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Thursday, November 02, 2017

New Mexico Chronic Wasting Disease CWD Figures 2016 - 2017 Update ???

-----Original Message-----
From: Terry Singeltary
To: bse-l ; nmdept.ofgameandfish
Cc: lance.cherry ; cjdvoice ; bloodcjd ; ispa ; jake.ingram ; melanie.sandoval2 ; William.Montoya ; karl.moffatt ; nmdept.ofgameandfish ; nmdgf.chairman
Sent: Tue, Oct 31, 2017 3:55 pm
Subject: New Mexico Chronic Wasting Disease CWD Figures 2016 - 2017 Update ???

New Mexico Chronic Wasting Disease CWD Figures 2016 - 2017 Update ???

Greetings everyone,

The great state of New Mexico has been notorious for keeping information about Chronic Wasting Disease CWD TSE prion aka Mad Deer Disease outdated and pretty much to themselves. urls to map links on cwd zones and such are not working anymore, that i can find. seems they are being mum again. so, i must give an outdated update as well, but here is what i have to date...




i sent out an email October 23, 2017, and nothing back yet. see email;

-----Original Message-----
From: Terry Singeltary <flounder9@verizon.net>
To: lance.cherry <lance.cherry@state.nm.us>
Sent: Mon, Oct 23, 2017 3:43 pm
Subject: cwd New Mexico ?

Greetings Officer Cherry, 

i am seeking the latest figures for Chronic Wasting Disease CWD TSE Prion for New Mexico Wild and for New Mexico Captive including WSMR. is there any way you might be able to give me a run down on these figures. i try and keep up to date on these figures from state to state, and the latest i have is;


and here is what i posted on Texas recently;



but any help Sir would be most appreciative. latest links if you have them, or just figures you have.

i don't advertise or make money from all this mess, it's just for education use. ...

many thanks, kindest regards, terry

you can go to the New Mexico state site and search cwd or cwd maps.

good luck...terry

end...tss


THURSDAY, SEPTEMBER 22, 2016 

New Mexico CWD confirmed in 5 McGregor Range deer during the 2015-16 hunting season



WEDNESDAY, MARCH 25, 2015 

Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015


i got this in an email years back...

Subject: New Mexico Chronic Wasting Disease CWD Statistics To Date Sample_Number GMU Sampling_Date DOK Zone Easting Northing Kill_Location CWD_Test SignsORComments Kill_Info Tissue Species_Type

NM02-09 19 6/1/2002 6/1/2002 13 359899 3583583 WSMR main post (first CWD Positive in NM) Positive First CWD positive deer in New Mexico CWD Area Obex Deer

NM03-50-12 19 11/4/2002 11/4/2002 13 361000 3582000 WSMR Post Positive Deer

NM03-50-16 19 11/12/2002 11/12/2002 13 361000 3582000 WSMR Post Positive Deer

NM03-232-42 19 12/17/2002 12/17/2002 13 361000 3581000 WSMR Positive took tonsil sample, eartag 476 purple Tonsil Biopsy Tonsil & Lymph node Deer

NM03-232-41 19 1/1/2003 1/1/2003 13 351000 3581000 Organ Mtns. Positive no signs Hunter Harvest Lymph node & Obex Deer

NM03-227-17 19 1/4/2003 1/4/2003 13 348000 3577900 Dripping Springs Positive looked healthy Hunter Harvest Lymph node Deer

NM04-BURKETT-1114-004 19 11/14/2003 11/14/2003 13 359919 3583574 WSMR MAIN POST, BLDG. 100 Positive DOE SEVERELY EMACIATED, CAUSE OF DEATH UNKN. CWD Area Lymph node Deer

NM05-232-07 34 1/13/2004 1/13/2005 13 463977 3608839 15 miles NE of Pinon Positive Hunter reported convulsions, vomit, death CWD Suspect Obex Deer

NM05-50-38 19 12/14/2004 12/14/2004 13 346464 3566415 West Organs, W of Massey Tank Positive Tonsil Biopsy, eartag 478 Orange Tonsil Biopsy Tonsil Deer

NM05-50-36 19 12/14/2004 12/14/2004 13 349493 3578747 West Organs, W of Dripping Spring Visitor Center Positive Tonsil Biopsy, eartag # 249 Orange, 1st recapture (doe found & put down on 5/5/2005) Tonsil Biopsy Tonsil Deer

NM06-48-16 19 4/5/2005 4/5/2005 13 347623 3579382 WSMR - Tag # 482 Positive Tonsil Biopsy Tonsil Deer

