Thursday, July 12, 2012


Brain-eating disease found in Texas deer

By Shannon Tompkins

Updated 05:47 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.

The agency also plans to require hunters who harvest deer from the containment area this hunting season take the animals to one of two check stations to be set up in the area. Tissue samples for Chronic Wasting Disease testing will be taken from those hunter-checked deer.

Similar to Mad Cow

No reliable live-animal test exists for the disease, which destroys the deer's brain. The disease can be confirmed only by testing the brain stem of the animal, requiring the animal be killed.

While the disease has not been shown to be transmissible to humans, it is highly contagious to members of the deer family. Caused by a prion, a mutated protein, Chronic Wasting Disease is a transmissible spongiform encephalopathy similar to Mad Cow Disease in bovines and Cruetzfeldt-Jakob Disease in humans. The disease, which can incubate for as long as five years before manifesting clinical symptoms, causes deterioration of the brain.

Texas among 19 states

In deer herds where the disease has become established, as many as half the animals test positive for it. The disease is passed from animal to animal through contact with body fluids such as saliva, urine and feces. Also, "shed" prions can remain viable in the soil for at least two years and perhaps much longer, and can infect deer that ingest the infectious agent while feeding on forbs or other low-growing vegetation.

The disease was first identified in 1967 in captive mule deer in Colorado.

It has since spread, through natural movement of wild deer and human transportation of infected captive deer, to 18 states and two Canadian provinces. Texas is the 19th state to document the disease in its free-ranging or captive deer herd.

The discovery of Chronic Wasting Disease in the Hueco Mountains mule deer was not unexpected, said Wolf. Earlier this year, New Mexico reported mule deer taken by hunters within a couple of miles of the Texas border were confirmed having the disease.

"We knew it was a possibility," Wolf said. The surveillance program that produced the two deer and the drafting of containment plans was a response to the New Mexico cases.

State monitors deer

For 10 years, Texas has had an aggressive Chronic Wasting Disease prevention and monitoring program. Wildlife agency regulations prohibit importing deer into the state, and the agency has tested more than 26,000 hunter-taken deer and 7,400 animals from the captive-deer industry. None of those deer tested positive.

Maintaining a healthy deer herd is an economic and environmental positive for Texas. Recreational deer hunting annually generates an estimated $1.5 billion in economic impact, with the captive-deer industry adding about $650 million.


Brain-eating disease found in Texas deer

By Shannon Tompkins

Updated 05:47 a.m., Wednesday, July 11, 2012


Sunday, November 30, 2008

Commentary: Crimes hurt essence of hunting


Nov. 29, 2008, 8:30PM

Tompkins: There are a lot of reasons to be concerned about CWD

Published 05:30 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.

I kindly submit the following ;

From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Sun, 10 Mar 2002 08:12:51 -0800
Content-Type: text/plain
Parts/Attachments text/plain (281 lines)
########  Bovine Spongiform Encephalopathy   #########

March 9, 2002, 6:29PM
Move on deer importing may be too late
Copyright 2002 Houston Chronicle

Texas wildlife officials propose sealing the state's borders to
importation of white-tailed deer as part of a program they hope helps
prevent the state's private and public deer herds from being exposed to
Chronic Wasting Disease, a close relative of the more well-known Mad Cow

But, officials admit, the move may be too late to prevent CWD-infected
deer from entering the state and potentially devastating Texas' $2
billion deer hunting and deer ranching industry.

While no cases of CWD have been documented in Texas, the state has no
monitoring program targeting discovery of infected deer, either in
penned or wild herds.

And thousands of deer, some from states with CWD in their herds, have
been imported into Texas over the past several years.

"Right now, we don't know if we have CWD in Texas," said Jerry Cooke,
director of TPWD's upland wildlife programs. "We know we've had no
documented cases, but that doesn't necessarily mean it's not here. But
we certainly hope it's not."

Chronic Wasting Disease, or CWD, an untreatable, always-fatal disease
affecting the brain, has been spreading as deer and elk have been moved
around the nation by buyers and breeders.

First identified in penned deer and elk Colorado in the 1960s, CWD was
initially noted in the state's wild deer population in the mid-1980s.
Since then it has spread to wild populations in Wyoming, South Dakota,
Nebraska, Saskatchewan and, just announced this past week, Wisconsin.

It also has been identified in penned deer or elk herds in Oklahoma and

CWD is a form of transmissible spongiform encephalopathy, the same
disease family as bovine spongiform enchephalopathy that causes the "Mad
Cow Disease" that resulted in the slaughter of millions of head of
livestock in Britain and killed approximately 80 humans who contracted
BSE from infected meat.

So far, CWD has proved transmissible only to deer and elk. Most
scientists believe the chance of it infecting cattle or humans is low,
but note there is no definitive evidence to support that theory.

While CWD's effects are known -- it results in degeneration of brain
tissue -- its causes and transmission are poorly understood by scientists.

But it is obvious that CWD-infected deer can and have passed the disease
to other deer, particularly when many animals are in close quarters or
high concentrations such as those seen in many deer ranches.

It can take years for the disease to manifest itself in an animal, and
scientists do not know whether CWD is transmittable during that
incubation period.

Until the recent documentation of CWD in two wild whitetail fawns in
Nebraska, it seemed CWD affected only adult animals.

Also, no test is available to detect CWD in live animals. The only
dependable CWD test involves use of brain tissue, and animals must be
dead to take the tissue sample.

"This is an issue that scares every wildlife biologist to death," Doug
Humphreys of the Texas Parks and Wildlife Department's wildlife division
said of CWD's spread and its little-understood methods of transmission.
"Not only do we not know how deer get it, we don't know how to get rid
of it."

The Texas Animal Health Commission this past November ordered a
prohibition on importing deer and elk from Colorado.

But TAHC and TPWD officials, who have been working together to address
the CWD issue, are looking for a more effective way to prevent any
CWD-infected deer from entering the state.

While TAHC is moving toward passing regulatory changes that will give
the agency's executive director authority to unilaterally take action
that could include prohibiting import of deer and elk from other states,
it will take at least a few months for any such change to be approved by
the agency's commission.

In the interim, TPWD is moving to "suspend" deer imports until TAHC is
in a position to take the regulatory lead.

Under TPWD proposals published in the March 1 issue of the Texas
Register and set for consideration April 4 by the Texas Parks and
Wildlife Commission, the agency would cease issuing permits allowing
deer to be imported into the state.

Any out-of-state deer already in the state at the time of the ban taking
effect would not be affected by the prohibition.

If the commission approves the proposal, the import ban could take
effect as early as April 25.

Currently, almost anyone owning deer habitat can obtain a TPWD-issued
permit allowing them to purchase and import deer from out-of-state. Most
of those permits are obtained by some of the 450 or so individuals in
Texas holding TPWD-issued "scientific breeder permits."

Most of the private landowners and permitted deer breeders obtain those
animals in an effort to produce buck deer with large antlers, a
commodity that can bring the deer's owner tens of thousands of dollars
should the buck be used for breeding, sold to another breeder or sold to
a person wanting to shoot a heavy-antlered deer.

Over the past decade, thousands of deer have been imported into Texas
from other states.

The pace of importation has accelerated in past months as Texas wildlife
and animal health officials have voiced concerns about the possibility
some of those imported deer could be carrying Chronic Wasting Disease.

That concern intensified over the past two weeks as wildlife officials
in Wisconsin reported finding CWD in that state's wild deer herd.

Since 1996, Wisconsin's natural resource agency has conducted disease
testing on blood and tissue samples from deer taken by hunters.

Of the approximately 400 hunter-killed deer checked this past season,
three have tested positive for CWD so far, Wisconsin officials announced
this past week. All three animals were taken from a two-county area near

The findings, the first CWD cases east of the Mississippi River, shocked
state wildlife officials. The closest confirmed cases of CWD in deer had
been more than 900 miles away, in Nebraska and South Dakota.

But Wisconsin, like Texas, holds hundreds of "game farms" where owners
import and release deer and elk bought from other states.

A Wisconsin wildlife official in 1998 had alerted supervisors in that
state's Department of Natural Resources, its agriculture agency and the
governor's office that unless the state issued a moratorium on
importation of all "game farm animals," they risked a CWD outbreak.

That warning went unheeded.

Julia Langenberg. Wisconsin DNR veterinarian and administrator of its
deer testing program, told the Denver Post that she is certain CWD's
arrival in her state's deer herd was "human assisted," indicating it
arrived via imported animals.

About half the states in the United States currently prohibit
importation of deer and/or elk -- seven prohibit importation of all
"cervids," and 17 outlaw importation of white-tailed deer.

That number is certain to grow as states such as Texas, which has had a
liberal deer importation policy, begin considering sealing their borders
to deer imports.

