How much longer before the feedlots are hit?
Nightmare “mad elk” or “mad deer” disease, the always lethal malady spread by prions (infectious proteins), keeps creeping ever closer the the Greater Yellowstone ecosystem in Wyoming and to the massive elk winter feedlots. In these, it is expected to spread like wildfire in cheatgrass.
According to Wyoming Game and Fish, CWD presence has now been confirmed in the lab and visually in the field in all the hunting units adjacent to the core of the Greater Yellowstone in NW Wyoming. The new, bad news is detailed in the Jackson Hole News and Guide, CWD keeps creeping closer to feedgrounds.
For years critics have wanted to close down the elk feedgrounds to prevent infection. Now it seems obvious the state game department will never do this. It is hypothesized that wolves are as close to an ideal way of taking out infected deer and elk just beginning to show symptoms as any natural method possible. Wolves, disproportionately target sick ungulate prey. The hypothesis has not been tested, however, and it is doubtful that it will, given Wyoming’s hostility to a natural density for the now restored predator.
As hunters wait for the axe to fall, they can have their moose, elk, or deer tested at Wyoming State Veterinary Lab at 307-766-9925.
CWD does not occur in Montana or Idaho. These states contain the rest of the Greater Yellowstone.
Comments
This is the real threat to the elk population!
I hope this will get through to people now. We need our predators.
Prions. Now prions concern me. Back in the mid-90’s when I worked at a hospital we had a patient admitted who died from Creutzfeldt-Jacob Disease. The autoclaves are useless to destroy prion; the pathologists were reluctant to autopsy; and basically, there was confusion on what to do or how to handle the medical waste.
I hope the CWD doesn’t spread into the other states. Let the four-legged predators take care of the problem. Isn’t there peer-reviewed studies out there have shown wolves will select for those with CWD?
Yvette,
Many observers believe that the winter range, and some other elk and deer range in Colorado and much of WYoming has been permanently contaminated with CWD prions because they are so resistant to natural degradation and they stay infectious indefinitely.
Two situations seem to lead to CWD in Elk – over crowding and lack of predators to take out the diseased animals.
How do the “Elk reduction” program in GTNP and feeding in the National Elk Refuge protect our threatened herds?
Lorin Nelson,
THe feeding going onk, on the National Elk Refuge does not protect the elk that winter there from CWD. The non-natural concentration of elk on the National Elk Refuge and on the nearby Wyoming state elk refuges are much of the problem. They bring the elk together so that CWD spreads more easily than were they not fed. For years conservationists have been trying to get these winter feeding operations shut down, but pressure from local businesses that want to have tourists come view the big concentration of elk keep them open. In addition, wintertime employees on the state feedgrounds is a political constituency to keep the feeding going. Finally, some hunting groups have downplayed the danger because they see closure of the feeding as the end of abundant elk.
Speaking of diseases, I think this is such a wonderful thing. In my area and other areas too:
http://www.capecodtoday.com/article/2014/10/24/27552-rabies-vaccine-distribution-started-week-sandwich-brewster
This is very sad and predictable. They blame the wolves and carnivores for the loss of elk or other large animals, but in fact poor practices and greed will ultimately wipe them out with the diesease but of course it will be blamed on the wolves so more can be hunted.
Sandy Lee – “Oh, what a tangled web we weave. When first we practise to deceive!”
>>> It is hypothesized that wolves are as close to an ideal way of taking out infected deer and elk just beginning to show symptoms as any natural method possible. Wolves, disproportionately target sick ungulate prey. The hypothesis has not been tested, however, and it is doubtful that it will, given Wyoming’s hostility to a natural density for the now restored predator. <<<
PLEASE be careful what you ask for.
recently, canine spongiform encephalopathy has been confirmed.
I proved this in 2005, with a letter from MAFF/DEFRA et al confirming my suspicions of the ‘hound study’ way back. this was covered up. see documents below.
also, recently, cwd to the domestic cat is a great concern.
even though to date, as far as I am aware of, the cwd study on the mountain lion has not produced any confirmation yet, we already know that the feline species is highly succeptible to the TSE prion. domestic cats and the exotic zoo big cats.
so in my honest opinion, any program that would use wild animals to prey on other wild animals, as a tool to help curb CWD TSE prion disease, would only help enhance the spread of disease, and it would only help spread the disease to other species. …TSS
Monday, February 14, 2011
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
NO, NO, NOT NO, BUT HELL NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011
http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
Monique David, Mourad Tayebi UT Health; Houston, TX USA
It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8 Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.
Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.
In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters.
If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).
References snip…end…tss
http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html
2005
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN: FAX:
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less
critical. For more details see- http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf
As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
======================================
HOUND SURVEY
I am sorry, but I really could have been a co-signatory of Gerald's minute.
I do NOT think that we can justify devoting any resources to this study, especially as larger and more important projects such as the pathogenesis study will be quite demanding.
If there is a POLITICAL need to continue with the examination of hound brains then it should be passed entirely to the VI Service.
J W WILESMITH Epidemiology Unit 18 October 1991
Mr. R Bradley
cc: Mr. G A H Wells
http://collections.europarchive.org/tna/20081106102318/http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf
3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would by the end of the year, indentify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.
http://collections.europarchive.org/tna/20080103034308/http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf
SEE FULL TEXT ;
http://caninespongiformencephalopathy.blogspot.com/
Monday, February 14, 2011
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
NO, NO, NOT NO, BUT HELL NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011
http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html
http://www.thewildlifenews.com/2011/11/03/jackson-hole-newsguide-retired-biologist-stop-feeding-make-elk-migrate/
Monday, March 8, 2010
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
http://caninespongiformencephalopathy.blogspot.com/
Saturday, October 18, 2014
Chronic wasting disease threatens Canadian agriculture, Alberta MLA says
http://chronic-wasting-disease.blogspot.com/2014/10/chronic-wasting-disease-threatens.html
Thursday, October 23, 2014
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
http://chronic-wasting-disease.blogspot.com/2014/10/first-case-of-chronic-wasting-disease.html
Tuesday, October 21, 2014
Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE
http://chronic-wasting-disease.blogspot.com/2014/10/pennsylvania-department-of-agriculture.html
Tuesday, October 07, 2014
Wisconsin white-tailed deer tested positive for CWD on a Richland County breeding farm, and a case of CWD has been discovered on a Marathon County hunting preserve
http://chronic-wasting-disease.blogspot.com/2014/10/wisconsin-white-tailed-deer-tested.html
Thursday, October 02, 2014
IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
http://chronic-wasting-disease.blogspot.com/2014/10/iowa-test-results-from-captive-deer.html
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets?
http://chronic-wasting-disease.blogspot.com/2014/07/how-chronic-wasting-disease-is.html
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND POTENTIAL RISK FACTORS THERE FROM
http://chronic-wasting-disease.blogspot.com/2014/07/chronic-wasting-disease-cwd-tse-prion.html
Saturday, October 25, 2014
118th USAHA Annual Meeting CWD and Captive Cerivds
http://chronic-wasting-disease.blogspot.com/2014/10/118th-usaha-annual-meeting-cwd-and.html
Saturday, October 25, 2014
Wyoming Chronic Wasting Disease Found in Two More Deer Hunt Areas
http://chronic-wasting-disease.blogspot.com/2014/10/wyoming-chronic-wasting-disease-found.html
SEE CWD VACCINE UPDATE ;
https://www.youtube.com/watch?v=czOSEWx7Hiw
Friday, November 16, 2012
Yellowstone elk herds feeding grounds, or future killing grounds from CWD
http://chronic-wasting-disease.blogspot.com/2012/11/yellowstone-elk-herds-feeding-grounds.html
TSS
Wolf family groups or packs, below high Arctic and Subarctic populations, tend to be violently intolerant of neighboring unrelated packs. In nature the wolf is less prone to communicable disease (excepting of course, the highly social propensity of dispersing, unattached wolves – some have been know to interact sociably with dogs, and others associated with family packs have exhibited this behavior also).
It is probable that any domestic-vectored disease will spread to wolves at some time, more likely through illegal off-leashing or perhaps the mere presence of infected dogs.
Prion diseases appear to be quite dangerous; the ultimate “crowd” disease, which me might expect to affect neural tissue of most vertebrates. Thus is may be difficult to conduct viability experiments (I hardly believe that molecule persistence can be as permanent as is claimed, but cannot deny possibility).
this appears to be a case contrasting the “Sleeping sickness” borne by tsetse flies in two parts of Africa, which has recently been controlled, leading to greater inmigration of humans and their domestics into the final areas of Africa safe for indigenous species.
Montana, Idaho, and Wyoming all (like Alaska) intend their wildlife to be intensively managed for maximum carrying capacity, to esentially farm ungulates for “harvest” via gun.
