Friday, June 02, 2017

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

Notice to Members Regarding Chronic Wasting Disease (CWD)

Posted on: 
To: MNA Members
From: Métis Nation of Alberta
Date: Wednesday, May 31, 2017
Métis Nation of Alberta (MNA) was made aware of a recent Canadian research study examining the transmission of Chronic Wasting Disease. The initial results of the study indicate that macaque monkeys (genetically similar to humans) can be infected with Chronic Wasting Disease (CWD) after eating deer that is infected with CWD. CWD is a prion disease, which are fatal, transmissible diseases characterized by abnormal proteins in the brain and nervous system. To date no research has shown that CWD can be passed on to humans, and no human cases of CWD have ever been identified. However, this new research indicates that it is a possibility. The Deputy Chief Medical Officer of Health has reached out to us to share with our Métis harvesters this important information.
For more information you can visit:


and


What the Alberta Government knows:
Necessary Precautions for Harvesters:
  1. Hunters and others who handle carcasses follow basic handling precautions (available here http://aep.alberta.ca/fish-wildlife/fishing-hunting-trapping/hunting-alberta/documents/CWDGuidelines-DeerCarcassTransportationHandling-Oct2009.pdf
  2. All deer, moose and elk harvested from CWD mandatory submission wildlife management units (WMUs) be tested for CWD; and
  3. A negative result (no CWD detected by the test) must be obtained before any part of an animal is eaten.

For more information, contact:
Amy Quintal
Métis Nation of Alberta
Métis Harvesting Liaison
Tel: (780) 455 – 2200
aquintal@metis.org



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


CWD Updates

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

We have completed the heads received to date from the 2016/17 hunting seasons. A total of 5112 heads were tested since September 1, 2016, and we detected CWD in 179 animals (3.5%; up from 2.4% in 2015/16). The positives included 178 deer (154 mule deer, 23 white-tail, 1 unknown deer; 136 males, 41 females, 1 unknown gender) and 1 male elk. As in previous years the majority of cases (119 of 179; 66%) were mule deer bucks.
Also as in previous years, species- and gender-specific differences are apparent in the surveillance data. In the 4944 heads that were suitable for determining disease status, CWD was detected in:
  • 5.4% of 2833 mule deer
  • 1.5% of 1494 white-tailed deer
  • 0.2% of 431 elk (primarily from CFB Suffield)
  • 0 of 176 moose (primarily from CFB Wainwright)
In the 4312 deer for which gender/sex was reported, CWD was detected in:
  • 8.1% of 1473 male mule deer
  • 2.6% of 1349 female mule deer
  • 1.7% of 1071 male whitetails
  • 1.3% of 473 female whitetails
The disease continues to expand further westward into central Alberta. In the 2016/17 surveillance sample, CWD was again detected beyond the known range in the province (further up the Red Deer River in Wildlife Management Unit (WMU) 158, in WMU 230 in the Battle River watershed, in WMU 254 in the Vermilion River watershed).
These units are adjacent to previous cases and indicate further geographic spread of CWD along major waterways. However, the finding of CWD in a white-tailed deer in WMU 250 northeast of Fort Saskatchewan is a significant westward extension of the known occurrence in the North Saskatchewan River watershed.
We also detected CWD in a bull elk from WMU 732 (Canadian Forces Base Suffield). Since 2012, we tested 1973 elk from WMU 732 and this is the first one found to have CWD (0.05%). The disease is well established in mule deer and white-tailed deer in areas outside the military base along the Red Deer and South Saskatchewan rivers.
Note that all CWD freezers have now been removed. However, any time throughout the year, heads can be submitted at any Fish and Wildlife office during their office hours. See page 14 of the 2016 Alberta Guide to Hunting Regulations for office locations and phone numbers.
Additional information about preparing and submitting heads and specific freezer locations can be found at:
The success of the CWD surveillance program relies heavily on participation by hunters, guides, and landowners to ensure a successful harvest that provides heads to be tested. We gratefully acknowledge the efforts of one and all.
The total number of CWD cases detected in wild deer in Alberta since September 2005 is 592.
Note that hunters receive NEGATIVE test results directly at the email address associated with their individual AlbertaRELM account. The email process is the only notification hunters receive when their animal is NEGATIVE for CWD.
As in the past, hunters who harvest a CWD POSITIVE deer are contacted directly by phone (see below).

Patterns of CWD in Alberta

There are significant overall patterns of disease occurrence in Alberta. CWD continues to occur primarily in mule deer in comparison to white-tailed deer despite testing large numbers of both species. Similarly males are more likely to be infected than females.
CWD Annual Prevalence 2010 to 2016
   
CWD Prevalence 1996 to 2016
Analyses of previous data determined the weighted CWD occurrence in Alberta is:
  • Mule Deer: male 1.00 female 0.4
  • White-tailed Deer: male 0.3 female 0.1
Thus male mule deer are the most likely, and female white-tailed deer the least likely to be infected with CWD.
The geographic distribution of CWD is clustered in some WMUs but continues to expand westward.
The finding of CWD in a moose near the South Saskatchewan River valley in 2012 is the first such case identified in Canada.
Specific information about the CWD hunter surveillance program is provided at:
The CWD Freezer Locations currently posted on the Information for Hunters page has all the correct information for 2016. Note that the freezers generally are available each year only between mid-October and late December. Current information also is available from any Fish and Wildlife office.
  • CWD surveillance is focused on the Alberta/Saskatchewan border; however, hunter-killed deer (and elk) are accepted from anywhere in the province (as in all previous years)
  • Ongoing NEGATIVE test results are made available to individual hunters; when test results are available, the hunter receives an email that provides the negative result
  • Ongoing POSITIVE test results are provided by phone directly to the hunter who harvested the infected deer

2015 Fall CWD Surveillance Results

We tested 4929 heads and detected CWD in 116 deer (2.4%). This is an increase in annual overall prevalence from the 2.1% in the 4163 heads tested in the 2014 surveillance program. The 116 cases in 2015 included 105 mule deer, 11 white-tailed deer; 84 males, 31 females, 1 of unknown gender. Majority of cases (77 of 116; 66%) were mule deer bucks.
As in previous years, species-and gender-specific differences are apparent in the surveillance data. In the 4798 heads that were suitable for determining disease status, CWD was detected in:
  • 3.8% of 2756 mule deer
  • 0.8% of 1420 white-tailed deer
  • 0 of 487 elk (primarily from CFB Suffield)
  • 0 of 135 moose (primarily from CFB Wainwright)
In the 4033 deer for which gender/sex was reported, CWD was detected in:
  • 5.9% of 1310 male mule deer
  • 2.0% of 1325 female mule deer
  • 0.7% of 991 male whitetails
  • 1.0% of 407 female whitetails
The geographic distribution of CWD continues to expand with the disease identified in the 2015/16 sample in 6 WMUs where CWD was not previously known to occur: WMU 116 in southeast; 158, 166, 238, and 242 in eastcentral; and 500 in northeast Alberta. These cases are in the Milk River, Red Deer River, Battle River, and North Saskatchewan River watersheds.
The most remarkable new case is the outlier in WMU 242 approximately 100 km further west than the closest known cases (in WMU 232 and 203). This was a mule deer buck harvested on the northern edge of the Battle River watershed west of Miquelon Lake and approximately 30 km southeast of Edmonton. Although we know CWD is well-established in the eastern reaches of the Battle River, the case in WMU 242 significantly expands the known distribution of CWD in central Alberta. Cumulatively we have tested 700 deer heads from the Battle River watershed between WMU 242 and WMU 203/232 and all were negative for CWD. Thus, until we have data to show otherwise, the case near Miquelon Lake appears to be an outlier.
Hunters continue to support the program and are providing a solid foundation on which we can monitor CWD as it becomes further established in eastern deer populations.
To learn more about CWD Surveillance in Alberta, see:
For past CWD surveillance results and a general timeline of CWD in Alberta, see:

Attention Hunters!

Submit deer heads for CWD testing at any Fish and Wildlife office during their office hours or any of the forty-five 24 hr freezers in Edmonton, Calgary, and across eastern Alberta during rifle seasons.
Submission of deer heads for CWD testing is MANDATORY in eastern Alberta from Cold Lake south to the US border.
For more details, see:

CWD Map and Statistics

News Releases and Information Bulletins

Page Information

Updated: Apr 19, 2017 
http://aep.alberta.ca/fish-wildlife/wildlife-diseases/chronic-wasting-disease/cwd-updates/default.aspx

Chronic Wasting Disease: CFIA Research Summary 

 Embargoed until May 23, 2017 

(OCR of a scanned original) 

Research Findings 

Chronic Wasting Disease (CWD) is a progressive, fatal disease of the nervous system of cervids including deer, elk, moose, and reindeer that is caused by abnormal proteins called prions. It is known as a transmissible spongiform encephalopathy (TSE). Other TSEs include scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle, and Creutzfeldt-Jakob disease (CJD) in humans.

