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Sunday, March 25, 2018

Texas Longer whitetail deer season in North Zone shot down Shannon Tompkins Houston Chronicle WHAT ABOUT CWD Mad Deer Disease?

Longer whitetail deer season in North Zone shot down

By Shannon Tompkins, Houston Chronicle Updated 9:54 pm, Saturday, March 24, 2018

This autumn, Texas hunters pursuing deer and most game other than migratory game birds will for the first time be allowed to use guns and bows employing compressed air to fire projectiles. Dove hunters in the state's South Dove Zone who for years have clamored for an earlier opening of the regular season will see their wishes granted with a Sept. 14 opener - the earliest for the zone since at least 1940. And anglers will see liberalized largemouth bass regulations on more than a dozen reservoirs.

But the overwhelming majority of the approximately 750,000 hunters participating in the state's general season for white-tailed deer will continue to see two fewer weeks of hunting opportunity than those in a 30-county region that, for no biological or wildlife management reason, has long benefited from more liberal deer-hunting rules than the remainder of the state.


Greetings Texas Hunters et al, 

Once again, another great article by a prolific outdoors writer Shannon Tompkins on whitetail deer in Texas, yet one must wonder, why Mr. Tompkins now has lockjaw about speaking about the recent 100th case of chronic wasting disease cwd tse prion, aka mad deer disease in Texas. seems the trace back cwd positives from breeders, seems the end is just not in sight for cwd positive cases. cwd just continues to spread around the globe, science and scientist raising alarm bells for possible mad deer disease in humans, as sporadic CJD, yet the houston chronicle seems to stay silent on this silent epidemic. one must ask yourself WHY? ($$$) the Houston chronicle, and Shannon Tompkins, use to write extensively about mad deer disease, when the shoe was on the other foot (cwd was in other states, NOT Texas yet), but when cwd was discovered in Texas, and began spreading, especially in the captive farming industry, the Houston Chronicle and Shannon Tompkins, imo, developed lock jaw. WHY? there must be a reason. when the world is so worried, Texas and the Houston Chronicle stays silent (please see history of this apparent case of lockjaw about speaking and warning the public about  cwd tse prion aka mad deer disease in links at bottom of this page) this cwd tse prion aka mad deer disease, not only have already infected humans as sporadic CJD, as science has shown via laboratory studies, but animal studies as well, including not only the squirrel monkey, but the macaque, the closest to humans, and this orally with muscle meat. yet the silence is deafening from the Houston Chronicle and Shannon Tompkins. WHY? hunters across Texas have exposing themselves to this mad deer disease, science and the CDC is warning hunters about this, yet the Houston Chronicle and Mr. Tompkins stay silent. WHY? Land Values could plummet due to CWD TSE Prion exposure in Texas, yet the silence is deafening. this is very disturbing to me. i guess i will have to give an update on the latest from Texas on the increasing numbers of mad deer disease in Texas, and most updated peer review science. ...


-----Original Message-----
From: Terry Singeltary <flounder9@verizon.net>
To: bse-l l@lists.aegee.org
>
Cc: cjdvoice <cjdvoice@yahoogroups.com>; bloodcjd <bloodcjd@yahoogroups.com>
Bcc:        xxxxx                                                                                                                         
Sent: Thu, Mar 22, 2018 4:00 pm
Subject: TEXAS CWD TSE PRION JUMP TO 100 POSITIVE, NEW CASES 17 BREEDER, 1 BREEDER RELEASE, AND 1 WILD SINCE JAN 31, 2018

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

CWD Positives in Texas

Show  entriesSearch:

CWD Positive

Year Confirmed CWD Positive

Confirmation Date Free Range / Captive County Source Species Sex Age

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 2.5

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 4.5

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5

2018 03/16/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5

2018 03/09/18 Release Site Uvalde Facility #3 Elk F 4.5

2018 02/28/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5

2018 02/13/18 Free Range Hudspeth Mule Deer M 4.5

2018 02/13/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 7.5

2018 02/13/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 3.5

2018 02/13/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 1.5

2018 02/02/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 7.5

2018 01/31/18 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 2.5

2018 01/29/18 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 6.5

2018 01/08/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 3.5

2018 01/08/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 3.5

2018 01/08/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 6.5

2018 01/08/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 5.5

2018 01/08/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 4.5

2018 01/08/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 4.5

2018 01/08/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 8.5

2018 01/08/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 3.5

2018 01/08/18 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 5.5

2018 01/08/18 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 4.5

2017 9/13/17 Breeder Deer Uvalde Facility #3 White-tailed Deer F 5

2017 7/6/17 Breeder Deer Medina Facility #5 White-tailed Deer M 4

2017 12/29/17 Free Range Hartley White-tailed Deer M 2.5

2017 12/22/17 Free Range Hartley Mule Deer M 2.5

2017 12/22/17 Free Range Hartley Mule Deer M 4.5

2017 12/18/17 Free Range El Paso Mule Deer M 5.5

2017 11/29/17 Breeder Release Site Medina Facility #3 White-tailed Deer M 4.5

2017 11/27/17 Breeder Release Site Medina Facility #4 White-tailed Deer M 4.5

2017 10/6/17 Release Site Medina Facility #3 Elk F 4

2017 10/6/17 Breeder Deer Uvalde Facility #3 White-tailed Deer F 1

2017 10/25/17 Breeder Deer Medina Facility #5 White-tailed Deer F 3

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer M 7

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 9

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 9

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 6

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer M 4

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2016 9/21/16 Breeder Release Site Medina Facility #3 White-tailed Deer M 3.5

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer F 1

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer M 1

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer F 1

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer M 1

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2016 6/29/16 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2nd page