"I would not be surprised to see a lot of other states take steps to
address deer imports in the wake of what's been happening over the past
year," said TPWD's Humphreys. "This (CWD) has a lot of people shaking in
their boots."

It also has a lot of Texas deer importers apparently rushing to get
out-of-state deer into the state before any prohibition takes effect.

In the 12-month period immediately prior to members of the TPW
Commission this past summer first publicly voicing concern over deer
imports, TPWD issued permits authorizing 470 white-tailed to be brought
into Texas from other states.

During the January-February 2001 reporting period, before talk of an
import ban, deer importers hauled 92 out-of-state deer into Texas.

During the just-ended January-February 2002 reporting period, that
number jumped to 243 deer, a 150 percent increase.

Those nearly 250 deer came from a dozen states and a Canadian province.

Two loads of them came from Wisconsin.

Shannon Tompkins


Greetings list Members,

did i read this correctly, did someone actually say;

[[So far, CWD has proved transmissible only to deer and elk. Most
scientists believe the chance of it infecting cattle or humans is low,
but note there is no definitive evidence to support that theory.]]

maybe they read this;-)

The EMBO Journal, Vol. 19, No. 17 pp. 4425-4430, 2000
© European Molecular Biology Organization

Evidence of a molecular barrier limiting
susceptibility of humans, cattle and sheep to
chronic wasting disease

G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O?Rourke3,
L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M.
and B. Caughey1,7

1NIAID/NIH Rocky Mountain Laboratories, Hamilton, MT 59840,
3USDA/ARS/ADRU, Pullman, WA 99164-7030, 4USDA/ARS/ABADRL,
Laramie, WY 82071, 5Colorado Division of Wildlife, Wildlife Research
Center, Fort Collins, CO 80526-2097, 6Department of Veterinary Sciences,
University of Wyoming, Laramie, WY 82070, USA and 2ID-Lelystad,
Institute for Animal Science and Health, Lelystad, The Netherlands
7Corresponding author e-mail: Received June 7, 2000;
revised July 3, 2000; accepted July 5, 2000.


Chronic wasting disease (CWD) is a transmissible
spongiform encephalopathy (TSE) of deer and elk,
and little is known about its transmissibility to other
species. An important factor controlling
interspecies TSE susceptibility is prion protein (PrP)
homology between the source and recipient
species/genotypes. Furthermore, the efficiency with which
the protease-resistant PrP (PrP-res) of one
species induces the in vitro conversion of the normal PrP
(PrP-sen) of another species to the
protease-resistant state correlates with the cross-species
transmissibility of TSE agents. Here we
show that the CWD-associated PrP-res (PrPCWD) of cervids
readily induces the conversion of recombinant cervid PrP-sen
molecules to the protease-resistant state in accordance
with the known transmissibility of CWD between cervids. In contrast,
PrPCWD-induced conversions of human and bovine PrP-sen were
much less efficient, and conversion of ovine PrP-sen was
intermediate. These results demonstrate a barrier at the
molecular level that should limit the susceptibility of these non-cervid
species to CWD.


Clearly, it is premature to draw firm conclusions about CWD
passing naturally into humans, cattle and sheep, but the present
results suggest that CWD transmissions to humans would be as
limited by PrP incompatibility as transmissions of BSE or sheep
scrapie to humans. Although there is no evidence that sheep
scrapie has affected humans, it is likely that BSE has caused variant
CJD in 74 people (definite and probable variant CJD cases to
date according to the UK CJD Surveillance Unit). Given the
presumably large number of people exposed to BSE infectivity,
the susceptibility of humans may still be very low compared with
cattle, which would be consistent with the relatively inefficient
conversion of human PrP-sen by PrPBSE. Nonetheless, since
humans have apparently been infected by BSE, it would seem prudent
to take reasonable measures to limit exposure of humans
(as well as sheep and cattle) to CWD infectivity as has been
recommended for other animal TSEs.


i remember when they said BSE aka MAD COW DISEASE would not
transmit to humans, they missed the boat on that one.
i hope they don't make the same assumption/mistake on CWDs.
these 6 different strains of sporadic CJDs that are killing
folks all across America, these CJDs are caused by something.
they have routes and a sources, and they are real. again, my
opinion of the CWD situation is only a small part, of a much
larger problem. _we must start testing cattle for TSEs in
sufficient numbers to find it_. one million annually, for the
next five years...

kind regards,
Terry S. Singeltary Sr., Bacliff, Texas USA

###########  ############
Subject: CWD aka MAD DEER $ ELK DISEASE $ TEXAS TROPHY HUNTERS ASSOC. $ TEXAS DEER ASSOC. (oh my God, stupidity knows no borders, as with CWD)
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Wed, 4 Sep 2002 22:34:09 -0700
Content-Type: text/plain
Parts/Attachments text/plain (274 lines)
########  Bovine Spongiform Encephalopathy   #########


I would like to take this opportunity to bring readers up to date as to
what's going on in the Deer Industry. I'm sure by now you have heard the
term "CWD," which is Chronic Wasting Disease. This supposed disease
situation appears to have originated in a state wildlife disease
research facility in Fort Collins, Colorado.

Since discovering CWD in Colorado during the 1960s, with elk being the
primary carrier, it has since appeared in several states, the latest of
which is Wisconsin whitetails. The CWD issue has basically taken on a
life of its own in terms of nationwide publicity. In my opinion, what we
have here is an example of the proverbial Chicken Little--the sky is
falling syndrome.

Even though there have been less than 300 confirmed cases out of the
30-plus million whitetails that we have nationwide, and although we know
very little about CWD, dramatic measures are being taken. In 40-plus
years there have been only 300 confirmed cases of the disease in the
entire U.S. and Canada.

The DNR of Wisconsin has become so hysterically concerned over the CWD
issue that they are carrying out a total depopulation of whitetails
across a nine-ten mile radius area. I've been told that they are using
helicopter gunships, as well as local sharpshooters, and have even
employed mobile incinerators to dispose of the carcasses, all because
they found 14 positive cases of "Clinical CWD" in a sampling of 578
hunter-killed whitetails.

In a recent visit with the Texas Animal Health Commission and the Texas
Deer Association, there were many direct and pointed questions asked
about the questionable disease itself. For what I heard, we very plainly
don't know very much about CWD at all. There is, however, evidence that
CWD is possibly what's called a "Spontaneous Disease," meaning it occurs
from time to time in nature when certain conditions exist, much like
anthrax occurrences. In other words, CWD, if it truly is a disease, per
say, is probably not a new disease at all. It has probably been around

You may have a question in your mind about this time. Is there any
possibility that a Depopulation Program could come into play in Texas if
the "disease" were discovered in the state? Ken Waldrup of the Texas
Animal Health Commission (TAHC) says, "Yes, that possibility does exist
under certain circumstances." Depopulation of even a small fraction of
our Texas deer herds could be harmful to our three billion dollar per
year hunting industry, as well as the economic hunting opportunities of
certain parts of Texas.

I pose the question, "Why has all this attention and concern been placed
solely on CWD when many other proven diseases which pose serious animal
and human threats are in the wild populations, and many times there are
more in our domestic livestock?" TAHC says it kills deer, but does it
kill as many as does our hysteria? Is it contagious to humans? TAHC at
this time says there is no indication. Is it highly contagious among
whitetail? TAHC doesn't know for sure, but it could be judging by
several models to that effect and studies in other states.

Here is my point.

CWD is only one of many diseases we are discovering in deer and other
wildlife. For instance, Rabies, Theileria, Lyme disease, Rocky Mountain

Spotted Fever, Bluetongue and E.H.D. have been around forever.

There probably is no more incidence (percentage wise of total
population) of these diseases in wild deer than have already been around
for a long time. The only difference is that there are more
opportunities for humans and deer to interact and secondly we are, of
course, looking more intensely for diseases these days.

Diseases are density dependent, meaning the more deer you have the more
likely it is to have a disease spread within the population.

A natural result of this is that in some cases states have mismanaged
deer (whitetails, mule deer and elk) for more than 50 years, allowing
under so-called traditional deer management (hunter opportunity/bucks
only harvest) deer populations to build up to dangerously high levels.
During the period of 1987-88, Texas lost about 40 percent of its deer
herd to disease--not CWD, but EHD, Bluetongue and probably some bacterial
diseases. Did we get hysterical over that? The die-offs in east Texas
may have happened because the state moved deer from south Texas, where
varieties of Bluetongue and bacterial disease abound, to restock East
Texas Type II Areas, spreading the diseases.

