A cool start to deer season, but challenges linger By Shannon Tompkins
A cool start to deer season, but challenges linger By Shannon
Tompkins
October 29, 2014 | Updated: October 29, 2014 11:00pm
another award winning article by Houston Chronicle Shannon Tompkins about
deer in Texas, and Mr. Tompkins absolutely refuses to acknowledge and about
warning/reminding hunters about Chronic Wasting Disease CWD in Texas. it seems
that since CWD was detected in Texas, Mr. Tomkins mind has completely forgot
about CWD. However, before CWD was detected in Texas, Mr. Tomkins found time to
write about how bad CWD was in other states. Just recently on October 22, 2014,
the TPWD released a news release stating ;
Mule Deer Hunters Reminded of CWD Testing Requirements
you would have thought the Houston Chronicle Shannon Tompkins would have
thought this an important enough news release to tell it’s readers about in this
full page article today A cool start to deer season, but challenges linger, but
not a word, not one single word. so I guess I might and try to update hunters in
Texas about CWD, since Mr. Tompkins and the Houston Chronicle refuse to do so.
oh, the silence is deafening...
Mule Deer Hunters Reminded of CWD Testing Requirements
News Release Media Contact: Steve Lightfoot, 512-389-4701,
steve.lightfoot@tpwd.texas.gov
Oct. 22, 2014
Mule Deer Hunters Reminded of CWD Testing Requirements AUSTIN – Wildlife
officials are reminding mule deer hunters and landowners in far West Texas about
the testing protocols required in the Texas Parks and Wildlife Department’s
(TPWD) Chronic Wasting Disease (CWD) Management Plan. The plan includes
mandatory check stations for susceptible species like elk and mule deer taken
inside the CWD Containment Zone, which covers portions of Hudspeth, Culberson,
and El Paso counties. A map of CWD zones can be found on the department’s
website at http://www.tpwd.state.tx.us/cwd.
The management plan was implemented after CWD was detected in tissue
samples from two mule deer in far West Texas during the summer of 2012. Those
were the first cases of CWD detected in Texas deer. Four more CWD-positive mule
deer were detected during the 2012-13 season, but no new CWD-positives were
detected last hunting season. Over 600 tissue samples have been collected for
CWD testing purposes from hunter-harvested deer and elk from the Trans Pecos
ecoregion the past two hunting seasons.
Texas Animal Health Commission (TAHC) and TPWD will also use the CWD check
stations in a cooperative effort to monitor for bovine tuberculosis (TB) in
Texas. The tissue samples used for this effort would be the same samples
currently collected as part of the ongoing CWD monitoring effort.
Hunters taking mule deer inside the Containment Zone during the 2014
general mule deer hunting season, Nov. 28 – Dec. 14, are required to submit
their harvest (unfrozen head) for CWD sampling at a check station within 24
hours of take.
“We recommend hunters in the Containment Zone and High Risk Zone quarter
deer in the field and leave all but the quarters, backstraps, and head at the
site of harvest if they are unable to bury the inedible carcass parts as deep as
possible on the ranch or take them to a landfill,” said Shawn Gray, Mule Deer
Program Leader for TPWD.
Mandatory check stations will be open from 9 a.m. to 9 p.m. Nov. 28 – Dec.
15. Stations will be located in Cornudas at May’s Café (on US 62-180) and in Van
Horn at the Van Horn Convention Center (1801 West Broadway).
Hunters who harvest deer in the Containment Zone outside the general season
under the authority of MLDP (Managed Lands Deer Permits) will need to call TPWD
at (512) 221-8491 the day the deer is harvested to make arrangements to have the
deer sampled for CWD.
In addition to protocols within the Containment Zone, TPWD has established
check stations for voluntary CWD sampling for susceptible species like elk and
deer harvested in other parts of West Texas. Biologists have been collecting
mule deer harvest data in the region since 1980 and this year CWD sampling will
once again be offered in addition to age and weight measurements.
