, 2017 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION



THIS April, 4, 2017 violation of the mad cow 21 CFR 589.2000 OAI is very serious for the great state of Michigan, some 20 years post FDA mad cow feed of August 1997. if would most likely take a FOIA request and a decade of wrangling to find out more. 

TUESDAY, JANUARY 17, 2017

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION 

I would kindly like to comment on this FDA BSE/Ruminant Feed Inspections Firms Inventory (excel format)4 format, for reporting these breaches of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters the fda use to put out for each violations. simply put, this excel format sucks, and the FDA et al intentionally made it this difficult to follow the usda fda mad cow follies. this is an intentional format to make it as difficult as possible to follow these breaches of the mad cow TSE prion safety feed protocols. to have absolutely no chronological or numerical order, and to format such violations in a way that they are almost impossible to find, says a lot about just how far the FDA and our fine federal friends will go through to hide these continued violations of the BSE TSE prion mad cow feed ban, and any breaches of protocols there from. once again, the wolf guarding the henhouse $$$

NAI = NO ACTION INDICATED

OAI = OFFICIAL ACTION INDICATED

VAI = VOLUNTARY ACTION INDICATED

RTS = REFERRED TO STATE

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

2016


ONE more thing, please remember, the label does not have to say ''deer ration'' for cervid to be pumped up with. you can get the same ''high protein'' from many sources of high protein feed for animals other than cattle, and feed them to cervid...

Saturday, August 29, 2009

FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009


Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009



FRIDAY, APRIL 20, 2018 

***> Scrapie Transmits To Pigs By Oral Route

what about the terribly flawed USA tse prion feed ban? 

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



TUESDAY, APRIL 17, 2018 

***> Chronic wasting disease: Bambi vs. the prion 

Research Project: Immunodiagnostics to Detect Prions and Other Important Animal Pathogens 

Location: Produce Safety and Microbiology Research



ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE ???

here is the latest;


SEE CZUB CWD TSE Prion Zoonosis to squirrel monkey by oral route to macaque, RACE et al study, and other studies that show that indeed CWD is a increasingly zoonosis risk factor for humans...terry



9:35 Candace Mathiason (Colorado State University): An Overview-Chronic Wasting
Disease mother to offspring transmission studies conducted at Colorado State University.

10:05 Hermann Schätzl/Sandor Dudas (University of Calgary): Oral transmission of CWD
into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in
macaques and bio-assayed transgenic mice.

16:30 Jo Moore (USDA, Ames): The agent of chronic wasting disease from pigs is infectious
in transgenic mice expressing human PRNP.




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


CDC CWD 2018 TRANSMISSION


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


see more cwd zoonosis risk factors from updated science below...terry

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 # 1R01NS088604-01A1 
Application # 9037884 
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 2015-09-30 
Budget End 2016-07-31 
Support Year 1 
Fiscal Year 2015 
Total Cost $337,507 
Indirect Cost $118,756 
Institution 
Name Case Western Reserve University 
Department Pathology 
Type Schools of Medicine 
DUNS # 077758407 
City Cleveland 
State OH 
Country United States 
Zip Code 44106 

http://grantome.com/grant/NIH/R01-NS088604-01A1 http://grantome.com/grant/NIH/R01-NS088604-01A1

CWD TSE Prion Zoonosis to squirrel monkey and macaque


Prion 2017 Conference Abstracts CWD

 2017 PRION CONFERENCE 

First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 

Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 

University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen 

This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. 

Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. 

At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. 

PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 

Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO 

PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS 

*** PRION 2017 CONFERENCE VIDEO 





TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT 

First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress



9:35 Candace Mathiason (Colorado State University): An Overview-Chronic Wasting
Disease mother to offspring transmission studies conducted at Colorado State University.

10:05 Hermann Schätzl/Sandor Dudas (University of Calgary): Oral transmission of CWD
into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in
macaques and bio-assayed transgenic mice.

16:30 Jo Moore (USDA, Ames): The agent of chronic wasting disease from pigs is infectious
in transgenic mice expressing human PRNP.



SATURDAY, JULY 29, 2017 

Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC 







ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION 

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

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

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

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

also, see; 

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

snip... 

The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure. 


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

***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116*** 


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...BSE INQUIRY

Summary and Recommendation: 

snip...

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

These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle. 



*** WDA 2016 NEW YORK *** 

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

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

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

Student Presentations Session 2 

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

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

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

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

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

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

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

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



CDC CWD 2018 TRANSMISSION


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



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”


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. 

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).*** 






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. 



I urge everyone to watch this video closely...terry 

*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***



P.97: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum

Justin Greenlee1, S JO Moore1, Jodi Smith1, M Heather WestGreenlee2 and Robert Kunkle1

1National Animal Disease Center; Ames, IA USA

2Iowa State University; Ames, IA USA

The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n = 5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the 2 inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. 

***In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, 2 distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.



*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA


White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation

snip...

It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that

1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and

2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.

This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.




2012

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

snip...

The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.

*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.

Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.


2011

*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.



***> CWD TO PIGS <***

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

Location: Virus and Prion Research

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

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

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

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

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

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

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

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

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



CONFIDENTIAL

EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY

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


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

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


snip...see much more here ;

WEDNESDAY, APRIL 05, 2017

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


WEDNESDAY, APRIL 05, 2017

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



cattle are highly susceptible to white-tailed deer CWD and mule deer CWD

***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, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.

SNIP...


price of prion poker goes up for cwd to cattle;

Monday, April 04, 2016

*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***


 TUESDAY, MAY 15, 2018 

CATTLE (BOS TAURUS) RESIST CHRONIC WASTING DISEASE FOLLOWING ORAL INOCULATION CHALLENGE OR TEN YEARS’ NATURAL EXPOSURE IN CONTAMINATED ENVIRONMENTS?

this is a different study than that of the Canadian Czub et al study...see my comments here;



THURSDAY, MARCH 08, 2018 

Cervid, Wild Hogs, Coyotes, Wolves, Cats, Rodents, Gut Piles and Scavengers, A Potential Risk as Regards Disease Transmission CWD TSE Prion



the tse prion aka mad cow type disease is not your normal pathogen. 

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

you cannot cook the TSE prion disease out of meat. 

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

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

the TSE prion agent also survives Simulated Wastewater Treatment Processes. 

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

you can bury it and it will not go away. 

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

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

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

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. 

Laboratory of Central Nervous System Studies, National Institute of 

Neurological Disorders and Stroke, National Institutes of Health, 

Bethesda, MD 20892. 

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. 

PMID: 8006664 [PubMed - indexed for MEDLINE] 



TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION 



 *** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION 



Infectious agent of sheep scrapie may persist in the environment for at least 16 years

*** Nine of these recurrences occurred 14–21 years after culling

Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3

Correspondence Gudmundur Georgsson ggeorgs@hi.is

1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland

2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland

3 Bethesda, Maryland, USA Received 7 March 2006 Accepted 6 August 2006

In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.

*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years *** 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 



Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. 

Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. 

Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.

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

***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.

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

Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. 


New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication 


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


Detection of protease-resistant cervid prion protein in water from a CWD-endemic area 


A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing 


Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals 


PPo4-4: 

Survival and Limited Spread of TSE Infectivity after Burial 



Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). 

Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). 

Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). 

Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. 

Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. 

Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). 

The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. 

When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. 

This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. 

Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. 

It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. 

Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. 

Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. 

Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. 

PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. 

In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. 

In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). 

As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. 

False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). 

This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. 

This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. 

In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. 

Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. 

The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. 

In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). 

A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). 

This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. 

Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. 

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. 

These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. 

Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification 

Wednesday, December 16, 2015 

*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** 


161: Prion soil binding may explain efficient horizontal CWD transmission 

Nathaniel Denkers1, Davin Henderson1, Shannon Bartelt-Hunt2, Jason Bartz3 and Edward Hoover1

1Colorado State University; Fort Collins, Colorado USA

2University of Nebraska-Lincoln; Omaha, Nebraska USA

3Creighton University; Omaha, Nebraska USA

Background Chronic wasting disease (CWD) is unique due to the facile spread in nature. The interaction of excreted CWD prions and soil is a hypothesized contributor in environmental transmission. The present study examines whether and to what degree CWD prions bind to silty clay loam (SCL) using an adapted version of real-time quaking-induced conversion (RT-QuIC) methodology.

Materials and Methods Varying amounts (50–3.12 mg) of SCL were incubated with 1 mL-serial dilutions of CWD (+), CWD (−), or no brain homogenate (BH). Samples were centrifuged, washed, diluted 1:10 in 0.1% SDS, and 2.5 uL seeded in RT-QuIC assays employing recombinant Syrian hamster prion PrP substrate. Multiple well replicates of sample and supernatant fractions were assayed for positive seeding activity (recorded as thioflavin T fluorescence emission; 480 nm). Samples were considered positive if they crossed a threshold of 25,000. Reaction rates (RR) were calculated, averaged, and expressed as 1/RR.

Results Positive seeding activity was detected for most SCL samples incubated with CWD (+) BH dilutions. Higher SCL concentrations (50 mg) produced low fluorescent readings due to optical interference. Lower SCL concentrations (6.25 mg) produced minimal optical interference and removed the vast majority of seeding activity from CWD+ BH in a concentration-dependent manner; determined by seeding activity in residual BH supernatants. Control SCL and supernatants produced minimal false-positive reactions (8 of 240 replicates; 3.3%). We estimated the prion binding capacity of SCL to be 0.16 ng/mg.

Conclusion Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.


