Originally posted by jbwhttail:
They are going to grow bigger antlers when they are farm raised because they are not parasitized, are vaccinated, treated for sickness and they eat better than any wild deer has the ability to. In the very near future there will be a live test for CWD and a vaccine.
Dominator:
I have talked with you at the State House, you are breeding typical whitetails, I wont reveal your location.
I want to address your quote above with two points. First, a whitetail can only metabolize 18% protein anything above that goes out their butts. So ....... every wild deer can get 18% here in the United States. Even drought times a deer in Texas can get 18% from browse with no interference from humans. Also there has been no studies that prove minerals will grow bigger antlers either.
Your claim that there will soon be a live test and vaccine for CWD is not true. Today when a dead deer is tested it is classified positve or "not positive". That "not positive" does not mean it is CWD free, just that CWD was not detected at the time of the test. Also can you explain how a vaccine can keep a protein from mutating to a prion? Not possible, I have asked several people who are fighting this disease. As one told me "This is Pandora's box, and it has been opened.
It is well documented the origin of CWD in Colorado at Colorado wildlife facility. Mule deer were trapped and used in a study(proving it did not help to feed deer under stress) sheep were the control animal. The sheep were found(or at least one sheep) had scrapie, the prion in fact jumped species to deer. For you or anyone in your line of work to say CWD will not jump species is bold lies. How has it got into the mink population?
Folks this gentleman(and I mean gentleman) sat for an hour and talked about deer, he is genuine and convinced in his mind. He needs the same respect here that we afford all of our members. We aren't going to change his mind but........
say there jbwhttail,
I hope you don't mind, but I would like to comment on a few topics you brought up, that I might think you will and some of the others, might find interest in. I must get a bit long winded again. but I think it's worth the read. here goes, I am gonna lay down some history on TME, CWD, and scrapie, potential vaccine for cwd, and test for cwd, with reference materials, as follows ;
Sunday, August 11, 2013
Development of an oral vaccine for chronic wasting disease
AD.24: Development of an oral vaccine for chronic wasting disease
Ryan Taschuk1,3 Kristen Marciniuk,1,2 Suresh Tikoo,1,3 Philip Griebel,1 Andrew Potter,1 Neil Cashman5 and Scott Napper1,2
1University of Saskatchewan; VIDO-lnterVac; Saskatoon, SK Canada; 2Department of Biochemistry; University of Saskatchewan; Saskatoon, SK Canada; 3School of Public Health; University of Saskatchewan; Saskatoon, SK Canada; 4Brain Research Centre; University of British Columbia; Vancouver, BC Canada; 5Brain Research Center; University of British Columbia; Vancouver, BC Canada
The prion protein is well conserved across mammals, and the misfolded protein is the causative agent in many animal-specific prion diseases, including chronic wasting disease (CWD) in deer and elk. Prion diseases are caused by misfolding of endogenously expressed prion protein from the native and homeostatic Prpc conformation to the infectious and pathogenic PrPsc conformation. Transmissible spongiform encephalopathies are of great interest for many reasons: the onset of disease inevitably leads to neurodegeneration and death, the potential of interference with food production through transmission both within and between agricultural species can have severe economic impacts, and the potential exists for zoonotic transmission. Our group has hypothesized that immunotherapeutic targeting of the PrPSc conformation would clear the infectious agent / infected cell while sparing native PrP, and vaccines may have potential application in prevention of CWD transmission or therapeutic treatment of disease.
Our research has focused upon identifying and optimizing three components of a potential CWD vaccine: a CWD-disease specific epitope (DSE) that induces antibody responses, a carrier protein to increase the magnitude and duration of antibody responses toward DSEs, and identification of delivery systems for oral delivery of the above DSE-carrier protein ro cervids. We have developed and optimized DSEs from three distinct regions of PrPc. Vaccination trials using iterations of these DSEs elicit high titers of epitope-specific serum antibody. A second generation carrier protein has increased both the duration and magnitude of antibody responses when compared with our previous carrier protein. Lastly, two delivery systems were effective in inducing antibody responses when administered orally to white-tailed deer. We have identified the vaccine components necessary for delivering a CWD vaccine to wild cervids. These findings will direct our final CWD vaccine formulation and delivery system.