A limited number of experimental studies have demonstrated that non-human primates, specifically squirrel monkeys, are susceptible to CWD prions. An ongoing research study has now shown that CWD can also be transmitted to macaques, which are genetically closer to humans. 

The study led by Dr. Stefanie Czub, a scientist at the Canadian Food Inspection Agency (CFIA), and funded by the Alberta Prion Research institute has demonstrated that by orally administering material under experimental conditions from cervids (deer and elk) naturally infected with CWD, the disease can be transmitted to macaques. 

in this project, which began in 2009, 18 macaques were exposed to CWD in a variety of ways: by injecting into the brain, through contact with skin, oral administration, and intravenously (into the bloodstream through veins). So far, results are available from 5 animals. At this point, two animals that were exposed to CWD by direct introduction into the brain, one that was administered infected brain material by oral administration and two that were given infected muscle by oral administration have become infected with CWD. The study is ongoing and testing continues in the remaining animals. The early results will be presented at PRlON 2017, the annual international conference on prion diseases, in Edinburgh, Scotland, May 23 to 26, 2017. 

Potential impacts of the new finding

Since 2003 Canada has a policy that recommends that animals and materials known to be infected with prions be removed from the food chain and from health products. Although no direct evidence of CWD prion transmission to humans has ever been recorded, the policy advocates a precautionary approach to managing CWD and potential human exposure to prions. These initial findings do not change Health Canada’s Health Products and Food Branch (HPFB) position on food and health products. A precautionary approach is still recommended to manage the potential risks of exposure to prions through food and health products. Measures are in place at federal, provincial and territorial levels to reduce human exposure to products potentially contaminated by CWD by preventing known infected animals from entering the marketplace. 

While Federal and P/T government’s animal disease control policies continue to divert known CWD-infected animals away from entering the food and feed supply, research and development of sensitive detection methods including live-animal sampling techniques remain crucial for ensuring an accurate diagnosis. In addition, consistent federal, provincial and territorial communications of appropriate precautionary measures for hunters and indigenous communities are required. 

Next Steps

The CFlA will continue to collaborate with national and international partners to develop and validate new diagnostic techniques. The CFlA will also continue to offer confirmatory testing services and reference laboratory expertise to provincial and territorial partners on demand. 

Currently, CFlA laboratories are leading or collaborating on several research projects to understand the potential for CWD to infect humans. These projects use non‐human primates, genetically modified mice, and cell-free amplification approaches. Given the present findings, CFiA encourages continued research into TSEs. 

The results of this study reinforce the need to redesign the federal program to foster greater adoption of risk mitigation measures for farmed cervids. Federal and provincial government collaboration will continue as new program options are assessed. 

The results of Dr. Czub’s research into CWD will be of interest to scientists, governments, industry and people who consume cervid products. After the presentation at PRION 2017, the research will follow the normal steps of completion, peer review and publication. The Government of Canada will monitor the response to this research and determine whether further review of the science is required. Other studies underway by other researchers may also become public as a result of the presentation of Dr. Czub’s research. 

The Public Health Agency of Canada, Health Canada, CFlA and other Federal partners are working together to assess what policies or programs need further review as well as preparing other communications about the research and health policy and advice to Canadian. 2017/04/28 

===end...UNOFFICIAL...NO URL LINK...TSS===

0:30 First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 

Dr Stefanie Czub University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency Canada 


WEDNESDAY, MAY 03, 2017
*** First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques


CANADA

Herds infected with Chronic Wasting Disease in Canada – 2016 The CFIA works with provincial governments and industry to conduct regular Chronic Wasting Disease (CWD) surveillance. Ongoing provincial surveillance for CWD varies with each particular province's perceived threat and infection status. Testing is mandatory in Manitoba, Saskatchewan, Alberta and the Yukon; it is voluntary elsewhere.

In addition, CWD is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.

Current as of: 2016-06-30

Domestic cervid herds confirmed to be infected with CWD in Canada in 2016 Date confirmed Location Animal type infected February 18 Saskatchewan Deer March 21 Saskatchewan Deer May 18 Saskatchewan Elk

Additional Information Main page - Chronic wasting disease Federally Reportable Diseases in Canada - 2016 Federally Reportable Diseases in Canada - 2015 Federally Reportable Diseases in Canada - 2014 Federally Reportable Diseases in Canada - 2013


Tuesday, February 10, 2015

Alberta Canada First case of chronic wasting disease found in farm elk since 2002


Saturday, February 14, 2015

Canadian Food Inspection Agency Confirms Bovine Spongiform Encephalopathy (BSE) in Alberta


 Monday, April 07, 2014

 Saskatchewan’s first chronic wasting disease case of the year has been confirmed 2014


 Saturday, October 18, 2014

 Chronic wasting disease threatens Canadian agriculture, Alberta MLA says


Wednesday, June 18, 2008

CHRONIC WASTING DISEASE FOUND IN 24 MORE DEER IN ALBERTA


ZOO ANIMALS AND TSE PRION DISEASE

The 82 zoo animals with BSE:

Id TSE Genus Species Subsp Birth Origin Death Place of Death

654 x Microcebus murinus - 1997 U.Montpellier 1998 U.Montpellier

656 x Microcebus murinus - 1997 U.Montpellier 1998 U.Montpellier

481 + Eulemur fulvus mayottensis 1974 Madagascar 1992 Montpellier zoo

474 + Eulemur fulvus mayottensis 1974 Madagascar 1990 Montpellier zoo

584 - Eulemur fulvus mayottensis 1984 Montpellier 1991 Montpellier zoo

455 + Eulemur fulvus mayottensis 1983 Montpellier 1989 Montpellier zoo

 - + Eulemur fulvus mayottensis 1988 Montpellier 1992 Montpellier zoo

 - + Eulemur fulvus mayottensis 1995 Montpellier 1996 Montpellier zoo

 - + Eulemur fulvus albifrons 1988 Paris 1992 Montpellier zoo

 - + Eulemur fulvus albifrons 1988 Paris 1990 Montpellier zoo

 - + Eulemur fulvus albifrons 1988 Paris 1992 Montpellier zoo

456 + Eulemur fulvus albifrons 1988 Paris 1990 Montpellier zoo

586 + Eulemur mongoz - 1979 Madagascar 1998 Montpellier zoo

 - p Eulemur mongoz - 1989 Mulhouse 1991 Montpellier zoo

 - p Eulemur mongoz - 1989 Mulhouse 1990 Montpellier zoo

 - p Eulemur macaco - 1986 Montpellier 1996 Montpellier zoo

 - p Lemur catta - 1976 Montpellier 1994 Montpellier zoo

 - p Varecia variegata variegata 1985 Mulhouse 1990 Montpellier zoo

 - p Varecia variegata variegata 1993 xxx 1994 Montpellier zoo

455 + Macaca mulatta - 1986 Ravensden UK 1992 Montpellier zoo

 - p Macaca mulatta - 1986 Ravensden UK 1993 Montpellier zoo

 - p Macaca mulatta - 1988 Ravensden UK 1991 Montpellier zoo

 - p Saimiri sciureus - 1987 Frejus France 1990 Frejus zoo

700 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo

701 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo

702 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo

703 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo

704 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo

705 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo

706 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

707 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

708 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

709 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

710 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

711 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

712 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

713 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

714 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

715 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

716 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

717 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo

 x p genus species - - Lille zoo 1996 Lille zoo

 y p genus species - - Lille zoo 1996 Lille zoo

 z p genus species - - Lille zoo 1996 Lille zoo 

1 + Actinonyx jubatus cheetah 1986 Marwell zoo 1991 Pearle Coast AU

Duke + Actinonyx jubatus cheetah 1984 Marwell zoo 1992 Colchester zoo? UK

Saki + Actinonyx jubatus cheetah 1986 Marwell zoo 1993 unknown UK

Mich + Actinonyx jubatus cheetah 1986 Whipsnade 1993 Whipsnade UK

Fr1 + Actinonyx jubatus cheetah 1987 Whipsnade 1997 Safari de Peaugres FR

Fr2 + Actinonyx jubatus cheetah 1991 Marwell zoo 1997 Safari de Peaugres Fr

xx + Actinonyx jubatus cheetah 19xx xxx zoo 199x Fota zoo IR

yy + Actinonyx jubatus cheetah 19xx yyy zoo 1996+ yyyy zoo UK

zz + Actinonyx jubatus cheetah 19xx zzz zoo 1996+ yyyy zoo UK

aaa + Felis concolor puma 1986 Chester zoo 1991 Chester zoo UK

yy + Felis concolor puma 1980 yyy zoo 1995 yyyy zoo UK

zz + Felis concolor puma 1978 zzz zoo 1995 zzzz zoo UK

xxx + Felis pardalis ocelot 1987 xxx 1994 Chester zoo UK

zzz + Felis pardalis ocelot 1980 zzz 1995 zzzz zoo UK

85 + Felis catus cat 1990+ various 1999+ various UK LI NO 

19 + Canis familia. dog 1992+ various 1999+ various UK 

Fota + Panthera tigris tiger 1981 xxx zoo 1995 xxxx zoo UK

yy + Panthera tigris tiger 1983 yyy zoo 1998 yyyy zoo UK

Lump + Panthera leo lion 1986 Woburn SP 1998 Edinburgh zoo UK [since 1994]