It is documented that not one time have any of these diseases been
caused because someone confined deer behind a fence or bred deer in
pens. The CWD source may have been in the wild or may have originated in
state-owned research facilities. Tuberculosis (Tb) in Michigan was
acquired by mixing of wild deer with cattle, not the other way around.

We are told by Dr. Ken Waldrup, with TAHC, and Dr. Jerry Cooke, with
TPWD, Texas state agencies are going to test Wildlife Management Areas
(WMA) and public lands and are considering hunter harvest, slaughter
house surveillance, etc. I am assuming TAHC will also test the deer at
the Kerr Wildlife Area Research pens north of Kerrville.

A recent economic study indicated Colorado could take a 300-400 million
dollar hit on their hunting industry economy as a result of overreaction
concerning the CWD issue.

Many states appear to only want to look for CWD in penned deer. Again,
why? Two answers: 1) It fits their agenda to find and blame a disease on
private management (power and funding); and 2) if it is found in a
fenced situation, it's easy to kill out the deer on the property and
declare victory, all the while the disease could be raging on outside
the fence.

The CWD hysteria is in response to a panic being created by some
agencies, university scientists and some outdoor writers to benefit
their political agendas.

In spite of all this, CWD is a manageable "disease" and has probably
been out there for a long time. Colorado's management plan now calls for
holding the incidence to a "natural" background level of less than one
percent. That means for every 1,000 deer harvested, 10 will have CWD! In
1923, we found and eradicated Hoof and Mouth Disease in California
blacktails. Why can't we do the same for CWD? Over time? Again, why the

The cause of CWD still is not certain. Yes, we are fairly sure that the
agent is a prion, but prions occur naturally in all mammals' nervous
systems. It is only rogue prions that cause problems, and what turns
them bad no one really knows. There is growing scientific evidence CWD
may be like cancer, being caused by many agents, such as mineral
deficiencies, altitude, diet, etc. As I mentioned before, a "spontaneous

If the "Chicken Little" hysteria about wildlife diseases continues at
its current pace, I can see the day coming when the only places where
you can safely hunt and eat deer will be on privately managed fenced
ranches. That is what has happened in Michigan, where all fenced
properties have been tested repeatedly for Tb and have been shown to be
the only places in that part of Michigan where there is no Tb. I can see
the day soon when a hunting operation advertises proudly that they are
free of disease!

It's time for all the deer people--state agencies, biologists, landowners
and especially the outdoor writers--to come together, be responsible, not
hysterical and quit pointing the finger at each other. We need to put
political and personal agendas aside and join forces, not only to deal
with this supposed new disease, but also to develop sound management and
opportunities for private landowners to manage their deer. Its time to
wake up and smell the coffee. Let's make our decisions on sound science,
not hysteria.

© 2002-Texas Deer Association

Hunting Seasons Are Here

Jerry Johnston
President and Founder


The recent hysteria about Chronic Wasting Disease (CWD) seems to be
dying down some, at least in Texas, as we gradually get to know more
about the disease. All deer tested in Texas so far have proven negative.
But even if we find a few positive cases in Texas deer herds, so what.
The disease has only affected about two percent of the deer tested on an
average across the country and few, if any, deer have died as a direct
result of the disease; nor has there been a serious herd die-off of elk
or deer anywhere in the U.S.A. going back to the late 1960s when it was
first discovered. According to numerous experts, the meat is not
affected by the disease. If two percent of our deer did die from CWD,
remember that we lose about 30 percent of our deer each year from
hunting and natural mortality. So what's the big concern? Other research
has been done to see if domestic livestock can catch CWD. A study was
conducted by putting livestock in pens with infected deer or elk and
there has been no cross-contamination to domestic livestock. This means
that CWD doesn't jump species. Myself, Horace Gore, TDA president Gene
Riser and our cameraman Brian Hawkins recently traveled to Madison,
Wisconsin, the latest "hot spot" for CWD, to document what's going on
with the attempt of both the Department of Natural Resources (DNR) and
the Department of Agriculture to depopulate some 25,000 whitetail deer.
You will see our TV program report on the Journal of the Texas Trophy
Hunters, most likely to be aired in September, on the Outdoor Channel,
which is available on the Dish Network. Let me mention that this
depopulation attempt in Wisconsin simply is not feasible in terms of a
total depopulation and the DNR and Department of Agriculture admits it.
I also report to you that it is not a very pretty sight seeing a doe
with her two fawns laying in the back of a truck after being shot for no
good scientific reason-not to mention, the great number of other fawns
left to starve to death because their mothers were depopulated. Locals
who were on site when hunters brought deer into a local check station
muttered with remarks like, "This is sick!" Another thing about the
Wisconsin DNR's decision and judgment concerning the CWD issue is the
fact that they estimate that they have a deer to every three acres in
the area where they discovered CWD a few years ago. Guess what? Hunters
there have always had a nine day hunting season and can only use
shotguns or bows! This sort of DNR logic is puzzling to me. Like I say,
depopulation is not a very pretty sight, and I can't visualize this
happening in Texas, where I hope we have a little better common sense.
(As quoted from Mike Leggett's July 30, 2002, Sunday news column) "I
honestly believe the Texas crisis over Chronic Wasting Disease is really
more related to personal feelings about high fences, breeding deer in
pens and the changes in deer hunting that have occurred in the past two
decades." To me it's a classic case of the media and a lot of scientific
types that apparently just love a crisis. After all, if you can get the
people and the government to believe that you really do have a crisis,
that means the scientific community will probably get some funding to
study this "deadly disease" that, in reality, is nothing more than the
latest "boogie man." I say, "Hogwash. The jig is up."


Jerry Johnston
President and Founder

Jerry Johnston
President and Founder



damn, just when you thought you have heard all the
stupidity, dumb and dumber goes hunting again. i am not
sure if it truly is the money (industry), or these hunters
are that ignorant of the disease, and the long term
circumstances that surrounds the disease. i don't
think they truly understand the agent (nobody really
does), but transmission studies do not lie.

and to think that the only TSE testing ever done on
deer/elk in TEXAS totals less than 50 animals.
that really tells us a lot$ but is comparable with
TSE testing in cattle;

with that said, i beg to differ with the president and founder
of the Texas trophy hunters assoc. and his knowledge
of Chronic Wasting Disease, and only hope that the
hunters and their families, will take the time to investigate
this disease and the ramifications that are sure to come
from people that know not what they speak of...


with that said, i beg to differ with the president and founder
of the Texas trophy hunters assoc. and his knowledge
of Chronic Wasting Disease, and only hope that the
hunters and their families, will take the time to investigate
this disease and the ramifications that are sure to come
from people that know not what they speak of.

please, just read the data, do _not_ risk you and your
families lives from a most hideous death, from something
they know absolutely nothing about.

please deer hunters, read the data and make your
own minds up. do not let an industry regulate you
and your families lives with false information and
false reassurances just to keep their industry going$

Chronic Wasting Disease Program

8. Why is herd depopulation the preferred option of a herd plan in the event of a positive diagnosis?

(II.A.) Given CWD's long incubation period, absence of a live animal,
pre clinical test and current state of knowledge on transmission, whole
herd depopulation with no restocking on contaminated premises presents
the least risk of further spread of the disease once a positive
diagnosis has been made. However, alternative approaches may be
necessary where depopulation is not possible or other overriding factors
make depopulation undesirable or impractical. These may reflect
limitations on indemnity funding, the desire to increase surveillance
and monitoring, and the need for flexibility in order to encourage
initial participation and reporting on the part of owners.

some concerns of mine about TEXAS CWD potential and TEXAS
policy on herd contamination and quarantine;

Dr. Baca said animals from a herd that _had_ a history of CWD
_could_ be accepted into TEXAS, as long as it was no longer
under a hold order or quarantine.

(Because CWD is slow to develop, the disease has not been seen
in younger deer and elk.)

what about sub clinical cases of CWD, and the fact that CWD
_does_ transmit orally to mule deer fawns;

Oral Transmission And Early Lymphoid Tropism Of Chronic Wasting Disease
Prpres In Mule Deer Fawns

In this study, mule deer fawns were orally fed an infectious homogenate
and sacrificed at intervals to examine the lymphoid tissue of the
alimentary tract for signs of infection. Prion protein was detected as
early as 42 days and was evident in all fawns after 53 days. This paper
provides an improved procedure for detecting prions in early infection,
establishes a protocol for accelerated study of transmission routes, and
supports the hypothesis that oral exposure may reflect the initial
pathway of CWD infection in deer.

PrP-res can be detected at least 16 months before clinical signs would
be expected to appear and may reflect the initial pathway of CWD
infection in deer.