http://www.prion2013.ca/tiny_uploads/forms/Scientific-Program.pdf www.landesbioscience.com Thursday, August 08, 2013
Characterization of the first case of naturally occurring chronic wasting disease in a captive red deer (Cervus elaphus) in North America
http://chronic-wasting-disease.blogspot.com/2013/08/characterization-of-first-case-of.html Friday, August 09, 2013
CWD TSE prion, plants, vegetables, and the potential for environmental contamination
http://chronic-wasting-disease.blogspot.com/2013/08/cwd-tse-prion-plants-vegetables-and.html Tuesday, February 28, 2012
newly developed injectable CWD vaccine, live rectal mucosa testing and Deer Game Farms Update
http://chronic-wasting-disease.blogspot.com/2012/02/newly-developed-injectable-cwd-vaccine.html EPIDEMIOLOGY
EFFICACY OF ANTEMORTEM RECTAL BIOPSIES TO DIAGNOSE AND ESTIMATE PREVALENCE OF CHRONIC WASTING DISEASE IN FREE-RANGING COW ELK (CERVUS ELAPHUS NELSONI) Ryan J. Monello 1,6, Jenny G. Powers 1, N. Thompson Hobbs 2, Terry R. Spraker 3, Katherine I. O’Rourke 4,5, and Margaret A. Wild 1 1 National Park Service, Biological Resource Management Division, 1201 Oak Ridge Drive, Suite 200, Fort Collins, Colorado 80525, USA
2 Natural Resource Ecology Laboratory and Graduate Degree Program in Ecology, Colorado State University, Fort Collins, Colorado 80523, USA
3 Colorado State Diagnostic Laboratory, College of Veterinary Medicine, Colorado State University, Fort Collins, Colorado 80523, USA
4 United States Department of Agriculture, Agricultural Research Service, Animal Disease Research Unit, 3003 Animal Disease Biotechnology Facility, Washington State University, Pullman, Washington 99164, USA
5 Current address: Department of Veterinary Microbiology and Pathology, School of Veterinary Medicine, Washington State University, Pullman, Washington 99164, USA
A reliable antemortem test is needed to understand the ecology of chronic wasting disease (CWD) in elk (Cervus elaphus nelsoni). We measured the ability of antemortem biopsy samples from the rectal mucosa to detect the abnormal prion protein associated with CWD (PrPCWD), the relationship between test results from the obex and rectal biopsies at varying stages of CWD progression, and the prevalence of CWD in free-ranging elk from Rocky Mountain National Park, Colorado, USA. We sampled and placed radio collars on 136 adult female elk in the winter of 2007–08. Elk with biopsy samples found positive for PrPCWD by immunohistochemistry (IHC) were euthanized and the obex and retropharyngeal lymph nodes were examined with IHC. We resampled, euthanized, and necropsied 20, 25, and 34 of the remaining study elk in each of the three following winters, respectively. Sensitivity of rectal biopsy samples increased in an asymptotic fashion with follicle count and was maximized at 85% (95% credible limits [CL]=60, 98) in the beginning of the study, when a greater proportion of elk were in a detectable stage of prion infection. However, maximum sensitivity was reduced to 72% (CL=46, 94) when we included resampled elk, which included recently infected elk that were initially negative using rectal biopsies and IHC. Test results were similar between rectal biopsies and the obex, but the earliest stages of prion infection were only detected by using retropharyngeal lymph nodes. Minimum CWD prevalence was estimated to be 9.9% (CL=5.7, 15.7) using rectal biopsies, but this rose to 12.9% (CL=8.0, 19.1) when we included four elk that were likely misdiagnosed at initial capture. Our results indicate rectal biopsies can provide a useful research tool for CWD in elk populations, but should be used with caution because they can miss individuals in early stages of infection and underestimate prevalence. Prevalence estimates from this population are the highest reported to date in elk and indicate that under appropriate conditions, CWD may be able to affect the dynamics of high-density elk populations.
http://www.jwildlifedis.org/doi/abs/10.7589/2011-12-362?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed
Tuesday, February 28, 2012
newly developed injectable CWD vaccine, live rectal mucosa testing and Deer Game Farms Update
http://chronic-wasting-disease.blogspot.com/2012/02/newly-developed-injectable-cwd-vaccine.html *** 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. ...
also, see where even decades back, the USDA had the same thought as they do today with CWD, not their problem...see page 27 below as well, where USDA stated back then, the same thing they stated in the state of Pennsylvania, not their **** business, once they escape, and they said the same thing about CWD in general back then ;
”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.
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
now, decades later ;
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.
http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf 2011
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.
http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)
Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National Animal Disease Center, ARS, USDA, Ames, IA
snip...
This highlights the facts that
1) prior to the onset of clinical signs PrPSc is widely distributed in the CNS and lymphoid tissues and
2) currently used diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical signs.