1 + Taurotragus oryx eland 1987 Port Lympne 1989 Port Lympne zoo UK

Moll + Taurotragus oryx eland 1989 xx UK 1991 not Port Lympne UK

Nedd + Taurotragus oryx eland 1989 xx UK 1991 not Port Lympne UK

Elec + Taurotragus oryx eland 1990 xx UK 1992 not Port Lympne Uk

Daph p Taurotragus oryx eland 1988 xx UK 1990 not Port Lympne UK

zzz + Taurotragus oryx eland 1991 zz UK 1994 zzz UK 

yyy + Taurotragus oryx eland 1993 yy UK 1995 yyy UK 

Fran p Tragelaphus strepsi. kudu 1985 London zoo 1987 London zoo UK

Lind + Tragelaphus strepsi. kudu 1987 London zoo 1989 London zoo UK

Karl + Tragelaphus strepsi. kudu 1988 London zoo 1990 London zoo UK

Kaz + Tragelaphus strepsi. kudu 1988 London zoo 1991 London zoo UK

Bamb pc Tragelaphus strepsi. kudu 1988 London zoo 1991 London zoo UK

Step - Tragelaphus strepsi. kudu 1984 London zoo 1991 London zoo UK

346 pc Tragelaphus strepsi. kudu 1990 London zoo 1992 London zoo UK

324 + Tragelaphus strepsi. kudu 1989 Marwell zoo 1992 London zoo UK

xxx + Tragelaphus angasi nyala 1983 Marwell zoo 1986 Marwell zoo UK

yy + Oryx gazella gemsbok 1983 Marwell zoo 1986 Marwell zoo UK

zz + Oryx gazella gemsbok 1994+ zzz zoo 1996+ zzzz zoo UK

xx + Oryx dammah scim oryx 1990 xxxx zoo 1993 Chester zoo UK

yy + Oryx leucoryx arab oryx 1986 Zurich zoo 1991 London zoo UK

yy + Bos taurus ankole cow 1987 yyy zoo 1995 yyyy zoo UK

zz + Bos taurus ankole cow 1986 zzz zoo 1991 zzzz zoo UK

xx + Bison bison Eu bison 1989 xxx zoo 1996 xxxx zoo UK






2016-2017

***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.


Technical Abstract:

***Cattle could be exposed to the agent of chronic wasting disease (CWD) through contact with infected farmed or free-ranging cervids or exposure to contaminated premises. The purpose of this study was to assess the potential for CWD derived from elk to transmit to cattle after intracranial inoculation. Calves (n=14) were inoculated with brain homogenate derived from elk with CWD to determine the potential for transmission and define the clinicopathologic features of disease.

Cattle were necropsied if clinical signs occurred or at the termination of experiment (49 months post-inoculation (MPI)).

Clinical signs of poor appetite, weight loss, circling, and bruxism occurred in two cattle (14%) at 16 and 17 MPI, respectively.

Accumulation of abnormal prion protein (PrP**Sc) in these cattle was confined to the central nervous system with the most prominent immunoreactivity in midbrain, brainstem, and hippocampus with lesser immunoreactivity in the cervical spinal cord.

*** The rate of transmission was lower than in cattle inoculated with CWD derived from mule deer (38%) or white-tailed deer (86%).

Additional studies are required to fully assess the potential for cattle to develop CWD through a more natural route of exposure, but a low rate of transmission after intracranial inoculation suggests that risk of transmission through other routes is low.

***A critical finding here is that if CWD did transmit to exposed cattle, currently used diagnostic techniques would detect and differentiate it from other prion diseases in cattle based on absence of spongiform change, distinct pattern of PrP**Sc deposition, and unique molecular profile.


Monday, April 04, 2016

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

see;

UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;



2017 PRICE OF PRION POKER GOES UP...PIGS, CWD, HUMANS, AND THE INFAMOUS FDA USDA MAD COW FEED BAN...SEE;

seems if my primitive education does not fail me, intracranial means inside the skull, and peroral means by the mouth. seems the price of tse prion poker just keeps going up...terry

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.
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. 
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. 
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. 
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
 snip...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

Porcine prion protein amyloid 

Per Hammarstr€om and Sofie Nystr€om* IFM-Department of Chemistry; Link€oping University; Link€oping, Sweden 

ABSTRACT. Mammalian prions are composed of misfolded aggregated prion protein (PrP) with amyloid-like features. 

Prions are zoonotic disease agents that infect a wide variety of mammalian species including humans. Mammals and by-products thereof which are frequently encountered in daily life are most important for human health. It is established that bovine prions (BSE) can infect humans while there is no such evidence for any other prion susceptible species in the human food chain (sheep, goat, elk, deer) and largely prion resistant species (pig) or susceptible and resistant pets (cat and dogs, respectively). PrPs from these species have been characterized using biochemistry, biophysics and neurobiology. Recently we studied PrPs from several mammals in vitro and found evidence for generic amyloidogenicity as well as cross-seeding fibril formation activity of all PrPs on the human PrP sequence regardless if the original species was resistant or susceptible to prion disease. Porcine PrP amyloidogenicity was among the studied. Experimentally inoculated pigs as well as transgenic mouse lines overexpressing porcine PrP have, in the past, been used to investigate the possibility of prion transmission in pigs. The pig is a species with extraordinarily wide use within human daily life with over a billion pigs harvested for human consumption each year. Here we discuss the possibility that the largely prion disease resistant pig can be a clinically silent carrier of replicating prions. 

KEYWORDS. prion, pig, amyloid fibril, misfolding, transmissibility, seeding, TSE, prion strain, strain adaptation

snip...

What about pigs? 

 In several recent papers which in our view have not received sufficient attention the notion of prion resistant pigs was challenged by generation of transgenic mice with knocked out endogenous PrP and overexpressed PoPrP. Different lines of tgPoPrP mouse were proven to be susceptible to clinical disease triggered by a variety of prion strains, suggesting that the surrogate host species (mouse) and prion strain are more important than what PrP sequence it expresses for neurotoxicity to commence. In more detail, Torres and colleagues experimentally subjected transgenic mouse lines expressing porcine PrP to a number of different TSE isolates.24-26 Their studies demonstrate that prion infection is strain specific when porcine PrP is overexpressed (4x) and used as in vivo substrate. PoTg001 mice inoculated with classical scrapie, regardless of donor genotype, resisted prion disease both at first and second passage (Fig. 3b). On the other hand, Nor98 scrapie (Atypical scrapie) as well as BSE from both cattle and BoTg mouse model resulted in clinical disease in the PoTg001 mice. However, in the first generation, disease progression was slow. Incubation time until death was as long as 600 d and the hit rate was low. This indicates that disease has barely developed by the time the mice reach their natural life span limit which in this study was set to 650 d Already in the second passage the hit rate was 100 % and the incubation time was cut in half (Fig. 3b). No further shortening of incubation time was observed upon third passage. This shows that PoPrP is capable of forming infectious and neurotoxic prions in vivo if triggered by a compatible prion strain and if given enough time to develop. Both BSE and Nor98 rapidly adapts to the PoPrP host sequence, resulting in higher penetrance as well as in markedly shorter life span already in the second passage, well within the limits of normal life span for a mouse.

There are several crucial variables which impact the susceptibility of prion diseases and transmission studies.27 PrP sequence of host, PrP sequence of prion, prion strain, prion dosage, PrP expression level of host, host genetic background, route of transmission and neuroinvasiveness if peripherally infected.28 Importantly the PrP expression level corresponds to the rate of prion disease onset.1 This likely reflects 2 converging variables: a) PrP as a substrate to the prion misfolding reaction i.e. selfcatalyzed conversion and b) PrP as a mediator of neurotoxicity through interactions with misfolded PrP within prions.

