Unfortantely you can't dictate tone on here. My point was one of education. Wether it be CWD or CJD... You are going to have to eat brain, eyes or spinal cord. When it comes to CWD although it's already shown to be different then mad cow think about how a deer is processed, and what meat is retained. It simplifies these threads even more.

The CWD discussion should always be one of facts and most up to date info. It should never have an agenda via misinformation

the august 1997 mad cow feed ban was nothing but ink on paper...

31 Jan 2015 at 20:14 GMT

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

31 Jan 2015 at 20:14 GMT

see Singeltary comment ;

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

SEE WHAT DEFRA MAFF ET AL SAID JUST LAST MONTH ABOUT THIS ;

Thursday, April 07, 2016

What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016

Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008).

***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.

snip...

For the purpose of the qualitative risk assessment developed here it is necessary to estimate the probability that a 30-ml bottle of lure contains urine from an infected deer. This requires an estimate of the proportion of deer herds in the USA which are infected with CWD together with the within herd prevalence.

The distribution map of CWD in US shows it is present mainly in central states (Figure 1). However, Virginia in the east of the country has recorded seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take steps to prevent urine being taken from infected animals eg by sourcing from farms where the deer are randomly tested for CWD (Anon 2015a). However, if disease is already present and testing is not carried out regularly, captive populations are not necessarily disease free (Strausser 2014). Urine-based deer lures have been known to be collected from domestic white-tailed deer herds and therefore there is a recognised risk. This is reflected by 6 US States which have

14

banned the use of natural deer urine for lures, as the deer urine may be sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For example, the US State of Virginia is banning the use of urine-based deer lures on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned urine-based deer lures and acknowledged that there is no way to detect their use (Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it appears that up to 50% of deer herds can be infected with 80-90% of animals infected within some herds.

*** It is therefore assumed that probability that a 30-ml bottle of deer urine lure imported from the USA is sources from an infected deer is medium.

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 cannot be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the very low tonnage of non-fish origin processed animal proteins that were imported from US into GB.

*** Overall, therefore, it is considered there is a greater than negligible risk that (non-ruminant) 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...

https://www.gov.uk/government/uploads/sy...ing-disease.pdf

Summary and MORE HERE ;

What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016

http://chronic-wasting-disease.blogspot.com/2016/04/what-is-risk-of-chronic-wasting-disease.html

10 years post mad cow feed ban August 1997

10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

PRODUCT

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

CODE

Cattle feed delivered between 01/12/2007 and 01/26/2007

RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.

REASON

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

42,090 lbs.

DISTRIBUTION

WI

___________________________________

PRODUCT

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

CODE

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

REASON

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

9,997,976 lbs.

DISTRIBUTION

ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm

16 years post mad cow feed ban August 1997

2013

Sunday, December 15, 2013

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

http://madcowusda.blogspot.com/2013/12/fda-part-589-substances-prohibited-from.html

17 years post mad cow feed ban August 1997

Monday, October 26, 2015

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015

http://madcowusda.blogspot.com/2015/10/fda-part-589-substances-prohibited-from.html

Tuesday, December 23, 2014

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

http://madcowusda.blogspot.com/2014/12/fda-part-589-substances-prohibited-from.html

2006 WAS A BANNER YEARS TOO FOR MAD COW PROTEIN IN COMMERCE IN USA. ...SNIP...END

Sunday, March 20, 2016

UPDATED MARCH 2016 Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission

http://www.fda.gov/downloads/AnimalVeter...rce=govdelivery

http://chronic-wasting-disease.blogspot.com/2016/03/docket-no-fda-2003-d-0432-formerly-03d.html

Subject: Re: TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES

***UDATED CORRECTION BY AUTHOR...SEE EMAIL TO ME...terry

From: Kyung-Min Lee Sent: Thursday, October 01, 2015 1:39 PM

To: Terry S. Singeltary Sr. ; BSE-L@LISTS.AEGEE.ORG

Cc: CJD-L@LISTS.AEGEE.ORG ; cjdvoice@yahoogroups.com ; bloodcjd@yahoogroups.com ; jcattanach@foodprotection.org ; cnc3@psu.edu ; dloynachan@foodprotection.org ; lhovey@foodprotection.org ; Timothy J. Herrman

Subject: RE: TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES

Dear Terry S. Singeltary Sr.

Thank for your interest and concern about our published article entitled “Evaluation of Selected Nutrients and Contaminants in Distillers Grains from Ethanol Production in Texas”. I should apologize you and others that there were some errors and misleading statements in this article due to inappropriate terminology. The statement you were concerned about was corrected to "One sorghum DDGS out of 168 DG samples was contaminated with animal protein prohibited for use in ruminant feed and was channeled to poultry feed." We requested the journal editor to correct some errors and the relevant statements, or to withdraw the article from the journal.

