Greetings,
I am amazed, and concerned, that the Houston Chronicle can put out a
complete paper magazine addition in the Sunday Paper about Deer Hunting in Texas
(and other hunting) Sunday 25, 2012, (32 pages), promoting it, ‘’come on down,
the water is fine” type mentality, but yet not mention a word of the fact that
after trying to hide CWD for a decade, by not testing properly, and only after
having New Mexico force Texas to finally test in the very place I told TAHC and
Shannon Thomkins and the Houston Chronicle some 10 years ago, and every year
there from, to date, they finally documented CWD, yet not a word, NOT A WORD
from the chronicle in this magazine about it. I find that very deceiving, and
very disturbing, that the Houston Chronicle and Shannon Thomkins, when in comes
to TEXAS and CWD, I find it very disturbing that you have decided to stick you
head in the sand, look the other way, and ignore this. that’s why we are in this
mess, TSE prion disease. Mr. Thomkins wrote a few good articles in the past,
when CWD was NOT documented in Texas, but where is your pen at now Mr. Thomkins,
when we finally are forced into documenting it ??? where is your pen now Sir ???
you are a prized and honored author of the wild, where is your ink now Sir, when
we need it the most? you may think ehd is more concerning than the TSE prion
disease CWD, but I can assure you, don’t let the incubation period, and the fact
of transmission between species, and the lateral transmission, environmental
factors, I can assure you, you will only fool yourself and your readers. they
are both deadly diseases.
A huge difference the type ink you have now Sir, when the shoe is on the
other foot, compared to years past, when Texas was one of the elites i.e. had
the gold card, i.e. CWD free. same as with BSE aka mad cow, everything was just
fine, as long as the other states, countries had it, but when the shoe was put
on the other foot there, my oh my, how things changed then.
it’s all about money, and that is what keeps spreading this damn disease
i.e. the TSE prion mad cow type disease.
I think (my opinion), you have done a great harm to your readers, by making
lite of the cwd recently discovered in Texas, and this recent magazine shows it.
It would have been a great opportunity to educate your readers, and even a word,
let alone a sentence, or maybe even a whole paragraph, wow, would that have been
nice, I know a complete page would have been too much$
big difference here in Texas when the TSE prion shoe is on the other foot.
...
Brain-eating disease found in Texas deer
By Shannon Tompkins Updated 5:47 a.m., Wednesday, July 11, 2012
Two mule deer taken recently from west Texas tested positive for Chronic
Wasting Disease, the first time the invariably fatal illness affecting deer and
other cervids has been documented in Texas, adding urgency to proposals by
wildlife and animal health officials to prohibit or severely restrict movement
of susceptible animals from that corner of the state.
"This is definitely not a crisis," Clayton Wolf, wildlife division director
for Texas Parks and Wildlife Department, said of the confirmation Monday from
the National Veterinary Services Laboratories that two of 31 mule deer shot
along the Texas/New Mexico border were infected with the incurable disease which
can be spread to other cervids. The wildlife agency shot the animals as part of
a plan monitoring the disease.
The agency and the Texas Animal Health Commission want to impose
regulations aimed at minimizing risks of the disease spreading to other parts of
Texas. The commission in June proposed regulations establishing a "containment
zone" covering El Paso County and portions of Hudspeth and Culberson counties
and a "high-risk zone" covering portions of Culberson and Reeves counties from
which movement of privately-owned cervids susceptible to the disease would be
prohibited or restricted. The deer that tested positive were taken from the
Hueco Mountains in El Paso and Hudspeth counties.
The wildlife agency plans later this month to officially propose similar
rules which would cover movement of wild deer or captive deer held under agency
permits.
what a difference a decade makes. seems to be different kind of ink. I know
the science has not found anything to change the CWD TSE prion agent, and risk
factors there from, only that it’s in Texas now. ...