Voluntary check stations will be established at the following locations
during the first three weekends of the general season, Saturday through Monday
(Nov. 29–Dec.1, Dec. 6–8, and Dec. 13–15), from 9 a.m. – 5 p.m. Saturday and
Sunday and 9 a.m. – 1 p.m. Monday:
Midland at Naturally Fresh (Deer Processor) (1501 Elwyn) Bakersfield at
Chevron Station (south of I10; Exit 294) Sanderson at Slim’s Auto Repair (823
West Oak; Intersection of US 90 and 285) Alpine at Hip-O Taxidermy (east side of
town on US 90, across from Dairy Queen) All deer brought to the check stations
this season will be aged as part of disease surveillance. Additional biological
information such as antler measurements and field dressed weights will also be
collected as time allows.
“CWD has not been detected anywhere outside of the Hueco Mountains,” said
Dr. Bob Dittmar, wildlife veterinarian with TPWD. “But adequate surveillance in
that part of West Texas depends on check stations and we appreciate the
cooperation and active participation of hunters and landowners in this
effort.”
For more information on CWD, please visit TPWD’s website at http://www.tpwd.state.tx.us/cwd or at
the Chronic Wasting Disease Alliance website, http://www.cwd-info.org.
Information on Bovine TB can be found on TAHC’ website, http://www.tahc.state.tx.us/animal_health/cattle_tb/cattle_tb.html
Saturday, November 23, 2013
TAHC REMINDS MULE DEER HUNTERS OF CWD TESTING REQUIREMENTS & CHECK
STATIONS November 22, 2013
Thursday, November 14, 2013
Deer don't disappoint after hunters' early optimism Houston Chronicle By
Shannon Tompkins November 13, 2013
CWD, Houston Chronicle, and CWD reporting, what happened ???
Thursday, December 27, 2012
CWD TSE PRION, dr. deer, shooting pen type game farms and ranchers, Texas,
TAHC, Houston Chronicle, all silent about disease ?
Thursday, December 13, 2012
HUNTERS FEELING THE HEAT Houston Chronicle December 13, 2012 OUTDOORS not
talking about CWD in Texas
Wednesday, November 07, 2012
Chronic Wasting Disease CWD, Texas, Houston Chronicle Shannon Thomkins 1998
- 2012 what happened ???
Thursday, July 12, 2012
CWD aka MAD DEER, ELK DISEASE TEXAS HOUSTON CHRONICLE Wednesday, July 11,
2012
CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS
Greetings TAHC et al,
A kind greetings from Bacliff, Texas.
In reply to ;
Texas Animal Health Commission (TAHC) Announcement October 27, 2011
I kindly submit the following ;
Sunday, November 30, 2008
Commentary: Crimes hurt essence of hunting
Commentary on Houston Chronicle article [below] by Dr. Thomas Pringle
From: tom@cyber-dyne.com
Date: Fri, 10 May 2002 11:03:29 –0800
To: shannon.tompkins@chron.com
Subject: nice cwd reporting Shannon,
My compliments on these superb CWD Houston Chronical articles: not mincing
words, they display an excellent -- and most rare -- journalistic understanding
of the origin and continuing spread of CWD. (A couple of technical points were
not quite on target, see bottom.)
It is really refreshing to see in print the probable origin as sheep
scrapie-to-penned cervids in 1967 at Foothills Research Station, after decades
of relentless PR out of Colorado DOW seeking to distance itself from
responsibility (and liability). Facility workers at Colorado Dept of Wildlife
commented on the similarity to scrapie already in 1967 but never autopsied any
of their many dead research animals until 1979, discovering immediately an
obvious spongiform encephalopathy.
By that time of course, release to the wild and transfer of surplus animals
to zoos, game farms, and sister facilities had seeded widespread dissemination
of the disease. This was subsequently aggravated by the explosive growth in game
farms and intra- and inter-state cervid shipping, which at industry insistence
was in essence unregulated (eg regulated by state ag dept boosters). It is not
just the shoot-deer-in-a-barrel industry --elk velvet nutriceutical was never
tested by anyone for abnormal prions despite its troublesome composition (the
market collapsed from live CWD exported to Korea).
DOW itself did nothing to change its practises or control the disease until
very recently. Only last year, in the face of published evidence [below] that
the disease is expected to transfer to humans at the same low efficency as BSE
(129 human deaths to date), did they back off from encouraging human consumption
of venison from the endemic area. Nebraska fish and game even offered a
deer-neck stew recipe on its web site, even though spinal cord was long known to
have high infectious titres.
