CJD,CWD are two very similar diseases, each acts like the other except the amount of consumption. How many pounds of beef are eaten in 1 year compared to venison. Comparisons not even in the ballpark, that's why CWD has not shown up in the human population. Added that active testing is not required at time of death for dementia, alzheimer's or any wasting disease and CWD. Please if you have a loved one that has died of dementia or alzheimer's get them tested. That way we will know, epidemiologists have followed people around that consume venison but the sample size is extremely small.
" CWD has never been found in a human." that statement is all the answers the industry tries to spin answer the question... My question is- Would you knowingly feed CWD positive WTD,MD,Elk,Sitka and Red Deer to your family,kids,grandkids? Like putting a bullet in a revolver and spinning the cylinder and putting it to their heads. [/quote]

Ok. When you say stuff like the above with absolutely no facts to back it up, you leave yourself wide open to statements about where you pulled it from.

Please link the research based on valid data that states what you're implying. That CWD is already in the human population masquarading as Alzheimers, dementia, etc.

Man, if you are really a biologist, it explains how state fish cop agencies get it wrong so much.

Again I agree that the deer had to come from somewhere as they just did not appear magically one day in any pens. My response about the 5 ranches was to your statement that every breeder was in it to sell deer, which I just stated 5 I know are not doing. Again I agree it only takes one deer, but is this deer the original carrier of CWD? If not then what is the carrier and how did it get into these pens? That is critical in my mind at this point, to find out to put a stop to it appearing in another location not even closely related to this one. This case and ranch would be the time to try to do the live test first then the kill test after to see if they can find a way to diagnose it in live animals IMO. We are still hung on it being started by WT deer and not by an Elk or some other source. I am not jumping on any one bandwagon yet. All I know is a deer or Elk with CWD did not walk from far West Texas and jump into a HF set of breeding pens in Medina County.
I am on the same band wagon as you about deer being fed off label pharmaceuticals. My statement again was not all ranches do that to begin with, just seems you and others want to label them all the same since once a deer breeder always a crooked deer breeder. I can't blame a ranch going thru a vet to get a script done to give to his deer so he can try save any of them, but I am not a fan of what some are doing you are referring to. Those are doing it without Vet supervision or regard for the animal. They are doing it solely for profit.
I am still not convinced that animal movement is the sole culprit of the spread of CWD across this country. Does it aid in it? Yes, but it does not explain how it got into the center of Texas inside a HF ranch inside HF breeding pens. Been CWD clean since 2006 and this deer was born in the pens. To many questions need answered and we might not ever know those answers if they just kill everyone without doing as much research and testing as that can be done.
So I take since we are in such a sad state with our hunting you will be leading the petition to stop the TBGA program from recognizing the landowners/managers and hunters first-third place by division in the state this coming year? I mean they are recognizing the landowner for managing his ranch and raising the biggest deer he can. Start the petition I will sign it since we do not want to go down that road in the future of just managing deer and habitat to improve the quality.
As far as the needy, I agree we should forbid a ranch using a MLD permit to remove off deer numbers to benefit their ranch and those dang needy families. Let those familis starve and let the killed deer just rot on the ground. Who started MLD again and why?
For the record I am not grandstanding either, just throwing out thoughts(thoughts that might be for what I believe or not) in a forum debate. I hate to see any disease start or outbreak...Anthrax, EHD, CWD etc...nothing good happens for wildlife when it does.

Then your research skills are poor. Wisconsin law states that "feeding deer and hunting over bait be banned in counties within a 10-mile radius of where a CWD-positive deer is found." And as of August, there will be 3 new counties added to the bait ban list (Eau Claire, Clark, and Jackson).

Yes, CWD is slow, but mortality is 100%. And it has done nothing but increase in distribution since its inception. It has more numerous reservoir species than does EHD or other diseases. So transmission is still very much a concern. This is a good article for you https://www.hcn.org/blogs/goat/chronic-wasting-disease-forgotten-but-not-gone


And yes, there is research being conducted that is demonstrating that Alzheimer's can be caused by prions. The source of these prions is yet to be determined. Maybe it's a variant of CWD, Kreuzfeldt-Jakob, or other unknown sources.