Tompkins: There are a lot of reasons to be concerned about CWD
SHANNON TOMPKINS, Copyright 2002 Houston Chronicle Published 5:30 a.m.,
Thursday, March 14, 2002
Today, most Texas deer hunters probably yawn at the mention of Chronic
Wasting Disease. After all, the number of wild deer documented as killed,
nationwide, by the unusual malady probably is less than annually are crushed by
tractor-trailer rigs scorching Interstate 10 between Kerrville and Fort
Stockton.
And, so far, no cases of the fatal, incurable, communicable,
brain-destroying cervid disease have been documented in Texas.
What's so bad about a little-understood disease responsible for the death
of scattered pockets of deer in a handful of Rocky Mountain states?
If Texas' deer herd survived screwworms and can thrive despite endemic
bluetongue and anthrax and even the constant gnawing away of habitat, then why
worry about a little Chronic Wasting Disease?
There is abundant reason to be concerned.
CWD carries potential for incredible impacts on Texas' 4 million deer, its
half-million deer hunters, the hunting-based economy of rural areas and private
landowners and even the future of the state agency responsible for overseeing
those deer and all other natural resources.
Just how seriously many Texas wildlife managers and those with economic or
other interest in deer take the CWD threat was manifestly evident over the past
week.
In the wake of news that Wisconsin officials had discovered CWD in three of
26 wild deer taken by hunters in a small area of that state, Katharine Armstrong
Idsal, presiding officer of the Texas Parks and Wildlife Commission, called an
emergency meeting of the TPW Commission to address the issue of deer importation
into Texas.
A proposal to suspend all imports of deer into Texas was, and is, on the
TPW Commission's agenda for its scheduled April 4 meeting, with the
recommendation having been triggered by discovery over the past few months of
CWD in wild deer in Nebraska and South Dakota.
The emergency TPW Commission meeting was arranged Friday, the day the Texas
Wildlife Association, a politically active, landowner-based organization, sent
to the governor, members of the Legislature and the TPW Commission a resolution
calling for sealing the state's borders to deer imports because of the chance
some might be carrying CWD.
At the TPW Commission's hastily called Monday meeting, the group approved
and adopted an emergency rule prohibiting importation of white-tailed and mule
deer into Texas.
That emergency rule, which is effective for 45 days, took effect Tuesday.
It is the first time the TPW Commission has used its emergency rule-making
authority.
Justifications for the emergency action were laid out in the preamble to
the regulation change. CWD, the document states, "constitutes a direct threat to
wild deer populations in Texas and therefore to the multi-billion dollar hunting
industry, as well as a potential threat to human health, safety and
welfare."
To understand the threat to deer and, perhaps, public health and the
subsequent potentially devastating impact on Texas' deer-based economy, it's
necessary to understand CWD.
CWD is one of a group of transmissible spongiform encephalopathies (TSE)
diseases that destroy brain cells. Triggering the destruction is a prion, an
abnormal form of protein. The prion mutates normal cellular protein into the
abnormal form.
This "eats away" at the brain and damages an infected animal's ability to
maintain normal functions such as converting food and body fat to energy.
Animals suffering from CWD begin wasting away as their body tries to
convert protein to energy, a very inefficient process.
Eventually, the animal loses motor control and even goes blind, giving rise
to the pitiful "blind staggers" seen in livestock suffering from CWD's close
relative, Bovine Spongiform Encephalopathy, better known as "Mad Cow
Disease."
Death is inevitable and horrible.
Scientists know relatively little about CWD.
"We don't really know what triggers it. Does the prion create the disease
or does the disease create the prion?" said Jerry Cooke, game mammal branch
chief of the Texas Parks and Wildlife Department's wildlife division. "What we
do know is that it is transmissible to other cervids."
First documented in the 1960s in penned herds in Colorado, CWD "jumped"
into the wild cervid population there, being confirmed in wild deer and elk in
the 1980s.
A common suspicion is that CWD is a mutated form of "scrapie," a TSE long
confined to sheep.