State fish and game depts are basically unfenced game farms. They have a
commercial concession that allows them earn a salary from sale of antler tags.
This motivates them to set up winter feeding stations, watering holes, salt
blocks, control predators, fight CWD testing, anything and everything that
increases numbers and leads to more or continued sales. Unfortunately, practises
leading to high cervid concentrations and testing avoidance are highly conducive
to the spread of CWD.
States such as Montana require testing of every game farm cervid dead for
any reason and an accounting of each animal's provenance and disposition; other
states adopt a "don't look, don't find" policy of testing avoidance with no
monitoring whatsoever of facilities. Absence of evidence is not evidence of
absence when it comes to TSEs. This disease just does not go away on its own, be
it kuru in New Guinea or scrapie in the US.
Given the numbers of Texas game farms, massive importation statistics, and
the high likelihood of trace-backs to affected facilities, it would be most
surprising if CWD were not already entrenched in Texas along the lines of
Wisconsin. It really questionable if stonewalling really is in the industry's
best interest -- who is going to hunt in a state that fears to test? The longer
infectious foci are allowed to operate, the greater the probability of multiple
introductions into wild deer. To ban imports (only after everyone has finished
importing all they want) just locks the barn door after the horse is long gone.
Half-measures on prion diseases are worse than no measures because they put
off the day of reckoning while exacerbating it immensely. Wisconsin's hasty
policy of culling 15,000 wild deer, yet business as usual (no testing, no
trace-backs, no inspection, no recordkeeping, no culls) at its sacrosanct 535
game farms. will result in CWD in perpetuity. The focus is on temporary
abatement for purposes of hunter reassurance. Dr. Charles Southwick
southwic@stripe.colorado.edu is a good source of scientific information on cwd
control strategies.
A few technical notes. First, the word mutation is reserved for genetic
change affecting DNA. It is not applicable to mere protein conformational
changes and fibril formation seen in amyloid diseases such as Alzheimer and CWD.
Mutation has been ruled out in CWD amplification. The prion gene of hundreds of
CWD and non-CWD animals have been sequenced by Dr. O'Rourke at Pullman. There is
no counterpart to the mutations that cause 15% of human CJD, much to the
disappointment of DOW.
No TSE has ever been seen in natural populations of any wild animal
anywhere in the world, making Colorado's story of a natural pocket (by
coincidence located adjacent to Foothills and Sybille research stations) a bit
far-fetched. Now by golly another natural pocket has flared up next to a game
farm in Wisconsin. How about the supposed natural pocket adjacent to the
massively infected game farm in the Black Hills -- despite its import history,
the industry PR firm in Ketchum turned this around 180 degrees -- now it's the
wild animals infecting innocent game farms!?! There has invariably been a nexus
to intensive livestock operations, be that cows fed rendered cows, mink farms
fed downer cows or deer quartered in a scrapie research facility.
Second, the "best available scientific evidence" upon which public policy
is normally based (more studies are needed, they always are, but something must
be used for the interim) is that published by Byron Caughey's group at Rocky Mtn
labs (after two years of delay by co-author Mike Miller of DOW who controlled
sample access). A proxy test was used since human volunteers cannot be
considered. Transmission efficiencies to human were similar to BSE -- low, but
hardly reassuring given England's experience.
Third, CWD has already been experimentally transferred to 6-7 species
including rodents, primates, and bovids, as published in peer-reviewed
scientific journals. The first round of transmission can be inefficient in TSEs;
after that, no species barrier. It is really the human-to-human second round
(plasma donation, childhood vaccines, cornea transplants) that has cause the
greatest consternation in England. A Ft. Collins hunter/blood donor with
preclinical cwd-induced CJD would have no idea he is ill.
It is currently impossible to test humans for cwd-induced CJD because there
is no known signature. Rises in baseline CJD cannot be monitored, contrary to
CDC, because of very large numbers of missed diagnoses, swings in ascertainment
effort, and diagnostic changes.
Best wishes and keep up the good work! Tom
Dr. Thomas Pringle Sperling Biomedical Foundation 3295 Kincaid St. Eugene,
OR 97405
CWD archives
Wisconsin latest to be hit by deer brain disease
May 10, 2002
The Houston Chronicle by Shannon Tompkins
Wisconsin drew the black bean in the continent's expanding war with chronic
wasting disease, and that simple twist of fate promises to be expensive and
painful for the state's deer and human populations. It also serves as a sobering
study for Texas in what can happen when the poorly understood but invariably
fatal brain disease shows up in a state's wild deer herd.