You're excessively criticizing people when it's clear that you are not well informed.

If you read a lot of CWD research it's often postulated that there may be some level of spontaneous development. It pays to pay attention to research developments with Scrapie another TSE disease that has had far more research over a longer period than CWD. There are genotypes of sheep ,that are highly resistant to Scrapi,e are there lines of deer that are also naturally resistant? They have a live test test for Scrapie that much better than any for CWD. Will the third eyelid tissue test work for deer. There are lots of questions but no definitive answers.

CJD,CWD are two very similar diseases, each acts like the other except the amount of consumption. How many pounds of beef are eaten in 1 year compared to venison. Comparisons not even in the ballpark, that's why CWD has not shown up in the human population. Added that active testing is not required at time of death for dementia, alzheimer's or any wasting disease and CWD. Please if you have a loved one that has died of dementia or alzheimer's get them tested. That way we will know, epidemiologists have followed people around that consume venison but the sample size is extremely small.
" CWD has never been found in a human." that statement is all the answers the industry tries to spin answer the question... My question is- Would you knowingly feed CWD positive WTD,MD,Elk,Sitka and Red Deer to your family,kids,grandkids? Like putting a bullet in a revolver and spinning the cylinder and putting it to their heads. [/quote]

Ok. When you say stuff like the above with absolutely no facts to back it up, you leave yourself wide open to statements about where you pulled it from.

Please link the research based on valid data that states what you're implying. That CWD is already in the human population masquarading as Alzheimers, dementia, etc.

Man, if you are really a biologist, it explains how state fish cop agencies get it wrong so much. [/quote]

You never answered my question, it was directed at your statement:" CWD has never been found in a human."

Would you knowingly feed CWD positive WTD,MD,Elk,Sitka and Red Deer to your family,kids,grandkids?
Just want to know where you stand.

Furthermore my statement about testing for CWD or CJD or any wasting type disease in individuals that have died of dementia or alzheimer's is testing severely lacking. When the sample sizes get to those of BSE induced testing levels then we may find a link. Never did I state CWD is in the human population.

We don't get it wrong we follow the data.

My point about Wisconsin is that they've tried to kill all the deer in areas and tried baiting restrictions with zero success.

You're point about new counties under a feeding ban because they've seen new cases just proves my point. The statement I made about relaxing bait restrictions was based on friends in Wisconsin who told me that in their areas.

So yes, I'll give you that they haven't relaxed restrictions. But they've been totally unsuccessful in their attempts to "control" CWD.

You jumping to the conclusion that because someone postulates that prions "might" cause Alzheimer's as meaning that CWD causes Alzheimer's is ridiculous.

Your statement that biologists "don't make mistakes, they follow the data" is pretty funny, considering the 19 times they've been wrong on spikes.

That's just one example of many where state biologists have made multiple mistakes.

And your question about feeding my family infected deer. I don't eat or let my family eat anything that is sick. Many many people in Wisconsin have eaten contaminated deer. I guess they are the ones who told me the laws on baiting were being relaxed.

Here's a link about the potential ante mortem test for CWD https://en.wikipedia.org/wiki/Surround_Optical_Fiber_Immunoassay

I suggest you do some research into the basic premises of epidemiology before you start criticizing other people. It has absolutely been proven that prions are deposited from feces and urine into soil, and are then taken up into plants, where they reside until eaten at which point they infect another animal. Because feeders represent a point at which numerous animals concentrate, so too does it represent a point at which their urine and feces are concentrated. Hence the increased transmission of prions in that area.

The only way to test the deer on those ranches is by first killing them. CWD will be taken very seriously by TPWD (hopefully) and therefore they will need to test all of those deer that came into contact with other potentially infected deer.[/quote]


I suggest you do some research ;


I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

======

In the USA, under the Food and Drug Administrations 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.