There is some evidence that the cervids in the Colorado pen where CWD was
first documented were fed protein feeds containing sheep parts and that those
parts could have contained brain material infected with scrapie.
One of the scrapie-triggering prions might have mutated just enough to
break the molecular barrier of a deer's brain cell, and the disease was off and
running.
Scientists are convinced CWD is spread by close contact between uninfected
and infected animals. That can happen between animals in a pen or behind a
fence, or by nose-to-nose contact between deer or elk inside the fence and those
outside the enclosure.
From Colorado, CWD spread throughout the northwest corner of the state into
wild herds in Wyoming and Nebraska.
Its spread was accelerated over the past decade by a burgeoning market in
deer and elk triggered by elk farming and deer ranching.
Thousands of deer and elk are bought and transported each year, most to
penned facilities where they are either raised for food or, in the case of
white-tailed deer, used in an effort to produce bucks with large antlers to feed
a market in trophy hunting.
To test for CWD, brain tissue is needed. And such tissue samples can be
obtained only if the animal is dead.
Plus, getting rid of the disease has proved difficult, if not impossible,
even in penned facilities.
In at least one case, a penned facility holding CWD-infected deer was
"depopulated" (the animals slaughtered and destroyed) and the site left with no
animals for three years.
When uninfected deer were placed in the pens, they contracted CWD.
As deer and elk from areas with CWD have been traded and transported across
the nation, they have brought the disease with them
Currently, CWD-infected, free-ranging deer have been confirmed in Colorado,
Nebraska, Wyoming, South Dakota and Wisconsin, plus the Canadian province of
Saskatchewan.
CWD has been found in captive herds in Saskatchewan, Colorado, South
Dakota, Nebraska, Kansas, Oklahoma and Montana.
Texas has been a big player in the deer trade over the past decade, as
hundreds of deer-breeding facilities have sprung up in the state to feed the
interest in building bucks with bigger antlers.
Today, more than 450 individuals in Texas hold a TPWD-issued "scientific
breeder permit" allowing them to manipulate deer. Some of these breeders and
other landowners over the past four years have imported 2,107 deer from outside
Texas.
Because deer can be traded so often -- a deer may be sold as a fawn in
Nebraska to a broker in Missouri who sells it to a breeder in Pennsylvania who
sells it to a landowner in Texas -- it often is nearly impossible to determine
the provenance of individual animals.
Whether any of the thousands of deer imported into Texas over the past
decade carried CWD remains an unsettling question.
Texas has no CWD-testing program for wild deer and only a voluntary program
for elk and other animals under the jurisdiction of the Texas Animal Health
Commission.
"Ten years ago, elk and deer (imported into Texas) were not regulated at
all," said Dr. Ken Waldrup, an epidemiologist with the Texas Animal Health
Commission and one of the agency's point men on CWD. "If Texas doesn't already
have CWD, then I say that proves that God is a Texan.
"For everyone's sake, I sure hope He is."
CWD has not been proved to be transmissible to any animal other than deer
and elk.
But that was the original thought with BSE, which did "jump" into humans
who ate BSE-infected meat in Europe and contracted Creutzfeldt-Jakob Disease
(CJD), the human form of TSE. CJD, like CWD and BSE, is fatal, incurable and
untreatable. It is blamed for at least 80 deaths in Europe.
While there is no proof CWD can jump to humans, there is no absolute proof
it can't if given enough opportunities.
And that issue scares wildlife managers.
If CWD shows up in a deer herd and the deer-hunting public gets spooked
about the possibility -- no matter how tiny -- that by cleaning or eating a deer
they will contract CJD and face a certain and horrible death, they could, en
masse, abandon deer hunting.
This could destroy the $2 billion-plus deer hunting economy in Texas.
Also, if deer hunters abandon their recreation, natural resource agencies
such as TPWD, which depend almost entirely on hunting license fees to fund their
diverse wildlife programs, would be maimed, perhaps mortally.
"It's not the immediate impact on the deer herds that (is) the most
frightening thing about CWD," Waldrup said. "It's the secondary impacts that are
really scary.