CWD Positive

Year Confirmed CWD Positive

Confirmation Date Free Range / Captive County Source Species Sex Age

2016 6-Jan Free Range Dallam Mule Deer M 2.5

2016 4/13/16 Breeder Deer Lavaca Facility #2 White-tailed Deer M 3

2016 4/13/16 Breeder Deer Lavaca Facility #2 White-tailed Deer M 3

2016 4/13/16 Breeder Deer Lavaca Facility #2 White-tailed Deer M 3

2016 4/13/16 Breeder Deer Lavaca Facility #2 White-tailed Deer M 3

2016 4/1/16 Breeder Deer Medina Facility #4 White-tailed Deer F 4.5

2016 3/29/16 Breeder Deer Medina Facility #3 White-tailed Deer M 3

2016 2/9/17 Free Range Hudspeth Mule Deer M 3.5

2016 2/9/17 Free Range Hudspeth Mule Deer M 7.5

2016 2/4/16 Breeder Release Site Medina Facility #3 White-tailed Deer M 3

2016 2/18/17 Breeder Release Site Medina Facility #4 White-tailed Deer M 3.5

2016 2/17/17 Free Range Hudspeth Mule Deer M 7.5

2016 2/17/17 Free Range Hudspeth Mule Deer M 5.5

2016 12/6/16 Free Range Dallam Elk M 8.5

2016 10/28/16 Breeder Deer Uvalde Facility #3 White-tailed Deer M 5.5

2016 10/28/16 Breeder Deer Uvalde Facility #3 White-tailed Deer F 4.5

2016 1/6/17 Free Range El Paso Mule Deer M 4.5

2016 1/24/17 Free Range Medina White-tailed Deer M 1.5

2016 1/18/17 Free Range Hartley Mule Deer M 4.5

2016 1/18/17 Breeder Release Site Uvalde Facility #3 White-tailed Deer M 5.5

2016 1/18/17 Breeder Release Site Uvalde Facility #3 White-tailed Deer M 3.5

2015 9/14/15 Breeder Deer Lavaca Facility #2 White-tailed Deer M 3

2015 8/6/15 Breeder Deer Medina Facility #1 White-tailed Deer M 2.5

2015 8/6/15 Breeder Deer Medina Facility #1 White-tailed Deer M 2.5

2015 8/12/15 Breeder Deer Medina Facility #1 White-tailed Deer M 2.5

2015 6/30/15 Breeder Deer Medina Facility #1 White-tailed Deer M 2.5

2015 3/25/16 Free Range Hartley Mule Deer M 3.5

2015 3/18/16 Free Range Hudspeth Mule Deer M 5.5

2014 12/4/14 Free Range Hudspeth Mule Deer M 4.5

2012 7/12/12 Free Range Hudspeth Mule Deer F 6.5

2012 7/12/12 Free Range Hudspeth Mule Deer F 4.5

2012 12/28/12 Free Range Hudspeth Mule Deer M 3.5

2012 12/2/12 Free Range Hudspeth Mule Deer M 5.5

2012 12/10/12 Free Range Hudspeth Mule Deer M 4.5

2012 12/1/12 Free Range Hudspeth Mule Deer M 4.5

Showing 66 to 100 of 100 entries



WEDNESDAY, FEBRUARY 21, 2018 

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

http://chronic-wasting-disease.blogspot.com/2018/02/texas-tpwd-cwd-tse-prion-2-more-from.html

CWD MAP


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


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

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.



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***



> 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).*** 




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

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

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

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

Summary and Recommendation: 

snip...

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

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


*** 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


PRION 2016 TOKYO Zoonotic Potential of CWD Prions: 

An Update 

Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions. 

PRION 2016 TOKYO In Conjunction with Asia Pacific Prion Symposium 2016 PRION 2016 Tokyo Prion 2016 


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. 


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.


Chronic Wasting Disease and Potential Transmission to Humans 

Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,† Michael W. Miller,‡ Pierluigi Gambetti,§ and Lawrence B. Schonberger*

Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected in other parts of the United States. Although detection in some areas may be related to increased surveillance, introduction of CWD due to translocation or natural migration of animals may account for some new foci of infection. Increasing spread of CWD has raised concerns about the potential for increasing human exposure to the CWD agent. The foodborne transmission of bovine spongiform encephalopathy to humans indicates that the species barrier may not completely protect humans from animal prion diseases. Conversion of human prion protein by CWDassociated prions has been demonstrated in an in vitro cellfree experiment, but limited investigations have not identified strong evidence for CWD transmission to humans. More epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.


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

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

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

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

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

From: "Belay, Ermias"

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

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

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

Dear Sir/Madam,

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

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

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

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


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 ;



 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 ***



*** 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. 



BSE INQUIRY


CJD9/10022

October 1994

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

BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

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

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

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

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

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.



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

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

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

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

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

snip...

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

snip...

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

snip...

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

snip...see full report ;



TUESDAY, SEPTEMBER 12, 2017 

CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat 



SATURDAY, JANUARY 27, 2018 

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



TUESDAY, MARCH 06, 2018 

ZOONOSIS OF CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE, who makes the final call?



Sunday, February 25, 2018 

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



MONDAY, MARCH 05, 2018 

Chronic Wasting Disease: Status, Science, and Management EXPLANATION U.S. Department of the Interior U.S. Geological Survey Open-File Report 2017–1138 March 2018



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

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

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

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

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

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

SPORADIC/SPONTANEOUS TSE HAS NEVER BEEN PROVEN.

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



CDC CWD TSE PRION UPDATE USA JANUARY 2018

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

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

snip.... 



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


Fatal deer disease would impact more than hunters in Alabama LAND VALUES

The impact

Alabama is a hunting crazy state.

“The economic impact, of course, is huge,” Sykes said. “Hunting is a major part of the economy in rural areas of Alabama. And hunting is a huge part of the culture in Alabama. It is a part of the fabric of so many people’s lives.”

Land values will likely be the first indicator of bad news if CWD comes to the state, said Jeff Roberts, a real estate agent who sells hunting land in the Black Belt.

“For farmers and landowners, leasing the hunting rights to their places is a huge secondary income for many,” he said. “If CWD comes to Alabama, the land values are going to go into the basement. I’ve had clients turn their backs on absolutely beautiful hunting tracts when they found out feral hogs were on the property. You can imagine what CWD would do to spook buyers.”


WEDNESDAY, MAY 17, 2017

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


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?


USAHA 2017 RESOLUTIONS

RESOLUTION NUMBER: 23 

APPROVED AS AMENDED SOURCE: COMMITTEE ON WILDLIFE AND CAPTIVE WILDLIFE 

SUBJECT MATTER: Annual Reporting on Chronic Wasting Disease Epidemiological Data 

BACKGROUND INFORMATION: Chronic wasting disease (CWD) has been recognized in wild cervids since the 1980’s. Availability of complete epidemiological information is critical for evaluating the effectiveness of science-based disease control programs. Access to pertinent information from epidemiological investigations across the country in wild populations is imperative to developing success strategies for managing the disease. More comprehensive information is needed on CWD epidemiology in the affected wild populations. Analysis of data from CWD affected populations across the country will improve risk assessment. Comprehensive epidemiological data evaluation may potentially identify factors contributing to the detection of CWD, enhance mitigation strategies to reduce the likelihood of CWD in new populations, and facilitate its earliest detection when it is present. 

RESOLUTION: The United States Animal Health Association (USAHA) requests the United States Department of Agriculture (USDA), Animal and Plant Health Inspection Service, Veterinary Services and other appropriate federal and state agencies to work cooperatively to assemble, analyze, summarize, and make available annually to the Committee on Wildlife and Captive Wildlife at the USAHA meeting all pertinent information from epidemiological investigations of Chronic Wasting Disease (CWD) in cervid populations (including wild, free-ranging, and captive). 

Specific information requested may include: 

1) Compiled CWD testing data from each state to include: 

a) Overall state testing numbers of each susceptible species tested; 

b) Number of CWD positive tests found annually in each state; 

c) Overall state testing in wild populations; 

d) Prevalence of CWD in positive populations; 

e) Population totals for each susceptible species of wild herds in each state; 

f) Demography of positive and negative animals in infected herds; 

g) Results from all tissues that were tested; 

h) Duration of monitoring prior to detection of the first case - including numbers of animals in the herd, numbers tested, and numbers not tested; 

i) Results of trace-forward and trace-back investigations; and 

j) All other pertinent data that will enhance risk assessment of CWD in cervids and identification of effective mitigation measures. 

2) Compiled data should also be posted on the USDA website.

http://www.usaha.org/upload/Resolution/2017/Resolution_23_CWD_Data.pdf

RESOLUTION NUMBER: 21 APPROVED SOURCE: COMMITTEE ON SHEEP, GOATS AND CAMELIDS SUBJECT MATTER: National Scrapie Eradication Program Funding 

BACKGROUND INFORMATION: Due to the success of the cooperative National Scrapie Eradication Program, no new cases of scrapie have been identified in the United States (US) in the past 18 months. There are key components of the program that have been critical to this success and the effort to have the US be recognized internationally as free from scrapie, which would open new markets to US sheep and goat products. Surveillance and traceability are vital to this eradication program. Program use of sheep and goat official tags have demonstrated that official plastic tags are preferred over metal tags for readability and to reduce safety concerns. Funding for tags that are readable, acceptable to producers and efficient for regulators is essential to continue identification compliance and progress of the program. 

RESOLUTION: The United States Animal Health Association urges the United States Secretary of Agriculture to request a congressional appropriation of five million additional dollars of new money to be added to the Equine, Cervid and Small Ruminant health line for the purpose of supporting Small Ruminant Health Programs to complete the eradication of scrapie and assure program success. It is vital that this new funding does not reduce other current United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services program funding lines. 



lol, drop in the bucket and a band-aid approach to something that needed a tourniquet decades ago...