Again I sincerely apologize for any confusion and inconvenience this may cause. Thanks.

best wishes,

Kyung-Min

Kyung-Min Lee, Ph. D. Research Scientist Office of the Texas State Chemist

Texas A&M AgriLife Research P.O. Box 3160, College Station, TX 77841-3160 Phone: 979-845-4113 (ext 132) Email:kml@otsc.tamu.edu Fax: 979-845-1389

snip...end...tss

my link corrected

Sunday, September 27, 2015

TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES

http://bovineprp.blogspot.com/2015/09/texas-confirmation-of-bovine-spongiform.html

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/09/29003001.pdf

A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY

http://collections.europarchive.org/tna/20081105185647/http://www.bseinquiry.gov.uk/files/sc/Seac10/tab06.pdf

4.21 Three cases of SE’s with an unknown infectious agent have been reported in ostriches (Struthio Camellus) in two zoos in north west Germany (Schoon @ Brunckhorst, 1999, Verh ber Erkeg Zootiere 33:309-314). These birds showed protracted central nervous symptoms with ataxia, disturbances of balance and uncoordinated feeding behaviour. The diet of these birds had included poultry meat meal, some of which came from cattle emergency slaughter cases.

http://web.archive.org/web/20030331182151/http://www.bseinquiry.gov.uk/files/ws/s113.pdf

SE1806

TRANSMISSION STUDIES OF BSE TO DOMESTIC FOWL BY ORAL EXPOSURE TO BRAIN HOMOGENATE

1 challenged [censored] bird was necropsied (41 months p.i.) following a period of ataxia, tremor, limb abduction and other neurological signs. Histopathological examination failed to reveal any significant lesions of the central or peripheral nervous systems...

1 other challenged [censored] bird is also showing ataxia (43 months p.i.).

snip...

94/01.19/7.1

http://collections.europarchive.org/tna/20020525205812/http://bseinquiry.gov.uk/files/yb/1994/01/19007001.pdf

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/01/19007001.pdf

Saturday, January 9, 2016

Transmission of sheep-bovine spongiform encephalopathy to pigs Research article

http://transmissiblespongiformencephalop...spongiform.html

Saturday, April 16, 2016

APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission

http://animalhealthreportpriontse.blogspot.com/2016/04/aphis-docket-no-aphis-2016-0029.html

shoot the messenger if you must, I am full of holes, it will not change the facts. I don’t make this stuff up, and not all folks want to stick their head in the sand and ignore it, or at least they should not, imo. ...

have a nice day...

terry

So we are in 2016 are Purina and Lyssy and Echels putting ruminants in their Deer protein pellets?

"Well. I'll just go ahead and get this one locked too."

Let the Democrats run Amok

As long as it factual debate no reason to lock it. It's obvious Mr flounder is very passionate about the topic. Unfortunately some of his information is mis-information

Terry,

You have to accept the fact that all cervids and bovines will never be eliminated to make sure they can't spread diseases like alzheimers.

It's not going to happen. Too much money involved and we don't know for a fact it will eliminate the disease. Use your energy and passion to help with LIVE animal research to try to understand how to possibly cure it one day.

BOBO, you read it all and then "splain" it to the class, I got lost in the jargon

BTW, I did read enough to come to one firm conclusion, I "aint" feeding deer,,to my deer

I'll be honest after I read he sent a letter about animal protein being found in grain sorghum that ended up chicken feed( which means quality wise it wasn't human grade anyways), I stopped reading. A) chicken isn't a ruminant b) I'm not going to harvest milo by hand so that a rat or rabbit doesn't get sucked into a combine. C) I'm not going to stop drinking grain based vodka or whiskey, no mater what poops on it in the field. Nor am I going to stop using a manure based fertilizer from a feed lot where there has never been a case of Mad cow found EVER since no body has ever found mad cow in a cow under 30 months old.

Im still waiting to find out where we in the United States Feed deer..... deer and not cotton speed, soybean, alafafa and other legume based proteins.

I just want him to tell us where it's been devastating to a wild cervid population, and then explain (without cutting and pasting an entirely irrelevant book), where a govt agency has been successful in eradicating or having a statistically significant effect on limiting it.

He won't/can't so don't get too worked up about it.

Locally (not statewide) it has had devastating effects in individual counties in several states. Locally here in Texas, with a 36 month effective window from contraction to mortality a high infection rate would have horrible consequences for trophy deer production. Tell me what a 50% infection rate for 1 and 2 year old deer would do to the age structure of our deer herds? It would make it MUCH more difficult to get deer to 6 and 7 years old. The population may not go down, but the age structure would be decimated.