TSE Scrapie, CWD, BSE, Prion, Soil

Clay content and pH: soil characteristic associations with the persistent presence of chronic wasting disease in northern Illinois

Sheena J. Dorak, Michelle L. Green, Michelle M. Wander, Marilyn O. Ruiz, Michael G. Buhnerkempe, Ting Tian, Jan E. Novakofski & Nohra E. Mateus-Pinilla

Scientific Reportsvolume 7, Article number: 18062(2017) doi:10.1038/s41598-017-18321-x

Download Citation

Ecological epidemiology Ecological modelling Infectious diseases Prions

Received: 21 August 2017

Accepted: 08 December 2017

Published online: 22 December 2017

Abstract

Environmental reservoirs are important to infectious disease transmission and persistence, but empirical analyses are relatively few. The natural environment is a reservoir for prions that cause chronic wasting disease (CWD) and influences the risk of transmission to susceptible cervids. Soil is one environmental component demonstrated to affect prion infectivity and persistence. Here we provide the first landscape predictive model for CWD based solely on soil characteristics. We built a boosted regression tree model to predict the probability of the persistent presence of CWD in a region of northern Illinois using CWD surveillance in deer and soils data. We evaluated the outcome for possible pathways by which soil characteristics may increase the probability of CWD transmission via environmental contamination. Soil clay content and pH were the most important predictive soil characteristics of the persistent presence of CWD. The results suggest that exposure to prions in the environment is greater where percent clay is less than 18% and soil pH is greater than 6.6. These characteristics could alter availability of prions immobilized in soil and contribute to the environmental risk factors involved in the epidemiological complexity of CWD infection in natural populations of white-tailed deer.


Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles

Author Summary

Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.


tse prion soil





cwd tse prion and soil, see more ;


MONDAY, JUNE 12, 2017

Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?


WEDNESDAY, MAY 17, 2017

*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***


MONDAY, MARCH 05, 2018 

TRUCKING AROUND AND SPREADING CHRONIC WASTING DISEASE CWD TSE PRION VIA MOVEMENT OF CERVID AND TRANSPORTATION VEHICLES


to date, there is no cervid that has been documented to be totally resistant to cwd tse prion. 

***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. 

P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion 

Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD 

In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible. 

***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. 

PRION 2016 CONFERENCE TOKYO 

http://prion2016.org/dl/newsletter_03.pdf 

''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.'' 

c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease. 

https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf

''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.'' 

c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease. 

https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf

Subject: cwd genetic susceptibility 

Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms§ 

Julie A. Blanchong a, *, Dennis M. Heisey b , Kim T. Scribner c , Scot V. Libants d , Chad Johnson e , Judd M. Aiken e , Julia A. Langenberg f , Michael D. Samuel g

snip...

Identifying the genetic basis for heterogeneity in disease susceptibility or progression can improve our understanding of individual variation in disease susceptibility in both free-ranging and captive populations. What this individual variation in disease susceptibility means for the trajectory of disease in a population, however, is not straightforward. For example, the greater, but not complete, resistance to CWD in deer with at least one Serine (S) at amino acid 96 of the Prnp gene appears to be associated with slower progression of disease (e.g., Johnson et al., 2006; Keane et al., 2008a). If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a). Alternatively, if the slower progression of disease in resistant deer is not associated with longer periods of infectiousness, but might instead indicate a higher dose of PrPCWD is required for infection, transmission rates in the population could decline especially if, as in Wisconsin, deer suffer high rates of mortality from other sources (e.g., hunting). Clearly, determining the relationship between genetic susceptibility to infection, dose requirements, disease progression, and the period of PrPCWD infectiousness are key components for understanding the consequences of CWD to free-ranging populations.

http:// http://forest.wisc.edu/files/pdfs/samuel/2009%20blanchong%20et%20al%20genetic%20susceptibility%20chronic%20wasting.pdf

http://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=1083&context=nrem_pubs

http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2017.4667/epdf

http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1115179

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964855/pdf/kprn-09-06-1115179.pdf

http://www.sciencedirect.com/science/article/pii/S1567134809001956?via=ihub 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964855/


MONDAY, NOVEMBER 20, 2017 

*** What ever happened to 'LUCKY' the Wapiti cow elk thought to be immune from CWD with LL genotype MIA? ***


Use of environmental sites by mule deer: a proxy for relative risk of chronic wasting disease exposure and transmission

MARIAFERNANDAMEJIA-SALAZAR,1,CHERYLL. WALDNER,2 YEENTENHWANG,1,3 AND TRENTK. BOLLINGER1,41 Department of Veterinary Pathology, University of Saskatchewan, 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4 Canada2 Department of Large Animal Clinical Sciences, University of Saskatchewan, 52 Campus Drive, Saskatoon,Saskatchewan S7N 5B4 Canada3 Fish and Wildlife Branch, Saskatchewan Ministry of Environment, Regina, Saskatchewan S4S 5W6 Canada4 Canadian Wildlife Health Cooperative (CWHC), 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4 Canada Citation:Mejıa-Salazar, M. F., C. L. Waldner, Y. T. Hwang, and T. K. Bollinger. 2018. 

Use of environmental sites by mule deer: a proxy for relative risk of chronic wasting disease exposure and transmission. 

Ecosphere 9(1):e02055.10.1002/ecs2.2055

Abstract.