Just three months after CWD was documented in a handful of white-tailed
deer taken by hunters in southwestern Wisconsin, the state is preparing to kill
thousands of deer; Gov. Scott McCallum is calling for a special session of the
state Legislature to address the issue; politicians are asking for millions of
dollars to fight CWD spread; and the hunting-based economies of the region are
preparing to take a stunning blow.
Add to that the uncertainty many of Wisconsin's 700,000 deer hunters are
expressing about the safety of eating venison, and you have the future of that
state's deer and deer hunting hanging in the balance. CWD is a recently
discovered transmissible spongiform encephalopathy that affects deer and elk. It
is similar to the TSE that causes "mad cow disease" in livestock, and which in
Europe "jumped" from infected livestock to humans as a variation of the TSE
Creutzfeldt-Jakob disease in humans.
The disease manifests itself via prions, or mutant proteins, which cause
deterioration of brain cells. The effects include loss of weight and muscle
control, blindness and dementia. There is no treatment and the disease is fatal.
CWD has been proved transmissible between deer and elk, but it has not been
shown to be transmittable to humans. But neither has it been proved
non-transmittable. The possibility, however minuscule, exists that a human could
contract the fatal disease.
Since it was discovered in 1967 in wild deer in the northeast corner of
Colorado, CWD has been a mystery. How it came to exist remains a question, but
the most accepted theory is that it is a mutation of a TSE called "scrapie"
found in sheep. A Colorado research facility that housed sheep, deer and elk in
close contact is assumed to have been the genesis of CWD.
The disease for most of the past three decades seems to have remained
localized in a small area of Colorado.
Interstate trade in "farmed" live elk and deer, some of which were infected
with CWD, is assumed to have begun the diseases' spread to other states.
CWD has been identified in a half-dozen states and a couple of Canadian
provinces, almost always associated with penned elk or deer.
The discovery of CWD in three wild deer in Wisconsin during a routine
sampling of hunter-taken animals stunned most wildlife scientists and managers.
The disease never had been documented east of the Mississippi River, and
never in an area where deer densities are as high as they are in Wisconsin.
The closest CWD cases were more than 900 miles from Wisconsin.
The discovery triggered a rush of states closing their borders to
importation of deer and elk.
Texas, which has for years been one of the major players in live deer and
elk traffic, shut its borders to all importation of deer and elk within a couple
of weeks of the Wisconsin discovery.
Wisconsin officials began addressing the issue by killing and testing 516
deer in the area that produced CWD-infected animals. (There is no certified
live-animal test for CWD; animals must be killed and brain or brain stem tissue
analyzed to document infection.)
When 11 of those 516 deer proved infected with CWD, the state's Department
of Natural Resources and politicians knew they had a severe problem.
In an effort to prevent the spread of CWD, Wisconsin wildlife officials are
proposing to kill every deer in a 287-square-mile (about 184,000 acres) area
where the infected deer have been found.
That will involve killing 14,000-15,000 deer, officials estimate.
Just how that will be accomplished remains a question. But the slaughter
almost certainly will begin next month.
CWD has become a white-hot political issue in the state, where fingers are
being pointed at agriculture officials who disregarded warnings about the
possibility of CWD-infected deer being brought into the state.
McCallum said this week he will call a special session of the state's
Legislature to address CWD-related issues such as regulation of feeding wild
deer, a practice that crowds deer together and is suspected of making it easier
for CWD to spread.
The Wisconsin Legislature has approved spending $ 4.4 million this year to
fight CWD. Officials say they need at least $ 22.5 million over the next three
years to contain CWD.
McCallum is asking the federal government for $ 18.5 million.
At least Wisconsin knows it has a CWD problem, and is addressing it. Other
states, including Texas, probably have CWD-infected deer within their borders.
But because they do no testing for the disease, they have no evidence of
its presence.
Other states are beginning to fashion CWD testing programs, though.