The non-homologous recPrPs presented here and in,12 easily adapt to each other and form amyloid fibrils in accordance with what is seen in vivo when inoculum composed of BoPrP used to challenge mice expressing PoPrP (Fig. 3b).24-26 A review of the literature showed that BSE strains have a high degree of penetrance in both experimental and accidental transmission. Over 50% of the species reported to be susceptible to prion disease were infected by a BSE strain.19 Recent data form our lab shows that the promiscuity of BoPrP fibrils holds true also in the case of recombinant in vitro experiments. When cross-seeding human, bovine, porcine, feline and canine PrPs with any of the other, the recBoPrP seed outcompetes the other seeds in all instances except when the HuPrP acted as substrate (Data not shown). In this case recPoPrP fibrils have the highest seeding efficiency (Fig. 1). These findings in combination with the Torres experiments,24-26 implicate that a PoPrP substrate in vivo (in pigs) could adapt to an amyloidogenic prion strain of bovine or ovine prion disease and hence replicate in the new host.

For adaptation of experimental strains through multiple passages, donors are selected based on neurotoxicity (that is on TSE disease phenotype) not on basis of amyloid fibril formation. Hence the traits of transmissible amyloidotypic prion strains may be largely unexplored if these strains require more time to transform to neurotoxic strains e.g. as proposed by Baskakov’s model of deformed templating.8 There is experimental evidence for BSE transmission into pig via parenteral routes.16 with an incubation period of 2–3 years, well within what is to be considered normal lifespan. For a breeding sow in industrial scale pig farming that is 3–5 y (Bojne Andersson, personal communication).29,30 In small scale and hobby farming both sows and boars may be kept significantly longer. Collinge and Clarke.31 describe how prion titers reach transmissibility levels well before the prion burden is high enough to be neurotoxic and cause clinical disease. It is known that prion strains need time and serial passages to adapt. Knowing that pigs in modern farming are rarely kept for enough time for clinical signs to emerge in prion infected pigs it is important to be vigilant if there is a sporadic porcine spongiform encephalopathy (PSE) as has been seen in cattle (BASE) and sheep (Nor98). Hypothetically such a sporadic and then infectious event could further adapt and over a few generations have reached the point where clinical PSE is established within the time frame where pigs are being slaughtered for human consumption (Fig. 4).

FIGURE 4. Potential prion strain adaptation in pig. The red horizontal gradient indicates the hietherto unkown prion toxicity tolerance threshold for pigs, the blue vertical line indicates normal slaughter age for industrial pig farming, the green vertical line indicates the normal lifespan of a breeding sow in industrial scale pig farming, orange areas indicate window of neurotoxic prions before onset of clinical disease (dark orange indicates subclinical BSE as reported by Wells et al,16 pale orange indicate hypothetic outcome of PSE and strain adaptation. On the outmost right a potential subclinical sporadic PSE.

USE OF MATERIALS DERIVED FROM PIG IN VIEW OF PORCINE PrP AMYLOID

The pig is the most versatile species used by humans for food and other applications. Over 1,5 billion pigs are slaughtered each year worldwide for human use.32 Besides juicy pork sirloin other parts from pig are used for making remarkably diverse things such as musical instruments, china, leather, explosives, lubricants etc. Pig offal is used for human medicine, e.g., hormone preparations such as insulin and cerebrolysin, in xenographs, sutures, heparin and in gelatin for drug capsules.33,34

And that means not only pork, it means your pigskin wallet, catgut surgical suture...in tallow, in butter. It is undoubtedly in the blood supply. DC Gajdusek (From R. Rhodes ''Deadly Feast'' 35)

While the late Carleton Gajdusek had strong views in diverse areas of prion biology, according to journalist Richard Rhodes,35 he was correct on his prediction on BSE prions (vCJD) in the blood supply18 (see text box above). An opinionated scientist can sometimes be ignored due to a judgment of character and Gajdusek was certainly provocative. Notwithstanding society should remain vigilant on the possibility that Gajdusek was also prophetic on porcine prions given the exceptionally wide spread use of pigs in everyday human life and medicine. As discussed previously it is currently not established what relations transmissible neurotoxic prion strains and amyloid morphotypic mature APrP strains have. Given the hypotheses that amyloidotypic PrP conformations can transmit with low neurotoxicity.7,36 it is interesting to reflect on possible implications. Pigs are slaughtered at 6–8 months of age. Because amyloid deposition is associated with old age, this is likely far too young for spontaneous development of APrP amyloid from PoPrP as well as other amyloidogenic proteins. From the perspective of seeded amyloidogenesis it is however a potential ideal case for highly transmissible titers of APrP (Fig. 4). In such a scenario the potential of porcine prions constitutes the perfect storm, clinically silent due to neurotoxic resistance and with high titers of transmissibility. When it comes to prions CNS material is most heavily infected. In addition, however, fat tissue (to make lard and tallow) is known to harbor extraordinary amounts of amyloid in systemic amyloidoses.37 Amyloid fibrils of misfolded large proteins (AA, AL, ATTR) are notoriously hydrophobic due to the abnormal exposure of hydrophobic residues which normally in the folded structure being hidden in the protein core. The amyloid accumulation in fat tissue is likely a phase-separation from a rather hydrophilic environment in circulation toward the hydrophobic environment provided by adipocytes. Adipose tissue could in addition represent an in vivo environment well suitable for fibril formation. What about APrP?

In analysis of mice expressing Glycophosphatidylinositol, (GPI)-anchorless PrP, abdominal fat contains appreciable amounts of infectious prions in APrP isoform stained with ThS.38 Notably mice overexpressing anchorless PrP provides a silent carrier status for a long time prior to presenting symptoms and is severely afflicted by amyloid fibril formation following scrapie (RML) infection.39 Recall that this study showed that GPI-anchored PrP is needed to present clinical neurotoxicity. Evidently circulating anchorless-PrP (analogous to recPrP) is more amyloidogenic compared to GPI-anchored PrP and is poorly neuroinvasive.28 Amyloidosis is systemic in anchorless-PrP mice and is not limited to fat but is also found as extensive cardiac amyloid deposits.39 Interestingly cardiac APrP was recently reported in one BSE inoculated rhesus macaque which showed symptoms of cardiac distress prior to death from prion neurotoxicity.40 It is noteworthy that transgenic mice expressing PoPrP appear sensitive to strains with biochemical features of amyloidogenic prion strains i.e., BSE and Nor98.25,26,36 (Fig. 3b). We recently adopted the parallel inregister intermolecular b-sheet structural model of the APrP fibril from the Caughey lab to rationalize cross-seeding between various PrP sequences.12,41 It is tempting to use this structural model to speculate on the adaptation of mono-N-glycolsylated PoPrP at the expense of double-N-glycolylated PrP in the original BSE inoculum reported in the Torres experiments.25,26 In this APrP model monoglycosylated PrP at N197 is structurally compatible while N181 is not, due to burial in the in-register intermolecular cross-beta sheet (Fig. 5).

It appears that amyloidotypic prion strains, APrP, are transmissible but associated with lower neurotoxicity compared to diffuse aggregated PrP associated with synaptic PrP accumulations. It is possible that the amino acid substitutions in PoPrP compared to HuPrP and BoPrP are important for neurotoxic signal transmission (Fig. 2b, 5). The main issue hereby is that transmissibility of APrP will remain undetected unless used for surveillance. AA amyloidosis is frequent in many animals (e.g. cattle and birds) but is exceptionally rare in pigs.42 suggesting that APrP should it reside in pig fat would be traceable using newly developed screening methods.37

CONCLUDING REMARKS 

Should the topic of porcine PrP amyloid be more of a worry than of mere academic interest? Well perhaps. Prions are particularly insidious pathogens. A recent outbreak of peripheral neuropathy in human, suggests that exposure to aerosolized porcine brain is deleterious for human health.43,44 Aerosolization is a known vector for prions at least under experimental conditions.45-47 where a mere single exposure was enough for transmission in transgenic mice. HuPrP is seedable with BoPrP seeds and even more so with PoPrP seed (Fig. 1), indicating that humans could be infected by porcine APrP prions while neurotoxicity associated with spongiform encephalopathy if such a disease existed is even less clear. Importantly transgenic mice over-expressing PoPrP are susceptible to BSE and BSE passaged through domestic pigs implicating that efficient downstream neurotoxicity pathways in the mouse, a susceptible host for prion disease neurotoxicity is augmenting the TSE phenotype.25,26 Prions in silent carrier hosts can be infectious to a third species. Data from Collinge and coworkers.21 propose that species considered to be prion free may be carriers of replicating prions. Especially this may be of concern for promiscuous prion strains such as BSE.19,48 It is rather established that prions can exist in both replicating and neurotoxic conformations.49,50 and this can alter the way in which new host organisms can react upon cross-species transmission.51 The na€ıve host can either be totally resistant to prion infection as well as remain non-infectious, become a silent non-symptomatic but infectious carrier of disease or be afflicted by disease with short or long incubation time. The host can harbor and/or propagate the donor strain or convert the strain conformation to adapt it to the na€ıve host species. The latter would facilitate infection and shorten the incubation time in a consecutive event of intra-species transmission. It may be advisable to avoid procedures and exposure without proper biosafety precautions as the knowledge of silence carrier species is poor. One case of iatrogenic CJD in recipient of porcine dura mater graft has been reported in the literature.52 The significance of this finding is still unknown. The low public awareness in this matter is exemplified by the practice of using proteolytic peptide mixtures prepared from porcine brains (Cerebrolysin) as a nootropic drug. While Cerebrolysin may be beneficial for treatment of severe diseases such as vascular dementia,53 a long term follow-up of such a product for recreational use is recommended.