The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in white-tailed deer 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 consistent with 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 white-tailed deer 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 scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. While two WB patterns have been detected in brain regions of deer inoculated by the natural route, unlike the IC inoculated deer, the pattern similar to the scrapie inoculum predominates.
http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf 2011 Annual Report
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research Unit
2011 Annual Report
In Objective 1, Assess cross-species transmissibility of transmissible spongiform encephalopathies (TSEs) in livestock and wildlife, numerous experiments assessing the susceptibility of various TSEs in different host species were conducted. Most notable is deer inoculated with scrapie, which exhibits similarities to chronic wasting disease (CWD) in deer suggestive of sheep scrapie as an origin of CWD.
snip...
4. Accomplishments
1. Deer inoculated with domestic isolates of sheep scrapie. Scrapie-affected deer exhibit 2 different patterns of disease associated prion protein. In some regions of the brain the pattern is much like that observed for scrapie, while in others it is more like chronic wasting disease (CWD), the transmissible spongiform encephalopathy typically associated with deer.
his work conducted by ARS scientists at the National Animal Disease Center, Ames, IA suggests that an interspecies transmission of sheep scrapie to deer may have been the origin of CWD. This is important for husbandry practices with both captive deer, elk and sheep for farmers and ranchers attempting to keep their herds and flocks free of CWD and scrapie.
http://ars.usda.gov/research/projects/projects.htm?ACCN_NO=411467&showpars=true&fy=2011 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
snip...
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 ;
http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other species
http://chronic-wasting-disease.blogspot.com/2012/11/chronic-wasting-disease-cwd-in-cervidae.html Sunday, March 09, 2014
*** Lesion Profiling and Subcellular Prion Localization of Cervid Chronic Wasting Disease in Domestic Cats
http://chronic-wasting-disease.blogspot.com/2014/03/lesion-profiling-and-subcellular-prion.html Saturday, March 09, 2013
Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest Incubation Time Model for Prion Diseases
http://chronic-wasting-disease.blogspot.com/2013/03/chronic-wasting-disease-in-bank-voles.html Thursday, November 21, 2013
*** Assessing the susceptibility of transgenic mice over-expressing deer prion protein to bovine spongiform encephalopathy
The present study was designed to assess the susceptibility of the prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy (BSE) prions, which have the ability to overcome species barriers. Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a 90-100% attack rates, BSE from cattle failed to transmit, indicating agent adaptation in the deer.
http://chronic-wasting-disease.blogspot.com/2013/11/assessing-susceptibility-of-transgenic.html Sunday, September 1, 2013
Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy
We previously described the biochemical similarities between PrPres derived from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations suggest a link between these two uncommon prion phenotypes in a primate model (it is to note that such a link has not been observed in other models less relevant from the human situation as hamsters or transgenic mice overexpressing ovine PrP [28]). We speculate that a group of related animal prion strains (L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion diseases in humans with a type 2 PrPres molecular signature (and more specifically type 2B for vCJD)
snip...
Together with previous experiments performed in ovinized and bovinized transgenic mice and hamsters [8,9] indicating similarities between TME and L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME outbreaks in North America and Europe during the mid-1900s.
http://transmissiblespongiformencep...evaluation-of-zoonotic-potential-of.html Tuesday, July 21, 2009
Transmissible mink encephalopathy - review of the etiology
http://transmissible-mink-encephalopathy.blogspot.com/2009/07/transmissible-mink-encephalopathy.html Saturday, December 01, 2007
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model
http://transmissible-mink-encephalo...notypic-similarity-of-transmissible.html Sunday, December 10, 2006
Transmissible Mink Encephalopathy TME
http://transmissible-mink-encephalo...ansmissible-mink-encephalopathy-tme.html TSE have been around for decades.
it’s not out of the question to think that CWD might have been here much sooner than it was documented.
have cwd and these other TSE been around for eons, or forever, I cannot answer that.
I know scarpie was first documented around 1947 here in the USA, how long it was here before that, I don’t know, some say over 250 years.
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m08b/tab64.pdf
TME in mink was documented in the early 1960s. it was first thought that the TME out break was from scrapie infected sheep, until a investigation was done on feed practices at these mink facilities, and it was later found that the mink had been fed 95%+ dead stock downer cows. and later, the Late Richard Marsh tried to warn the feds of the pending mad cow debacle. they refused to listen. ...
some interesting reading on pages 26 to 33
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
http://www.jwildlifedis.org/content/16/1/89.long 1979
TME originates from feeding mink, scrapie infected materials...
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m08/tab016.pdf
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 ***
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09/tab05.pdf
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09a/tab01.pdf
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf
http://transmissible-mink-encephalopathy.blogspot.com/ Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html Saturday, July 6, 2013
Small Ruminant Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy
Research Article
http://nor-98.blogspot.com/2013/07/small-ruminant-nor98-prions-share.html kind regards, terry