PRION CONFERENCE 2015, 2016, 2017, ON potential for CWD TSE PRION ZOONOSIS, if it has not happened already...

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. 


MONDAY, MARCH 05, 2018 

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

Sunday, February 25, 2018 

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


WEDNESDAY, MARCH 21, 2018 

World Animal Organization (OIE) Appoints Veterinary Institute as first European reference laboratory for land animal health field of CWD or skrantesjuke scratch disease



MONDAY, MARCH 05, 2018 

Chronic Wasting Disease: Status, Science, and Management EXPLANATION U.S. Department of the Interior U.S. Geological Survey Open-File Report 2017–1138 March 2018


WEDNESDAY, MARCH 07, 2018 

Addressing deer disease: DNR, MSU collaborate on deer movement study in south-central Michigan


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 ***


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 *** 

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 ***



USAHA 2017 RESOLUTIONS

RESOLUTION NUMBER: 23 

APPROVED AS AMENDED SOURCE: COMMITTEE ON WILDLIFE AND CAPTIVE WILDLIFE 

SUBJECT MATTER: Annual Reporting on Chronic Wasting Disease Epidemiological Data 

BACKGROUND INFORMATION: Chronic wasting disease (CWD) has been recognized in wild cervids since the 1980’s. Availability of complete epidemiological information is critical for evaluating the effectiveness of science-based disease control programs. Access to pertinent information from epidemiological investigations across the country in wild populations is imperative to developing success strategies for managing the disease. More comprehensive information is needed on CWD epidemiology in the affected wild populations. Analysis of data from CWD affected populations across the country will improve risk assessment. Comprehensive epidemiological data evaluation may potentially identify factors contributing to the detection of CWD, enhance mitigation strategies to reduce the likelihood of CWD in new populations, and facilitate its earliest detection when it is present. 

RESOLUTION: The United States Animal Health Association (USAHA) requests the United States Department of Agriculture (USDA), Animal and Plant Health Inspection Service, Veterinary Services and other appropriate federal and state agencies to work cooperatively to assemble, analyze, summarize, and make available annually to the Committee on Wildlife and Captive Wildlife at the USAHA meeting all pertinent information from epidemiological investigations of Chronic Wasting Disease (CWD) in cervid populations (including wild, free-ranging, and captive). 

Specific information requested may include: 

1) Compiled CWD testing data from each state to include: 

a) Overall state testing numbers of each susceptible species tested; 

b) Number of CWD positive tests found annually in each state; 

c) Overall state testing in wild populations; 

d) Prevalence of CWD in positive populations; 

e) Population totals for each susceptible species of wild herds in each state; 

f) Demography of positive and negative animals in infected herds; 

g) Results from all tissues that were tested; 

h) Duration of monitoring prior to detection of the first case - including numbers of animals in the herd, numbers tested, and numbers not tested; 

i) Results of trace-forward and trace-back investigations; and 

j) All other pertinent data that will enhance risk assessment of CWD in cervids and identification of effective mitigation measures. 

2) Compiled data should also be posted on the USDA website.

http://www.usaha.org/upload/Resolution/2017/Resolution_23_CWD_Data.pdf

RESOLUTION NUMBER: 21 APPROVED SOURCE: COMMITTEE ON SHEEP, GOATS AND CAMELIDS SUBJECT MATTER: National Scrapie Eradication Program Funding 

BACKGROUND INFORMATION: Due to the success of the cooperative National Scrapie Eradication Program, no new cases of scrapie have been identified in the United States (US) in the past 18 months. There are key components of the program that have been critical to this success and the effort to have the US be recognized internationally as free from scrapie, which would open new markets to US sheep and goat products. Surveillance and traceability are vital to this eradication program. Program use of sheep and goat official tags have demonstrated that official plastic tags are preferred over metal tags for readability and to reduce safety concerns. Funding for tags that are readable, acceptable to producers and efficient for regulators is essential to continue identification compliance and progress of the program. 

RESOLUTION: The United States Animal Health Association urges the United States Secretary of Agriculture to request a congressional appropriation of five million additional dollars of new money to be added to the Equine, Cervid and Small Ruminant health line for the purpose of supporting Small Ruminant Health Programs to complete the eradication of scrapie and assure program success. It is vital that this new funding does not reduce other current United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services program funding lines. 



lol, drop in the bucket and a band-aid approach to something that needed a tourniquet decades ago...

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

Volume 23, Number 9—September 2017

Research Letter

Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion

Allen Herbst1, Camilo Duque Velásquez1, Elizabeth Triscott, Judd M. Aiken, and Debbie McKenzieComments to Author Author affiliations: University of Alberta, Edmonton, Alberta, Canada Cite This Article

Abstract

Human and mouse prion proteins share a structural motif that regulates resistance to common chronic wasting disease (CWD) prion strains. Successful transmission of an emergent strain of CWD prion, H95+, into mice resulted in infection. Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.

Chronic wasting disease (CWD) is a contagious prion disease of cervids that is spreading globally. CWD is enzootic in multiple cervid species, including deer and elk; the major foci of disease are Colorado/Wyoming (USA), Wisconsin/Illinois (USA), and Alberta/Saskatchewan (Canada). CWD is also present in captive cervids in South Korea and wild reindeer and moose in Norway (https://www.nwhc.usgs.gov/images/cwd/cwd_map.jpg). CWD results from the conformational transformation of the host-encoded cellular prion protein (PrPC) into protease-resistant, detergent-insoluble, β-sheet rich, amyloidogenic conformers, termed prions (PrPCWD). Within their conformation, prion strains encipher the information that directs the templated misfolding and aggregation of PrPC molecules into additional prions (1).

Although the sequence homology of PrP among mammals is high, the ability of particular prion strains to cause disease in different species is determined by the conformational compatibility between a given strain and the host PrPC (2). We previously identified 2 strains of CWD prion in white-tailed deer (3), Wisc-1 and H95+; these strains exhibit distinct biological properties in deer and transgenic cervidized mice. To ascertain the host range of different strains from cervids, we inoculated CWD prions isolated from experimentally infected deer with different PRNP genotypes (Q95G96 [wild type (wt)], S96/wt, H95/wt, and H95/S96) and from elk (CWD2 strain) into hamsters and mice. All isolates have been successfully transmitted into transgenic mice expressing wt cervid PrP and contain high titers of CWD prions (3).

Mice inoculated with H95+ CWD prions succumbed to clinical disease at 575 ± 47 or 692 ± 9 days, depending on the H95+ isolate (Table). Mice inoculated with Wisc-1 or elk CWD or uninfected deer homogenates were euthanized at day 708 after infection with no signs of prion disease. Clinical signs of H95+ CWD in C57Bl/6 mice included ataxia, lethargy, tail rigidity, and dermatitis. Protease-resistant PrPCWD was present in all mice infected with H95+ prions and was not detected in mice infected with Wisc-1 or CWD2 (Technical Appendix[PDF - 1.04 MB - 6 pages]).

In contrast to mice, hamsters succumbed to clinical disease when inoculated with Wisc-1 CWD prions but were less susceptible to H95+ CWD prions (Table). Clinical signs of CWD in hamsters began with lethargy and, upon arousal, retrocollis; as the disease progressed, lethargy declined with increased dystonic movement including ataxia and tremors. Hyperesthesia was not observed. Subclinical disease (no clinical signs but PrP-res positive by Western blot) was observed in a subset of hamsters (Technical Appendix[PDF - 1.04 MB - 6 pages]).