Date: Sat, 29 Jun 2002 18:12:35 -0700
From: "Terry S. Singeltary Sr."
MAY 2002 431 NEWS

TSE threat to US increases
The US Department of Agriculture last month confirmed that two sheep
taken from a farm in Vermont were infected with a form of
transmissible spongiform encephalopathy (TSE). Further tests are being
carried out to determine whether the disease is bovine spongiform
encephalopathy (BSE) or scrapie. The sheep were imported from the
Netherlands (Nature Med. 6, 1301; 2000). Analysis will take at least
two years, and if the prion is that which causes BSE, this would be
the first case of disease in the US.

Aguzzi warns of CWD danger
The TSE family of diseases also includes chronic wasting disease (CWD)
in deer, a condition that has spread in the US in recent years (Nature
416, 569; 2002). Speaking at the Days of Molecular Medicine conference
in La Jolla in March, prion expert Adriano Aguzzi issued a strong
warning against underestimating this form of TSE.

"For more than a decade, the US has by-and-large considered mad cows
to be an exquisitely European problem. The perceived need to protect
US citizens from this alien threat has even prompted the deferral of
blood donors from Europe," he said. "Yet the threat-from-within
posed by CWD needs careful consideration, since the evidence that CWD
is less dangerous to humans than BSE is less-than-complete. Aguzzi
went on to point out that CWD is arguably the most mysterious of all
prion diseases.

"Its horizontal spread among the wild population is exceedingly
efficient, and appears to have reached a prevalence unprecedented even
by BSE in the UK at its peak. The pathogenesis of CWD, therefore,
deserves a vigorous research effort. Europeans also need to think
about this problem, and it would be timely and appropriate to increase
CWD surveillance in Europe too." Aguzzi has secured funding from the
National Institutes of Health to investigate CWD, and the effort will
be lead by Christina Sigurdson in his department at the University of

Tachygrams show heart rate variability in BSE animals
Chris Pomfrett and colleagues at the University of Manchester, UK, may
have found the Holy Grail of prion research: a simple, non-invasive
test to diagnose patients with variant Creutzfeldt-Jakob disease
(vCJD) before clinical symptoms show themselves. The technique, a
high-resolution electrocardiogram (ECG), can identify a unique heart
rate variability signature caused by the early stages of infection.
The test successfully predicted bovine spongiform encephalopathy (BSE)
infection in cows before they showed signs of disease, and will now be
tested on suspected human vCJD patients in the UK. Currently, the
only definitive means to diagnose BSE and vCJD, which are among a
group of prion-based infections known as transmissible spongiform
encephalopathies (TSEs), is by postmortem examination of brain
tissue. Detecting vCJD before patients show clinical symptoms is an
urgent priority, as it could dramatically reduce the risk of
contaminating blood supplies and hospital equipment and give patients
and families time to prepare for illness. There have been 110 deaths
to date from vCJD in the UK Designing TSE diagnostic tests has been a
challenge not only because it is difficult to find antibodies that
penetrate the complex, folded structure of the abnormal prion, but
also because prions have no genetic material to identify. The ECG
test, called Fathom, aims to circumvent these problems by detecting a
condition called respiratory sinus arrhythmia (RSA). Fathom measures
beat-to-beat variability in heart rate with respect to breathing, and
was originally designed to assess depth of anesthesia during
surgery. Pomfrett decided to test whether RSA was affected in
BSE-infected animals, on the basis of the idea Heartbeat clue to
diagnosing vCJD that TSE infection passes from the gut along the vagus
nerve into an area of the brain stem called the solitary nucleus, an
area that controls RSA. The team measured the heart-rate variability
under laboratory conditions of 150 cows that had received either
single low dose, a single high dose or no dose of BSE. Pomfrett told
Nature Medicine that 2 animals that later died from the disease both
showed increased levels of RSA as compared with controls, and this ECG
pattern was detected 8 months before the animals died. Also, the
higher-dose animals showed a statistically higher level of RSA than
those that had received the lower dose.

"Of the 700 patients that I have seen under anesthesia, I've never
seen the effect to be so dramatic," said Pomfrett.

BSE appears to be the only brain-stem disease that increases sinus
arrhythmia -- other neurodegenerative diseases, such as Parkinson's
disease, reduce it -- making Fathom a potentially invaluable
diagnostic tool.

"One possible reason for this [may be] that once the dorsal vagal
motor nucleus, which is involved in blood pressure control, is knocked
out by TSE infection, the brain stem becomes unstable and the
autonomic nervous system compensates by inducing sinus arrhythmia to
try and maintain the blood pressure control," suggests Pomfrett.

For human trials, a 5-minute ECG recording and breathing information
will be taken from the 7 people currently suspected of having vCJD in
the UK, who will be monitored to see if the worsening of symptoms can
be predicted. The study is one of 22 being funded through a P million
($10 million) grant from the UK Public Funders of TSEs Research and
Development group. Five other projects will try to identify whether
"surrogate markers", such as levels of manganese and tau protein in
cerebrospinal fluid, are linked to TSEs. Other studies will look more
closely at infectivity, at how possible transmission risk can be
assessed and at methods to assess the effectiveness of decontamination
procedures for surgical instruments.

Simon Frantz, London

B) 2002 Nature Publishing Group

Volume 42 Issue 5 Page 513 - May 2002 Brain and buffy coat transmission
of bovine spongiform encephalopathy to the primate
MicrocebusmurinusNöelle Bons, Sylvain Lehmann, Nadine Mestre-Francès,
Dominique Dormont, and Paul Brown

BACKGROUND : More than 100 cases of variant CJD resulting from
infections with bovine spongiform encephalopathy (BSE) have accumulated
in the United Kingdom since 1995. Concern about the possibility of
secondary transmissions via blood and blood components donated by
infected individuals has prompted a variety of international donor
deferral policies that will continue until laboratory and epidemiologic
evidence provides a consensus about potential risk.

STUDY DESIGN AND METHODS: BSE was passaged through macaque monkeys and
then adapted to the prosimian microcebe (Microcebus murinus ). Brain
homogenate and buffy coat from an affected microcebe were separately
inoculated intracerebrally into three healthy microcebes (two animals
received brain and one received buffy coat).

RESULTS: All three inoculated microcebes became ill after incubation
periods of 16 to 18 months. Clinical, histopathologic, and
immunocytologic features were similar in each of the recipients.

CONCLUSION: Buffy coat from a symptomatic microcebe infected 17 months
earlier with BSE contained the infectious agent. This observation
represents the first documented transmission of BSE from the blood of an
experimentally infected primate, which in view of rodent buffy coat
infectivity precedents and the known host range of BSE is neither
unexpected nor cause for alarm.

From the Laboratory of Functional Neuropathology, School of Advanced
Studies, University of Montpellier II; Institute of Human Genetics,
National Center of Scientific Research, Montpellier; Neurovirology
Service, Atomic Energy Commission, Fontenay-aux-Roses, France; National
Institute of Neurological Disorders and Stroke, National Institutes of
Health, Bethesda, Maryland.

BSE = bovine spongiform encephalopathy; PrP = prion protein; PrPsc =
abnormal prion protein; vCJD= variant CJD.

Supported in part by the Region Languedoc-Roussillon, Ministry of
National Education, Research, and Technology, and Naturalia et Biologia.
To cite this article:
Bons, Nöelle, Lehmann, Sylvain, Mestre-Francès, Nadine, Dormont,
Dominique & Brown, Paul
Brain and buffy coat transmission of bovine spongiform encephalopathy to
the primate Microcebusmurinus.
Transfusion 42 (5), 513-516.
Available from:

Health & Science: Study examines venison eaters' risk of contracting
brain disease

By LOU KILZER, Rocky Mountain News of Colorado
(July 1, 2002 8:27 p.m. EDT) - The race is on to find out whether a
fatal brain disease in deer and elk poses a risk to human venison eaters.

"That's what everybody is trying to find out," said Dr. Pierluigi
Gambetti, head of a national team studying the occurrence of the deadly
protein disease.

Meanwhile, Gambetti's group and others are gearing up for studies of
genetically manipulated mice to see if they can be infected with chronic
wasting disease.

"We don't know whether it can be transmitted to humans and, if it is
transmitted, what it's going to look like," Gambetti said.

There are no proven cases of chronic wasting disease infecting humans,
but concern has intensified as the disease has spread from its endemic
areas in Colorado and Wyoming to several other states and two Canadian

There have been several cases reported in which human venison eaters
have contracted Creutzfeldt-Jakob disease (CJD), which, like chronic
wasting disease, is a transmissible spongiform encephalopathy (TSE), but
one that occurs naturally in humans.

Gambetti said that these cases seem to fit into known subtypes of CJD,
but he added that the assumption that human cases from deer or elk would
look different upon microscopic examination than ordinary CJD is just
that - _an assumption_.