Prions that cause chronic wasting disease (CWD) in cervids can remain infective for years out-side the host. Infectious cervids shed prions for a long time, consequently depositing prions in frequently used areas. These environmental prions are important in CWD epidemiology. Unfortunately, effective tools for quantifying CWD prions in soil, water, and other environmental sources are not currently available. Our goal was to investigate relative differences in visits by mule deer (Odocoileus hemionus hemionus) to various environmental site types as an indicator of the relative risk of prion contamination and disease transmission.For this, we deployed a system of triggered-by-movement cameras at eight site types in a CWD-endemic area in Saskatchewan, Canada. We first assessed whether the relative differences among site types in the frequency of visits by mule deer of any sex-and-age class, males, and females varied by season and site type.We then assessed whether the rate of behaviors with a high risk of environmental prion transmission (either contamination or acquisition) differed by season and site type. Finally, we assessed whether the intensity of visitation, based on the number of animals per picture, differed by season and site type. We found that grain sources and beds were key attractants for mule deer: 

(1) The greatest number of pictures with mule deer per camera-day occurred at grain sources across all seasons, except in fawning, when beds were the most visited sites; 

(2) during pre-rut and early gestation, mule deer visited grain sources at least twice as often as most other sites; 

(3) females were more likely to visit beds and grain sources, but there was no significant site preferences for males after accounting for season; 

(4) mule deer were most likely to be pictured contacting the environment at grain sources in early gestation; and 

(5) beds and grain sources were the most intensively visited sites. We also found that environmental contacts at waterholes were more frequent during spring. 

We discuss the potential importance of various sites in the transmission of CWD and how their modification could potentially reduce the risk of prion environmental exposure among mule deer.

snip...

CONCLUSIONS

In CWD-endemic areas, prion accumulation is most likely at environmental sites that are used frequently by large numbers of deer (Miller et al. 2004, Georgsson et al. 2006, Mathiason et al. 2009, Gough and Maddison 2010). The potential for CWD transmission both from prions in the environment and directly from infected deer is, therefore, also relatively higher at these locations. We demonstrated that mule deer in our study area preferentially and more intensively visited grain sources, particularly during pre-rut and early gestation, and that contacts with the environment occurred more commonly at such sites, especially during early gestation. Our findings suggest that grain sources could play a central role in the potential for CWD transmission and control. Based on these findings, limiting access to grain spills and other artificial feed sites during winter (mid-December to the end of March) is likely to help reduce CWD transmission in wild cervid populations in areas with similar characteristics to our study site. Similar recommendations have been made for management of tuberculosis in wild cervids (Miller et al. 2003).Moreover, as previously noted by Potapov et al.(2013) and Habib et al. (2011), the applicability of CWD dynamic models can be greatly improved by expanding these models by considering both the non-random social interactions between individuals (Mejıa-Salazar et al. 2017a) and the environmental dynamics of prion transmission. Until such time that analytical techniques are developed to detect concentrations of CWD prions in the environment, our results can be immediately used to rank the relative importance of various environmental sources of CWD prions in future epidemic models for this region. Without formal initiatives to address the unintentional creation of concentrated and localized attractive feeding sources for deer, such as grain spills, CWD will most likely be perpetuated, and the success of other suggested control efforts targeting population density or size (Uehlinger et al. 2016) will most likely be jeopardized.

Key words:artificial feeding; bed sites; carcass; chronic wasting disease; disease management; environmental prion contamination; frequency of visitation; grain; intensity of visitation; mule deer; prion; remote photography.Received14 September 2017; accepted 17 November 2017. Corresponding Editor: Andrew W. Park.Copyright:©2018 Mejıa-Salazar et al. This is an open access article under the terms of the Creative Commons AttributionLicense, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.E-mail:mihicoltia@gmail.com


December 2014, Volume 36, Issue 6, pp 1049–1061 | Cite as

Mineral licks: motivational factors for visitation and accompanying disease risk at communal use sites of elk and deer 

Authors Authors and affiliations Michael J. LavelleEmail authorGregory E. PhillipsJustin W. FischerPatrick W. BurkeNathan W. SewardRandal S. StahlTracy A. NicholsBruce A. WunderKurt C. VerCauteren 1. 2. 3. 4. 
Article First Online: 08 April 2014 258 Downloads 1 Citations 