Successful interspecies prion transmission at the molecular level depends on the compatibility of the invading prion conformers and structural determinants imposed by host PrPC. One structural motif is the loop region between β sheet 2 and α helix 2 of PRPC at aa 170–174 (Technical Appendix[PDF - 1.04 MB - 6 pages]). Host species containing PrPC molecules with a flexible β2-α2 loop (mice and humans) are hypothesized to be incompatible with prions derived from species containing a rigid loop (deer and elk) (4,5). Previous attempts to transmit CWD to mice have failed (6,7). Our data show that prions from a prototypic rigid-loop species (deer) can transmit to a flexible-loop species (mice). The transmission is strain dependent. H95+ overrides the conformational restriction imposed by the mouse PrP flexible loop that Wisc-1 and CWD2 cannot overcome, suggesting that the invading prion strain is a dominant contributor to the species/transmission barrier. How the N terminal amino acid polymorphism (Q95H) affects the conformation of PrP, altering the deer-to-mouse transmission barrier, is unknown. Further structural studies may clarify the effect of N terminal residues on β2-α2 loop rigidity.

Transmission of H95+ CWD prions to mice further confirms the value of specifying strain when defining species barriers. Experimental transmission of CWD prion into macaques and transgenic mice expressing human PrP suggests a considerable transmission barrier to CWD prions (although squirrel monkeys are susceptible), and human prion protein is converted inefficiently in vitro (8,9). Successful infection of a flexible-loop species (mice) with H95+ CWD raises concerns for the potential pathogenicity of H95+ prions to other flexible-loop species. Transmission studies with Wisc-1 and H95+ in transgenic humanized and bovinized mice are ongoing.

The increasing prevalence of CWD indicates selection for cervids with resistance alleles, such as S96 and H95. Genetic resistance to a given prion strain selects for the emergence of novel prion strains with altered properties such as H95+ and Nor98 (3,10). The iterative transmission of CWD prions to cervids with protective alleles of PrPC and the consequent emergence of new CWD prion strains highlights the dynamics of the CWD panzootic and the value of characterizing the host range of emergent CWD prion strains.

Dr. Herbst is a research associate and Dr. Duque Velásquez is a postdoctoral fellow at the University of Alberta. Their primary research interest is the mechanism(s) of pathogenicity underlying neurodegeneration, as exemplified by prion diseases in animals and humans.


see also;


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/

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

”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

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


PRION CONFERENCE 2015, 2016, 2017, ON potential for CWD TSE PRION ZOONOSIS, if it has not happened already...

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. 


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

http://chronic-wasting-disease.blogspot.com/2018/02/texas-tpwd-cwd-tse-prion-2-more-from.html

CWD MAP


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


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

January 14, 2018

MONDAY, NOVEMBER 27, 2017 TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING 63 CASES CONFIRMED TO DATE NOVEMBER 27, 2017 http://chronic-wasting-disease.blogspot.com/2017/11/texas-chronic-wasting-disease-cwd-tse.html FRIDAY, DECEMBER 01, 2017 TEXAS TAHC CWD TSE PRION SURVEILLANCE AND REPORTING UNDER QUESTION, 14 CAPTIVE CASES CWD DETECTED 2017 SO FAR http://chronic-wasting-disease.blogspot.com/2017/12/texas-tahc-cwd-tse-prion-surveillance.html SATURDAY, DECEMBER 02, 2017 TEXAS TAHC CWD TSE PRION Trace Herds INs and OUTs Summary Minutes of the 399th and 398th Commission Meeting – 8/22/2017 5/9/2017 http://chronic-wasting-disease.blogspot.com/2017/12/texas-tahc-cwd-tse-prion-trace-herds.html WEDNESDAY, OCTOBER 18, 2017 TEXAS Medina County Elk Tests Positive for Chronic Wasting Disease CWD TSE PRION harvested on a high-fenced premises http://chronic-wasting-disease.blogspot.com/2017/10/texas-medina-county-elk-tests-positive.html

WEDNESDAY, SEPTEMBER 27, 2017

TEXAS, TPWD, WIN CWD COURT CASE AGAINST DEER BREEDERS CAUSE NO. D-1-GN-15-004391

THURSDAY, SEPTEMBER 21, 2017

TEXAS TPWD CWD mandatory check stations for Chronic Wasting Disease in the South Central, Panhandle, and Trans-Pecos areas



WEDNESDAY, MAY 31, 2017

Texas New Exotic CWD Susceptible Species Rules Now in Effect



MONDAY, MAY 15, 2017 

TEXAS New CWD TSE PRION 50th Case Discovered at Fifth Captive Deer Breeding Facility 



SUNDAY, MAY 14, 2017 

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



FRIDAY, MARCH 31, 2017 

TPWD UPDATE CWD TSE Prion 49 confirmed cases and unwanted firsts for Texas 



THURSDAY, JANUARY 26, 2017 

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



WEDNESDAY, NOVEMBER 07, 2012 Thursday, November 26, 2015

TEXAS CWD TSE PRION REPORTING TURKEY OF THE YEAR AWARD GOES TO SHANNON TOMPKINS OF THE HOUSTON CHRONICLE



Thursday, October 30, 2014

A cool start to deer season, but challenges linger By Shannon Tompkins



THURSDAY, DECEMBER 13, 2012 

HUNTERS FEELING THE HEAT Houston Chronicle December 13, 2012 OUTDOORS not talking about CWD in Texas HUNTERS FEELING THE HEAT 

Houston Chronicle 

December 13, 2012 

OUTDOORS 

 A break in the unusually warm, dry weather could bolster late deer-season prospects 

 by Shannon Tompkins 



WEDNESDAY, NOVEMBER 07, 2012 

Chronic Wasting Disease CWD, Texas, Houston Chronicle Shannon Thomkins 1998 - 2012 what happened ???



SUNDAY, JANUARY 22, 2017 

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



FRIDAY, JANUARY 20, 2017 

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



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, November 18, 2016 

IMPORTANT: SAWCorp CWD Test is NOT APHIS Approved 



Wednesday, November 09, 2016 

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



Wednesday, September 28, 2016 

TPWD CWD Sample Collector Trainings in the Trans Pecos and Panhandle 



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 



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 



SATURDAY, JULY 09, 2016 

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


 
Friday, July 01, 2016 

*** TEXAS Thirteen new cases of chronic wasting disease (CWD) were confirmed at a Medina County captive white-tailed deer breeding facility on June 29, 2016 



Thursday, June 09, 2016 

Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964 

How Did CWD Get Way Down In Medina County, Texas? 

Confucius ponders... 

Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)? 

Epidemiology of Scrapie in the United States 1977 

snip... 

Scrapie Field Trial Experiments Mission, Texas A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. 

It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease. 

The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. 

They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. 

Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. 

The station was divided into 2 areas: 

(1) a series of pastures and-pens occupied by male animals only, and 

(2) a series of pastures and pens occupied by females and young progeny of both sexes. 

... snip...

see full text ; 



Thursday, June 09, 2016 

Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964 How Did CWD Get Way Down In Medina County, Texas? 




SUNDAY, MAY 22, 2016 

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



Wednesday, May 04, 2016 

TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99 Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment Submission 



*** Hartley County Sheep with Scrapie, and CWD in Hartley county ??? 

*** Friday, April 22, 2016 

*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer 



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 



Friday, February 05, 2016 

*** TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER RELEASE SITE 



SATURDAY, JANUARY 23, 2016 

Texas Chronic Wasting Disease Response Update and Interim Deer Management Permit Rules Recommended Adoption of Proposed Rules 



Monday, November 16, 2015 

*** TEXAS PARKS AND WILDLIFE DEPARTMENT EXECUTIVE DIRECTOR ORDER NO. 015-006 

*** Chronic Wasting Disease (CWD) immediate danger to the white-tailed deer and mule deer resources of Texas

http://chronic-wasting-disease.blogspot.com/2015/11/texas-parks-and-wildlife-department.html


Saturday, November 14, 2015 

TEXAS CAPTIVE BREEDER CHRONIC WASTING DISEASE CWD 2 MORE SUSPECTS DECTECTED BRINGING NUMBER TO 7 DETECTED IN CAPTIVE BREEDER (if/when the last two are confirmed). 



