Friday, November 27, 2015

Wyoming Game and Fish finds CWD in new Deer Hunt Area near Sheridan

Game and Fish finds CWD in new Deer Hunt Area near Sheridan

Wyoming Game & Fish Department sent this bulletin at 11/27/2015 11:00 AM MST

Fall3

Game and Fish finds CWD in new Deer Hunt Area near Sheridan

SHERIDAN - The Wyoming Game and Fish Department recently euthanized a white-tailed deer exhibiting signs of chronic wasting disease (CWD). The deer tested positive for CWD, which is a fatal neurological disease of deer, elk and moose. The white-tailed deer was found in deer hunt area 24 - an area flanked on three sides by deer hunt areas where CWD was previously documented.

The buck was euthanized by Game and Fish personnel on November 16, 2016 about 2.5 miles southwest of the town of Big Horn.

“We appreciate anyone reporting an animal that appears to be sick and appreciate the help of the public in monitoring the health of the public’s wildlife,” Scott Edberg, Deputy Chief of the Wildlife Division, said. Consistent with the Centers for Disease Control Game and Fish does not recommend people eat deer, elk or moose that test positive for CWD.

Game and Fish personnel continue to watch for cervids that appear sick. Game and Fish also continues to collect samples of deer, elk and moose through hunter field checks and at CWD sampling stations. Game and Fish personnel collect and analyze more than 1,600 CWD samples annually throughout the state.

Hunters who wish to have their deer, elk or moose tested for CWD outside of the department’s CWD surveillance program can to do so by contacting the Wyoming State Veterinary Lab at (307) 766-9925. Hunters should be aware that it may take a few weeks after their animal is sampled to get their test results.

For more information on chronic wasting disease transmission and regulations on transportation and disposal of carcasses please visit the Game and Fish website at:


-WGFD-


Wyoming WGF Commission Meeting 11/6/2015 Afternoon Edition Video

CWD starts at minute 58:51 of first hour of meeting discussion of previous models predicting extinction of deer population and elk population.

please mark hour 1:02 where remarks were made about potential resistant genes and prolonged survival, however a recent study (I posted directly next after youtube link) where it states ;

‘’Our study also demonstrates that mice expressing the deer S96-PRNP allele, previously shown to be resistant to various cervid prions, are susceptible to H95+ CWD prions. The potential for the generation of novel strains raises the possibility of an expanded host range for CWD. ‘’

hour minute mark 1:03

captive Elk study

39 femail elk calves captured on National Elk Refuge In Jackson, WY

Transported to WGFD Thorne-Williams Wildlife Research Unit (Sybille, TWWRU)

Worst-case scenario for prion exposure

Genotypes

-27 M/M132 (69.2%)

-11 M/L132 (28.2%)

-1 L/L132 (2.6%)

38 of 39 elk died over 10-year study

1 remaining elk was L/L132

still alive and remained negative for PrPCWD by rectal biopsy

Appears healthy, weighs 242kg, and bore healthy calf in May, 2012

CWD infection rate in this study ???



> During the analysis, 37 of 39 elk died, all of which were positive for CWD.



*** Our study also demonstrates that mice expressing the deer S96-PRNP allele, previously shown to be resistant to various cervid prions, are susceptible to H95+ CWD prions. ***

 
*** The potential for the generation of novel strains raises the possibility of an expanded host range for CWD. ***

 
Deer Prion Proteins Modulate the Emergence and Adaptation of Chronic Wasting Disease Strains

 
Camilo Duque Velásqueza,b, Chiye Kima,c, Allen Herbsta,b, Nathalie Daudea,d, Maria Carmen Garzaa,e, Holger Willea,e, Judd Aikena,b and Debbie McKenziea,c aCentre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada bDepartment of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada cDepartment of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada dDepartment of Medicine, University of Alberta, Edmonton, Alberta, Canada eDepartment of Biochemistry, University of Alberta, Edmonton, Alberta, Canada

 
B. Caughey, Editor

 
+ Author Affiliations

 
ABSTRACT

 
Transmission of chronic wasting disease (CWD) between cervids is influenced by the primary structure of the host cellular prion protein (PrPC). In white-tailed deer, PRNP alleles encode the polymorphisms Q95 G96 (wild type [wt]), Q95 S96 (referred to as the S96 allele), and H95 G96 (referred to as the H95 allele), which differentially impact CWD progression. We hypothesize that the transmission of CWD prions between deer expressing different allotypes of PrPC modifies the contagious agent affecting disease spread. To evaluate the transmission properties of CWD prions derived experimentally from deer of four PRNP genotypes (wt/wt, S96/wt, H95/wt, or H95/S96), transgenic (tg) mice expressing the wt allele (tg33) or S96 allele (tg60) were challenged with these prion agents. Passage of deer CWD prions into tg33 mice resulted in 100% attack rates, with the CWD H95/S96 prions having significantly longer incubation periods. The disease signs and neuropathological and protease-resistant prion protein (PrP-res) profiles in infected tg33 mice were similar between groups, indicating that a prion strain (Wisc-1) common to all CWD inocula was amplified. In contrast, tg60 mice developed prion disease only when inoculated with the H95/wt and H95/S96 CWD allotypes. Serial passage in tg60 mice resulted in adaptation of a novel CWD strain (H95+) with distinct biological properties. Transmission of first-passage tg60CWD-H95+ isolates into tg33 mice, however, elicited two prion disease presentations consistent with a mixture of strains associated with different PrP-res glycotypes. Our data indicate that H95-PRNP heterozygous deer accumulated two CWD strains whose emergence was dictated by the PrPC primary structure of the recipient host. These findings suggest that CWD transmission between cervids expressing distinct PrPC molecules results in the generation of novel CWD strains.