Iowa, which abuts the southwest corner of Wisconsin where the CWD-infected
deer have been found, this week announced it will begin collecting brain tissue
samples from road-killed deer and submitting them for CWD testing.
Iowa officials said they hope to collect 100-200 road-killed deer for
sampling each month.
Texas has no CWD testing program.
But the Texas Deer Association, a trade group representing many of the
state's 400-plus state-permitted deer and elk ranches, this past month promised
to put together a voluntary CWD monitoring program in cooperation with the Texas
Parks and Wildlife Department and Texas Animal Health Commission.
If the voluntary program is not accepted by TPWD and TAHC, the agencies
could issue regulations for mandatory CWD testing.
The issue will be discussed at May 29-30 TPW Commission meetings in Austin.
============end============
Mr. Thomkins, and Houston Chronicle, I think your disregard for concern
NOW, at least the same concern now, than you had back when the CWD TSE prion
disease was not on the other foot, I think your silence is deafening now, and
very disturbing, and is doing an injustice to your readers.
I wasted 12 years trying to get them to test, where New Mexico forced them
to test, i.e. White Sands Missle range side of Texas, and there about. course, I
did the same with mad cow disease too. to no avail. $$$
2001 – 2002
Subject: CWD testing in Texas
Date: Sun, 25 Aug 2002 19:45:14 –0500
From: Kenneth Waldrup
To: flounder@wt.net
CC: mcoats@tahc.state.tx.us
Dear Dr. Singletary,
In Fiscal Year 2001, seven deer from Texas were tested by the National
Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed
deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer).
During these two years, an additional six elk and one white-tailed deer were
tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal
Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least
eight other white-tailed deer have been tested at TVMDL. One elk has been tested
at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke
of the Texas Parks and Wildlife Department also has records of 601 clinically
ill white-tailed deer which were necropsied at Texas A&M during the late
1960's and early 1970's, and no spongiform encepalopathies were noted.
Thank you for your consideration.
Ken Waldrup, DVM, PhD Texas Animal Health Commission
========================
TEXAS CWD STATUS
Captive Cervids
There have been no reported CWD infections of captive elk or deer in Texas.
There is currently no mandatory surveillance program for susceptible cervids
kept on game farms, although, there has been voluntary surveillance since 1999,
which requires owners of participating herds to maintain an annual herd
inventory and submit samples for all mortalities of animals over 16 months of
age.
snip...
SO, i thought i would just see where these Ecoregions were, and just how
the CWD testing was distributed. YOU would think that with the cluster of CWD
bordering TEXAS at the WPMR in NM, you would have thought this would be where
the major CWD testing samples were to have been taken? wrong! let's have a look
at the sample testing. here is map of CWD in NM WPMR bordering TEXAS;
NEW MEXICO 7 POSITIVE CWD WHITE SANDS MISSILE RANGE MAP
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging
Cervids and see where the CWD cluster in NM WSMR borders TEXAS;
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
Ecoregions of TEXAS
IF you look at the area around the NM WSMR where the CWD cluster was and
where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my
Geography and my Ciphering is correct ;-) that region only tested 55% of it's
goal. THE most important area on the MAP and they only test some 96 samples,
this in an area that has found some 7 positive animals? NOW if we look at the
only other border where these deer from NM could cross the border into TEXAS,
this area is called the High Plains ecoregion, and again, we find that the
sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD
sampling was met, only 16 samples were tested from some 175 that were suppose to
be sampled.
AS i said before;
> SADLY, they have not tested enough from the total population to
> know if CWD is in Texas or not.
BUT now, I will go one step further and state categorically that they are
not trying to find it. just the opposite it seems, they are waiting for CWD to
find them, as with BSE/TSE in cattle, and it will eventually...
snip...end...TSS
===============================
2005
SEE MAP OF CWD ON THE BORDER OF NEW MEXICO VERY CLOSE TO TEXAS ;
NO update on CWD testing in Texas, New Mexico that i could find. I have
inquired about it though, no reply yet...
-------- Original Message --------
Subject: CWD testing to date TEXAS ?
Date: Mon, 09 May 2005 12:26:20 –0500
From: "Terry S. Singeltary Sr."