NM05-50-85 19 4/11/2005 13 358175 3588385 WSMR, SW of Antelope Hill Positive eartag: 484 Purple CWD Area Tonsil Deer

NM05-50-59 19 4/15/2005 4/15/2005 13 346855 3577310 SW of Dripping springs Positive eartag: 490 Purple CWD Area Tonsil Deer

NM05-12-02 34 6/6/2005 6/5/2005 13 435000 3611500 Timberon Positive Very Poor BC, old doe CWD Suspect Lymph node Deer

NM06-10-01 34 10/1/2005 10/1/2005 13 445449 3623454 Hughes Canyon Positive Poor condition, could not stand CWD Suspect Obex Elk

NM06-206-03 34 10/3/2005 10/3/2005 13 440452 3625273 Wayland Canyon Positive Healthy, herding cows Hunter Harvest Obex Elk

NM06-48-05 19 12/10/2005 13 360273 3587275 Antelope Hill Positive 708 Tonsil Biopsy Tonsil Deer

NM06-127-15 34 3/24/2006 3/24/2006 13 433877 3612203 123 Waialae Dr. Timberon Positive Drooling, wobbly, and losing weight CWD Suspect Lymph node Deer

NM06-50-09 19 4/21/2006 4/21/2006 13 346665 3563768 N of sewage plant (Bishops Cap) Positive Capture #224, Game and fish tag 575 purple, 207 orange CWD Area Tonsil Deer

NM06-WSMR-08 19 6/2/2006 6/2/2006 13 343263 3743696 WSMR SW of Red Butte-Stallion range Positive Lion depredation study animal #19, Game and fish tag #246, orange lymph nodes collected Found Dead Lymph node Deer

NM06-147-02 34 8/12/2006 8/12/2006 13 432633 3612182 Abbyville St. Timberon, NM Positive Stumbling, foaming at mouth, disoriented CWD Area Deer

NM07-WMD-70 34 10/27/2006 10/27/2006 13 445000 3608000 West of Pinon Positive NA Hunter Harvest Lymph node Deer 07-16149 19 7/13/2007 7/13/2007 13 349000 3564000 South of Bishop's Cap Positive Sick, emaciated, salivating, urinating. Collectey by Richard McDonald. CWD Suspect Deer

NM08-0145 28 10/14/2007 10/14/2007 13 427000 3598000 Mc Gregor Positive none Hunter Harvest Deer

NM08-0528 34 10/30/2007 10/28/2007 13 451000 3578000 Southern Cross Ranch Positive Hunter Harvest Deer

NM07-WSMR-81 19 12/13/2007 12/13/2007 13 361084 3588638 MAIN POST Positive RECAPTURE DOE SEQ #80 CWD Area Deer

NM08-0630 28 10/12/2008 10/12/2008 13 441500 3599300 McGregor Range Positive Hunter Harvest Deer

NM08-0635 28 10/13/2008 10/12/2008 13 442600 3600300 McGregor Positive Hunter Harvest Deer

NM09-321 34 10/29/2008 10/25/2008 13 443000 3603000 Chuck Brown's Ranch Positive Small, emaciated, tick infested Hunter Harvest Deer

NM09-241 34 3/2/2009 3/1/2009 13 439367 3634869 Rio Penasco Positive Sick, reported by landowner, collected by Ben Byrd CWD Suspect Elk

NM10-302 34 12/6/2009 12/6/2009 13 439522 3632464 Wills Canyon Positive Sunken hips, Drewling, Not moving well (possible wounded) CWD Suspect Elk

NM09-339 28 5/9/2010 13 435976 3598058 Positive R 44 Ylw Lft 149.244 CWD Area Deer

NM09-182 28 10/10/2010 10/10/2010 13 434000 3602000 TA 13, GU4 Positive Hunter Harvest Deer

NM11-201 28 11/17/2010 11/17/2010 13 432402 3595093 McGregor Positive R ear 12 purple l ear 149.484 CWD Area Deer

NM08-0253 34 11/27/2010 11/27/2010 13 431000 3621000 Sac. Lookout Positive Hunter Harvest Elk

NM11-364 28 3/12/2011 3/12/2011 13 435747 3599058 McGregor Positive Rt ear: 10 pur Lft ear: 149.323 CWD Area Deer

NM11-367 28 3/13/2011 3/13/2011 13 430236 3596459 McGregor Positive Rt ear: 9 pur Lft ear: 149.426 CWD Area Deer

NM11-368 28 3/13/2011 3/13/2011 13 436668 3594474 McGregor Positive Rt ear: 25 Blue Lft ear: 149.184 CWD Area Deer