DISCLOSURE OF POTENTIAL CONFLICTS OF INTEREST

No potential conflicts of interest were disclosed

FUNDING

This work was supported by G€oran Gustafsson foundation, the Swedish research council Grant #2011-5804 (PH) and the Swedish Alzheimer association (SN).

REFERENCES



THURSDAY, MARCH 30, 2017 

Norway CWD Skrantesjuke: VKM report supports the National Veterinary Institute perception management 


Terry S. Singeltary Sr. Declares a DECLARATION OF EXTRAORDINARY EMERGENCY DUE TO A FOREIGN ANIMAL DISEASE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION CHRONIC WASTING DISEASE CWD IN THE UNITED STATES AND NORTH AMERICA.

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

Hay/Straw

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


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

Feed Grains Data: Yearbook Tables Created March 10, 2016 Updates of this data, and data covering more years and countries, can be found at 


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


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

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

snip...see full text ;


TUESDAY, APRIL 18, 2017 

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


TUESDAY, JANUARY 17, 2017 

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



2016

Monday, May 02, 2016 
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo *** 

2017

10:30 First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 

Dr Stefanie Czub University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency Canada 


WEDNESDAY, MAY 03, 2017 

*** First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques


News Release Media Contact: TPWD News, news@tpwd.texas.gov, 512-389-8030 May 26, 2017 

New Chronic Wasting Disease Management Response Rules Adopted

AUSTIN – The Texas Parks and Wildlife Commission has approved amendments to chronic wasting disease (CWD) management response rules based in part on discovery of the disease in a free-ranging white-tailed deer west of San Antonio. The changes address containment and surveillance measures, and permitted movement of live deer, in portions of Bandera, Medina, and Uvalde counties as well as zone delineations in the northwest Panhandle.

Last year, the Commission established a CWD Surveillance Zone (SZ) in portions of Bandera, Medina, and Uvalde counties as a result of CWD being confirmed in permitted deer breeding facilities in the area. A containment Zone (CZ) was not established in this area because the disease had been detected only in permitted deer breeding facilities or their adjacent release sites, all of which had been issued hold orders or quarantines by Texas Animal Health Commission; these measures included requirements that satisfied the need for a CZ. This particular SZ was exempted from mandatory sampling and carcass movement restrictions in lieu of a local voluntary hunter and landowner effort to submit samples.

However, CWD was subsequently detected in a free-ranging white-tailed deer within that SZ, which introduced an epidemiological imperative to designate that area as a CZ by emergency rule and require CWD testing and restrictions on movement of live deer and hunter-harvested deer. The new rules replace the emergency rules and establish as a CZ all land located within two miles of the property boundaries where CWD has been detected in permitted deer breeding facilities, and within five miles of the approximate location where the CWD-positive free-ranging whitetail was harvested. A SZ is proposed for all land that does not fall within the proposed CZ, but is surrounded on the north by F.M. 470, on the east by F.M. 462, on the south by U.S. Highway 90 and the west from the intersection of U.S. 90 and the Sabinal river, following the river north to the intersection of F.M. 187 and north along F.M. 187 to F.M. 470.

Amendments to the SZ delineations in the northwest Panhandle extending the zone east of the cities of Amarillo and Dumas have also been adopted by the Commission to make sample submission and carcass disposal more convenient for hunters.

The new rules also provide greater latitude for permitted movement of live deer as it relates to CWD containment and surveillance zones. Under these new provisions, permitted movement of captive deer into a CZ or SZ may occur, as well as movement within the zones by permit holders having Transfer Category 1 or 2 status provided certain guidelines are met. Harvest on release sites must be equal to or exceed the number of breeder deer introduced that year and deer may be released from TC 2 facilities to an adjacent release site once “Not Detected” tonsil biopsy test results are obtained.

2017-05-26


Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A
Technical Abstract: 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 two 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, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.
*** 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.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.
see full text ;
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.

This next bit of science is very important, please study this...terry

TUESDAY, MARCH 28, 2017 

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


snip...see much more here;

WEDNESDAY, MAY 17, 2017

CWD, TSE, PRION, Cattle, Pigs, Sheep, and Humans aka Mad Cow Disease


CWD TSE PRION ROUNDUP

CWD of deer and elk is spreading across North America and cannot be stopped.

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.

cwd to humans, consumption, exposure, sub-clinical, iatrogenic, what if ?

i strenuously urge you all to rethink this cutting of funds for research of the TSE Prion disease. 

*** 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 


Title: Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission 


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. 

***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. 



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 *** 


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

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 


with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion...tss
 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
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.
>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.
>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.
snip...
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 ***
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
***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 CWO
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 


Pathways of Prion Spread during Early Chronic Wasting Disease in Deer 

Clare E. Hoover1, Kristen A. Davenport1, Davin M. Henderson1,Nathaniel D. Denkers1, Candace K. Mathiason1, Claudio Soto2, Mark D. Zabel1and Edward A. Hoover1# +Author Affiliations

1Prion Research Center, Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, Colorado, USA 2Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas, Houston, Texas, USA ABSTRACT

Among prion infections, two scenarios of prion spread are generally observed: (a) early lymphoid tissue replication or (b) direct neuroinvasion without substantial antecedent lymphoid amplification. In nature, cervids are infected with chronic wasting disease (CWD) prions by oral and nasal mucosal exposure, and studies of early CWD pathogenesis have implicated pharyngeal lymphoid tissue as the earliest sites of prion accumulation. However, knowledge of chronological events in prion spread during early infection remains incomplete. To investigate this knowledge gap in early CWD pathogenesis, we exposed white-tailed deer to CWD prions by mucosal routes and performed serial necropsies to assess PrPCWD tissue distribution by real-time quaking-induced conversion (RT-QuIC) and tyramide signal amplification immunohistochemistry (TSA-IHC). Although PrPCWD was not detected by either method in the initial days (1 and 3) post-exposure, we observed PrPCWD seeding activity and follicular immunoreactivity in oropharyngeal lymphoid tissues at 1 and 2 months post-exposure (MPE). At 3 MPE, PrPCWD replication had expanded to all systemic lymphoid tissues. By 4 MPE, the PrPCWD burden in all lymphoid tissues had increased, and approached levels observed in terminal disease, yet there was no evidence of nervous system invasion. These results indicate the first site of CWD prion entry is in the oropharynx and the initial phase of prion amplification occurs in the oropharyngeal lymphoid tissues followed by rapid dissemination to systemic lymphoid tissues. This lymphoid replication phase appears to precede neuroinvasion.

IMPORTANCE Chronic wasting disease (CWD) is a universally fatal transmissible spongiform encephalopathy affecting cervids and natural infection occurs through oral and nasal mucosal exposure to infectious prions. Terminal disease is characterized by PrPCWD accumulation in the brain and lymphoid tissues of affected animals. However, the initial sites of prion accumulation and pathways of prion spread during early CWD infection remain unknown. To investigate the chronological events of early prion pathogenesis, we exposed deer to CWD prions and monitored the tissue distribution of PrPCWD over the first 4 months of infection. We show CWD uptake occurs in the oropharynx with initial prion replication in the draining oropharyngeal lymphoid tissues, rapidly followed by dissemination to systemic lymphoid tissues without evidence of neuroinvasion. This data highlights the two phases of CWD infection: a robust prion amplification in systemic lymphoid tissues prior to neuroinvasion or establishment of a carrier state.

FOOTNOTES

↵#Address correspondence to Edward A. Hoover, edward.hoover@colostate.edu Copyright © 2017 American Society for Microbiology. All Rights Reserved. 