Abstract 

Free-ranging cervids acquire most of their essential minerals through forage consumption, though occasionally seek other sources to account for seasonal mineral deficiencies. Mineral sources occur as natural geological deposits (i.e., licks) or as anthropogenic mineral supplements. In both scenarios, these sources commonly serve as focal sites for visitation. We monitored 11 licks in Rocky Mountain National Park, north-central Colorado, using trail cameras to quantify daily visitation indices (DVI) and soil consumption indices (SCI) for Rocky Mountain elk (Cervus elaphus) and mule deer (Odocoileus hemionus) during summer 2006 and documented elk, mule deer, and moose (Alces alces) visiting licks. Additionally, soil samples were collected, and mineral concentrations were compared to discern levels that explain rates of visitation. Relationships between response variables; DVI and SCI, and explanatory variables; elevation class, moisture class, period of study, and concentrations of minerals were examined. We found that DVI and SCI were greatest at two wet, low-elevation licks exhibiting relatively high concentrations of manganese and sodium. Because cervids are known to seek Na from soils, we suggest our observed association of Mn with DVI and SCI was a likely consequence of deer and elk seeking supplemental dietary Na. Additionally, highly utilized licks such as these provide an area of concentrated cervid occupation and interaction, thus increasing risk for environmental transmission of infectious pathogens such as chronic wasting disease, which has been shown to be shed in the saliva, urine, and feces of infected cervids.
Keywords Cervus elaphus Chronic wasting disease Elk Geophagy Mineral lick Mule deer Odocoileus hemionus 

https://rd.springer.com/article/10.1007/s10653-014-9600-0

Elk and Deer Use of Mineral Licks: Implications for Disease Transmission 

Kurt C. VerCauteren1*, Michael J. Lavelle1, Gregory E. Phillips1, Justin W. Fischer1, and Randal S. Stahl1 1United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 4101 LaPorte Avenue, Fort Collins, CO 80521-2154, USA *Cooresponding author e-mail: kurt.c.vercauteren@aphis.usda.gov 

North American cervids require and actively seek out minerals to satisfy physiological requirements. Minerals required by free-ranging cervids exist within natural and artificial mineral licks that commonly serve as focal sites for cervids. Ingestion of soils contaminated with the agent that causes chronic wasting disease (CWD) may result in risk of contracting CWD. Our objective was to evaluate the extent and nature of use of mineral licks by CWD-susceptible cervid species. We used animal-activated cameras to monitor use of 18 mineral licks between 1 June and 16 October 2006 in Rocky Mountain National Park, north-central Colorado. We also assessed mineral concentrations at mineral licks to evaluate correlations between visitation rates and site-specific characteristics. We collected > 400,000 images of which 991 included elk, 293 included deer, and 6 included moose. We documented elk and deer participating in a variety of potentially risky behaviors (e.g., ingesting soil, ingesting water, defecating, urinating) while at mineral licks. Results from the mineral analyses combined with camera data revealed that visitation was highest at sodium-rich mineral licks. Mineral licks may play a role in disease transmission by acting as sites of increased interaction as well as reservoirs for deposition, accumulation, and ingestion of disease agents. 

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf 

http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html


Sunday, January 06, 2013

USDA TO PGC ONCE CAPTIVES ESCAPE

*** "it‘s no longer its business.”

http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no.html

COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. 

IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989

http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;

''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.

https://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

SHOOTING PENS (HIGH/LOW FENCE), CAPTIVE CERVID FARMING, BREEDING, SPERM MILLS, ANTLER MILLS, URINE MILLS, a petri dish for cwd tse prion disease...

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. 

https://web.archive.org/web/20170126060744/http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. 

IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989

http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

Subject: CWD TSE PRION 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised


Saturday, February 04, 2012

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


also see;

Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm and 15 of 22 fawns aged 6 to 9 months (68.2%) were positive.



specific susceptibility? 194. It is probable, based on age-class specific prevalence data from wild cervids and epidemiological evidence from captive cervids in affected research centres, that both adults and fawns may become infected with CWD (Miller, Wild & Williams, 1998; Miller et al., 2000). 198. In Odocoileus virginianus – white tailed deer, out of 179 white-tailed deer which had become enclosed by an elk farm fence, in Sioux County, northwestern Nebraska, four fawns only eight months old were among the 50% of CWD-positive animals; these fawns were not showing any clinical signs of CWD (Davidson, 2002).


SCWDS BRIEFS

Volume 17 January 2002 Number 4

CWD News from Nebraska and Kansas

Infection with the chronic wasting disease (CWD) agent recently was found in 28 of 58 formerly wild white-tailed deer in a high-fenced enclosure adjacent to a pen containing CWDaffected captive elk in northern Sioux County, Nebraska.

***Four of the positive deer were fawns approximately 8 months old, which is unusually young for animals testing positive for CWD.



CWD in adult deer and fawns

***Five of the CWD-positive deer were fawns, less than 1 year of age.

Early CWD (PrPd detected in the tonsil or retropharyngeal node but not brain) was diagnosed in 14 deer (12 adults ranging from 1?5 to more than 5 years of age and two fawns). Late CWD (PrPd detectable in brain as well as lymphoid tissues) was diagnosed in 53 deer (50 adults ranging in age from 1?5 to 7 years of age and three fawns). None of the CWD-positive deer showed clinical signs of the disease (weight loss, hypersalivation, disorientation) or gross changes consistent with CWD (serous atrophy of fat) at necropsy.


Illinois CWD, see where there 2003 sampling showed 2. % of fawns tested had CWD i.e. 1 positive out of 51 samples.