 
IMPORTANCE CWD prions are contagious among wild and captive cervids in North America and in South Korea. We present data linking the amino acid variant Q95H in white-tailed deer cellular prion protein (PrPC) to the emergence of a novel CWD strain (H95+). We show that, upon infection, deer expressing H95-PrPC molecules accumulated a mixture of CWD strains that selectively propagated depending on the PRNP genotype of the host in which they were passaged. Our study also demonstrates that mice expressing the deer S96-PRNP allele, previously shown to be resistant to various cervid prions, are susceptible to H95+ CWD prions. The potential for the generation of novel strains raises the possibility of an expanded host range for CWD.

 
http://jvi.asm.org/content/89/24/12362.abstract?etoc

 

*** Our study also demonstrates that mice expressing the deer S96-PRNP allele, previously shown to be resistant to various cervid prions, are susceptible to H95+ CWD prions. ***

 

*** The potential for the generation of novel strains raises the possibility of an expanded host range for CWD. ***

 

UPDATE CWD VACCINE ELK minute mark 1:22:00

 

VACCINE

 

RECOMBINANT PROTEIN FUSION VACCINE

 

Hedlin, PD et al ‘’Design and delivery of a cryptic PrP c epitope for induction of Prp Sc-specific antibody responses.’’ Vaccine 28.4 (2010) 981-988.

 

PAN-PROVINCIAL VACCINE ENTERPRISES (PREVENT)

 

Dose: 2ml IM CWD VACCINE UPDATE IS A FAILURE, I REPEAT, A NEGATIVE RESULTS FOR CWD VACCINE. .tss

 


 

Monday, November 16, 2015

 

*** Wyoming Latest round of testing CWD surveillance program has found the disease in three new hunt areas

 


 

Saturday, November 14, 2015

 

Wyoming Chronic Wasting Disease CWD Surveillance Results 2014 reported in 2015

 


 

cwd to humans ?

 

now, let’s see what the authors said about this casual link, personal communications years ago.

 

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

 

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

 

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 ;

 


 

So far, says NIH researcher Race, the two Wisconsin cases pinpointed by the newspaper look like spontaneous CJD. "But we don't know how CWD would look in human brains. It probably would look like some garden-variety sporadic CJD." What the CDC will do with these cases and four others (three from Colorado and Schwan from Upper Michigan), Race says, is "sequence the prion protein from these people, inject it into mice and wait to see what the disease looks like in their brains. That will take two years."

 

CJD is so rare in people under age 30, one case in a billion (leaving out medical mishaps), that four cases under 30 is "very high," says Colorado neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in the newspaper], six cases of CJD in people associated with venison is very, very high." Only now, with Mary Riley, there are at least seven, and possibly eight, with Steve, her dining companion. "It's not critical mass that matters," however, Belay says. "One case would do it for me." The chance that two people who know each other would both contact CJD, like the two Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in 140 years.

 

Given the incubation period for TSEs in humans, it may require another generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting disease pass into humans? We'll be able to answer that in 2022," says Race. Meanwhile, the state has become part of an immense experiment.

 


 

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

 

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

 


 

*** 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).***

 


 

*** PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS ***

 

*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***

 

O18

 

Zoonotic Potential of CWD Prions

 

Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA

 

***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***

 

P.105: RT-QuIC models trans-species prion transmission

 

Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

 

Additionally, human rPrP was competent for conversion by CWD and fCWD.

 

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***

 


 

From: Terry S. Singeltary Sr.

 

Sent: Saturday, November 15, 2014 9:29 PM

 

To: Terry S. Singeltary Sr.

 

Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984

 

THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE

 

R. G. WILL

 

1984

 

*** 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). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;

 

snip...

 


 

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

 

Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.

 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),

 

***is the third potentially zoonotic PD (with BSE and L-type BSE),

 

***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

 

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

 

***thus questioning the origin of human sporadic cases...TSS

 

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

 


 

Monday, November 16, 2015

 

Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission

 


 


 

Thursday, November 26, 2015

 

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

 


 

Terry S. Singeltary Sr.

posted by Terry S. Singeltary Sr. at 2:48 PM

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