"People better just pray it doesn't show up here. If it does, things could
get very ugly."
Shannon Tompkins covers the outdoors for the Chronicle. His column appears
Thursdays, Fridays and Sundays.
now, don’t get me wrong Mr. Thompkins, you have written some great articles
on the wild and on the fisheries.
snip...tss
but Mr. Thomkin Sir, you have written some great articles. a few here ;
Sunday, November 30, 2008
Commentary: Crimes hurt essence of hunting
Commentary on Houston Chronicle article [below] by Dr. Thomas Pringle
Date: Fri, 10 May 2002 11:03:29 –0800
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
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 ;
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
Saturday, August 25, 2012
Missouri Suspends Issuing Permits for New Deer Breeders and Big-game
Hunting Facilities
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B). SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5).
PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B).
Friday, August 24, 2012
Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting
disease within white-tailed deer (Odocoileus virginianus) herds in North America
Tuesday, June 05, 2012
Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012
Legislative Session
Saturday, June 09, 2012
USDA Establishes a Herd Certification Program for Chronic Wasting Disease
in the United States
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol
Needs To Be Revised
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
Monday, November 14, 2011
WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Sunday, November 13, 2011
COLORADO CWD CJD TSE PRION REPORTING 2011
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation,
although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This
finding raised concerns that CWD prions might be transmitted to cattle grazing
in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight,
revealed abnormal clinical signs, and were euthanatized. Laboratory tests
revealed the presence of a unique pattern of the disease agent in tissues of
these animals. These findings demonstrate that when CWD is directly inoculated
into the brain of cattle, 86% of inoculated cattle develop clinical signs of the
disease.
" although the infection rate was low (4 of 13 animals [Hamir et al.
2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly
as possible all updates/comments that contribute substantially to the topic
under discussion.
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author
Affiliations
1Institute for Neurodegenerative Diseases, University of California, San
Francisco, San Francisco, California 94143 2Department of Neurology, University
of California, San Francisco, San Francisco, California 94143 Correspondence:
stanley@ind.ucsf.edu
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As
the only prion disease identified in free-ranging animals, CWD appears to be far
more communicable than other forms of prion disease. CWD was first described in
1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of
histopathology of the brain. Originally detected in the American West, CWD has
spread across much of North America and has been reported also in South Korea.
In captive populations, up to 90% of mule deer have been reported to be positive
for prions (Williams and Young 1980). The incidence of CWD in cervids living in
the wild has been estimated to be as high as 15% (Miller et al. 2000). The
development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible
to CWD, has enhanced detection of CWD and the estimation of prion titers
(Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces,
even in presymptomatic deer, has been identified as a likely source of infection
for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD
has been transmitted to cattle after intracerebral inoculation, although the
infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding
raised concerns that CWD prions might be transmitted to cattle grazing in
contaminated pastures.
snip...