This brings in financialsupport for management agencies, in a corrupt twist of the word, “wildlife.”
In any case, this is a density-dependent result.
With humans CJD was understood as possibly slow-progressing.
The prion itself exists in two forms, one commonly present in cells and benign, serving transport and possibly other purposes. I am not sure how the other form has manifested, but occurs sporadically, except in the case of the few arising from a genetic mutation.
Over here in teh Klamath ecosystems, I have noted that the endemic Roosevelt Elk are only able to disperse quickly through the patchy ecological conditiions resulting from logging. You will probably one day hear of the spreading population, although I hav enot yet seen any work on what I have visually observed.
I presume Rocky Mt Elk are somewhat like Mule Deer, remaining in their watersheds with little inter-herd dispersal.
There have been no reports of CWD generating a human infection. This has been attributed to the elk and human proteins being sufficiently different as to not allow transmission (unlike the cow and human proteins which do allow for transfer as Mad Cow Disease). But as CWD moves deeper into elk and deer populations and human consumption thus increases, it will be interesting to see if this infectious barrier persists.
Food for thought from some background research I conducted last year:
Prions persist in soils and ungulate feces and are taken up by green plants:
http://www.loe.org/content/2013-10-04/prions-in-plants.mp3
http://aevm.tamu.edu/files/2010/06/10322-Vet-Quarterly-Review-Fall-2009.pdf
a.) SUBCLINICAL SYMPTOMS AND PUBLIC HEALTH
Abstract
“Prion diseases of humans and animals are associated with the accumulation of an abnormal isoform (PrP(Sc)) of the host-encoded prion protein (PrP(C)). Transmission of these diseases between mammalian species is usually limited by a ‘species barrier’, which can be mediated by differences in primary sequence of the prion protein between donor and host species. Studies on species barriers usually rely on the development of clinical disease in inoculated animals as an assessment of susceptibility in a particular host. Recent studies by a number of groups have demonstrated that the absence of clinical symptoms does not necessarily exclude transmission of prion disease across a species barrier. Such results indicate that subclinical or carrier states exist in these diseases, which has public health implications regarding human exposure to BSE prions and iatrogenic transmission from apparently healthy humans. Here the issue of subclinical prion diseases is reviewed and implications are discussed.”
SOURCE: http://www.ncbi.nlm.nih.gov/pubmed/12064255
b.) SUBCLINICAL PRION INFECTION IN HUMANS AND ANIMALS
Abstract
“Transmission of prion diseases between mammalian species is limited by a so-called ‘species’ or ‘transmission’ barrier. Recognition of prion transmission usually relies on the appearance of clinical symptoms in inoculated animals and the interval between inoculation and appearance of clinical disease is designated incubation period. At some point during this clinically silent period, neuropathological and biochemical changes as well as accumulation of prions in the brain can be detected and this stage can be called preclinical prion disease. Recently, several lines of evidence have suggested that subclinical forms of prion disease exist, in which high levels of infectivity and PrP(Sc) are found in animals that do not develop clinically apparent disease during a normal life-span. Such asymptomatic prion ‘carrier’ states challenge our current understanding of pathogenesis as well as of the molecular basis of barriers to transmission. Subclinical as well as preclinical/clinical prion disease may be relevant when analysing the risk to public health of potential sources of prion exposure.”
SOURCE: http://www.ncbi.nlm.nih.gov/pubmed/14522857
c.) BIG GAME HUNTERS WARY OF PRION TRANSMISSION
“Because prions aren’t living organisms, they remain infectious indefinitely, whether they’re in soil or living matter. And although CWD prions were once thought confined to the brain, spleen, tonsils, lymph nodes and spinal cord of deer and elk, they’ve since been found at lower levels in their eyes, heart, blood, urine, saliva and muscles.
So far, science has found no evidence that CWD can infect humans who eat contaminated venison, but the World Health Organization and most state wildlife agencies advise people not to eat CWD-positive animals.
The state of Wyoming adds this warning: “Until more is known about the human health risk, individuals may want to consider the theoretical possibility that a yet-to-be-determined human health risk may exist before consuming CWD-infected animals.”
Johnson’s findings raise concerns beyond deer hunting’s world. One unknown is whether plants alter CWD prions in ways that make them increasingly infectious. Laboratory tests show that prions injected into mice can change enough that even though the first mouse doesn’t die, its tissues kill mice in subsequent injections.” …
“You might recall Hall’s farm, otherwise known as Buckhorn Flats, was once a commercial deer-breeding and shooting preserve. After the state of Wisconsin closed the 80-acre operation in 2005 and killed the 76 deer in its breeding pen in January 2006, tests revealed 60 of the whitetails, 80 percent, carried CWD.