10:30 First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 

Dr Stefanie Czub University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency Canada 


WEDNESDAY, MAY 03, 2017 

*** First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques


*** 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. 
Key Molecular Mechanisms of TSEs 
Zabel, Mark D. 
Colorado State University-Fort Collins, Fort Collins, CO, United States 
Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs), are fatal neurodegenerative diseases affecting humans, cervids, bovids, and ovids. The absolute requirement of PrPC expression to generate prion diseases and the lack of instructional nucleic acid define prions as unique infectious agents. Prions exhibit species-specific tropism, inferring that unique prion strains exist that preferentially infct certain host species and confront transmission barriers to heterologous host species. However, transmission barriers are not absolute. Scientific consensus agrees that the sheep TSE scrapie probably breached the transmission barrier to cattle causing bovine spongiform encephalopathy that subsequently breached the human transmission barrier and likely caused several hundred deaths by a new-variant form of the human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease of cervids, overcoming similar human transmission barriers. A groundbreaking discovery made last year revealed that mice infected with heterologous prion strains facing significant transmission barriers replicated prions far more readily in spleens than brains6. Furthermore, these splenic prions exhibited weakened transmission barriers and expanded host ranges compared to neurogenic prions. These data question conventional wisdom of avoiding neural tissue to avoid prion xenotransmission, when more promiscuous prions may lurk in extraneural tissues. Data derived from work previously funded by NIH demonstrate that Complement receptors CD21/35 bind prions and high density PrPC and differentially impact prion disease depending on the prion isolate or strain used. Recent advances in live animal and whole organ imaging have led us to generate preliminary data to support novel, innovative approaches to assessing prion capture and transport. We plan to test our unifying hypothesis for this proposal that CD21/35 control the processes of peripheral prion capture, transport, strain selection and xenotransmission in the following specific aims. 
1. Assess the role of CD21/35 in splenic prion strain selection and host range expansion. 
2. Determine whether CD21/35 and C1q differentially bind distinct prion strains 
3. Monitor the effects of CD21/35 on prion trafficking in real time and space 
4. Assess the role of CD21/35 in incunabular prion trafficking 
Public Health Relevance Transmissible spongiform encephalopathies, or prion diseases, are devastating illnesses that greatly impact public health, agriculture and wildlife in North America and around the world. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease (CWD) of cervids, overcoming similar human transmission barriers. Early this year Canada reported its first case of BSE in over a decade audits first case of CWD in farmed elk in three years, underscoring the need for continued vigilance and research. Identifying mechanisms of transmission and zoonoses remains an extremely important and intense area of research that will benefit human and other animal populations. 
PMCA Detection of CWD Infection in Cervid and Non-Cervid Species 
Hoover, Edward Arthur 
Colorado State University-Fort Collins, Fort Collins, CO, United States 
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).*** 


Molecular Barriers to Zoonotic Transmission of Prions

 *** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.

 *** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.



SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY
***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.***

Envt.07: 

Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease 

***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans. 

Yet, it has to be noted that our assessments of PrPTSE levels in skeletal muscles were based on findings in presumably pre- or subclinically infected animals. Therefore, the concentration of PrPTSE in skeletal muscles of WTD with clinically manifest CWD may possibly exceed our estimate which refers to clinically inconspicuous animals that are more likely to enter the human food chain. Our tissue blot findings in skeletal muscles from CWD-infected WTD would be consistent with an anterograde spread of CWD prions via motor nerve fibres to muscle tissue (figure 4A). Similar neural spreading pathways of muscle infection were previously found in hamsters orally challenged with scrapie [28] and suggested by the detection of PrPTSE in muscle fibres and muscle-associated nerve fascicles of clinically-ill non-human primates challenged with BSE prions [29]. Whether the absence of detectable PrPTSE in myofibers observed in our study is a specific feature of CWD in WTD, or was due to a pre- or subclinical stage of infection in the examined animals, remains to be established. In any case, our observations support previous findings suggesting the precautionary prevention of muscle tissue from CWD-infected WTD in the human diet, and highlight the need to comprehensively elucidate of whether CWD may be transmissible to humans. While the understanding of TSEs in cervids has made substantial progress during the past few years, the assessment and management of risks possibly emanating from prions in skeletal muscles of CWD-infected cervids requires further research. 



Prions in Skeletal Muscles of Deer with Chronic Wasting Disease 

Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ + Author Affiliations

1 Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, KY 40536, USA. 2 Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA. 3 Department of Neurology, University of Kentucky, Lexington, KY 40536, USA. 4 Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5 Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA. ↵§ To whom correspondence should be addressed. E-mail: gtell2@uky.edu ↵* These authors contributed equally to this work. 

↵† Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, FL 33458, USA. 

↵‡ Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. 

Abstract The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. 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. 


Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic Wasting Disease 

Contact: Exotic Meats USA 1-800-680-4375

FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). The meat with production dates of December 29, 30 and 31, 2008 was purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk Farm LLC in Pine Island, MN and was among animals slaughtered and processed at USDA facility Noah’s Ark Processors LLC.

Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease found in elk and deer. The disease is caused by an abnormally shaped protein called a prion, which can damage the brain and nerves of animals in the deer family. Currently, it is believed that the prion responsible for causing CWD in deer and elk is not capable of infecting humans who eat deer or elk contaminated with the prion, but the observation of animal-to-human transmission of other prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has raised a theoretical concern regarding the transmission of CWD from deer or elk to humans. At the present time, FDA believes the risk of becoming ill from eating CWD-positive elk or deer meat is remote. However, FDA strongly advises consumers to return the product to the place of purchase, rather than disposing of it themselves, due to environmental concerns.

Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was packaged in individual vacuum packs weighing approximately 3 pounds each. A total of six packs of the Elk Tenderloins were sold to the public at the Exotic Meats USA retail store. Consumers who still have the Elk Tenderloins should return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX 78209. Customers with concerns or questions about the Voluntary Elk Recall can call 1-800-680-4375. The safety of our customer has always been and always will be our number one priority.

Exotic Meats USA requests that for those customers who have products with the production dates in question, do not consume or sell them and return them to the point of purchase. Customers should return the product to the vendor. The vendor should return it to the distributor and the distributor should work with the state to decide upon how best to dispose. If the consumer is disposing of the product he/she should consult with the local state EPA office.

#


COLORADO: Farmer's market meat recalled after testing positive for CWD

24.dec.08 9News.com Jeffrey Wolf

Elk meat that was sold at a farmer's market is being recalled because tests show it was infected with chronic wasting disease. The Boulder County Health Department and Colorado Department of Public Health and Environment issued the recall Wednesday after the meat was sold at the Boulder County Fairgrounds on Dec. 13. Although there isn't any human health risk connected with CWD, the recalled was issued as a precaution. About 15 elk were bought from a commercial ranch in Colorado in early December and processed at a licensed plant. All 15 were tested for CWD and one came up positive. The labeling on the product would have the following information: *Seller: High Wire Ranch *The type of cut: "chuck roast," "arm roast," "flat iron," "ribeye steak," "New York steak," "tenderloin," "sirloin tip roast," "medallions" or "ground meat." *Processor: Cedaredge Processing *The USDA triangle containing the number "34645" People with questions about this meat can contact John Pape, epidemiologist at the Colorado Department of Public Health and Environment at 303-692-2628. 


COULD NOT FIND any warning or recalls on these two sites confirming their recall of CWD infected meat. ...TSS 



Wednesday, April 06, 2011 

Presence and Seeding Activity of Pathological Prion Protein (PrPTSE) in Skeletal Muscles of White-Tailed Deer Infected with Chronic Wasting Disease 


Prion Infectivity in Fat of Deer with Chronic Wasting Disease

Brent Race,# Kimberly Meade-White,# Richard Race, and Bruce Chesebro* Rocky Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840

Received 2 June 2009/ Accepted 24 June 2009

ABSTRACT Top ABSTRACT TEXT REFERENCES

Chronic wasting disease (CWD) is a neurodegenerative prion disease of cervids. Some animal prion diseases, such as bovine spongiform encephalopathy, can infect humans; however, human susceptibility to CWD is unknown. In ruminants, prion infectivity is found in central nervous system and lymphoid tissues, with smaller amounts in intestine and muscle. 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.

snip...

The highest risk of human contact with CWD might be through exposure to high-titer CNS tissue through accidental skin cuts or corneal contact at the time of harvest and butchering. However, the likelihood of a human consuming fat infected with a low titer of the CWD agent is much higher. It is impossible to remove all the fat present within muscle tissue, and fat consumption is inevitable when eating meat. Of additional concern is the fact that meat from an individual deer harvested by a hunter is typically consumed over multiple meals by the same group of people. These individuals would thus have multiple exposures to the CWD agent over time, which might increase the chance for transfer of infection.

In the Rocky Mountain region of North America, wild deer are subject to predation by wolves, coyotes, bears, and mountain lions. Although canines such as wolves and coyotes are not known to be susceptible to prion diseases, felines definitely are susceptible to BSE (9) and might also be infected by the CWD agent. Deer infected with the CWD agent are more likely to be killed by predators such as mountain lions (11). Peripheral tissues, including lymph nodes, muscle, and fat, which harbor prion infectivity are more accessible for consumption than CNS tissue, which has the highest level of infectivity late in disease. Therefore, infectivity in these peripheral tissues may be important in potential cross-species CWD transmissions in the wild.

