that is only for nvCJD. cwd in humans will not be nvCJD. most likely it will be a strain of the sporadic CJD's. ...



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 ;


http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html


http://chronic-wasting-disease.blogspot.com/2006_12_01_archive.html



*** 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.

http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf




Sunday, July 21, 2013

*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?

http://chronic-wasting-disease.blogspot.com/2013/07/as-chronic-wasting-disease-cwd-rises-in.html



Sunday, August 25, 2013

Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission





HD.13: CWD infection in the spleen of humanized transgenic mice

Liuting Qing and Qingzhong Kong

Case Western Reserve University; Cleveland, OH USA

Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals. These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.




Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system

Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1

1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK

Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.

Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.

Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.

Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay.


***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.





http://www.prion2013.ca/tiny_uploads/forms/Scientific-Program.pdf



www.landesbioscience.com




http://chronic-wasting-disease.blogspot.com/2013/08/prion2013-chronic-wasting-disease-cwd.html






Thursday, August 12, 2010

Seven main threats for the future linked to prions

First threat

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

Second threat

snip...

http://www.neuroprion.org/en/np-neuroprion.html




kind regards,
terry

there are still cannibal cervids still running loose, because man is still feeding them ruminant protein. that's why DEFRA is so concerned...


Friday, December 14, 2012

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

snip...

In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

Animals considered at high risk for CWD include:

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

snip...

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

snip...

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

snip...

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

snip...

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

snip...

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

snip...

http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf


SNIP...SEE ;

Friday, December 14, 2012

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

http://chronic-wasting-disease.blogspot.com/2012/12/defra-uk-what-is-risk-of-chronic.html



Wednesday, September 25, 2013

Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE PRION 2013

http://madcowusda.blogspot.com/2013/09/inspections-compliance-enforcement-and.html




DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability


Date: Fri, 16 May 2003 11:47:37 –0500


EMC 1 Terry S. Singeltary Sr. Vol #: 1


http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm


http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm



PLEASE SEE FULL TEXT SUBMISSION ;


http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html



kind regards,
terry

pens, pens, PENS ???

*** 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.

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. This 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




Tuesday, September 17, 2013

USAHA 116TH ANNUAL MEETING October 18 – 24, 2012 CWD, Scrapie, BSE, TSE prion (September 17, 2013)

http://transmissiblespongiformencephalop...october-18.html



kind regards,
terry

Wednesday, September 25, 2013

USDA Officials: CWD Standards Going to Public Comment Soon

http://chronic-wasting-disease.blogspot.com/2013/09/usda-officials-cwd-standards-going-to.html


kind regards,
terry

On another site where I am a moderator, flounder also post these CWD Prion related posts.

As moderator I at first cautioned him that it was off topic for the area it was being posted in and for using links that took the reader to other sites, something most sites do not want, is for their members to be redirected off their site to another. I didn't mind links for sourcing information but did mind for taking the member away for the entire post.

I eventually gave in because several other members seemed to be able to understand the Highly scientific....biologic language and discussed it. It reads like the insert that comes with your prescription drugs to me!! LOL

A plus was we had a member that would basically translate into laymans terms what flounder was trying to get across and it was actually pretty interesting.

My opinion, flounder is trying to do a service and I welcome him, but still don't understand all the techy necky language.

hell i'm just paranoid , i've fussed with ARA so much and for so many years that post like this and the way they are posted makes me thing ,,,,,, hummmmmmmm thats a ARA trying to stir the pot . it's a tactic i've seen used many times .

same with anti gunners . lol

sorry Flounder if i'm wrong ????

no problem, we're good. I understand this is all complicated, and I don't understand it all myself, I am layman also, I just followed the science daily as it comes out, for 15+ years. just made a promise to mom, back then there was no information. I have been on the BSE-L (mostly scientist studying TSE prion disease around the world since about 1999), and at one point, they suggested I put all this science and stuff via FOIA on the www somewhere when I reference the peer review scientific transmission studies and such, and some of the stuff they send me, so I put it all in blogs now (before that, it's scattered all over the www), and I do NOT advertise or make money from doing this. I just think to help stop the further spread of TSE prion disease, everyone must first have all the science to date. so, that's just what I try to do. my opinions are my opinions, based on the science to date I present from the scientist working on the TSE prion disease. you must read this, maybe more times than once, to understand for yourself, and then make your decisions there from. I just think when folks are trying to make policy decision making, when making policy for CWD prion regulations, they must have all the science. ...


just recently made this up for the hospitals and media in NH about the CJD exposure there. this nightmare goes much further than the mad cow bovines, cervids, sheep or caprines, and the rest of the species et al now, because it's in our medical arenas now. gonna be hard to get it out. ...just saying.


Thursday, September 26, 2013

Minimise transmission risk of CJD and vCJD in healthcare settings Guidance

http://creutzfeldt-jakob-disease.blogspot.com/2013/09/minimise-transmission-risk-of-cjd-and.html





Saturday, September 21, 2013

CJD CONFIRMED in patient at New Hampshire Department of Health and Human Services (DHHS), Catholic Medical Center (CMC), and the Manchester Health Department (MHD)

http://creutzfeldt-jakob-disease.blogspot.com/2013/09/cjd-confirmed-in-patient-at-new.html



SOMETHING I must add, that if you read carefully, you can see just what I am speaking of here in this old study I always go back to. this brings it all home for me. and remember, all iatrogenic CJD (medical surgical transmitted TSE CJD prion disease), all iatrogenic CJD is, is sporadic CJD, until route and source of agent is confirmed and documented. this rarely happens due to incubation period.



> 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]
>
> http://www.ncbi.nlm.nih.gov/entrez/query...p;dopt=Abstract

>
>





kind regards,
terry