In it, hamster prions were injected into mice, which then showed no
outward or microscopic sign of the disease. However, when brain matter
from those mice is injected into another set of mice and hamsters, they
become sick from mutant prions and die.

No one knows how these "sleeper carriers" stay healthy, or why
subsequent test animals become sick. But it raises the concern that if
CWD infected other animals, it is possible that at least the first
generation of the infected species might not get sick.

"It used to be thought the hamster (prion disease) didn't go into mice.
There was a species barrier," said Anne Raines, a fellow scientist at
Rocky Mountain Laboratory. "And now we have some of those mice going
down in a short amount of time - 100 days or so."
Date: May 25, 2002 at 4:48 pm PST ######## Bovine Spongiform Encephalopathy #########
8420-20.5% Antler Developer
For Deer and Game in the wild
Guaranteed Analysis Ingredients / Products Feeding Directions
Crude Protein (min) 20.50%
Crude Fat (min) 2.50%
Crude Fiber (max) 15.00%
Calcium (min) 1.50%
Calcium (max) 1.90%
Phosphorus (min) 1.25%
Potassium (min) 1.00%
Magnesium (min) 0.45%
Zinc (min) 450ppm
Manganese (min) 250ppm
Copper (min) 40ppm
Copper (max) 60ppm
Selenium (min) 0.30ppm
Vitamin A (min) 25,000IU/LB
Vitamin E (min) 20IU/LB Plant Protein, Soybean
Hulls (16%), Grain, Processed Grain By-Products, Dehydrated Alfalfa
Meal, Molasses, Defluorinated Phosphate, Monocalcium Phosphate,
Dicalcium Phosphate, Calcium Carbonate, Sodium Bicarbonate,
__Animal Protein__, Vitamin A Supplement, Vitamin D3 Supplement,
Vitamin E Supplement, Magnesium Oxide, Soybean Oil, DL-Mdethionine, Zinc
Sulfate, Manganese Sulfate, Copper Sulfate, Ferrous Sulfate,
Ethylenediamine Dihydriodide, Cobalt Carbonate, Sodium Selenite and
Artificial Flavoring Feed to wildlife as a supplement to pasture and
browse, or hay. Feed at a rate to maintain desired growth rate and body
condition, antler development and fawn survival. For optimal results
feed during times of nutrient stress, such as drought or when nutrient
requirements are elevated such as lactation antler growth, or rapid fawn
growth. Provide animals access to fresh clean water at all times.
CAUTION: This product contains high levels of copper. Do not feed to
animal sterol????????????????TSS
Grain Products, Plant Protein Products, Forage Products, Roughage
Products 30%, Calcium Carbonate, Processed Grain By-Products,
Deflourinated Phosphate, Salt, Molasses Products, Vitamin A Acetate with
D-activated Animal Sterol (source of Vitamin D3, di-alpha-Tocopheryl
Acetate, Artificial flavors added.
22.6 KG.
Crude Protein (Min) 15.5%
Crude Fat (Min) 2.0%
Crude Fiber (Max) 8.0%
Calcium (Min) 0.30%
Calcium (Max) 0.70%
Phosphorus (Min) 0.30%
Salt (Min) 0.05%
Salt (Max) 0.25%

Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products 15%, Molasses Products, Animal
Protein Products, Monocalcium Phosphate, Dicalcium Pyosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol (
source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement,
Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, Choline
Chloride, Folic Acid, Menadione Soduim Bisulfite Complex, Pyridoxine
Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.
CORN 666.67 LBS
PEAS 666.67 LBS
F# 3153 666.67 LBS
Feed Free Choice
Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products 15%, Molasses Products, Animal
Protein Products, Monocalcium Phosphate, Dicalcium Pyosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol (
source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement,
Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, Choline
Chloride, Folic Acid, Menadione Soduim Bisulfite Complex, Pyridoxine
Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.
Bode's #1 Game Pellets
Crude Protein (Min) 16%
Crude Fat (Min) 2.0%
Crude Fiber (Max) 19%
Calcium (Ca) (Min) 1.25%
Calcium (Ca) (Max) 1.75%
Phosphorus (P) (Min) 1.0%
Salt (Min) .30%
Salt (Max) .70%

Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products, 15% Molasses Products, Animal
Protein Products, Monocalcium Phosphate, Dicalcium Phosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol (
source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement,
Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, Choline
Chloride, Folic Acid, Menadione Sodium Bisulfite Complex, Pyridoxine
Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.
Feed as Creep Feed with Normal Diet
Selling Tips
* Designed to improve the nutritional health of your herd
* Provides consistent protein source
* High levels of Vitamin E and Selenium
* Yeast culture
* Available in pellet form

Profile^(TM) Deer Builder Pellets
Product Features: Product Benefits:
* High quality protein
* Balanced for demanding nutritional stages of post and pre rut deer
* Extremely palatable
* Keeps deer coming to the feeding area
* Quality ingredients
* Assures that the deer is receiving a consistent source of quality
* Yeast culture
* For increased feed efficiency and increased fiber digestion
* Fortified with the proper balance of vitamins and minerals
* Especially Vitamin E and Selenium for reproduction efficiency,
prevent white muscle disease and boost the immune system under stress
General Description:
For deer with higher nutrient needs.
Deer Builder Pellets
Crude Protein, Not less
Crude Fat, Not less
Crude Fiber, Not more
Calcium (Ca), Not less
Calcium (Ca), Not more
Phosphorus (P), Not less
Salt (NaCl), Not less
Salt (NaCl), Not more
Potassium (K), Not less
Selenium (Se), ppm, Not less
Copper (Cu), ppm, Not less
Zinc (Zn), ppm, Not less
Vitamin A, I.U./lb, Not less
Vitamin D3, I.U./lb, Not less
Vitamin E, I.U./lb, Not less

Grain Products, Roughage Products (not more than 35%), Processed Grain
By-Products, Plant Protein Products, Forage Products, Animal Protein
Products, L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium
Phosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic
Copper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite,
Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide,
Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A
Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium
Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite
Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,
Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate
Deer Builder Pellets is designed to be fed to deer under range
conditions or deer that require higher levels of protein. Feed to deer
during gestation, fawning, lactation, antler growth and pre-rut, all
phases which require a higher level of nutrition. Provide adequate
amounts of good quality roughage and fresh water at all times.
Selling Tips
* Elk Lactation Cow Gest is for elk cows from 45 days prior to
calving through weaning
* Provides needed protein, energy, vitamins and minerals created by
calving and milk production.

Profile^(TM) Elk Lactation Cow Gest
Product Features: Product Benefits:
* High quality plant protein
* Supply protein requirements during this high demand period
* Complex carbohydrates and fats
* Provide needed energy to help maintain body condition
* Highly digestible fiber
* Lowers risk of acidosis, while providing a high level of energy
* Highly fortified; complete vitamins and trace minerals with
Zinpro organic trace minerals
* Meets trace nutrient requirements during this period of
high-nutrient demand even in the presence of interfering trace elements
* Diamond V's XP Yeast
* Increases palatability and forage digestibility
* Pelleted
* Convenient and easy for the producer to handle
* Mold Inhibitor
* Feed stays fresh longer
* Apple Flavored

General Description:
For elk cows from 45 days prior to calving through weaning.
Elk Lactation Cow Gest
Crude Protein, Not less
Crude Fat, Not less
Crude Fiber, Not more
Calcium (Ca), Not less
Phosphorus (P), Not less
Salt (NaCl), Not less
Salt (NaCl), Not more
Potassium (K), Not less
Magnesium (Mg), Not less
Zinc (Zn), ppm, Not less
Copper (Cu), ppm, Not less
Selenium (Se), ppm, Not less
Vitamin A, I.U./lb, Not less
Vitamin D3, I.U./lb, Not less
Vitamin E, I.U./lb, Not less