To the second question, look at the New York positive. There was CWD detected immediately outside the positive breeder facility in the wild. A cull was done, and to date no other positives have been found.

By devastating I mean on par with the effects of anthrax or EHD.

Please show me hard data stating that CWD (not govt snipers) has destroyed a wild population anywhere close to 80%.

In fact, the areas hardest hit in Wisconsin and Wyoming have been naturally rebounding in population.

And on the second, when a 100% cull is done l, how is that preferable to the natural process where CWD takes a small amount of deer? The killemall method really isn't preferable is it?

We have CWD in wild deer in Texas. Have for quite some time. It hasn't been a problem so far. My bet is it won't be. And nowhere near the level of anthrax/EHD. We have those periodically and guess what, we recover each time there's an outbreak.

Amazing huh? So please post the hard data to support your statements above, and tell me why CWD requires goverment intervention, when the really devastating diseases don't.

This is the first CWD post I've opened. I was wondering why they always get locked. Now I know and can continue to ignore them. Pardon the interruption.

Exactly. Why lock them when big boys and girls can choose to ignore what they want to ignore?

290 tests in one county one year. Last few years they average around 1933 tests state wide. With a harvest # of 238,672 white tails last year that's less then a percentage point of total harvest tested.

Are you sure they are looking for it?

In 50 years of CWD is there any area in the country where CWD has had a majority % of population die off from disease?

If I can recover from a 30% loss from EHD, I'm not sweating CWD. Especially since CO still has elk and mule deer 50years after they first observed it.

You don't understand statistics and epidemiology.

It's very easy to say "test the same percentage" etc etc

The fact of the matter is, in larger populations you dont have to test as many animals to find disease at a percentage prevalence.

If you only have 100 animals in a population you have to test all of them to determine a 1% prevalence. It's 1 animal.

In a herd of 4 million 1% prevalence is 40,000 animals. You don't have to test all 4 million before you find a positive.

The actual number is much smaller, and the testing done has greatly exceeded the requirements for the confidence levels.

For reference to how this is done look here: Specifically section 4.4.1

http://www.fao.org/wairdocs/ilri/x5436e/x5436e06.htm

There is a lot of misinformation out there. A lot of people are angry, but sound science is being followed.

As to EHD and Anthrax, I don't really get the argument. Anthrax is confined locally due to environmental conditions. EHD burns itself out because it kills so fast and the population can locally rebound. (It's less of a problem in Texas since our native deer are highly resistant)

One disease's ability to kill deer doesn't make another disease that kills deer less of a problem.

It's a problem we have a chance to get ahead of, and the prudent thing to do is to monitor and restrict artificial movement of deer to those practices that have been screened with the necessary safeguards to give us a high degree of confidence that that movement isn't spreading this disease.

Has nothing to do with understanding, you are either looking for CWD or You are appeasing. .8 of a percent is appeasing

Only mass herd loss CWD is responsible for is by Goverment extermination.

In that event the only plausible course of action via you and Flounder is mass elimination to extinction of a local population. On top of that with the affirmanation that grass can transport it, restocking an area after mass extermination is not feasible if you want to further prevent, there for half of CO and Wyoming should barren of ruminants until the ground is considered clean correct?

*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

http://jgv.sgmjournals.org/content/87/12/3737.full

***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.

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

Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

see ;

Potential role of soil properties in the spread of CWD in western Canada

Alsu Kuznetsova, Debbie McKenzie, Pamela Banser, Tariq Siddique & Judd M. Aiken

http://www.tandfonline.com/doi/pdf/10.4161/pri.28467

Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted Infectivity from Complex Solutions (BASICS)

Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted Infectivity from Complex Solutions (BASICS) A. Christy Wyckoff, Krista L. Lockwood, Crystal Meyerett-Reid, Brady A. Michel, Heather Bender, Kurt C. VerCauteren, Mark D. Zabel PLOS x Published: March 4, 2013 http://dx.doi.org/10.1371/journal.pone.0058630

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630

Behavior of Prions in the Environment: Implications for Prion Biology

Shannon L. Bartelt-Hunt1*, Jason C. Bartz2*

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf

Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of Prion Infection A. Christy Wyckoff1, 2 n1 , Nathan Galloway3 n1 , Crystal Meyerett-Reid1 , Jenny Powers4 , Terry Spraker1 , Ryan J. Monello4 , Bruce Pulford1 , Margaret Wild4 , Michael Antolin3 , Kurt VerCauteren2 […] & Mark Zabel1 - Show fewer authors Scientific Reports 5, Article number: 8358 (2015) doi:10.1038/srep08358 Download Citation