To: kristen.everett@tpwd.state.tx.us
Hello Mrs. Everett,
I am most curious about the current status on CWD testing in Texas. could
you please tell me what the current and past testing figures are to date and
what geographical locations these tests have been in. good bust on the illegal
deer trapping case. keep up the good work there.........
thank you, with kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
-------- Original Message --------
Subject: CWD testing in New Mexico
Date: Mon, 09 May 2005 14:39:18 –0500
From: "Terry S. Singeltary Sr."
To: ispa@state.nm.us
Greetings,
I am most curious of the current and past CWD testing in New Mexico, and
there geographical locations...
thank you,
Terry S. Singeltary SR. CJD Watch
#################### https://lists.aegee.org/bse-l.html
####################
2006
----- Original Message -----
From: "Terry S. Singeltary Sr." flounder9@VERIZON.NET
To: BSE-L@aegee.org
Sent: Saturday, December 23, 2006 1:47 PM
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing
sampling figures -- what gives TAHC ???
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing
sampling figures -- what gives TAHC ???
Date: December 23, 2006 at 11:25 am PST
Greetings BSE-L members,
i never know if i am going crazy or just more of the same BSe. several
years ago i brought up the fact to the TAHC that CWD was literally at the Texas
borders and that the sample size for cwd testing was no where near enough in the
location of that zone bordering NM. well, i just wrote them another letter
questioning this again on Dec. 14, 2006 (see below) and showed them two
different pdf maps, one referencing this url, which both worked just fine then.
since then, i have NOT received a letter from them answering my question, and
the url for the map i used as reference is no longer working? i had reference
this map several times from the hunter-kill cwd sampling as of 31 August 2005
pdf which NO longer works now??? but here are those figures for that zone
bordering NM, for those that were questioning the url. the testing samples
elsewhere across Texas where much much more than that figure in the zone
bordering NM where CWD has been documented bordering TEXAS, near the White Sands
Missile Range. SO, why was the Texas hunter-kill cwd sampling as of 31 August
2005 document removed from the internet??? you know, this reminds me of the
infamous TEXAS MAD COW that i documented some 7 or 8 months before USDA et al
documented it, when the TAHC accidentally started ramping up for the
announcement on there web site, then removed it (see history at bottom). i am
not screaming conspiracy here, but confusious is confused again on the ciphering
there using for geographical distribution of cwd tissue sample size survey, IF
they are serious about finding CWD in TEXAS. common sense would tell you if cwd
is 35 miles from the border, you would not run across state and have your larger
samples there, and least samples 35 miles from where is what
found..........daaa..........TSS
THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of
Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare
to the other sample locations ;
snip...see full text ;
here are a few of my pleas to the TAHC about CWD waltzing into Texas for
over a decade. see history of my failed attempts to get the TAHC to start
testing for CWD in far west Texas started back in 2001 – 2002 ;
Saturday, July 07, 2012
TEXAS Animal Health Commission Accepting Comments on Chronic Wasting
Disease Rule Proposal
Considering the seemingly high CWD prevalence rate in the Sacramento and
Hueco Mountains of New Mexico, CWD may be well established in the population and
in the environment in Texas at this time.
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Thursday, March 14, 2013
TEXAS DEER BREEDERS CHEER TWO NEW BILLS SB 1444 AND HB 2092 THAT COULD HELP
POTENTIALLY ENHANCE CHRONIC WASTING DISEASE CWD
Thursday, October 03, 2013
*** TAHC ADOPTS CWD RULE THAT the amendments _REMOVE_ the requirement for a
specific fence height for captives
Texas Animal Health Commission (TAHC)
ANNOUNCEMENT
October 3, 2013
Wednesday, October 23, 2013
Steve Lightfoot: West Texas Mule Deer rules CWD Management Plan mandatory
check stations for harvested mule deer taken inside the CWD Containment Zone
*** 2014 CHRONIC WASTING DISEASE CWD UPDATE ***
Saturday, October 18, 2014
Chronic wasting disease threatens Canadian agriculture, Alberta MLA
says
Thursday, October 23, 2014
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
Tuesday, October 21, 2014
Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer
Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE
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
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
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets?
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM
Saturday, October 25, 2014
118th USAHA Annual Meeting CWD and Captive Cerivds
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature. Acknowledgments.
Supported by NIH grant RO1-NS-061902 and grant D12ZO-045 from the Morris Animal
Foundation.