Thursday, November 05, 2015 

*** TPW Commission Adopts Interim Deer Breeder Movement Rules 



Thursday, September 24, 2015

TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE Prion Testing 

*** I cannot stress enough to all of you, for the sake of your family and mine, before putting anything in the freezer, have those deer tested for CWD. ...terry 

see Shannon Tomkins;

State seeks help from hunters in monitoring deer disease

By Shannon Tompkins

Updated 8:40 pm, Saturday, September 26, 2015



Friday, October 09, 2015 

Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October 2015 


 
Saturday, October 03, 2015 

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015 


WARNING

***raw and uncut***

(i was just fed up at this point, the sheer ignorance of it all...tss)

Sunday, August 23, 2015 

TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas 



Thursday, August 20, 2015 

TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks and CWD



Friday, August 07, 2015 

*** Texas CWD Captive, and then there were 4 ? 



Thursday, August 06, 2015 

*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY 



Wednesday, July 22, 2015 

Texas Certified Chronic Wasting Disease CWD Sample Collector, like the Wolf Guarding the Henhouse 



Tuesday, July 21, 2015 

*** Texas CWD Medina County Herd Investigation Update July 16, 2015 *** 



Thursday, July 09, 2015 

TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed Herd with Testing of Exposed Animals 



Wednesday, July 01, 2015 

*** TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer 

http://chronic-wasting-disease.blogspot.com/2015/07/texas-chronic-wasting-disease-detected.html


TUESDAY, DECEMBER 16, 2014

Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION 



SUNDAY, DECEMBER 14, 2014

TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry

http://chronic-wasting-disease.blogspot.com/2014/12/texas-84th-legislature-commencing-this.html


TUESDAY, OCTOBER 21, 2014

Texas Pair Convicted in Illegal Deer Breeding Operation TPWD



THURSDAY, MAY 08, 2014

TEXAS Game Wardens Investigate Deer Breeding Facility, Seize Animals, for disease and criminal investigation


 
FRIDAY, MARCH 14, 2014

TEXAS 2013-2014 CWD TESTING FINDS NO POSITIVES ! 

this is good news, however, with the limited testing, I would not sit back and give the all clear. we must remain vigilant. with past testing history for cwd, it is a very real likelihood cwd has been established in Texas, especially, with as many game farms and such. but this is good news.


http://chronic-wasting-disease.blogspot.com/2014/01/texas-cwd-testing-2013-2014-to-date.html


MONDAY, FEBRUARY 11, 2013

TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos



Tuesday, July 10, 2012 

Chronic Wasting Disease Detected in Far West Texas 

http://www.tpwd.state.tx.us/newsmedia/releases/?req=20120710a

http://chronic-wasting-disease.blogspot.com/2012/07/chronic-wasting-disease-detected-in-far.html


Tuesday, July 10, 2012 

Dr. James C. Kroll Texas deer czar final report on Wisconsin 

http://chronic-wasting-disease.blogspot.com/2012/07/dr-james-c-kroll-texas-deer-czar-final.html


Saturday, July 07, 2012 

TEXAS Animal Health Commission Accepting Comments on Chronic Wasting Disease Rule Proposal 

Considering the seemingly high CWD prevalence rate in the Sacramento and Hueco Mountains of New Mexico, CWD may be well established in the population and in the environment in Texas at this time. 

http://chronic-wasting-disease.blogspot.com/2012/07/texas-animal-health-commission.html


Wednesday, June 13, 2012 

TAHC Modifies Entry Requirements Effective Immediately for Cervids DUE TO CWD 

FOR IMMEDIATE RELEASE 

http://chronic-wasting-disease.blogspot.com/2012/06/tahc-modifies-entry-requirements.html


Friday, June 01, 2012 

*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS 

http://chronic-wasting-disease.blogspot.com/2012/06/texas-deer-czar-to-wisconsin-ask-to.html


Thursday, March 29, 2012 

TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT CALLING KETTLE BLACK 

http://chronic-wasting-disease.blogspot.com/2012/03/texas-deer-czar-says-wisconsin-dnr-not.html


Monday, March 26, 2012 

Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West Texas 

http://chronic-wasting-disease.blogspot.com/2012/03/texas-prepares-for-chronic-wasting.html


Monday, March 26, 2012 

3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILS FROM TEXAS BORDER 

http://chronic-wasting-disease.blogspot.com/2012/03/3-cases-of-cwd-found-new-mexico-mule.html


Saturday, June 09, 2012 

USDA Establishes a Herd Certification Program for Chronic Wasting Disease in the United States 

http://chronic-wasting-disease.blogspot.com/2012/06/usda-establishes-herd-certification.html

 
2011 – 2012 

Friday, October 28, 2011 

CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS 

Greetings TAHC et al, 

A kind greetings from Bacliff, Texas. 

In reply to ; 

Texas Animal Health Commission (TAHC) Announcement October 27, 2011 

I kindly submit the following ; 



TUESDAY, JUNE 14, 2011

Texas deer smuggler to pay $1.5 million in fines, restitution

http://chronic-wasting-disease.blogspot.com/2011/06/texas-deer-smuggler-to-pay-15-million.html

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

CWD TEXAS TAHC OLD FILE HISTORY

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

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

Date: Sun, 25 Aug 2002 19:45:14 –0500

From: Kenneth Waldrup


snip...see ;


i am not a Doctor and never anywhere have i implied i was, or have implied nothing more than who i am, and why i do it...terry

 Subject: CWD SURVEILLANCE STATISTICS TEXAS (total testing figures less than 50 in two years) Date: Sun, 25 Aug 2002 21:06:49 –0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de

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

greetings list members,

here are some figures on CWD testing in TEXAS...TSS

Dear Dr. Singletary,

In Fiscal Year 2001, seven deer from Texas were tested by the National Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer). During these two years, an additional six elk and one white-tailed deer were tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least eight other white-tailed deer have been tested at TVMDL. One elk has been tested at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke of the Texas Parks and Wildlife Department also has records of 601 clinically ill white-tailed deer which were necropsied at Texas A&M during the late 1960's and early 1970's, and no spongiform encepalopathies were noted. Thank you for your consideration.

xxxxxxx

Texas Animal Health Commission

(personal communication...TSS)

Austin 8 news

snip...

"There's about 4 million deer in the state of Texas, and as a resource I think we need to be doing as much as we can to look for these diseases," said Doug Humphreys with Texas Parks and Wildlife. "Right now Texas is clear. We haven't found any, but that doesn't mean we don't look."


With approximately 4 million animals, Texas has the largest population of white-tailed deer in the nation. In addition, about 19,000 white-tailed deer and 17,000 elk are being held in private facilities. To know if CWD is present in captive herds, TPWD and Texas Animal Health Commission are working with breeders to monitor their herds.


How is it spread?

It is not known exactly how CWD is spread. It is believed that the agent responsible for the disease may be spread both directly (animal to animal contact) and indirectly (soil or other surface to animal). It is thought that the most common mode of transmission from an infected animal is via saliva, feces, and urine.


some surveillance?

beyond the _potential_ methods of transmissions above, why, not a single word of SRM of various TSE species in feed as a source?

it's a known fact they have been feeding the deer/elk the same stuff as cows here in USA.

and the oral route has been documented of CWD to mule deer fawns in lab studies.

not to say that other _potential_ transmission mechanisms are possible, but why over look the obvious?