Grain Products, Roughage Products (Not more than 50%), Processed Grain
By-Products, Forage Products, Plant Protein Products, Molasses Products,
Animal Fat (Preserved with BHA and Citric Acid), Monocalcium/Dicalcium
Phosphate, Calcium Carbonate, Salt, Potassium Chloride, Sodium Selenite,
Copper Sulfate, Potassium Iodide, Cobalt Carbonate, Basic Copper
Chloride, Manganese Sulfate, Manganous Oxide, Zinc Sulfate, Zinc Oxide,
Ethylenediamine Dihydriodide, Manganese Amino Acid Complex, Zinc
Methionine Complex, Copper Amino Acid, Complex, Cobalt Glucoheptonate,
Mineral Oil, Propionic Acid, Vitamin A Supplement, Vitamin D3
Supplement, Vitamin E Supplement, Sodium Propionate, Natural &
Artificial flavors
Feed at 1 to 1.5 lb per 100 lb body weight (ideally 3 to 8 lb) per head
daily to lactating elk cows. Always provide adequate forage and fresh,
clean water. If body condition is not being maintained at these
recommended feeding rates, evaluate forage quality and health status
before increasing the amount of Elk Lactation Gest fed beyond 8 lb per
head per day. The maximum feeding rate for this product is 13 lb per
head daily. Always follow good feeding and health management procedures.
Previous Product Next Product
considering 1/2 to 1 gram of TSE material is lethal;
April 9, 2001 WARNING LETTER
Brian J. Raymond, Owner
Sandy Lake Mills
26 Mill Street
P.O. Box 117
Sandy Lake, PA 16145
Tel: 215-597-4390
Dear Mr. Raymond:
Food and Drug Administration Investigator Gregory E. Beichner conducted
an inspection of your animal feed manufacturing operation, located in
Sandy Lake, Pennsylvania, on March 23,
2001, and determined that your firm manufactures animal feeds including
feeds containing prohibited materials. The inspection found significant
deviations from the requirements set forth in
Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins
Prohibited in Ruminant Feed. The regulation is intended to prevent the
establishment and amplification of Bovine Spongiform Encephalopathy
(BSE) . Such deviations cause products being manufactured at this
facility to be misbranded within the meaning of Section 403(f), of the
Federal Food, Drug, and Cosmetic
Act (the Act).
Our investigation found failure to label your
swine feed with the required cautionary statement "Do Not Feed to cattle
or other Ruminants" The FDA suggests that the statement be
by different type-size or color or other means of highlighting the
statement so that it is easily noticed by a purchaser.
In addition, we note that you are using approximately 140 pounds of
cracked corn to flush your mixer used in the manufacture of animal
feeds containing prohibited material. This
flushed material is fed to wild game including deer, a ruminant animal.
Feed material which may potentially contain prohibited material should
not be fed to ruminant animals which may become part of the food chain.
The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal
feed use, you are responsible for assuring that your overall operation
and the products you manufacture and distribute are in compliance with
the law. We have enclosed a copy of FDA's Small Entity Compliance Guide
to assist you with complying with the regulation... blah, blah, blah...
now, what about those 'deer scents' of 100% urine',
and the prion that is found in urine, why not just
pass the prion with the urine to other deer...
Mrs. Doe Pee Doe in Estrus
Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urine
collected at the peak of the rut, blended with Fresh Doe Urine for an
extremely effective buck enticer. Use pre-rut before the does come into
heat. Use during full rut when bucks are most active. Use during
post-rut when bucks are still actively looking for does. 1 oz.
Works anytime of the year
100 % Cow Elk-in-Heat urine (2oz.)
Economical - mix with water in spray mist bottle
Use wind to your advantage
Product Code WP-ESB $9.95
prions in urine?
Subject: Cervid (Deer) Meat from BSE Countries
Effective immediately, deer meat from all countries the USDA considers
to be affected with bovine spongiform encephalopathy (BSE) may be
allowed entry into the US if each shipment is accompanied by a
certificate endorsed by an official of the National Veterinary Service
of the country of origin certifying that the meat was derived from
either wild cervidae or from farm raised cervidae that have never been
fed ruminant origin meat and bone meal. Previously, the only
BSE-affected country which was allowed to export deer to the US was
Ronald B. Caffey
Assistant to the Deputy Administrator
Plant Protection and Quarantine
(If a location in your jurisdiction cannot access the PPQ Bulletin
Board, please forward a copy of this notice to that location.)
Subject: Importation of Cervid (deer) Antlers from BSE Countries
Effective immediately, processed and unprocessed deer antlers from all
countries that USDA considers to be affected with bovine spongiform
encephalopathy (BSE) may be allowed entry into the US if each shipment
is accompanied by a certificate endorsed by an official of the National
Veterinary Service of the country of origin certifying that the antlers
were derived from either wild cervidae or farm raised cervidae that have
never been fed ruminant origin meat and bone meal.
Elizabeth A. Klontz
Veterinary Medical Officer
Plant Protection and Quarantine
Greetings List Members,
wonder what species these animal proteins and fats
are? some more of that non-species coding i imagine?
that non-species coding system comes in real handy i
would imagine on both exports, imports and even
home grown...
kind regards,
Terry S. Singeltary Sr., Bacliff, Texas USA
########### ############
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Thu, 29 Nov 2001 19:42:38 -0800
Content-Type: text/plain
######## Bovine Spongiform Encephalopathy #########
NEWS RELEASE Texas Animal Health Commission Box l2966 *Austin, Texas 78711 *(800) 550-8242* FAX (512) 719-0719 Linda Logan, DVM, PhD* Executive Director For info, contact Carla Everett, information officer, at 1-800-550-8242, ext. 710, or
For Immediate Release-- Texas "Fences Out" Colorado Deer and Elk
Texas animal health officials have shut the door on the importation of live elk and several species of deer from Colorado after cases of Chronic Wasting Disease (CWD), a fatal, degenerative brain disease of elk and deer, were confirmed earlier this fall in farmed elk herds in that state. CWD belongs to the family of transmissible spongiform encephalopathies or TSEs, Other similar, but unique diseases, include BSE, or bovine spongiform encephalopathy, which affects cattle; and scrapie, a disease that can affect sheep and goats.
"The TAHC issued the quarantine on the entire state of Colorado, prohibiting the entry into Texas of live elk, mule deer, white-tailed and black-tailed deer. The quarantine is to prevent exposure to CWD and will remain in effect until it is modified or rescinded by the 12-member TAHC commission. The restrictions do not include hunter-killed animals," said Dr. Linda Logan, Texas state veterinarian and head of the TAHC. Texas has not had a case of CWD, and we want to provide as much protection against this disease as possible, while maintaining safe marketing and movement opportunities."
"The TAHC quarantine on Colorado was redundant until late November, when Colorado animal health officials lifted a movement ban that had been in place on domestic elk since October. Colorado officials will continue to restrict the movement of animals from quarantined facilities and any domestic elk that originate in the northeast corner of the state, where the disease is endemic.
Dr. Wayne Cunningham, Colorado state veterinarian, said his staff has nearly completed the disease investigation. As of end of November, they have detected 11 positive elk, resulting in the quarantine of nine herds, involving about 1,550 animals. The infected herds will be depopulated, beginning in the non-endemic area of Colorado.
Veterinarians from the Texas Animal Health Commission (TAHC), the state's livestock health regulatory authority, also have traced a dozen elk that were imported to Texas from two of the Colorado herds, prior to the detection of disease.
"Colorado officials acted swiftly to notify other states when they confirmed disease in the herds. Although this is extremely unfortunate, it's an indication that the detection and reporting system works among states, and we're handling this issue quickly to prevent potential exposure to Texas hoof stock," said Dr. Logan. "It should be noted that the ranchers who had imported the elk to Texas complied with all health regulations."
Dr. Logan said, before being imported into Texas, deer and elk must meet a number of health requirements. Besides entry permits, the animals must have had a certificate of veterinary inspection issued within the previous 30 days, meet stringent tuberculosis testing requirements and test negative for brucellosis, a bacterial disease that can affect cattle. The deer and elk also must come from a state with a CWD program that requires disease reporting and which imposes movement restrictions on suspicious or positive herds. If the animals originate in a state that has CWD in its wildlife, the animals must come from a herd enrolled in a CWD monitoring program for at least a year.
"We've located all of the imported elk, 11 of which were moved to a ranch in the Panhandle, and the 12th animal, which was sent to a facility in the Hill Country," commented Ken Waldrup, TAHC veterinarian and field epidemiologist. "When our veterinarians inspected these imported elk, they had no clinical signs of CWD, which can include extreme weight loss, unusual behavior, excessive salivation, weakness, and loss of body function."
Dr. Waldrup explained that the ranchers involved have excellent sale and movement records, making epidemiology work much easier for the TAHC veterinarians. The 11 elk on the Panhandle ranch were imported from Colorado prior to l998 or earlier,
Two had been killed, and two each had been transported to Pennsylvania and Missouri. One had been returned to Colorado. Because there is no live-animal test for CWD, the four Colorado-imports remaining on the ranch were euthanized Friday, November 9, and their brain tissue was submitted to the National Veterinary Services Laboratory (NVSL) in Ames, Iowa, for examination. The carcasses were incinerated as an extra biosecurity measure, Dr Waldrup said.
"We've also notified Pennsylvania and Missouri animals health officials, so that they can locate the four Colorado animals that were transported to their states," said Dr. Waldrup. "While we await the report from NVSL regarding the health status of the Colorado-imported elk, the other animals in the Panhandle herd will be quarantined. If disease is detected, we'll take appropriate measures to cull and remove animals that may have been exposed."
Dr. Waldrup said the Colorado elk taken to the Hill Country ranch also is quarantined, along with its herd mates, while negotiations are finalized for the purchase of the imported animal for testing. "Federal CWD indemnity funds are limited to $3,000 per animal, and since many of these animals are worth much more, it is difficult to let go of an animal for testing," he said. "This animal has been in Texas less than three months, so there is little chance that this animal poses a threat to the rest of its herd."
Dr. Logan explained that Colorado officials have required mandatory CWD monitoring of farmed deer and elk herds in the state since May l998, due to the incidence of the disease in wildlife in the northeastern corner of the state. The monitoring program involves testing animals that die, regardless of the cause of death.
The TAHC offers a voluntary CWD monitoring program in Texas, encompassing all cervids, including fallow and white-tailed deer. About 20 herds are enrolled, added Dr. Waldrup. He said TAHC veterinarians are working with staff from the Texas Parks and Wildlife Department to determine ways to increase surveillance for Texas white-tailed deer raised under permit by scientific breeders.
Dr. Logan said wildlife officials in Colorado, Wyoming and Nebraska also have collected brain samples for testing from hunter-killed animals in the targeted "endemic area," involving a small portion of northeastern Colorado, southeastern Wyoming and southwestern Nebraska. Hunters are notified when an infected carcass is detected. In Wyoming and Colorado, less than one percent of the elk and less than five percent of the deer have been found to be infected. Two hunter-killed infected mule deer have been detected in Nebraska.
"At this time, there is no evidence that CWD is transmissible to other hoof stock, such as axis or fallow deer. In the endemic area of Colorado, there has been no evidence of spread to cattle, sheep or pronghorn antelope," said Dr. Waldrup. "Experiments and monitoring are continuing in the area, so the veterinary and producer community can better understand this disease, which was unknown until 1967, when it was first seen in a captive wildlife research center in northeastern Colorado," he said.
Dr. Waldrup said that the first CWD-positive farmed elk herd was detected in 1997 in South Dakota. Since then, 16 other herds have been found: five more in South Dakota; three in Nebraska, five in Colorado, and one each in Oklahoma and Montana. By late October 2001, 10 of these herds had been depopulated, six remained quarantined, and one herd had been released from quarantine after rigorous testing and surveillance revealed no further evidence of disease. He said the disease also has been detected in several farmed elk herds and free-ranging mule deer in the Canadian province of Saskatchewan.
"All animal movement and trade entails a degree of risk," said Dr. Logan. "Besides disease eradication, our main duty is to assess and reduce risks to our state's herds and flocks. We cannot construct a fence around Texas, but we can set realistic standards, testing and monitoring requirements for imported animals. After Colorado officials complete the epidemiological work on these herds, the TAHC commissioners may want to revisit the issue of the prohibition on Colorado deer and elk imports in a year or more."
########### ############