Molecular ecology Proteins Statistics Received: 27 June 2014

http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217

CELL REPORTS

Report

Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions

http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4

PRION UPDATE VIA VEGETABLE PLANTS FROM THE SOIL

56. Members considered that there is no evidence that crops grown on the land which received composted excreta from BSE-challenged animals pose a TSE risk to humans or animals. One member suggested that, as some of these animals are orally challenged with high doses of BSE-infected materials, and the distribution of infectivity in the digestive system is not completely understood, it might be premature to conclude that there is no infective agent in the manure.

Furthermore, an unpublished study had indicated low level absorption of PrP from soil by tomato plants although it should be noted that this study had not been repeated. Details of this work would be sent to the SEAC Secretary. Dr Matthews explained that most of the manure from animals challenged with high doses of BSE had already been composted and used for coppicing. Members agreed that the risks from disposal of residual manure from experimental animals would be much less than historic risks of on farm contamination from naturally infected animals at the height of the BSE epidemic. ...SNIP...END

http://www.seac.gov.uk/minutes/final91.pdf

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.

Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification

http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full

The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.

http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.

SUMMARY:

http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf

For Immediate Release Thursday, October 2, 2014

Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov

*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).

http://www.iowaagriculture.gov/press/2014press/press10022014.asp

*** see history of this CWD blunder here ;

http://www.iowadnr.gov/Portals/idnr/uploads/Hunting/070313_consent_order.pdf

On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.

http://www.iowadnr.gov/Portals/idnr/uploads/Hunting/060613_consent_order.pdf

The overall incidence of clinical CWD in white-tailed deer was 82%

Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)

https://cpw.state.co.us/Documents/Hunting/BigGame/CWD/PDF/ResearchArticles/JWDEpiCWD.pdf

”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.

http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

Wednesday, April 20, 2016

TVMDL hosts legislative representatives, discusses CWD

http://chronic-wasting-disease.blogspot.com/2016/04/tvmdl-hosts-legislative-representatives.html


kind regards, terry

I'm not in that camp.

We have not detected CWD in wild WTD populations in Texas that are unaffiliated with artificial transport of deer. This doesn't mean we won't.

The Mule Deer positives in West and North Texas are another issue, but lets use them here for a second. The state has not proposed large depopulation in West Texas. There are 3 stratified zones of risk with live animal and carcass movement restrictions.

The CWD issue in Whitetails has to this point been handled differently in Texas. CWD is scary for biologists, hunters, and landowners alike. All the tools for slowing the spread of the disease need to be on the table, but large scale depopulations (counties wide) have never eliminated the disease, only kept the prevalence rate in check. When those efforts stopped, prevalence rates went up.

Now do you destroy hunting opportunity in order to do that? That's a very hard balancing act.


It's a complicated problem. Just because it's complicated doesn't mean we can't do ANYTHING about it.

There you go AIM small. Per flounder Once CWD is found in a county the county and borders areas should be eradicated and barren of deer and elk for atleast 17 years!!!


So after looking at a map, a good quarter of native US deer and elk population should be exterminated.

Yeah, like I said, I don't agree with that. I was specifically making counterpoints to the arguments that you and therancher were making.

Transportation and carcass restrictions are the only feasible thing I support. Extermination doesn't work.

More we test the more counties in Texas will have positive hits. When you want to find something you test until you find it. History of ground zero has shown that CWD will not eliminate our herds.

I just saw that .

But same token if we where to eliminate it, assuming there isn't a genetic aspect to it(Arkansas/medina), it would take extermination of a massive level. At that point we are done as hunters and will have to rely on a 100% ag production. When that happens US will fail.

It will do what I said though, which is make it much harder to carry age classes to maturity.

How much of a shame would it be, after 70 years of topping off our age classes by harvesting young bucks, we finally learned our lesson, implemented antler restrictions and saw the success we have in the last 8 years all over the state. Only then, we ended up with a pervasive creeping disease that took us almost all the way back to where we started.

No one said that the deer POPULATION was a problem in east texas before antler restrictions. It was the age structure that was the problem.

Saying that it isn't going to be a problem, because we would have the same number of deer doesn't make sense. I personally am not interested in hunting 2 and 3 year olds.

South Carolina has a persistent problem that causes age structure destruction. It gives them problems raising many mature bucks at all, regardless of how little hunting pressure they put on them.

It's called a brain abscess.

http://www.deerandforests.org/resources/do-brain-abcesses-hinder-quality-deer-management-programs