----- Original Message -----
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor
Department of Chemical Engineering University of Delaware
====================END...TSS==============
SNIP...SEE FULL TEXT ;
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
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that 1) infected deer could serve
as a reservoir to infect sheep with scrapie offering challenges to scrapie
eradication efforts and 2) CWD spread need not remain geographically confined to
current endemic areas, but could occur anywhere that sheep with scrapie and
susceptible cervids cohabitate. This work demonstrates for the first time that
white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation
with a high attack rate and that the disease that results has similarities to
CWD. These experiments will be repeated with a more natural route of inoculation
to determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. The purpose
of these experiments was to determine susceptibility of white-tailed deer (WTD)
to scrapie and to compare the resultant clinical signs, lesions, and molecular
profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD
intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral
and intranasal (IN); n = 5) with a US scrapie isolate. All deer were inoculated
with a 10% (wt/vol) brain homogenate from sheep with scrapie (1ml IC, 1 ml IN,
30 ml oral). All deer inoculated by the intracranial route had evidence of PrPSc
accumulation. PrPSc was detected in lymphoid tissues as early as 7
months-post-inoculation (PI) and a single deer that was necropsied at 15.6
months had widespread distribution of PrPSc highlighting that PrPSc is widely
distributed in the CNS and lymphoid tissues prior to the onset of clinical
signs. IC inoculated deer necropsied after 20 months PI (3/5) had clinical
signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural
and lymphoid tissues. The results of this study suggest that there are many
similarities in the manifestation of CWD and scrapie in WTD after IC inoculation
including early and widespread presence of PrPSc in lymphoid tissues, clinical
signs of depression and weight loss progressing to wasting, and an incubation
time of 21-23 months. Moreover, western blots (WB) done on brain material from
the obex region have a molecular profile similar to CWD and distinct from
tissues of the cerebrum or the scrapie inoculum. However, results of microscopic
and IHC examination indicate that there are differences between the lesions
expected in CWD and those that occur in deer with scrapie: amyloid plaques were
not noted in any sections of brain examined from these deer and the pattern of
immunoreactivity by IHC was diffuse rather than plaque-like. After a natural
route of exposure, 100% of WTD were susceptible to scrapie. Deer developed
clinical signs of wasting and mental depression and were necropsied from 28 to
33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB.
Similar to IC inoculated deer, samples from these deer exhibited two different
molecular profiles: samples from obex resembled CWD whereas those from cerebrum
were similar to the original scrapie inoculum. On further examination by WB
using a panel of antibodies, the tissues from deer with scrapie exhibit
properties differing from tissues either from sheep with scrapie or WTD with
CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive
when probed with mAb P4, however, samples from WTD with scrapie are only weakly
immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from
sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from
WTD with scrapie are strongly positive. This work demonstrates that WTD are
highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is
differentiable from CWD.
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
*** 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.
(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN,
AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY
PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF
FILE...TSS)
White-tailed Deer are Susceptible to Scrapie by Natural Route of
Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
LANCET INFECTIOUS DISEASE JOURNAL
Volume 3, Number 8 01 August 2003
Previous
Next
Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.
49-year-old Singeltary is one of a number of people who have remained
largely unsatisfied after being told that a close relative died from a rapidly
progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease
(CJD). So he decided to gather hundreds of documents on transmissible spongiform
encephalopathies (TSE) and realised that if Britons could get variant CJD from
bovine spongiform encephalopathy (BSE), Americans might get a similar disorder
from chronic wasting disease (CWD)the relative of mad cow disease seen among
deer and elk in the USA. Although his feverish search did not lead him to the
smoking gun linking CWD to a similar disease in North American people, it did
uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the
occurrence of CJD and CWD in the USA. Only a few states have made CJD
reportable. Human and animal TSEs should be reportable nationwide and
internationally, he complained in a letter to the Journal of the American
Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue
to expect us to still believe that the 85% plus of all CJD cases which are
sporadic are all spontaneous, without route or source.
Until recently, CWD was thought to be confined to the wild in a small
region in Colorado. But since early 2002, it has been reported in other areas,
including Wisconsin, South Dakota, and the Canadian province of Saskatchewan.
Indeed, the occurrence of CWD in states that were not endemic previously
increased concern about a widespread outbreak and possible transmission to
people and cattle.
To date, experimental studies have proven that the CWD agent can be
transmitted to cattle by intracerebral inoculation and that it can cross the
mucous membranes of the digestive tract to initiate infection in lymphoid tissue
before invasion of the central nervous system. Yet the plausibility of CWD
spreading to people has remained elusive.
Getting data on TSEs in the USA from the government is like pulling teeth,
Singeltary argues. You get it when they want you to have it, and only what they
want you to have.
SNIP...FULL TEXT ;
now, a few things to ponder about those said double fences that will
supposedly stop those deer from escaping.
what about water that drains from any of these game farms. surrounding
water tables etc., are the double fences going to stop the water from becoming
contaminated? where does it drain? who's drinking it?
Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic
Area
65
Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal
Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and
M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of
Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort
Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services,
United States Department of Agriculture, Fort Collins, Colorado, 80521, USA
3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA
4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory,
University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology,
Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging,
University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author-
tracy.a.nichols@aphis.usda.gov
Chronic wasting disease (CWD) is the only known transmissible spongiform
encephalopathy affecting free-ranging wildlife. Experimental and epidemiological
data indicate that CWD can be transmitted horizontally and via blood and saliva,
although the exact mode of natural transmission remains unknown. Substantial
evidence suggests that prions can persist in the environment, implicating it as
a potential prion reservoir and transmission vehicle. CWD- positive animals can
contribute to environmental prion load via biological materials including
saliva, blood, urine and feces, shedding several times their body weight in
possibly infectious excreta in their lifetime, as well as through decomposing
carcasses. Sensitivity limitations of conventional assays hamper evaluation of
environmental prion loads in water. Here we show the ability of serial protein
misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions
in spiked water samples at a 1:1 x106 , and protease-resistant prions in
environmental and municipal-processing water samples from a CWD endemic area.
Detection of CWD prions correlated with increased total organic carbon in water
runoff from melting winter snowpack. These data suggest prolonged persistence
and accumulation of prions in the environment that may promote CWD transmission.
snip...
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels. snip...end...full text at ;
what about rodents there from? 4 American rodents are susceptible to CWD to
date. are those double fences going to stop these rodents from escaping these
game farms once becoming exposed to CWD?
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A.
Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel
J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary
Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI
53706, USA 2US Geological Survey, National Wildlife Health Center, 6006
Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural
Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary
Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author
email: cjohnson@svm.vetmed.wisc.edu
We intracerebrally challenged four species of native North American rodents
that inhabit locations undergoing cervid chronic wasting disease (CWD)
epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed
mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles
(Myodes gapperi). The inocula were prepared from the brains of hunter-harvested
white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles
proved to be most susceptible, with a median incubation period of 272 days.
Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the
brains of all challenged meadow voles. Subsequent passages in meadow voles lead
to a significant reduction in incubation period. The disease progression in
red-backed voles, which are very closely related to the European bank vole (M.
glareolus) which have been demonstrated to be sensitive to a number of TSEs, was
slower than in meadow voles with a median incubation period of 351 days. We
sequenced the meadow vole and red-backed vole Prnp genes and found three amino
acid (AA) differences outside of the signal and GPI anchor sequences. Of these
differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is
particularly intriguing due its postulated involvement in "rigid loop" structure
and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5
years post-inoculation, but appear to be exhibiting a high degree of disease
penetrance. White-footed mice have an even longer incubation period but are also
showing high penetrance. Second passage experiments show significant shortening
of incubation periods. Meadow voles in particular appear to be interesting lab
models for CWD. These rodents scavenge carrion, and are an important food source
for many predator species. Furthermore, these rodents enter human and domestic
livestock food chains by accidental inclusion in grain and forage. Further
investigation of these species as potential hosts, bridge species, and
reservoirs of CWD is required.
please see ;
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. www.landesbioscience.com Prion
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.
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
Sunday, July 27, 2008
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer
and Elk in Animal Feed; Availability
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material
From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov
Greetings FDA,
i would kindly like to comment on;
Docket 03D-0186
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed; Availability
Several factors on this apparent voluntary proposal disturbs me greatly,
please allow me to point them out;
1. MY first point is the failure of the partial ruminant-to-ruminant feed
ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials
being fed back to cattle is terribly flawed. without the _total_ and _mandatory_
ban of all ruminant materials being fed back to ruminants including cattle,
sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for
human/animal consumption), this half ass measure will fail terribly, as in the
past decades...
2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of
deer fawns being infected with CWD, how many could possibly be sub-clinically
infected. until we have a rapid TSE test to assure us that all deer/elk are free
of disease (clinical and sub-clinical), we must ban not only documented CWD
infected deer/elk, but healthy ones as well. it this is not done, they system
will fail...