Mad cow disease: Could it be here? / Man's stubborn crusade attracts experts' notice


SUN 08/05/2001 Houston Chronicle, Section A, Page 37 Metfront, 4 STAR Edition

Like Paul Revere with e-mail, Terry Singeltary Sr. is on a mission to sound an alarm: Beware of mad cow disease.
As is true of many crusaders, however, his pleas often fall on deaf ears. Health officials here and abroad insist that bovine spongiform encephalopathy - popularly known as mad cow disease, a fatal brain disorder that can make cows shake uncontrollably - has been kept out of this country through surveillance of the cattle industry.
But since his mother's death in December 1997, the Galveston County man has been obsessed with possible connections between her deadly brain disorder, sporadic Creutzfeldt-Jakob Disease, and mad cow disease.
And after much persistence on his part, people are taking notice of this former machinist and high school dropout who jokes that he has a Ph.D. - a Pool Hall Degree.
"They called me Chicken Little for four years," he said. "Now they're calling back, asking for more information."
For the past year he has been U.S. co-coordinator of an international monitoring group called CJD Watch. He regularly gets e-mail from scientists and journalists around the world.
Debora MacKenzie, a reporter for the British magazine New Scientist, described Singeltary, 47, as a "dogged unearther and tabulator of government documents."
Singeltary monitors "every word written about CJD/BSE," said Anita Manning of USA Today, also by e-mail.
"He's passionate, opinionated and not always tactful, although I like him because he's such a character and he is so transparent," Manning said. "He is what he appears to be."
Science and environment writer Jonathan Leake of the Sunday Times in London said Singeltary has helped him track down families of people with CJD along with academic research papers.
"I strongly suspect he is right in thinking the USA has had BSE cases," Leake said by e-mail.
"The American government is making the same mistake as the British in putting the short-term commercial interests of its farmers before health considerations," he added.
"It should start formal and widespread testing of cattle plus compulsory autopsies for all human CJD victims at the state's expense. If there is BSE, then leaving it to spread will kill people - and that would eventually destroy the industry, too."
Texas Department of Health epidemiologist Julie Rawlings said Singeltary's careful monitoring of the disease had proven useful.
"Terry has been helpful in providing contact information regarding suspect CJD cases so that the Health Department can initiate case investigations and learn more about CJD in Texas," she said.
Noting that the department cannot release records on individual patients, she added, "I think we learn more from him than he does from us."
Mad cow disease surfaced in England in 1986 and quickly became an epidemic. It since has been reported in 15 European countries, most recently Greece on July 2, and the Czech Republic on June 14. Two German-born cows tested positive for BSE in November.
Singeltary said he became convinced that BSE is here as he watched his mother, Barbara Poulter of Crystal Beach, dying of sporadic Creutzfeldt-Jakob Disease. The rare, fatal brain disease is sometimes accompanied by severe jerking.
"She would jerk so bad at times, it would take three of us to hold her down," Singeltary said. "They can call it whatever they want, but I know what I saw, and what she went through. `Sporadic' simply means they don't know."
Poulter, a retired telephone-company field worker, had a form of sporadic CJD - Haidenhain variant - that is even less common than the typical sporadic case. One of its first symptoms is loss of vision.
She started seeing brown spots in September 1997 and was virtually blind within two weeks. By the eighth week of the illness Poulter was bedridden, and in the 10th week she died. Before that she had been in good health.
In many countries and most U.S. states, physicians are not required to report CJD cases to health officials. Texas made the disease reportable in 1998. Through 2000, there were 17 probable or confirmed cases, according to the Texas Department of Health.
In mid-June, a case of sporadic CJD was confirmed through brain biopsy at Christus Spohn Hospital Shoreline in Corpus Christi, said Jane Bakos, hospital vice president. The patient has since died, the hospital reported.
CJD and mad cow disease leave their victims' brains full of holes like a sponge. Although not contagious, the illnesses are thought to be transmissible through prions, or nearly indestructible abnormal proteins.
Because the prion protein is not killed by standard sterilization, sporadic CJD can be spread by contaminated surgical instruments.
In March 1996, the British government announced the discovery of a new variant of CJD, most likely explained by exposure to bovine spongiform encephalopathy.
Through June, 101 cases of new-variant CJD have been reported in the United Kingdom, three in France and one in Ireland. In contrast to sporadic CJD, the new variant usually affects younger patients and lasts longer.
No cases of new-variant CJD or BSE have been reported in the United States. No relationship has been shown between sporadic CJD and mad cow disease.
There is no indication that new-variant CJD can be spread through blood transfusions, but a U.S. Food and Drug Administration advisory committee voted in June to broaden the categories for excluding potential donors. The recommendations have not yet been approved by the FDA.
The American Red Cross has announced that on Sept. 17 it will begin rejecting potential blood donors who, since 1980, have spent at least three months in the United Kingdom or at least six months in any European country or combination of countries. Those who have received a blood transfusion in Britain since 1980 also will be rejected.
The primary collector of local blood donations is the Gulf Coast Regional Blood Center, which will follow the FDA's guidelines, said Bill Teague, president and chief executive officer.
Singeltary said it's naive to think that U.S. prevention efforts have kept mad cow and new-variant CJD out of the United States.
"They haven't found it," he said, "because they haven't looked."
For one thing, he said, too few cows are tested for the disease. In the first six months of this year, the European Union tested more than 3.2 million cows, David Byrne of the European Commission said in a speech last month.
By contrast, it took the U.S. Department of Agriculture nearly 10 years to analyze about 13,000 cow brains, according to the department's Web site.
With more than 68 million cattle slaughtered since 1990 in the United States, according to the USDA, checking about 13,000 falls far short, Singeltary said.
Though not a scholar, Singeltary has collected voluminous material on mad cow and CJD. Disabled from a neck injury, Singeltary never used a computer until 1998. He now spends hours each day on the Internet while his wife, Bonnie Singeltary, runs a flower shop in their home in Bacliff, in north Galveston County.
His challenge to the CJD/BSE establishment is courageous and refreshing, said Dr. Lynette Dumble, former visiting professor of surgery at University of Texas Medical School at Houston and a former senior research fellow in the history and philosophy of science at the University of Melbourne in Australia.
"I certainly have no problem with Terry's ideas on BSE/CJD," said Dumble, who coordinates the Global Sisterhood Network, a computer service that posts media reports on developments affecting women. "His research skills are excellent, and he is abreast of each and every development in the field."
Among Singeltary's worries now, he said, are widespread violations of an August 1997 ban on feeding animal products to U.S. cattle. The FDA reported in January that hundreds of feed manufacturers were not complying with regulations designed to keep BSE out of this country.
(That same month, a Purina Mills feedlot near San Antonio told the FDA that a "very low level" of cow parts had been found in cattle feed. The company voluntarily removed 1,222 animals who had been fed the prohibited materials.)
He obtained copies of FDA letters to various feed mills that had been found in violation of the regulations and immediately sent them by e-mail to hundreds of people around the world.
Singeltary might not be so zealous in getting the word out if he weren't convinced that someone is covering up the truth.
"They used to say BSE would never transmit to humans," he said, "and it has. They lied about the feed ban being in place.
"I've lost faith in the whole process. I've discovered too many things."
2012 JULY
Media Contacts:
Steve Lightfoot, TPWD, 512-389-4701,
Yvonne "Bonnie" Ramirez, TAHC, 512-719-0710,