2003

Boone-Winnebago Unit Fawn 51 1 2.0%


2011 FAWN CWD POSITIVE ILLINOIS

1/26/11 WINNEBAGO 344N 2E S36 F FAWN SHARPSHOOTING

2/10/11 OGLE 341N 1E S7 F FAWN SHARPSHOOTING

3/9/11 OGLE 341N 1E S7 M FAWN SHARPSHOOTING


For example, in 2008 a fawn tested positive and in 2010 an infected yearling buck was detected in Smith County



P172 Multigenerational transmission of CWD prions from mother to offspring

Erin Mcnulty1, MS Amy Nalls1, Dr Clare Hoover1, Dr Jenny Powers2, Dr Edward Hoover1, Dr Candace Mathiason1 1Colorado State University, Fort Collins, United States, 2National Park Services, Fort Collins, United States

Aims: Chronic wasting disease (CWD) continues to demonstrate geographic expansion, now found in captive and/or free-range cervid populations in North America, South Korea and Norway. While horizontal transmission is credited for much of the spread of CWD, few studies have monitored the transmission of this disease from mother-to-offspring.

CWD-infected muntjac dams are able to become pregnant, carry, deliver and rear offspring during the long asymptomatic phase of prion infection. We have demonstrated that CWD prions can be transmitted from mother to first-generation offspring leading to prion infection and subsequent development of TSE disease, and that transmission occurs during gestation (Nalls 2013). We have also observed fecundity in first-generation offspring. In fact, one first-generation female muntjac gave birth to two nonviable second-generation offspring. Tissues harvested from these nonviable second-generation offspring harbor protein misfolding cyclic amplification (PMCA) competent prions.

Recently we revealed PrPC seeding activity and infectious prions within the reproductive milieu (uterus, ovaries, placentomes, amniotic fluid) of CWD-infected Reeve’s muntjac dams by PMCA, real time quaking-induced conversion (RT-QuIC) and bioassay. The presence of CWD prions in the pregnancy microenvironment begs the question: Is it possible CWD is transmitted from one generation to the next via intrauterine or germline exposure to infectious prions?

Methods: To begin to address this question we assessed tissues harvested from full-term second-generation nonviable muntjac offspring for infectivity by mouse bioassay. Transgenic mice expressing the cervid prion protein, Tg(CerPrP-E226)5037+/- (n=6/cohort), were IP-inoculated with PMCA-amplified lung, mammary gland, kidney or uterus from nonviable 2nd generation muntjac offspring (n=2) born to a first generation dam (n=1), or PMCA-amplified age and tissue-matched negative control second-generation offspring (n=2). Mice from all cohorts were examined for prions by western blot and RTQuIC.

Results: All mice (n=20) inoculated with PMCA-amplified tissue from “gestational CWD-exposed” second-generation offspring developed signs consistent with TSE disease, including severe ataxia and weight loss between 209-373 days pi, and were confirmed CWD positive by western blot and RT-QuIC. Negative control mice (n=9) receiving PMCA-amplified negative age and tissue-matched homogenates remained healthy and TSE-free for the same duration. Studies have been initiated to further assess the relationship between prions in ovaries and CWD transmission.

Conclusions: Our data indicates that: (1) multigenerational transmission of infectious CWD prions from mother-to-offspring may be possible and (2) early and persistent exposure of the developing embryo to infectious CWD prions in the uterine microenvironment may help explain the facile transmission of CWD in the native host.

=====

P176 Infectious CWD prions at the fetal-maternal interface

Ms. Amy Nalls1, Ms. Erin McNulty1, Ms. Laura Pulscher1, Dr. Clare Hoover1, Dr. Edward Hoover1, Dr. Candace Mathiason1 1Colorado State University, Fort Collins, United States

Aims: Ample evidence exists for the trafficking of infectious agents across the placenta, often with grave outcomes to the developing fetus (i.e. zika, brucella, cytomegalovirus). While less studied, pregnancy-related transmissible spongiform encephalopathies (TSEs) have been implicated in several species, including humans.

Our previous work demonstrated that prions can be transferred from mother-to-offspring resulting in the development of clinical TSE disease in offspring born to CWD-infected muntjac dams (Nalls 2013). We also revealed PMCA-prion seeding activity in maternal and fetal tissues harvested in utero from muntjac dams at various stages of pregnancy and CWD infection. What remained unknown was whether the prions detected at the fetal-maternal interface were infectious. In addition, we were interested to determine if the ultrasensitive RT-QuIC methodology may enhance our ability to detect prion seeding activity within the pregnancy microenvironment.

We undertook this study to assess CWD infectivity and RT-QuIC PrPc seeding activity in in utero harvested— (1) female reproductive tissues and fluids associated with the pregnancy microenvironment; the ovary, uterus and birthing fluids, and (2) the semipermeable interface between cervid mother and fetus throughout pregnancy; the placentome.