3. WE must ban not only CNS (SRMs specified risk materials), but ALL
tissues. recent new and old findings support infectivity in the rump or ass
muscle. wether it be low or high, accumulation will play a crucial role in
TSEs.
4. THERE are and have been for some time many TSEs in the USA. TME in mink,
Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has
been proven, but the TSE in USA cattle has been totally ignored for decades. i
will document this data below in my references.
5. UNTIL we ban all ruminant by-products from being fed back to ALL
ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient
numbers to find (1 million rapid TSE test in USA cattle annually for 5 years),
any partial measures such as the ones proposed while ignoring sub-clinical TSEs
and not rapid TSE testing cattle, not closing down feed mills that continue to
violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely
available those violations, will only continue to spread these TSE mad cow
agents in the USA. I am curious what we will call a phenotype in a species that
is mixed with who knows how many strains of scrapie, who knows what strain or
how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling
how many strains there), but all of this has been rendered for animal feeds in
the USA for decades. it will get interesting once someone starts looking in all
species, including humans here in the USA, but this has yet to happen...
6. IT is paramount that CJD be made reportable in every state (especially
''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family
of a victim of TSE. only checking death certificates will not be sufficient.
this has been proven as well (see below HISTORY OF CJD -- CJD
QUESTIONNAIRE)
7. WE must learn from our past mistakes, not continue to make the same
mistakes...
REFERENCES
snip...see full text ;
Saturday, May 26, 2012
Are USDA assurances on mad cow case 'gross oversimplification'?
SNIP...
What irks many scientists is the USDA’s April 25 statement that the rare
disease is “not generally associated with an animal consuming infected
feed.”
The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown,
one of the world’s experts on this type of disease who retired recently from the
National Institutes of Health. "(The agency) has no foundation on which to base
that statement.”
“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an
official with the USDA during the Clinton Administration now at Mississippi
State.
In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the
origins of atypical cases of BSE,” she said
The argument about feed is critical because if feed is the cause, not a
spontaneous mutation, the California cow could be part of a larger outbreak.
SNIP...
==============================================
Saturday, August 4, 2012
Final Feed Investigation Summary - California BSE Case - July 2012
=============================================
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE
INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
in the url that follows, I have posted
SRM breaches first, as late as 2011.
then
MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until
2007, when they ceased posting them.
then,
MAD COW SURVEILLANCE BREACHES.
Friday, May 18, 2012
Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy
(BSE) in the United States Friday May 18, 2012
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Monday, August 06, 2012
Atypical neuropathological sCJD-MM phenotype with abundant white matter
Kuru-type plaques sparing the cerebellar cortex
Wednesday, August 01, 2012
Behavioural and Psychiatric Features of the Human Prion Diseases:
Experience in 368 Prospectively Studied Patients
Monday, July 23, 2012
The National Prion Disease Pathology Surveillance Center July 2012
Monday, August 20, 2012
CASE REPORTS CREUTZFELDT-JAKOB DISEASE: AN UNDER-RECOGNIZED CAUSE OF
DEMENTIA
Friday, August 24, 2012
Iatrogenic prion diseases in humans: an update
kind regards, terry
layperson
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
flounder9@verizon.net
Friday, October 26, 2012
CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT PRODUCTS, BAITING, AND MINERAL LICKS
http://chronic-wasting-disease.blogspot.com/2012/10/chronic-wasting-disease-cwd.html
CWD TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the CWD TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the CWD TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
CWD TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
see full text ;
Friday, October 12, 2012
Texas Animal Health Commission (TAHC) is Now Accepting Comments on Rule Proposals for “Chronic Wasting Disease (CWD)”
TO:
comments@tahc.state.tx.us;
Texas Animal Health Commission (TAHC)
http://chronic-wasting-disease.blogspot.com/2012/10/texas-animal-health-commission-tahc-is.html
TSS
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