July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
AUSTIN -- Samples from two mule deer recently taken in far West Texas have been confirmed positive for Chronic Wasting Disease (CWD). These are the first cases of CWD detected in Texas deer. Wildlife officials believe the event is currently isolated in a remote part of the state near the New Mexico border.
The Texas Parks and Wildlife Department (TPWD) and the Texas Animal Health Commission (TAHC) implemented regionally-focused deer sample collection efforts after the disease was detected in the Hueco Mountains of New Mexico during the 2011-12 hunting season. With the assistance of cooperating landowners, TPWD, TAHC, and USDA-APHIS-Wildlife Services biologists and veterinarians collected samples from 31 mule deer as part of a strategic CWD surveillance plan designed to determine the geographic extent of New Mexico's findings. Both infected deer were taken from the Hueco Mountains of northern El Paso and Hudspeth counties.
CWD is a member of the group of diseases called transmissible spongiform encephalopathies (TSEs). Other diseases in this group include scrapie in sheep, bovine spongiform encephalopathy (BSE or mad cow disease) in cattle, and Cruetzfeldt-Jakob disease in humans. CWD among cervids is a progressive, fatal disease that commonly results in altered behavior as a result of microscopic changes made to the brain of affected animals. An animal may carry the disease for years without outward indication, but in the latter stages, signs may include listlessness, lowering of the head, weight loss, repetitive walking in set patterns, and a lack of responsiveness. CWD is not known to affect humans.
Tissue samples were initially tested by the Texas Veterinary Medical Diagnostic Laboratory in College Station, with confirmation by the National Veterinary Services Laboratory in Ames, Iowa.
"Now that we have detected CWD in Texas, our primary objective is to contain this disease," said Carter Smith, TPWD Executive Director. "Working collaboratively with experts in the field we have developed protocols to address CWD and implementation is already under way."
There is no vaccine or cure for CWD, but steps have been taken to minimize the risk of the disease spreading from beyond the area where it currently exists. For example, human-induced movements of wild or captive deer, elk, or other susceptible species will be restricted and mandatory hunter check stations will be established.
"This is obviously an unfortunate and rather significant development," said TPW Commission Chairman, T. Dan Friedkin. "We take the presence of this disease very seriously and have a plan of action to deal with it. The Department will do whatever is prudent and reasonable to protect the state's deer resources and our hunting heritage."
Although wildlife officials cannot say how long the disease has been present in Texas or if it occurs in other areas of the state, they have had an active CWD surveillance program for more than a decade.
"We have tested more than 26,500 wild deer in Texas since 2002, and the captive-deer industry has submitted more than 7,400 CWD test results as well," said Mitch Lockwood, Big Game Program Director with TPWD. "But that part of West Texas is the toughest place to conduct an adequate CWD surveillance program because so few deer are harvested out there each hunting season. Thanks to the cooperation and active participation of several landowners, we were able to begin getting an idea of the prevalence and geographic distribution of the disease without needing to remove many deer."
The TAHC regulates cervid species not indigenous to Texas such as elk, red deer, and sika deer. TAHC oversees a voluntary CWD herd monitoring status program with the intent to facilitate trade and marketability for interested cervid producers in Texas. Cervid herds under either TPWD or TAHC authority may participate in the commission's monitored CWD program. The basis of the program is that enrolled cervid producers must provide an annual herd inventory, and ensure that all mortalities during the previous year were tested for CWD and the disease was not detected.
Wildlife biologists, hunters, and landowners would certainly have preferred for Texas mule deer populations to have not been dealt this challenge, but TPWD and TAHC have developed a CWD Management Plan that includes management practices intended to contain the disease. The management plan includes input from the CWD Task Force, which is comprised of deer and elk producers, wildlife biologists, veterinarians and other animal-health experts from TPWD, Texas Animal Health Commission, Department of State Health Services, Texas A&M College of Veterinary Medicine, and USDA.
The disease was first recognized in 1967 in captive mule deer in Colorado. CWD has also been documented in captive and/or free-ranging deer in 19 states and 2 Canadian provinces, including neighboring New Mexico.
"We know that elk in southern New Mexico are also infected with CWD," said Dr. Dee Ellis, State Veterinarian and TAHC Executive Director. "It will take a cooperative effort between hunters, the cervid industry, and state/federal animal health and wildlife agencies to ensure we keep this disease confined to southern New Mexico and far West Texas. I am confident however that will be able to do that, and thus protect the rest of the Texas cervid industry."
More information on CWD can be found on TPWD's website, or at the Chronic Wasting Disease Alliance website,
More information about the TAHC CWD herd monitoring status program may be found at
Founded in 1893, the Texas Animal Health Commission works to protect the health of all Texas livestock, including: cattle, swine, poultry, sheep, goats, equine animals, and exotic livestock.
The fact of the matter is, CWD has been waltzing across Texas for over a decade from the WSMR at New Mexico border, and the state of Texas, in my opinion, knew this. in my opinion, the state of Texas purposely tested the least amount of cervids in that area for years, why, they knew it was there, and I warned you of this in 2001, 2005, and year after year after year. now, it’s too late. Game farms and ranchers i.e. high fence operations here in Texas are out of control in my opinion, with the TAHC not having a clue as to the infection rate of CWD (if any) at these high fence operations. it has been proven in the past, they are nothing but a petri dish for CWD infection rates, with the highest infection rate in Wisconsin at the Buckhorn Flats Game farm toping out at 80%. TAHC actions now on CWD, as I finally applaud them, may well be much too late, and not near enough. I pray that I am wrong. However, because of this, I think the movement restrictions on cervids in Texas should include every region in the state of Texas, until a very large cwd sampling over a period of 7 to 10 years. ...
here are a few of my pleas to the TAHC about CWD waltzing into Texas for over a decade ;
2001 – 2002
Subject: CWD testing in Texas
Date: Sun, 25 Aug 2002 19:45:14 –0500
From: Kenneth Waldrup
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
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
Volume 3, Number 8 01 August 2003
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.
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
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-
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.
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:
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:
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. Prion
----- Original Message -----
From: David Colby
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 ProfessorDepartment of Chemical EngineeringUniversity of Delaware
Wednesday, September 08, 2010

Tuesday, June 19, 2012

Experimental Oral Transmission of Chronic Wasting Disease to Reindeer (Rangifer tarandus tarandus)

Monday, June 18, 2012

natural cases of CWD in eight Sika deer (Cervus nippon) and five Sika/red deer crossbreeds captive Korea and Experimental oral transmission to red deer (Cervus elaphus elaphus)

Wednesday, June 27, 2012

First US BSE Case Since 2006 Underscores Need for Vigilance

Neurology Today 21 June 2012

Tuesday, June 05, 2012

Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012 Legislative Session

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

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).
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).
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).
Thursday, February 09, 2012

Wednesday, April 25, 2012


Tuesday, July 29, 2008
Heidenhain Variant Creutzfeldt Jakob Disease Case Report
I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
SKROLL down a bit for Mom's autopsy of hvCJD. ...
MOM, I’M STILL HERE DAMN’T................
with sad regards,


Post a Comment

Subscribe to Post Comments [Atom]

<< Home