TSS


From: Ken Waldrup, DVM, PhD (host25-207.tahc.state.tx.us)

Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border)

Date: December 15, 2003 at 3:43 pm PST

In Reply to: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border) posted by TSS on December 12, 2003 at 2:15 pm:

Dear sirs:

With regard to your comment about Texas NOT looking for CWD along the New Mexico border, it is painfully obvious that you do not know or understand the natural distribution of mule deer out there or the rights of the land owners in this state. As of 15 December 2003, a total of 42 deer had been sampled from what we call "Trans-Pecos", beyond the Pecos River. Mule deer are very widely dispersed through this area, sometimes at densities of one animal per 6 square miles. The Texas Parks and Wildlife Department does not have the legal authority to trepass on private property to collect deer. Some landowners are cooperative. Some are not. Franklin State Park is at the very tip of Texas, and deer from the park have been tested (all negative). One of the single largest land owners along the border is the National Park Service. Deer and elk from the Guadalupe Peak National Park cannot be collected with federal permission. The sampling throughout the state is based on the deer populations by eco-region and is dictated by the availability of funds. I am concerned about your insinuation that CWD is a human health risk. We are at a stand-off - you have no proof that it is and I have no definitive proof that it isn't. However I would say that the inferred evidence from Colorado, Wyoming and Wisconsin suggests that CWD is not a human health concern (i.e. no evidence of an increased incidence of human brain disorders within the CWD "endemic" areas of these states). From my professional interactions with the Texas Parks and Wildlife Department, I can definitely say that they want to do a thorough and sound survey throughout the state, not willy-nilly "look here, look there". There are limitations of manpower, finances and, in some places, deer populations. I would congratulate TPWD for doing the best job with the limitations at hand rather than trying to browbeat them when you obviously do not understand the ecology of West Texas. Thank you for your consideration.

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

From: TSS (216-119-139-126.ipset19.wt.net)

Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border)

Date: December 16, 2003 at 11:03 am PST

In Reply to: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border) posted by Ken Waldrup, DVM, PhD on December 15, 2003 at 3:43 pm:

HEllo Dr. Waldrup,

thank you for your comments and time to come to this board.

Ken Waldrup, DVM, PhD states;

> it is painfully obvious that you do not know or understand the natural distribution of mule deer out there or the rights of the land owners in this state...

TSS states;

I am concerned about all deer/elk not just mule deer, and the rights of land owners (in the case with human/animal TSEs) well i am not sure of the correct terminology, but when the States deer/elk/cattle/sheep/humans are at risk, there should be no rights for land owners in this case. the state should have the right to test those animals. there are too many folks out there that are just plain ignorant about this agent. with an agent such as this, you cannot let landowners (and i am one) dictate human/animal health, especially when you cannot regulate the movement of such animals...

Ken Waldrup, DVM, PhD states;

> Deer and elk from the Guadalupe Peak National Park cannot be collected with federal permission. TSS states;

I do not understand this? so there is no recourse of action even if every deer/elk was contaminated with CWD in this area (hypothetical)?

Ken Waldrup, DVM, PhD states;

> I am concerned about your insinuation that CWD is a human health risk. We are at a stand-off - you have no proof that it is and I have no definitive proof that it isn't. However I would say that the inferred evidence from Colorado, Wyoming and Wisconsin suggests that CWD is not a human health concern (i.e. no evidence of an increased incidence of human brain disorders within the CWD "endemic" areas of these states)...

 TSS states;

NEXT, let's have a look at the overall distribution of CWD in Free-Ranging Cervids and see where the CWD cluster in NM WSMR borders TEXAS;

Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids


NOW, the MAP of the Exoregion where the samples were taken to test for CWD;

CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS


Ecoregions of TEXAS


IF you look at the area around the NM WSMR where the CWD cluster was and where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my Geography and my Ciphering is correct ;-) that region only tested 55% of it's goal. THE most important area on the MAP and they only test some 96 samples, this in an area that has found some 7 positive animals? NOW if we look at the only other border where these deer from NM could cross the border into TEXAS, this area is called the High Plains ecoregion, and again, we find that the sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD sampling was met, only 16 samples were tested from some 175 that were suppose to be sampled.

AS i said before;

 > SADLY, they have not tested enough from the total population to

> know if CWD is in Texas or not.

 BUT now, I will go one step further and state categorically that they are not trying to find it. just the opposite it seems, they are waiting for CWD to find them, as with BSE/TSE in cattle, and it will eventually...

snip...end...TSS

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

2005

SEE MAP OF CWD ON THE BORDER OF NEW MEXICO VERY CLOSE TO TEXAS ;



NO update on CWD testing in Texas, New Mexico that i could find. I have inquired about it though, no reply yet...

 -------- Original Message --------

Subject: CWD testing to date TEXAS ?

Date: Mon, 09 May 2005 12:26:20 –0500

From: "Terry S. Singeltary Sr."


 Hello Mrs. Everett,

I am most curious about the current status on CWD testing in Texas. could you please tell me what the current and past testing figures are to date and what geographical locations these tests have been in. good bust on the illegal deer trapping case. keep up the good work there.........

thank you, with kindest regards,

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

 -------- Original Message --------

Subject: CWD testing in New Mexico

Date: Mon, 09 May 2005 14:39:18 –0500

From: "Terry S. Singeltary Sr."


Greetings,

I am most curious of the current and past CWD testing in New Mexico, and there geographical locations... thank you,

Terry S. Singeltary SR. CJD Watch

#################### https://lists.aegee.org/bse-l.html ####################

 2006

 ----- Original Message -----

From: "Terry S. Singeltary Sr." flounder9@VERIZON.NET

To: BSE-L@aegee.org

Sent: Saturday, December 23, 2006 1:47 PM

Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing sampling figures -- what gives TAHC ???

Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing sampling figures -- what gives TAHC ???

Date: December 23, 2006 at 11:25 am PST

Greetings BSE-L members,

i never know if i am going crazy or just more of the same BSe. several years ago i brought up the fact to the TAHC that CWD was literally at the Texas borders and that the sample size for cwd testing was no where near enough in the location of that zone bordering NM. well, i just wrote them another letter questioning this again on Dec. 14, 2006 (see below) and showed them two different pdf maps, one referencing this url, which both worked just fine then. since then, i have NOT received a letter from them answering my question, and the url for the map i used as reference is no longer working? 

i had reference this map several times from the hunter-kill cwd sampling as of 31 August 2005 pdf which NO longer works now??? 

but here are those figures for that zone bordering NM, for those that were questioning the url. 

the testing samples elsewhere across Texas where much much more than that figure in the zone bordering NM where CWD has been documented bordering TEXAS, near the White Sands Missile Range. 

SO, why was the Texas hunter-kill cwd sampling as of 31 August 2005 document removed from the internet??? 

you know, this reminds me of the infamous TEXAS MAD COW that i documented some 7 or 8 months before USDA et al documented it, when the TAHC accidentally started ramping up for the announcement on there web site, then removed it (see history at bottom). 

i am not screaming conspiracy here, but confusious is confused again on the ciphering there using for geographical distribution of cwd tissue sample size survey, IF they are serious about finding CWD in TEXAS. 

common sense would tell you if cwd is 35 miles from the border, you would not run across state and have your larger samples there, and least samples 35 miles from where is what found..........daaa..........TSS

 THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare to the other sample locations ;



TPWD has been conducting surveys of hunter-kill animals since 2002 and has collected more than 7300 samples (as of 31 August 2005). In total, there have been over 9400 samples, both hunter-kill and private samples, tested in Texas to date, and no positives have been found.


SO, out of a total of 9,400 samples taken for CWD surveillance in TEXAS since 2002 of both hunter-kill and private kill, ONLY 191 samples have been taken in the most likely place one would find CWD i.e. the border where CWD has been documented at TEXAS and New Mexico latest map NM cwd old data



CWD in New Mexico ;

What is the Department doing to prevent the spread of CWD?