NM08-062 28 10/9/2011 10/9/2011 13 406700 3544700 McGregor Range South End Positive Hunter Harvest Deer

NM08-061 28 10/9/2011 10/9/2011 13 463900 3598800 McGregor Range Positive Hunter Harvest Deer

NM08-066 28 10/10/2011 10/9/2011 13 405238 3542644 McGregor Range Positive Hunter Harvest Deer

NM11-388 28 2/17/2012 2/17/2012 13 403607 3546117 Ft Bliss- McGregor Positive Left ear 60 yellow, Pregnant Collar 150.662 Rectal Biopsy Deer

NM11-391 28 2/18/2012 2/18/2012 13 416507 3576920 McGregor Positive Rt ear 56 yellow Collar 151.761 4 dars 1 stick 1 break 1 miss Rectal Biopsy Deer

NM14-4 28 12/11/2013 12/9/2013 13 432000 3606000 McGregor Positive Hunter Harvest Elk

NM14-6 28 12/11/2013 12/11/2013 13 431000 3604000 McGregor Positive Hunter Harvest Elk

NM14-5 28 12/11/2013 12/11/2013 13 431000 3604000 McGregor Positive Hunter Harvest Elk

NM14-62 19 2/12/2014 2/12/2014 13 348333 3598384 NASA Positive CWD Suspect Deer

NM14-343 19 4/6/2014 4/5/2014 13 343000 3575000 Mathis home Positive Suspect- near water, sick. Study deer. Collected by Pat Mathis. CWD Suspect Deer 

*** 2017 CHRONIC WASTING DISEASE ZOONOTIC REPORT UPDATE

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

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

Chronic Wasting Disease (CWD) 

Prevention 

If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people. 

Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat. 

Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD. 

To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD: 

Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD. 

Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP) 


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

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

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

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** 



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. 


TUESDAY, SEPTEMBER 12, 2017 

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


Subject: Prion 2017 Conference Abstracts CWD

 2017 PRION CONFERENCE 

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

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

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

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

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

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

PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 

Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO 

PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS 

*** PRION 2017 CONFERENCE VIDEO 



TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT 

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


TUESDAY, JULY 04, 2017

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


TUESDAY, JUNE 13, 2017

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


Wednesday, May 24, 2017 

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


SATURDAY, JULY 29, 2017 

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


Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ 

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

Rocky Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840 Next Section ABSTRACT

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.


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,§ ↵* 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. + See all authors and affiliations Science 24 Feb 2006: Vol. 311, Issue 5764, pp. 1117 DOI: 10.1126/science.1122864 Article Figures & Data Info & Metrics eLetters PDF You are currently viewing the abstract.

View Full Text

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.


*** 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 


you can see more evidence here ; 


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

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

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02). The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

snip...

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

snip...

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

snip...

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

snip...see full report ;


you can see more evidence here ;


*** 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. 


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

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

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


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

snip... 

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

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

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

This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. 

These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis. 


2012 PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer 

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

snip... 

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

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

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


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


FRIDAY, OCTOBER 20, 2017 

Wisconsin Two white-tailed deer Waupaca County Hunting Ranch Positive for Chronic Wasting Disease CWD TSE Prion


TUESDAY, OCTOBER 03, 2017

Wisconsin CWD-positive white-tailed deer found on Shawano County hunting ranch


SUNDAY, OCTOBER 01, 2017 

WISCONSIN CHRONIC WASTING DISEASE CWD SAMPLING UPDATE 


THURSDAY, AUGUST 03, 2017

Wisconsin CWD Showing Up in Northern Wisconsin Deer Farms


MONDAY, MARCH 20, 2017 

Wisconsin CWD TSE Prion Annual Roundup 441 positive


WISCONSIN CWD CASES OUT OF CONTROL

Monday, May 16, 2016 

Governor Walker Announces Several Initiatives to Combat Chronic Wasting Disease in Wisconsin 


Sunday, May 08, 2016 

WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE ABYSS UPDATE 


Wednesday, March 16, 2016 

Wisconsin CWD sample survey 2015 confirms 290 cases of Chronic Wasting Disease TSE Prion 


 Wednesday, February 10, 2016

*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD ***


Monday, May 16, 2016 

Governor Walker Announces Several Initiatives to Combat Chronic Wasting Disease in Wisconsin 


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

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

SUMMARY: 


J Vet Diagn Invest 20:698–703 (2008) 

Chronic wasting disease in a Wisconsin white-tailed deer farm 

Delwyn P. Keane,1 Daniel J. Barr, Philip N. Bochsler, S. Mark Hall, Thomas Gidlewski, Katherine I. O’Rourke, Terry R. Spraker, Michael D. Samuel 

Abstract. 