Methods: RT-QuIC: A total of 12 replicates/sample of ovary (n=6), uterus (n=6), placentome (n=5-6 placentomes each from n=2 pregnancies) and birthing fluids (n=4) were analyzed. Bioassay: Transgenic mice expressing the cervid prion protein, Tg(CerPrP-E226)5037+/- (n=9/cohort), were IC-inoculated with 30μl 10% homogenate of uterus (n=2), placentome (n=2) or 5-fold concentrated birthing fluids (n=3).

Results: RT-QuIC: PrPC seeding activity was consistently detected in 5/6 ovary, 6/6 uterus, 9/11 placentomes, 2/2 amniotic and 0/2 allantoic fluids. Bioassay: Clinical TSE disease (ataxia, weight loss and stiff tail) was observed in mice inoculated with uterus, placentome and amniotic fluid, but not allantoic fluid between 180-343 day pi while negative control cohorts remained healthy. Bioassay mice were confirmed TSE positive: brain (uterus 7/8, placentome 8/8, amniotic fluid 1/9, allantoic fluid 0/9) and spleen (uterus 7/8, placentome 7/8, amniotic fluid 2/9, allantoic fluid 0/0) by western blot and RT-QuIC.

Conclusions: Here, using a native CWD susceptible host, we have— for the first time— demonstrated infectious prions in the cervid pregnancy microenvironment and placental structure at the fetal-maternal interface. These findings reveal a source of infectious prions that the developing fetus is exposed to long before the birthing process, maternal grooming, or encounter with contaminated environments. Thus suggesting that CWD mother-to-offspring transmission may contribute to the facile transmission of CWD and be underappreciated for all TSEs.


FRIDAY, MARCH 30, 2018 

Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018

Terry S. Singeltary Sr., Bacliff, Texas USA 77518 flounder9@verizon..net 

Attachments (1) Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary View Attachment:View as format pdf 



https://www.regulations.gov/docketBrowser?rpp=25&so=DESC&sb=commentDueDate&po=0&dct=PS&D=APHIS-2018-0011


SUNDAY, JUNE 3, 2018 

Clinical, pathological, and molecular features of classical and L-type atypical-BSE in goats


WEDNESDAY, JUNE 13, 2018 

National Scrapie Eradication Program April 2018 Monthly Report Fiscal Year 2018



ONE DECADE POST MAD COW FEED BAN OF AUGUST 1997...2007
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
see page 176 of 201 pages...tss
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply;
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT

Of the 143 million pounds involved with the recall, we have about 50.3 million pounds that went to federal nutrition programs. Of that 50.3 million pounds, we have 19.6 million pounds were consumed. We know that 15.2 million pounds are currently on hold. And we know that 15.5 million pounds are actively being traced. And these numbers will be updated as states are able to ascertain the location of the remainder of these products.



SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE

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

DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???

this recall was not for the welfare of the animals. ...tss

you can check and see here ;

(link now dead, does not work...tss)


try this link ;




NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES

NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIES

Subject: Prion Disease in Dromedary Camels, Algeria

Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.



Wednesday, May 30, 2018 

Dromedary camels in northern Africa have a neurodegenerative prion disease that may have originated decades ago


Saturday, April 14, 2018


Dromedary Camels Algeria Prion (Mad Camel Disease) TSE BSE MRR Import Export Risk Factors Excluding Grains and Plants

Dromedary Camels Algeria Prion (Mad Camel Disease) TSE BSE MRR Import Export Risk Factors Excluding Grains and Plants

(Grains and Plants Materials Could Harbor the Transmissible Spongiform Encephalopathy TSE Prion agent...TSS)

Dromedary Camels Algeria Prion (Mad Camel Disease) TSE BSE MRR Import Export Risk Factors Excluding Grains and Plants

*** please see files of U.K. exports of M.B.M. AND OTHER MEAT PRODUCTS (metric tonnes), and to the countries (including Germany), they went to; 



TUESDAY, DECEMBER 12, 2017 

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



Tuesday, December 12, 2017 

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



MONDAY, OCTOBER 02, 2017 

Creutzfeldt Jakob Disease United States of America USA and United Kingdom UK Increasing and Zoonotic Pontential From Different Species



THURSDAY, AUGUST 17, 2017 

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



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. 



Tracking spongiform encephalopathies in North America

Xavier Bosch

Published: August 2003

DOI: http://dx.doi.org/10.1016/S1473-3099(03)00715-1

Summary;

“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.”

49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.

Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). "I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source."

Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.

To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.

Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.

Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.

"Getting data on TSEs in the USA from the government is like pulling teeth", Singeltary argues. "You get it when they want you to have it, and only what they want you to have."

Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that "current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings"; adding that, "the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure". The USA should develop a system modelled on that established in the UK, he points out.

Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters "two of whom were friends" who died from pathologically confirmed CJD, says that "at present there are insufficient data to claim transmission of CWD into humans"; adding that "[only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further". Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.

CDC spokesman Ermias Belay says that the CDC "will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat". He notes that although "the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100%" and that "[we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited". 




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? 