======

31 Jan 2015 at 20:14 GMT

*** Ruminant feed ban for cervids in the United States? ***

31 Jan 2015 at 20:14 GMT

http://www.plosone.org/annotation/listThread.action?root=85351

Saturday, January 31, 2015

European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route

http://transmissiblespongiformencephalop...us-elaphus.html

Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus)

The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species. ...



These results indicate that CWD PrPres can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species....

http://vir.sgmjournals.org/content/80/10/2757.full.pdf

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://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf

Wednesday, March 18, 2009

Noah’s Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html

P.108: Successful oral challenge of adult cattle with classical BSE

Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada

Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults.

Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease.

At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.

Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. We are further examining explanations for the unusual disease presentation in the third challenged animal.

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

***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***

-----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

*** 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).***

https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249

*** 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

Friday, May 22, 2015

*** Chronic Wasting Disease and Program Updates - 2014 NEUSAHA Annual Meeting 12-14 May 2014 ***

http://chronic-wasting-disease.blogspot.com/2015/05/chronic-wasting-disease-and-program.html


kind regards, terry

CJD,CWD are two very similar diseases, each acts like the other except the amount of consumption. How many pounds of beef are eaten in 1 year compared to venison. Comparisons not even in the ballpark, that's why CWD has not shown up in the human population. Added that active testing is not required at time of death for dementia, alzheimer's or any wasting disease and CWD. Please if you have a loved one that has died of dementia or alzheimer's get them tested. That way we will know, epidemiologists have followed people around that consume venison but the sample size is extremely small.
" CWD has never been found in a human." that statement is all the answers the industry tries to spin answer the question... My question is- Would you knowingly feed CWD positive WTD,MD,Elk,Sitka and Red Deer to your family,kids,grandkids? Like putting a bullet in a revolver and spinning the cylinder and putting it to their heads. [/quote]


just because cwd has not been detected in humans, does not mean it does not exist. cwd in humans will not look like nvcjd in humans from typical c-BSE from cattle. ...


*** 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

Chronic wasting disease (CWD) is a widespread and expanding prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern. Current literature generated with in vitro methods and in vivo animal models (transgenic mice, macaques and squirrel monkeys) reports conflicting results. The susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. In our earlier bioassay experiments using several humanized transgenic mouse lines, we detected protease-resistant PrPSc in the spleen of two out of 140 mice that were intracerebrally inoculated with natural CWD isolates, but PrPSc was not detected in the brain of the same mice. Secondary passages with such PrPSc-positive CWD-inoculated humanized mouse spleen tissues led to efficient prion transmission with clear clinical and pathological signs in both humanized and cervidized transgenic mice. Furthermore, a recent bioassay with natural CWD isolates in a new humanized transgenic mouse line led to clinical prion infection in 2 out of 20 mice. ***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.

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

***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

The propensity for trans-species prion transmission is related to the structural characteristics of the enciphering and heterologous PrP, but the exact mechanism remains mostly mysterious. Studies of the effects of primary or tertiary prion protein structures on trans-species prion transmission have relied primarily upon animal bioassays, making the influence of prion protein structure vs. host co-factors (e.g. cellular constituents, trafficking, and innate immune interactions) difficult to dissect. As an alternative strategy, we used real-time quakinginduced conversion (RT-QuIC) to investigate trans-species prion conversion.

To assess trans-species conversion in the RT-QuIC system, we compared chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions, as well as feline CWD (fCWD) and feline spongiform encephalopathy (FSE). Each prion was seeded into each host recombinant PrP (full-length rPrP of white-tailed deer, bovine or feline). We demonstrated that fCWD is a more efficient seed for feline rPrP than for white-tailed deer rPrP, which suggests adaptation to the new host.

Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. 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.

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

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

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

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, Valerie 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

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

https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf

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

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

PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;

Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011. http://transmissiblespongiformencephalop...nd-venison.html

NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;

Wednesday, March 18, 2009

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html

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

*** 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).

https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249

*** 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

Terry S. Singeltary Sr.

What if's and what if's

Until there is a 100% accurate live testing method this will always be circular argument.