The present finding of CWD infectivity in deer fat tissue raises the possibility that prion infectivity might also be found in fat tissue of other infected ruminants, such as sheep and cattle, whose fat and muscle tissues are more widely distributed in both the human and domestic-animal food chains. Although the infectivity in fat tissues is low compared to that in the CNS, there may be significant differences among species and between prion strains. Two fat samples from BSE agent-infected cattle were reported to be negative by bioassay in nontransgenic RIII mice (3, 6). However, RIII mice are 10,000-fold-less sensitive to BSE agent infection than transgenic mice expressing bovine PrP (4). It would be prudent to carry out additional infectivity assays on fat from BSE agent-infected cattle and scrapie agent-infected sheep using appropriate transgenic mice or homologous species to determine the risk from these sources.


Chronic Wasting Disease Susceptibility of Four North American Rodents 

Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: cjohnson@svm.vetmed.wisc.edu 

We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required. 


please see ; 


Oral.29: Susceptibility of Domestic Cats to CWD Infection 

Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason† Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu 

Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature. 


Prion 


see more recent science abstracts from the Prion 2011 on CWD here;


PAGE 25 

Transmission Studies 

Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculam (?saline). 

Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in all of these species with the shortest incubation period in the ferret. 


Generation of a New Form of Human PrPScin Vitro by Interspecies Transmission from Cervid Prions* 

Marcelo A. Barria‡, Glenn C. Telling§, Pierluigi Gambetti¶, James A. Mastrianni‖ and Claudio Soto‡,1 

+ Author Affiliations 

From the ‡Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Medical School at Houston, Houston, Texas 77030, 

the §Departments of Microbiology, Immunology, and Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky Medical Center, Lexington, Kentucky 40506, 

the ¶Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, and 

the ‖Department of Neurology, The University of Chicago, Chicago, Illinois 60637 

1 To whom correspondence should be addressed: University of Texas Medical School at Houston, 6431 Fannin St., Houston, TX 77030. Tel.: 713-500-7086; Fax: 713-500-0667; E-mail: claudio.soto@uth.tmc.edu. 

Abstract 

Prion diseases are infectious neurodegenerative disorders that affect humans and animals and that result from the conversion of normal prion protein (PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. Determining the risk of transmission of CWD to humans is of utmost importance, considering that people can be infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the misfolded form by CWD PrPSc, we performed experiments using the protein misfolding cyclic amplification technique, which mimics in vitro the process of prion replication. Our results show that cervid PrPSc can induce the conversion of human PrPC but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct biochemical pattern that differs from that of any of the currently known forms of human PrPSc. Our results also have profound implications for understanding the mechanisms of the prion species barrier and indicate that the transmission barrier is a dynamic process that depends on the strain and moreover the degree of adaptation of the strain. If our findings are corroborated by infectivity assays, they will imply that CWD prions have the potential to infect humans and that this ability progressively increases with CWD spreading. 

snip... 

Interestingly, when the Western blot profile of this newly generated form of human PrPSc (termed CWD-huPrPSc) was compared with known strains of human prions, it was clear that CWD-huPrPSc exhibited a different pattern (Fig. 4A). The electrophoretic migration of this protein after PK-digestion is similar to the type 1 strain of sCJD, but its glycosylation profile is clearly different, showing a highly predominant diglycosylated form (Fig. 4A and B). This result suggests that CWD hu-PrPSc corresponds to a new human prion strain. Interestingly, a detailed previous study from Gambetti’s group comparing the biochemical characteristics of PrPSc from cervids and humans showed that CWD PrPSc is similar to sCJDMM1 in terms of electrophoretic mobility (6). However, the misfolded protein associated with CWD is predominantly di-glycosylated, whereas PrPSc from type 1 sCJD is mostly monoglycosylated (6). Based on the fact that transmission of BSE prions to humans resulted in a new form of PrPSc very similar to the one in cattle (6;27), these authors predicted that if humans were infected by CWD it is likely that PrPSc would be of type 1 and with a predominance of the diglycosylated isoform (6). Our results agree with that prediction and suggest that the newly generated CWD-huPrPSc acquires the biochemical properties of the cervid infectious material (Fig. 4A and B). 

snip... 

Our results have far-reaching implications for human health, since they indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc, suggesting that CWD might be infectious to humans. Interestingly our findings suggest that unstable strains from CWD affected animals might not be a problem for humans, but upon strain stabilization by successive passages in the wild, this disease might become progressively more transmissible to man. 

Reference List 

snip... 

please see full text and many thanks to the Professor Soto and the other Authors of this study AND to The Journal Of Biological Chemistry for the free full text !!! 

Amyloid Neurodegeneration Neurological Diseases Prions Protein Conformation Prion Diseases 



see full text and more here ; 


0C7.04

North American Cervids Harbor Two Distinct CWD Strains

Authors

Angers, R. Seward, T, Napier, D., Browning, S., Miller, M., Balachandran A., McKenzie, D., Hoover, E., Telling, G. 'University of Kentucky; Colorado Division of Wildlife, Canadian Food Inspection Agency; University Of Wisconsin; Colorado State University.

Content

Despite the increasing geographic distribution and host range of CWD, little is known about the prion strain(s) responsible for distinct outbreaks of the disease. To address this we inoculated CWD-susceptible Tg(CerPrP)1536+/· mice with 29 individual prion samples from various geographic locations in North America. Upon serial passage, intrastudy incubation periods consistently diverged and clustered into two main groups with means around 210 and 290 days, with corresponding differences in neuropathology. Prion strain designations were utilized to distinguish between the two groups: Type I CWD mice succumbed to disease in the 200 day range and displayed a symmetrical pattern of vacuolation and PrPSc deposition, whereas Type II CWD mice succumbed to disease near 300 days and displayed a strikingly different pattern characterized by large local accumulations of florid plaques distributed asymmetrically. Type II CWD bears a striking resemblance to unstable parental scrapie strains such as 87A which give rise to stable, short incubation period strains such as ME7 under certain passage conditions. In agreement, the only groups of CWD-inoculated mice with unwavering incubation periods were those with Type I CWD. Additionally, following endpoint titration of a CWD sample, Type I CWD could be recovered only at the lowest dilution tested (10-1), whereas Type II CWD was detected in mice inoculated with all dilutions resulting in disease. Although strain properties are believed to be encoded in the tertiary structure of the infectious prion protein, we found no biochemical differences between Type I and Type II CWD. Our data confirm the co·existence of two distinct prion strains in CWD-infected cervids and suggest that Type II CWD is the parent strain of Type I CWD.

see page 29, and see other CWD studies ;


Sunday, November 23, 2008

PRION October 8th - 10th 2008 Book of Abstracts


ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD

Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5

The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.


>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO CONVERSION OF THE HUMAN PRION PROTEIN<<<

*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***

Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014

Wednesday, January 01, 2014

Molecular Barriers to Zoonotic Transmission of Prions

*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.

*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.



*** 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 ;


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. ...


snip...see full text ;


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




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


The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province! ...page 26. 


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



MONDAY, MAY 15, 2017 

TEXAS New CWD TSE PRION 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 


SUNDAY, MAY 21, 2017 

Arkansas Chronic Wasting Disease CWD TSE Prion Roundup 212 Cases Confirmed To Date 


THURSDAY, MAY 18, 2017

Minnesota Four more farmed white-tailed deer test positive for Chronic Wasting Disease CWD TSE Prion


MONDAY, MARCH 27, 2017 

Wyoming CWD Postive Mule Deer Doe Near Pinedale 


MONDAY, MARCH 20, 2017 

Wisconsin CWD TSE Prion Annual Roundup 441 positive 


TUESDAY, MARCH 14, 2017 

Iowa 12 deer test positive for chronic wasting disease from 2016-17 hunting seasons 


MONDAY, MARCH 13, 2017 

CHRONIC WASTING DISEASE CWD TSE PRION UDATE March 13, 2017 


FRIDAY, MARCH 10, 2017 

Nebraska Tests confirm spread of CWD to Lancaster County 


SATURDAY, MAY 20, 2017

Missouri CWD TSE PRION Surveillance and Monitoring


THURSDAY, MARCH 09, 2017 

Missouri MDC REPORTS TWO CASES OF CWD IN ST. CLAIR COUNTY 


SATURDAY, MARCH 04, 2017 

Maryland DNR Six Deer Test Positive for Chronic Wasting Disease 


WEDNESDAY, MARCH 01, 2017 

South central Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease 


MONDAY, MAY 15, 2017 

Pennsylvania 25 more deer test positive for CWD TSE PRION in the wild


MONDAY, MAY 15, 2017 

TEXAS New CWD TSE PRION 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 


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 


MONDAY, APRIL 17, 2017 

Wildlife advocates see wolves as 'best natural defense' against chronic wasting disease

NO WAY! this is an extremely stupid move, and very, very, dangerous... 