***> 2001 FDA CJD TSE Prion Singeltary Submission 



Sent: Monday, January 08,2001 3:03 PM

WOW, my submission held up on the www for 17 years, and was proven to be true, and now, it has been removed from the www, the same url does not work anymore and it was just working this year. nothing like the FDA et al cleaning up any evidence of truth with their mad cow debacle and sporadic cjd cover up contineus...so sad$$$

let's review the truth about sporadic cjd shall we;



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

[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



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. 



Singeltary on CWD TSE Prion video



Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy 

>>> The only tenable public line will be that "more research is required’’ <<< 

>>> possibility on a transmissible prion remains open<<< 

O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ? 

Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy 

Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015) 

snip...see full Singeltary Nature comment here; 

Alzheimer's disease

let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease... 

Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy






Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease 

*** Singeltary comment PLoS *** 

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

Posted by flounder on 05 Nov 2014 at 21:27 GMT 



IN CONFIDENCE

5 NOVEMBER 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. 

There are also results to be made available shortly 

(1) concerning a farmer with CJD who had BSE animals, 

(2) on the possible transmissibility of Alzheimer’s and 

(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]






snip...see full Singeltary Nature comment here; 

re-Evidence for human transmission of amyloid-? pathology and cerebral amyloid angiopathy Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)


I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.

First, I applaud Nature, the Scientist and Authors of the Nature paper, for bringing this important finding to the attention of the public domain, and the media for printing said findings.

Secondly, it seems once again, politics is getting in the way possibly of more important Transmissible Spongiform Encephalopathy TSE Prion scientific findings. findings that could have great implications for human health, and great implications for the medical surgical arena. but apparently, the government peer review process, of the peer review science, tries to intervene again to water down said disturbing findings.

where have we all heard this before? it's been well documented via the BSE Inquiry. have they not learned a lesson from the last time?

we have seen this time and time again in England (and other Country's) with the BSE mad cow TSE Prion debacle.

That 'anonymous' Lancet editorial was disgraceful. The editor, Dick Horton is not a scientist.

The pituitary cadavers were very likely elderly and among them some were on their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients, who got pooled extracts injected from thousands of cadavers, were 100% certain to have been injected with both seeds. No surprise that they got both diseases going after thirty year incubations.

That the UK has a "system in place to assist science journalists" to squash embargoed science reports they find 'alarming' is pathetic.

Sounds like the journalists had it right in the first place: 'Alzheimer's may be a transmissible infection' in The Independent to 'You can catch Alzheimer's' in The Daily Mirror or 'Alzheimer's bombshell' in The Daily Express

if not for the journalist, the layperson would not know about these important findings.

where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?

when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.

to date, as far as documented body bag count, with all TSE prion named to date, that count is still relatively low (one was too many in my case, Mom hvCJD), however that changes drastically once the TSE Prion link is made with Alzheimer's, the price of poker goes up drastically.

so, who makes that final decision, and how many more decades do we have to wait?

the iatrogenic mode of transmission of TSE prion, the many routes there from, load factor, threshold from said load factor to sub-clinical disease, to clinical disease, to death, much time is there to spread a TSE Prion to anywhere, but whom, by whom, and when, do we make that final decision to do something about it globally? how many documented body bags does it take? how many more decades do we wait? how many names can we make up for one disease, TSE prion?

Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.

FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.

in my opinion, it's one of the reasons we are at where we are at to date, with regards to the TSE Prion disease science i.e. money, industry, politics, then comes science, in that order.

greed, corporate, lobbyist there from, and government, must be removed from the peer review process of sound science, it's bad enough having them in the pharmaceutical aspect of healthcare policy making, in my opinion.

my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer's of some type (no autopsy?). just made a promise, never forget, and never let them forget, before I do.

I kindly wish to remind the public of the past, and a possible future we all hopes never happens again. ...




2012

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

Background

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.

Methods

Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.

Results

I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.

Conclusions

There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.

end...tss

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

source references ...end...tss 

Hello Nicole,

by all means, please do use my poster. but I thought this was already taken care of, and I could not attend for my poster presentation, therefore, it was not going to be presented. I have some health issues and could not make the trip.

please see old correspondence below...

From: Nicole Sanders Sent: Tuesday, April 10, 2012 5:37 PM To: Terry S. Singeltary Sr. Subject: RE: re-submission

Dear Terry,

The decline of proposal number 30756 is registered in the system. Thank you for your consideration.

Best Regards,

Nicole

Nicole Sanders

Senior Specialist, Membership & Conference Programming

______________________________________


From: xxxx 

To: Terry Singeltary 

Sent: Saturday, December 05, 2009 9:09 AM 

Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'

Your preliminary abstract number: 670

Dear Mr. Singeltary,

On behalf of the Scientific Committee, I am pleased to inform you that your abstract

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

WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.

Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.

Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE

#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Author: T. Singeltary; Bacliff, TX/US

Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange

This abstract has been ACCEPTED.

#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Authors: T. Singeltary; Bacliff, TX/US

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

Body: Background

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

Methods

12 years independent research of available data

Results

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

Conclusion

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.

I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion

page 114 ;

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

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

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

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



Terry S. Singeltary Sr.

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