Until this issue is resolved let's ban CO alfalfa and Yankee alfalfa......

Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.

"This is the first intensive sampling for CWD in fawns anywhere," said Dr. Julie Langenberg, Department of Natural Resources wildlife veterinarian, "and we are trying to learn as much as we can from these data".

http://www.cwd-info.org/index.php/fuseaction/news.detail/ID/a4b4e5e8749d729af242e253ac742084

Saturday, February 04, 2012

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

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-16-age-limit-on-testing-dead.html

Articles of Significant Interest Selected from This Issue by the Editors Next Section Prions in the Blood of Infected Hosts: Early and Persistent Prions circulate in the blood of prion-infected hosts, including humans with variant Creutzfeldt-Jakob disease. Determining the parameters of blood-borne prions during the long asymptomatic phase of disease characteristic of all prion diseases has been a long-standing problem in prion biology. Elder et. al (p. 7421–7424) have demonstrated amyloid formation, a biomarker for prions, in the blood of prion-infected rodent and cervid hosts as early as 15 minutes post-mucosal or -intravenous infection. This prionemia persists throughout the disease course, indicating a role for hematogenous prions throughout the preclinical stage of illness.

http://jvi.asm.org/content/89/14/6973.full

***Immediate and Ongoing Detection of Prions in the Blood of Hamsters and Deer following Oral, Nasal, or Blood Inoculations

Alan M. Eldera, Davin M. Hendersona, Amy V. Nallsa, Edward A. Hoovera, Anthony E. Kincaidb,c, Jason C. Bartzb and Candace K. Mathiasona aDepartment of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, USA bMedical Microbiology and Immunology, Creighton University, Omaha, Nebraska, USA cDepartment of Pharmacy Sciences, Creighton University, Omaha, Nebraska, USA S. Perlman, Editor + Author Affiliations

http://jvi.asm.org/content/89/14/7421.abstract?etoc



kind regards, terry

CWD HAS been waltzing across the Texas border from the WSMR in New Mexico since around 2002. I was warning the TAHC about this back in 2002, to know avail...


Wednesday, March 18, 2015

Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015

http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-confirmed.html


Wednesday, March 25, 2015

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

http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-cases.html

Monday, February 11, 2013

TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos

http://chronic-wasting-disease.blogspot.com/2013/02/texas-chronic-wasting-disease-cwd-four.html

Tuesday, July 10, 2012

Chronic Wasting Disease Detected in Far West Texas

http://chronic-wasting-disease.blogspot.com/2012/07/chronic-wasting-disease-detected-in-far.html


kind regards, terry

Careful you don't get sand in your ears Every endeavor has been solved with "what if's" much to naysayers chagrin. There is definitely "something in the water" (used as a figure of speech).

Ok. When you say stuff like the above with absolutely no facts to back it up, you leave yourself wide open to statements about where you pulled it from.

Please link the research based on valid data that states what you're implying. That CWD is already in the human population masquarading as Alzheimers, dementia, etc.

Man, if you are really a biologist, it explains how state fish cop agencies get it wrong so much. [/quote]



Alzheimer's disease, and other neurological disease have now been linked to the Transmissible Spongiform Encephalopathy TSE Prion disease. ...just saying...kind regards, terry


Singeltary comment ;

http://www.plosone.org/annotation/listThread.action?root=82860




http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0111492&representation=PDF

Singeltary comment ;

http://www.plosone.org/annotation/listThread.action?root=82860

Wednesday, May 16, 2012

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Background

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.

Methods

Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.

Results

I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.

Conclusions

There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.

end...tss

SEE FULL TEXT AND SOURCE REFERENCES ;

Wednesday, May 16, 2012

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Proposal ID: 29403 ‘accepted’

http://betaamyloidcjd.blogspot.com/2012/05/alzheimers-disease-and-transmissible.html

Ann N Y Acad Sci. 1982;396:131-43.

Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).

Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.