Chronic wasting disease (CWD) was recently detected in a mule deer from Unit 34. Until 2005, CWD had only been found in Unit 19. With this discovery, the Department will increase its surveillance of deer and elk harvested in Units 29, 30 and 34.

Lymph nodes and/or brain stems from every harvested deer and brain stems from all elk taken in Unit 34 will be sampled.

snip...







CWD SURVEILLANCE TEXAS


SNIP...SEE FULL TEXT ;

2011 – 2012

Friday, October 28, 2011

CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS

Greetings TAHC et al,

A kind greetings from Bacliff, Texas.

In reply to ;

Texas Animal Health Commission (TAHC) Announcement October 27, 2011

I kindly submit the following ;



MONDAY, AUGUST 14, 2017

TEXAS CREUTZFELDT JAKOB DISEASE CJD TSE PRION

http://cjdtexas.blogspot.com/2017/07/

SATURDAY, DECEMBER 02, 2017 TEXAS 

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


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.


FRIDAY, FEBRUARY 09, 2018 
Mississippi Chronic Wasting Disease confirmed in a White-tailed Deer

TUESDAY, FEBRUARY 13, 2018 
*** MISSISSIPPI STATE DEPARTMENT OF HEALTH Chronic Wasting Disease: Public Health Recommendations ***

FRIDAY, MARCH 23, 2018 
Mississippi MDWFP Chronic Wasting Disease: Present, Past, and Future

SATURDAY, MARCH 03, 2018 

Minnesota CWD All seven of the remaining white-tailed deer on farm Positive


FRIDAY, NOVEMBER 24, 2017 

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


SATURDAY, MARCH 03, 2018 

WISCONSIN CHRONIC WASTING DISEASE TSE Prion DNR Study Finds CWD-Infected Deer Die At 3 Times Rate Of Healthy Animals


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


USA MAD DEER ROUNDUP

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


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:


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 ???

For Immediate Release Thursday, October 2, 2014

 Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov

 *** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease ***

 DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). 


For Immediate Release

Thursday, October 2, 2014

Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov Share on facebook Share on twitter Share on email Share on print More Sharing Services 1

TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected

CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.

On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.

The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.

The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.

Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.

Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.

The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.

-30-


79.8 percent of the deer tested positive for the disease

DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected

CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.

On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.

The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.

The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.

Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.

Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.

The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.


PENNSYLVANIA NEW CWD MANAGEMENT AREA ESTABLISHED
HARRISBURG, PA - People who live and hunt deer within parts of Lancaster, Lebanon and Berks counties now need to comply with special rules intended to slow the spread of chronic wasting disease (CWD).
The Pennsylvania Game Commission today established Disease Management Area 4 (DMA 4) in response to a CWD-positive deer recently detected at a captive deer farm in Lancaster County.
DMA 4 encompasses 346 square miles in northeastern Lancaster County, southeastern Lebanon County and western Berks County. The northern part of DMA 4 runs roughly between the cities of Lebanon and Reading. The DMA includes the boroughs of Adamstown, Denver, Ephrata, Mohnton, Richland, Womelsdorf and Wyomissing. State Game Lands 46, 220, 225, 274 and 425 are included in DMA 4.
Within DMAs, special rules apply. The intentional feeding of deer is prohibited. Hunters may not use urine-based deer attractants or possess them while afield. And hunters who harvest deer within a DMA may not transport the carcass outside the DMA without first removing and properly disposing of all high-risk deer parts, including the head and backbone.
While the rules might pose an inconvenience, they are meant to slow the spread of CWD, which so far has been detected in only a few parts of the state.
“CWD is an increasing problem in Pennsylvania, and as the disease emerges in new areas, more Pennsylvanians are impacted,” said Game Commission Executive Director Bryan Burhans. “To this point, however, CWD has been detected in captive or free-ranging deer only in a few, isolated areas of the state. That’s good news for all Pennsylvanians who enjoy deer and deer hunting. And we continue to focus our resources on ways to minimize CWD’s impacts statewide.”
CWD, which is always fatal to deer, elk and other cervids, first was detected in Pennsylvania in 2012 at a captive deer farm in Adams County. CWD has been detected among free-ranging deer in two areas of the state.
In addition to establishing DMA 4, the Game Commission will increase its CWD sampling there.
Within DMA 4, the agency will begin testing all known road-killed deer for CWD. Come hunting season, bins for the collection of deer heads and other high-risk deer parts will be placed in areas for the public to use. Hunters who deposit the heads of the deer they harvest in designated collection bins will be able to have their deer tested, free of charge. And DMAP permits for use within DMA 4 will be available for purchase.
Wayne Laroche, the Game Commission’s special assistant for CWD response, said increased sampling within DMA 4 is necessary to find out whether CWD exists among free-ranging deer there, and adjust the response accordingly.
“We need to know the full extent of the CWD problem in any area where the disease exists,” Laroche said. “We have not detected CWD among free-ranging deer in DMA 4, and maybe we won’t. But if CWD is out there, we surely need to know about it to confront it head-on.”
Information on CWD and Pennsylvania’s DMAs, including maps of all DMAs, is available at www.pgc.pa.gov.
 DMA 4 boundary
The exact boundary of DMA 4 is as follows: Beginning in the northwestern extent of the DMA in the city of Lebanon, at the intersection of state Route 897 and U.S. Route 422, proceed east on U.S. Route 422 for 12.3 miles to state Route 419. Turn left on state Route 419 and proceed north for 2.3 miles to Christmas Village Road (state Route 4010). Turn right, proceeding east on Christmas Village Road for 5.1 miles to North Heidelberg Road (state Route 3033). Turn left on North Heidelberg Road, proceeding northeast for 0.6 miles to state Route 183. Turn right on state Route 183, proceeding southeast for 7.7 miles to the U.S. 222. Turn right on U.S. 222 proceeding southwest for 3.2 miles to the interchange with U.S. Route 422 Bypass. Proceed on U.S. Route 422 Bypass for 2.4 miles to intersection with Business Route 222E (Lancaster Avenue). Proceed south on Business 222E for 0.6 miles to the intersection with state Route 625. Turn left onto state Route 625 and proceed south for 16.7 miles to the intersection with Route 23. Turn right on Route 23, proceeding westerly for 9.7 miles to intersection with state Route 772 (Glenbrook Road). Turn right on state Route 772, proceeding northwest for 9.3 miles to state Route 501 (Furnace Hills Pike). Turn right on state Route 501, proceeding northerly for 5 miles to the intersection with U.S. Route 322 (West 28th Division Highway). Turn left on U.S. Route 322, proceeding westerly for 1.3 miles to the Pennsylvania Turnpike (U.S. Route 76). Move right along U.S. Route 76, proceeding east for 0.7 miles to the western boundary of State Game Lands 46. Proceed north, then east for 1.2 miles along the game lands boundary to state Route 501 (Furnace Hills Pike). Turn left on state Route 501, proceeding north for 4.1 miles to the intersection with state Route 419. Turn left, proceeding west for 0.1 miles to state Route 897 (South 5th Street). Turn right on state Route 897, proceeding northwest for 6.2 miles to the starting point at the intersection of state Route 897 and U.S. Route 422.
CWD in Pennsylvania
In Pennsylvania, the Game Commission oversees the management and protection of all free-ranging deer, while farm-raised deer and facilities are overseen by the state Department of Agriculture. The agencies work together to monitor chronic wasting disease.
After CWD was detected in 2012 at a captive deer farm in Adams County, the Game Commission established Disease Management Area 1 (DMA 1), a nearly 600-square-mile area in Adams and York counties, in which restrictions regarding the hunting and feeding of deer applied.
CWD was detected among free-ranging deer a few months later, in three deer harvested by hunters in Bedford and Blair counties in the 2012 firearms season. The deer were detected through the Game Commission’s ongoing CWD surveillance program.
Those CWD-positive deer resulted in the creation of DMA 2, which initially encompassed nearly 900 square miles in parts of Bedford, Blair, Cambria and Huntingdon counties, but since has expanded annually due to the detection of additional free-ranging and captive CWD-positive deer. DMA 2 now encompasses more than 2,845 square miles in parts of Adams, Bedford, Blair Cambria, Clearfield, Cumberland, Franklin, Fulton, Huntingdon and Somerset counties.
So far, 104 free-ranging CWD-positive deer, and 46 of CWD-positive captive deer, have been detected within DMA 2.
In 2014, CWD was detected at a captive deer farm in Jefferson County, leading to the creation of DMA 3, which encompasses about 350 square miles in parts of Clearfield, Indiana and Jefferson counties. In July 2017, a sick-looking adult buck euthanized a month earlier on state game lands in Clearfield County, within DMA 3, was confirmed as CWD-positive. An additional CWD-positive deer was detected within DMA 3 in the 2017-18 hunting season.
In 2017, the Game Commission eliminated DMA 1 after five years of monitoring, which included the testing of 4,800 wild deer; CWD never was found in the wild within DMA 1.
Hunters harvesting deer within DMAs are prohibited from transporting the high-risk parts of those deer (head and backbone) outside the DMA. If those hunters live outside the DMA, and are processing the deer themselves, they must remove and properly dispose of the high-risk parts before taking other parts of the deer home.
Deer meat may be transported outside a DMA so long as the head and backbone have been removed. Antlers may also be transported from a DMA if the skull plate is free of visible brain material.
Hunters using professional meat processors to process the meat from deer they harvest within a DMA must take the deer to processors within the DMA, or otherwise included on the list of approved processors associated with that DMA. There’s also a list of approved taxidermists associated with each DMA.
The feeding of deer and the use or field possession of urine-based deer lures while hunting also are prohibited within DMAs.
MEDIA CONTACT: Travis Lau - 717-705-6541
# # #
FRIDAY, FEBRUARY 23, 2018