*** We conclude that TSE infectivity is likely to survive burial for long
time periods with minimal loss of infectivity and limited movement from the
original burial site. However PMCA results have shown that there is the
potential for rainwater to elute TSE related material from soil which could lead
to the contamination of a wider area. These experiments reinforce the importance
of risk assessment when disposing of TSE risk materials.
*** The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
Sunday, November 3, 2013 Environmental Impact Statements; Availability,
etc.: Animal Carcass Management [Docket No. APHIS-2013-0044]
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
UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION
CONGRESS SEPTEMBER 8-11 2010
Sunday, August 19, 2012
Susceptibility of cattle to the agent of chronic wasting disease from elk
after intracranial inoculation 2012
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
Thursday, November 21, 2013
*** Assessing the susceptibility of transgenic mice over-expressing deer
prion protein to bovine spongiform encephalopathy
The present study was designed to assess the susceptibility of the
prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy
(BSE) prions, which have the ability to overcome species barriers.
Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a
90-100% attack rates, BSE from cattle failed to transmit, indicating agent
adaptation in the deer.
*** 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.
NOW, what is the latest on human risk factors to CWD strains ???
*** 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.
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.
>>>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.
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 to 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
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 ;
***********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 for all exposures), while the other exposures ceased
to be 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 ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb**************
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
*** 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. ***
snip...see full text ;
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
*** We hypothesize that both BSE prions and CWD prions passaged through
felines will seed human recPrP more efficiently than BSE or CWD from the
original hosts, evidence that the new host will dampen the species barrier
between humans and BSE or CWD. The new host effect is particularly relevant as
we investigate potential means of trans-species transmission of prion disease.
Monday, August 8, 2011
*** Susceptibility of Domestic Cats to CWD Infection ***
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M.
Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K.
Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness.
*** Two of these cats have developed rear limb ataxia. Although the limited
data from this ongoing study must be considered preliminary, they raise the
potential for cervid-to-feline transmission in nature.
AD.63:
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado
State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN
USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to
the domestic cat, thus raising the issue of potential cervid-to- feline
transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
FELINE SPONGIFORM ENCEPHALOPATHY FSE
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose
DOCUMENT ID: APHIS-2006-0118-0411
***Singeltary submission
Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program
Standards
>>>The CWD herd certification program is a voluntary, cooperative
program that establishes minimum requirements for the interstate movement of
farmed or captive cervids, provisions for participating States to administer
Approved State CWD Herd Certification Programs, and provisions for participating
herds to become certified as having a low risk of being infected with
CWD<<<
Greetings USDA/APHIS et al,
I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting
Disease Herd Certification Program and Interstate Movement of Farmed or Captive
Deer, Elk, and Moose; Program Standards.
I believe, and in my opinion, and this has been proven by scientific facts,
that without a validated and certified test for chronic wasting disease cwd,
that is 100% sensitive, and in use, any voluntary effort will be futile. the
voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow
surveillance program has failed terribly, as well as the testing for bse tse
prion in cattle, this too has failed terrible. all this has been proven time and
time again via OIG reports and GOA reports.
I believe that until this happens, 100% cwd testing with validated test,
ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO
INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.
In my opinion, and the opinions of many scientists and DNR officials, that
these so called game farms are the cause of the spreading of chronic wasting
disease cwd through much negligence. the game farms in my opinion are not the
only cause, but a big factor. I kindly wish to submit the following to show what
these factors are, and why interstate movement of cervids must be banned.
...
snip...see full text and PDF ATTACHMENT HERE ;
Sunday, June 23, 2013
National Animal Health Laboratory Network Reorganization Concept Paper
(Document ID APHIS-2012-0105-0001)
***Terry S. Singeltary Sr. submission
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population CWD TSE PRION
disease in cervids
***SINGELTARY SUBMISSION
The Scottish Parliament’s Rural Affairs, Climate Change and Environment
Committee has been looking into deer management, as you can see from the
following press release,
***and your email has been forwarded to the committee for information:
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population
Sunday, July 21, 2013
Welsh Government and Food Standards Agency Wales Joint Public Consultation
on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations
2013
*** Singeltary Submission WG18417
TSS
posted by Terry S. Singeltary Sr. at
11:05 AM
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