Abstract

Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.

http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1982.tb26849.x/abstract

CJD1/9 0185 Ref: 1M51A

IN STRICT CONFIDENCE

Dr McGovern From: Dr A Wight Date: 5 January 1993 Copies: Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray

TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES

1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC. 2. Briefly, the meeting agreed that:

i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;

ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and

iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion. 93/01.05/4.1

http://collections.europarchive.org/tna/20080102191246/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf

BSE101/1 0136

IN CONFIDENCE

5 NOV 1992 CMO From: Dr J S Metters DCMO 4 November 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.

2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. What are the implications for public health?

3. The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.

92/11.4/1-1 BSE101/1 0137

4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.

JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 121/YdeS 92/11.4/1.2

http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf

BSE101/1 0136

IN CONFIDENCE

CMO

From: Dr J S Metters DCMO

4 November 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf

CJD1/9 0185

Ref: 1M51A

IN STRICT CONFIDENCE

From: Dr. A Wight Date: 5 January 1993

Copies:

Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray

TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES

http://collections.europarchive.org/tna/20080102191246/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf

Tuesday, November 26, 2013

Transmission of multiple system atrophy prions to transgenic mice

‘’Our results provide compelling evidence that α-synuclein aggregates formed in the brains of MSA patients are transmissible and, as such, are prions.’’

http://www.pnas.org/content/110/48/19555.abstract.html?etoc

Transmission of a neurodegenerative disorder from humans to mice

The findings suggest that the α-synuclein deposits that form in the brains of patients with MSA behave like prions and are transmissible under certain circumstances, according to the authors. — N.Z.

α-Synuclein deposits in the brainstems of inoculated mice.

http://www.pnas.org/content/110/48/19175.full.pdf+html

http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0111492&representation=PDF

http://www.plosone.org/annotation/listThread.action?root=82860


TSS


Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease

Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014

http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0111492&representation=PDF

Singeltary comment ;

http://www.plosone.org/annotation/listThread.action?root=82860




Tuesday, June 30, 2015

visual variant of Alzheimer’s disease VVAD vs Heidenhain Variant Creutzfeldt Jakob Disease hvCJD

http://betaamyloidcjd.blogspot.com/2015/06/visual-variant-of-alzheimers-disease.html



PRION2015 Alzheimer’s disease

*** P.34: Preliminary study of Alzheimer’s disease transmission to bank vole

Guido Di Donato1, Geraldina Riccardi1, Claudia D’Agostino1, Flavio Torriani1, Maurizio Pocchiari2, Romolo Nonno1, Umberto Agrimi1, and Michele Angelo Di Bari1

1Department of Food Safety and Veterinary Public Health Istituto Superiore di Sanita, Rome, Italy; 2Department of Cellular Biology and Neuroscience; Istituto Superiore di Sanita, Rome, Italy

Extensive experimental findings indicate that prion-like mechanisms underly the pathogenesis of Alzheimer disease (AD). Transgenic mice have been pivotal for investigating prionlike mechanisms in AD, still these models have not been able so far to recapitulate the complex clinical-pathological features of AD. Here we aimed at investigating the potential of bank vole, a wild-type rodent highly susceptible to prions, in reproducing AD pathology upon experimental inoculation.

Voles were intracerebrally inoculated with brain homogenate from a familial AD patient. Animals were examined for the appearance of neurological signs until the end of experiment (800 d post-inoculation, d.p.i.). Brains were studied by immunohistochemistry for pTau Prion 2015 Poster Abstracts S29 (with AT180 and PHF-1 antibodies) and b-amyloid (4G8).

Voles didn’t show an overt clinical signs, still most of them (11/16) were found pTau positive when culled for intercurrent disease or at the end of experiment. Interestingly, voles culled as early as 125 d.p.i. already showed pTau aggregates. Deposition of pTau was similar in all voles and was characterized by neuropil threads and coiled bodies in the alveus, and by rare neurofibrillary tangles in gray matter. Conversely, b-amyloid deposition was rather rare (2/16). Nonetheless, a single vole showed the contemporaneous presence of pTau in the alveus and a few Ab plaque-like deposits in the subiculum. Uninfected age-matched voles were negative for pTau and Ab.