Pennsylvania NEW CWD MANAGEMENT AREA TO BE ANNOUNCED


MONDAY, FEBRUARY 12, 2018 

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


FRIDAY, MARCH 23, 2018 
Michigan Chronic wasting disease could be a serious problem for U.P. deer

WEDNESDAY, FEBRUARY 21, 2018 

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

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

SATURDAY, FEBRUARY 17, 2018 

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

FRIDAY, FEBRUARY 09, 2018 

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


MONDAY, FEBRUARY 05, 2018 

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


SATURDAY, FEBRUARY 03, 2018 

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


THURSDAY, FEBRUARY 08, 2018 

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


TUESDAY, JANUARY 30, 2018 

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


THURSDAY, JANUARY 25, 2018 

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


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


WEDNESDAY, JANUARY 24, 2018 

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


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


January 14, 2018

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


MONDAY, JANUARY 29, 2018 

Wyoming, Hanna, WGFD diagnosed chronic wasting disease (CWD) for the first time in Deer Hunt Area 161


MONDAY, JANUARY 29, 2018 

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


SUNDAY, FEBRUARY 18, 2018 

Chronic Wasting Disease CWD TSE Prion RoundUp February 18, 2018


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


trucking and spreading cwd around...tss

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.


spreading cwd around...tss

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





Friday, May 13, 2011

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



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)


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

http://chronic-wasting-disease.blogspot.com/2017/12/norway-30000-deer-animals-have-so-far.html

THURSDAY, NOVEMBER 30, 2017 

Norway Animal welfare surveillance at Nordfjella Skrantesjuke CWD TSE Prion Update

http://chronic-wasting-disease.blogspot.com/2017/11/norway-animal-welfare-surveillance-at.html

WEDNESDAY, NOVEMBER 29, 2017

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

http://chronic-wasting-disease.blogspot.com/2017/11/norway-another-case-of-skrantesjuke-cwd.html

FRIDAY, NOVEMBER 24, 2017 

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

https://chronic-wasting-disease.blogspot.com/2017/11/norwegian-food-safety-authority-makes.html

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.

http://chronic-wasting-disease.blogspot.com/2017/11/norway-detects-more-chronic-wasting.html

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;

http://chronic-wasting-disease.blogspot.com/2017/11/norway-detects-cwd-skrantesjuke-deer.html

http://chronic-wasting-disease.blogspot.com/2017/11/norway-cwd-ny-informasjon-om.html

FRIDAY, OCTOBER 13, 2017 

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

http://chronic-wasting-disease.blogspot.com/2017/10/norway-two-more-new-cases-of-chronic.html

TUESDAY, OCTOBER 10, 2017

Norway detects another case of CWD TSE PRION Skrantesjuke

http://chronic-wasting-disease.blogspot.com/2017/10/norway-detects-another-case-of-cwd-tse.html

SATURDAY, SEPTEMBER 30, 2017 

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

http://chronic-wasting-disease.blogspot.com/2017/09/norway-cwd-tse-prion-humans-zoonosis.html

MONDAY, AUGUST 14, 2017 

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

http://chronic-wasting-disease.blogspot.com/2017/08/norway-cwd-sheep-grazing-and-scrapie.html

TUESDAY, JUNE 20, 2017 

Norway Confirms 6th Case of Skrantesjuke CWD TSE Prion Disease

http://chronic-wasting-disease.blogspot.com/2017/06/norway-confirms-6th-case-of.html

Tuesday, December 13, 2016

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

http://chronic-wasting-disease.blogspot.com/2016/12/norway-chronic-wasting-disease-cwd-tse.html

Thursday, September 22, 2016

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

http://chronic-wasting-disease.blogspot.com/2016/09/norway-detects-5th-case-of-chronic.html

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

http://chronic-wasting-disease.blogspot.com/2016/09/norway-regulation-concerning-temporary.html

Wednesday, August 31, 2016

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

http://chronic-wasting-disease.blogspot.com/2016/08/norway-confirms-4th-case-of-chronic.html

Wednesday, August 31, 2016

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

http://chronic-wasting-disease.blogspot.com/2016/08/norway-confirms-4th-case-of-chronic.html

Tuesday, August 02, 2016

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

http://chronic-wasting-disease.blogspot.com/2016/08/chronic-wasting-disease-of-deer-is.html

Tuesday, June 14, 2016

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

http://chronic-wasting-disease.blogspot.com/2016/06/chronic-wasting-disease-cwd-in-moose.html

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

http://chronic-wasting-disease.blogspot.com/2016/07/norway-reports-third-case-chronic.html

Tuesday, April 12, 2016

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

http://chronic-wasting-disease.blogspot.com/2016/04/the-first-detection-of-chronic-wasting.html

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

http://transmissiblespongiformencephalopathy.blogspot.com/2016/04/the-norwegian-veterinary-institute-nvi.html

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 ??? 

https://web.archive.org/web/20161027181651/http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1982/07/05001001..pdf 

https://web.archive.org/web/20161027182246/http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1982/07/28001001..pdf 

https://web.archive.org/web/20161027181712/http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1983/03/01001001..pdf 

Clinical Communication Enzootic ataxia in Red deer 

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

http://www.tandfonline.com/doi/pdf/10.1080/00480169.1979.34665

SEE FULL TEXT ;

http://chronic-wasting-disease.blogspot.com/2016/07/chronic-wasting-disease-in-deer-cwd-or.html

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


Singeltary submission ;

Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose

DOCUMENT ID: APHIS-2006-0118-0411

***Singeltary submission



Singeltary submission ;

Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose

*** DOCUMENT ID: APHIS-2006-0118-0411



*USA USDA CWD BSE SCRAPIE TSE PRION?
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...


Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. snip... The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle... 

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells 3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ... 


The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite its 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.



Terry S. Singeltary Sr.

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