It’s North America’s worst CWD infection. In fact, its soils are so tainted the state had to buy the property. The Wisconsin Department of Natural Resources intends to make it a research facility, so what better place to test how efficiently potatoes, parsnips, carrots, lettuce, zucchini, broccoli, green beans and other common food plants pull prions from CWD-tainted soils, and pass them along? …
“But this much is certain: As Wisconsin and other states with CWD slowly assembled the disease’s puzzle piece by piece since 2002, the picture has only grown uglier.”
SOURCE: http://www.bowhunting.com/blog/2013/10/23/plants-could-be-spreading-cwd-prions/
You do understand, of course, that should ungulate populations significantly fall, there will be political calls to exterminate predators, as the more confused among humans revalue the less numerous “game” species.
The most comon response to rarity of game animals is greater desire and demand for individuals of that species as trophy.
This cognitive evil is endemic among our kind, and can be as deadly to Wolf and Griz, as competitors, as a bite of a spongy brain.
jdubya says:
October 29, 2014 at 11:40 am There have been no reports of CWD generating a human infection. This has been attributed to the elk and human proteins being sufficiently different as to not allow transmission (unlike the cow and human proteins which do allow for transfer as Mad Cow Disease). …end
please see ;
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***
let’s review some science to date from the prion Gods on the potential for CWD transmission to humans, and what it might look like ;
human risk factors from cwd
NOW, what is the latest on human risk factors to CWD strains ???
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
http://chronic-wasting-disease.blogspot.com/2014/06/prion-2014-chronic-wasting-disease-cwd.html
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.
https://www.landesbioscience.com/journals/prion/Prion4-3-PPo2.pdf
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.
http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm
http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
***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 ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
http://chronic-wasting-disease.blogspot.com/2013/08/prion2013-chronic-wasting-disease-cwd.html
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
continued…
there is in fact evidence that the potential for cwd transmission to humans can NOT be ruled out.
I thought your readers and hunters and those that consume the venison, should have all the scientific facts, personally, I don’t care what you eat, but if it effects me and my family down the road, it should then concern everyone, and the potential of iatrogenic transmission of the TSE prion is real i.e. ‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there from…like deer antler velvet and TSE prions and nutritional supplements there from, all a potential risk factor that should not be ignored or silenced. …
the prion gods at the cdc state that there is ;
”no strong evidence”
but let’s see exactly what the authors of this cwd to human at the cdc state ;
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
http://chronic-wasting-disease.blogspot.com/2014/04/iowa-chronic-wasting-disease-detected.html
***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD…tss)
These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. …
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
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).
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 ;
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and venison and lamb**************
http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-report-1994-increased-risk-for.html
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** 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
*** our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions. ***
http://www.jbc.org/cgi/content/abstract/M704597200v1?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Cross-sequence+transmission+of+sporadic+Creutzfeldt-Jakob+disease+creates+a+new+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
snip…see full text ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/cwd-tse-prion-in-cervids-to-htgmice.html
Wednesday, December 11, 2013
*** Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease ***
http://creutzfeldt-jakob-disease.blogspot.com/2013/12/detection-of-infectivity-in-blood-of.html
Sunday, April 06, 2014
SPORADIC CJD and the potential for zoonotic transmission there from, either directly or indirectly via friendly fire iatrogenic mode, evidence to date
http://creutzfeldt-jakob-disease.blogspot.com/2014/04/sporadic-cjd-and-potential-for-zoonotic.html
Wednesday, July 23, 2014
*** After the storm? UK blood safety and the risk of variant Creutzfeldt-Jakob Disease
http://vcjd.blogspot.com/2014/07/after-storm-uk-blood-safety-and-risk-of.html
Saturday, August 02, 2014
Structural effects of PrP polymorphisms on intra- and inter-species prion transmission
http://chronic-wasting-disease.blogspot.com/2014/08/structural-effects-of-prp-polymorphisms.html
TSE prion disease, a disease that is 100% fatal, once clinical, but with an incubation period anywhere from 10 to 50 years, never say never…
Sunday, November 23, 2014
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case *NOT* European
http://vcjd.blogspot.com/2014/11/confirmed-variant-creutzfeldt-jakob.html