*** These findings corroborate and extend previous evidences on the transmissibility of pTau and Ab aggregation. Furthermore, the observation of a vole with contemporaneous propagation of pTau and Ab is intriguing and deserves further studies.

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

P.155: Quantitative real-time analysis of disease specific tau amyloid seeding activity

Davin Henderson and Edward Hoover Prion Research Center; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; Fort Collins, CO USA

A leading hypothesis for the cause of neurodegenerative diseases is the templated misfolding of cellular proteins to an amyloid state. Spongiform encephalopathies were the first diseases discovered to be caused by a misfolded amyloid-rich protein. It is now recognized that the major human neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and chronic traumatic encephalopathy (CTE), also are associated with amyloid formation. Moreover, AD and PD amyloids have been shown competent to transmit disease in experimental animal models, suggesting shared mechanisms with traditional prion diseases. Sensitive detection of prion disease has been advanced by in vitro amplification of low levels of disease specific amyloid seeds, e.g. serial protein misfolding amplification (sPMCA), amyloid seeding (ASA) and real-time quaking induced conversion (RT-QuIC), thereby replicating the disease process in vitro. In addition, measurement of the amyloid formation rate can estimate the level of disease-associated seed by using methods analogous to quantitative polymerase chain reaction (qPCR). In the present work, we apply these principles to show that seeding activity of in vitro generated amyloid tau and AD brain amyloid tau can be readily detected and quantitated.





Tuesday, June 30, 2015

PRION2015 Alzheimer’s disease

http://betaamyloidcjd.blogspot.com/2015/06/prion2015-alzheimers-disease.html






kind regards, terry

If all of the brain pinion diseases are inter-chanable and not animal specific then the dairy, feedlot cattle, cubed fed cattle, deer, or any animal supplemented....are doomed!!!!!!!! Stop the importation of CWD area alfalfa

Are you ready to un-retire? I can teach you to run a swather

Retired I wish! Lets cut it man!!, Colorado and a few other states have issues with foreign hay already, but they don't have a problem shipping the crap out. Yeah, regulating feed by state, would be a start up nightmare for everybody, likely turn a lot of feeders into kill all the cervids off types IDK

They'd definitely request a lot more landowner vouchers and cheaper AUM fees.

Thursday, July 09, 2015

TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed Herd with Testing of Exposed Animals

http://chronic-wasting-disease.blogspot.com/2015/07/texas-chronic-wasting-disease-cwd-herd.html

You missed this part


• If the epidemiological investigation determines that the herd was not commingled with an animal from the CWD-positive herd, the herd will be reinstated to its former status, and the time spent in Suspended status be counted in its herd status.



• Animals are commingled if they have direct contact with each other, have less than 10 feet of physical separation, or share equipment, pasture, or water sources/watershed.

Did you armchair Biologist and Chemist solve this yet??

Tuesday, July 14, 2015

Texas Parks and Wildlife Commission Special Meeting Thursday on Chronic Wasting Disease CWD

http://chronic-wasting-disease.blogspot.com/2015/07/texas-parks-and-wildlife-commission.html


kind regards, terry

how did the deer czar from Texas Dr. Dough do for Wisconsin in regards to CWD $


Tuesday, July 14, 2015

TWO Escaped Captive Deer on the loose in Eau Claire County Wisconsin CWD postive farm Yellow ear tag

http://chronic-wasting-disease.blogspot.com/2015/07/two-escaped-captive-deer-on-loose-in.html


kind regards, terry

I read years back that it was caused by a copper deficiency in the brain. Didn't read the 7 pages ahead of this, may of learnt something haha. No need to go slaughtering our deer on some kind of witch hunt. I think we have killed more deer looking for the disease than the disease itself could of done.

I'm at the meeting today. Tons of people have showed up. There will be a live broadcast.
tpwd.texas.gov/business/feedback/meetings/

I got in the audio only room with about 50 more people, at least.