In September 2002, chronic wasting disease (CWD), a prion disorder of captive and wild cervids, was diagnosed in a white-tailed deer (Odocoileus virginianus) from a captive farm in Wisconsin. The facility was subsequently quarantined, and in January 2006 the remaining 76 deer were depopulated. 

Sixty animals (79%) were found to be positive by immunohistochemical staining for the abnormal prion protein (PrPCWD) in at least one tissue; the prevalence of positive staining was high even in young deer. 

Although none of the deer displayed clinical signs suggestive of CWD at depopulation, 49 deer had considerable accumulation of the abnormal prion in the medulla at the level of the obex. Extraneural accumulation of the abnormal protein was observed in 59 deer, with accumulation in the retropharyngeal lymph node in 58 of 59 (98%), in the tonsil in 56 of 59 (95%), and in the rectal mucosal lymphoid tissue in 48 of 58 (83%). The retina was positive in 4 deer, all with marked accumulation of prion in the obex. One deer was considered positive for PrPCWD in the brain but not in the extraneural tissue, a novel observation in white-tailed deer. The infection rate in captive deer was 20- fold higher than in wild deer. Although weakly related to infection rates in extraneural tissues, prion genotype was strongly linked to progression of prion accumulation in the obex. Antemortem testing by biopsy of recto– anal mucosal-associated lymphoid tissue (or other peripheral lymphoid tissue) may be a useful adjunct to tonsil biopsy for surveillance in captive herds at risk for CWD infection. 

Key words: Cervids; chronic wasting disease; prion; transmissible spongiform encephalopathy. 


State pays farmer $298,000 for infected deer herd Jan. 16, 2016 8:05 p.m. 

The State of Wisconsin paid nearly $300,000 to the Eau Claire County farmer whose deer herd was depopulated after it was found to be infected with chronic wasting disease. Rick Vojtik, owner of Fairchild Whitetails in Fairchild, received an indemnity payment of $298,770 for 228 white-tailed deer killed on his farm, according to officials with the Department of Agriculture, Trade and Consumer Protection. 

The money was taken from the agency's general program revenue funded by Wisconsin taxpayers. 


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

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. 

RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site. 

SUMMARY: 


Saturday, February 04, 2012

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


FRIDAY, FEBRUARY 03, 2012 

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


Monday, January 16, 2012

9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD 


IOWA

For Immediate Release Thursday, October 2, 2014 Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov 

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

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


*** see history of this CWD blunder here ; 


On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises. 


The overall incidence of clinical CWD in white-tailed deer was 82% Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo) 


MONDAY, SEPTEMBER 25, 2017

Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosis

(see origin of cwd in Colorado debate and evidence there from...tss)


THURSDAY, NOVEMBER 02, 2017 

Texas deer hunting season looks inviting By Shannon Tompkins Houston Chronicle also see updated CWD cases and science


WEDNESDAY, SEPTEMBER 27, 2017

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


THURSDAY, SEPTEMBER 21, 2017

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


MONDAY, AUGUST 14, 2017

*** Texas Chronic Wasting Disease CWD TSE Prion History


SUNDAY, AUGUST 06, 2017 

USA Chronic Wasting Disease CWD TSE Prion Emergency Response Plan Singeltary et al 


TUESDAY, MARCH 28, 2017 

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


URINE

SUNDAY, JULY 16, 2017

*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***


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


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


*** INFECTIOUS AGENT OF SHEEP SCRAPIE MAY PERSIST IN THE ENVIRONMENT FOR AT LEAST 16 YEARS *** 

GUDMUNDUR GEORGSSON1, SIGURDUR SIGURDARSON2 AND PAUL BROWN3 


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

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

you cannot cook the TSE prion disease out of meat. 

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

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

the TSE prion agent also survives Simulated Wastewater Treatment Processes. 

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

you can bury it and it will not go away. 

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

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

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

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

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

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

Laboratory of Central Nervous System Studies, National Institute of 

Neurological Disorders and Stroke, National Institutes of Health, 

Bethesda, MD 20892. 

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

PMID: 8006664 [PubMed - indexed for MEDLINE] 


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


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


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


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


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


PPo4-4: 

Survival and Limited Spread of TSE Infectivity after Burial 



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 


MONDAY, JUNE 12, 2017 

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


 WEDNESDAY, MAY 17, 2017 

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


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




Terry S. Singeltary Sr.
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