>>>Consider the potential role of predators and scavengers to remove CWD infected animals and carcasses to reduce CWD transmission (Krumm, 2010; Wild, 2011).<<<

ABSOLUTELY A BAD DECISION, BASED ON THE FACT THAT THE CANINE AND FELINE SPECIES ARE SUSCEPTIBLE TO THE TSE PRION, AND THE FACT THAT THE TSE PRION SURVIVES THE Digestive System OF THE American crows (Corvus brachyrhynchos) AND THE Coyotes (Canis latrans).

ALSO, it was well documented that domestic feline and big cage cats in zoos contracted the TSE Prion disease.

ALSO, it was well documented that HOUNDS were susceptible to a TSE PRION, and later science shows the same thing for canines.

THIS CONSIDERATION SHOULD BE TABLED AND NEVER MENTIONED AGAIN FOR THE FOLLOWING REASONS ;

Saturday, December 05, 2015

CWD Prions Remain Infectious after Passage Through the Digestive System of Coyotes (Canis latrans)


Wednesday, October 17, 2012

Prion Remains Infectious after Passage through Digestive System of American Crows (Corvus brachyrhynchos)


Sunday, November 01, 2009

AS THE CROW FLIES, SO DOES CWD

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases


Monday, July 13, 2009

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease


Sunday, July 07, 2013

Could avian scavengers translocate infectious prions to disease-free areas initiating new foci of chronic wasting disease?

Prion. 2013 Jul 3;7(4). [Epub ahead of print]


Monday, February 14, 2011

THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER

NO, NO, NOT NO, BUT HELL NO !

Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011


OR-09: Canine spongiform encephalopathy—A new form of animal prion disease

Monique David, Mourad Tayebi UT Health; Houston, TX USA

It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8 Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.

Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.

In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters.

If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).

References 1. Colchester AC, Colchester NT. The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61; PMID:16139661; http:// dx.doi.org/10.1016/S0140-6736(05)67218-2.

2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation. PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal. ppat.1000156.

3. Collinge J. Human prion diseases and bovine spongiform encephalopathy (BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/ hmg/6.10.1699.

4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233.

5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514.

6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu (Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.

7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317- 75-11-2947.

8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102.

9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30; PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121.


Monday, March 26, 2012

CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE


MONDAY, MARCH 8, 2010 

Canine Spongiform Encephalopathy aka MAD DOG DISEASE


Monday, March 8, 2010

Canine Spongiform Encephalopathy aka MAD DOG DISEASE


TUESDAY, APRIL 18, 2017 

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


WEDNESDAY, MAY 17, 2017 

*** SHIC FUNDED STUDY SUGGESTS POTENTIAL FOR PATHOGEN TRANSMISSION VIA FEED



WEDNESDAY, MAY 17, 2017

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


TUESDAY, APRIL 04, 2017

Please Support Funding for CDC and NPDPSC's Prion Disease Programs


Wednesday, May 24, 2017 

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


FRIDAY, MAY 26, 2017 

OIE World Assembly of OIE Delegates distributed SCOTLAND, NORTHERN IRELAND, AND POLAND BSE NEGLIGIBLE RISK STATUS


2001 - 2002 

 TEXAS OLD STATISTICS BELOW FOR PAST CWD TESTING; 

Subject: CWD testing in Texas 

Date: Sun, 25 Aug 2002 19:45:14 –0500 

From: Kenneth Waldrup 



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. 

Ken Waldrup, DVM, PhD Texas Animal Health Commission 

======================== 

TEXAS CWD STATUS 

Captive Cervids 

There have been no reported CWD infections of captive elk or deer in Texas. There is currently no mandatory surveillance program for susceptible cervids kept on game farms, although, there has been voluntary surveillance since 1999, which requires owners of participating herds to maintain an annual herd inventory and submit samples for all mortalities of animals over 16 months of age. 

 snip... 

 SO, i thought i would just see where these Ecoregions were, and just how the CWD testing was distributed. YOU would think that with the cluster of CWD bordering TEXAS at the WPMR in NM, you would have thought this would be where the major CWD testing samples were to have been taken? wrong! let's have a look at the sample testing. here is map of CWD in NM WPMR bordering TEXAS; 

NEW MEXICO 7 POSITIVE CWD WHITE SANDS MISSILE RANGE MAP 


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




Subject: cwd Texas

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 ; 



Sunday, October 04, 2009

CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009 2009 Summary of Chronic Wasting Disease in New Mexico New Mexico Department of Game and Fish


Monday, March 26, 2012

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


Tuesday, July 10, 2012

Chronic Wasting Disease Detected in Far West Texas


Monday, February 11, 2013

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


***for anyone interested, here is some history of CWD along the Texas, New Mexico border, and my attempt to keep up with it...terry

snip...

see history CWD Texas, New Mexico Border ;

Monday, March 26, 2012

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


Texas 84th Legislative Session 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 


TUESDAY, DECEMBER 16, 2014 

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


Wednesday, July 01, 2015 

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


Thursday, July 09, 2015 

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


Tuesday, July 21, 2015 

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


Wednesday, July 22, 2015 Texas 

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


Thursday, August 06, 2015 

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


Friday, August 07, 2015 

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


***raw and uncut*** 

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 


Saturday, October 03, 2015 

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


Friday, October 09, 2015 

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


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 


Thursday, November 05, 2015 

*** TPW Commission Adopts Interim Deer Breeder Movement Rules 


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). 


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 


SATURDAY, JANUARY 23, 2016 

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


Friday, February 05, 2016 

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


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, April 22, 2016 

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


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 


SUNDAY, MAY 22, 2016 

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


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? 



SATURDAY, JULY 09, 2016 

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


Monday, 

July 18, 2016 

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


TUESDAY, AUGUST 02, 2016 

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


Wednesday, September 28, 2016 

TPWD CWD Sample Collector Trainings in the Trans Pecos and Panhandle 


Wednesday, November 09, 2016 

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


Friday, November 18, 2016 

IMPORTANT: SAWCorp CWD Test is NOT APHIS Approved 


Thursday, December 08, 2016 

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


Saturday, December 03, 2016 

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


FRIDAY, JANUARY 20, 2017 

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


SUNDAY, JANUARY 22, 2017 

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


WEDNESDAY, JANUARY 25, 2017 

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


THURSDAY, JANUARY 26, 2017 

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


SATURDAY, MAY 27, 2017

TEXAS New Chronic Wasting Disease Management Response Rules Adopted


Terry S. Singeltary Sr.

WEDNESDAY, MAY 31, 2017

Texas New Exotic CWD Susceptible Species Rules Now in Effect


WEDNESDAY, MARCH 01, 2017 

South central Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease 



FRIDAY, JANUARY 13, 2017 

Pennsylvania Deer Tests Positive for Chronic Wasting Disease four-year-old white-tailed deer Franklin County Hunting Preserve


Wednesday, May 11, 2016 

PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL CONTROL MEASURES 


Sunday, October 18, 2015
*** Pennsylvania Game Commission Law and Law Makers CWD TSE PRION Bans Singeltary 2002 from speaking A smelly situation UPDATED 2015
Saturday, November 07, 2015
PENNSYLVANIA CHRONIC WASTING DISEASE CWD TSE PRION RULES EXPAND
Saturday, November 07, 2015
Pennsylvania 2015 September Minutes CWD Urine Scents
Tuesday, May 05, 2015
Pennsylvania CWD DETECTED IN SIX MORE FREE-RANGING DEER Disease Management Area 2 again expanded due to new cases Release #030-15
Sunday, July 13, 2014
Louisiana deer mystery unleashes litigation 6 does still missing from CWD index herd in Pennsylvania Great Escape
Saturday, June 29, 2013
PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA
Tuesday, June 11, 2013
*** CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013
*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
”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.
Wednesday, November 14, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO LOUISIANA and INDIANA
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
Thursday, October 11, 2012
Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests Positive

 Friday, February 05, 2016

 *** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION Detections in Farmed Cervids and Wild ***

 http://chronic-wasting-disease.blogspot.com/2016/02/report-of-committee-on-wildlife.html

 Wednesday, February 10, 2016

 Wisconsin Two deer that escaped farm had chronic wasting disease CWD

 http://chronic-wasting-disease.blogspot.com/2016/02/wisconsin-two-deer-that-escaped-farm.html

MONDAY, MAY 15, 2017 

Pennsylvania 25 more deer test positive for CWD TSE PRION in the wild


THURSDAY, JUNE 01, 2017

PENNSYLVANIA Third Case of CWD Discovered in a Captive Deer Farm in Four Months



Terry S. Singeltary Sr.

posted by Terry S. Singeltary Sr. at 11:02 AM

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