######## Bovine Spongiform Encephalopathy #########
March 9, 2002, 6:29PM
Move on deer importing may be too late
By SHANNON TOMPKINS
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
Disease.
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
Kansas.
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
Madison.
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
http://www.chron.com/cs/CDA/story.hts/outdoors/tompkins/1288304
==================
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.
Smits2
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: bcaughey@nih.gov Received June 7, 2000;
revised July 3, 2000; accepted July 5, 2000.
Abstract
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.
snip...
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.
snip...
http://www.emboj.org/current.shtml
==================================
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
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
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######## Bovine Spongiform Encephalopathy #########
LET'S "GET A GRIP" ON CWD !
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
forever.
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
hysteria?
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
disease."
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
http://www.texasdeerassociation.com/jj_letter.htm
http://www.texasdeerassociation.com/news.htm
Hunting Seasons Are Here
FROM THE PRESIDENT
Jerry Johnston
President and Founder
snip...
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."
snip...
Jerry Johnston
President and Founder
Respectfully,
Jerry Johnston
President and Founder
http://209.221.152.85/framesets/presidentindex.html
http://209.221.152.85/index.php
=================
Greetings,
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;
http://www.testcowsnow.com/
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...
snip...
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
snip...
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.
snip...
http://www.aphis.usda.gov/vs/nahps/cwd/cwd-program.html
some concerns of
mine about TEXAS CWD potential and TEXAS
policy on herd contamination and
quarantine;
snip...
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.
snip...
(Because CWD is slow
to develop, the disease has not been seen
in younger deer and elk.)
snip...
http://www.tahc.state.tx.us/News/Press_Releases/1999.04_Chronic_Wasting.pdf
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
snip...
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.
snip...
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.
snip...
http://nps.ars.usda.gov/publications/publications.htm?lognum=0000103091
Subject: TSE
THREAT TO USA INCREASES, AGUZZI WARNS OF CWD DANGER TO HUMANS
Date: Sat, 29
Jun 2002 18:12:35 -0700
From: "Terry S. Singeltary Sr."
To: BSE-L
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
Zurich. KAREN BIRMINGHAM, LONDON
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 medicine.nature.com
NUMBER 5 R VOLUME 8 RNATURE MEDICINE
R
============================================
Transfusion
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.
Affiliations
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.
ABBREVIATIONS:
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:
http://dx.doi.org/10.1046/
j.1537-2995.2002.00098.x
http://www.blackwell-synergy.com/servlet/useragent?func=synergy&synergyAction=showAbstract&doi=10.1046/j.1537-2995.2002.00098.x
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.
snip...
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
provinces.
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_.
snip...
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."
http://www.nandotimes.com/healthscience/story/453225p-3628137c.html
CONTINUED...TSS
Subject: MAD DEER/ELK
DISEASE CWD AND POTENTIAL SOURCES IN USA !!!
Date: May 25,
2002 at 4:48 pm PST
######## Bovine Spongiform Encephalopathy #########
MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
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
sheep.
http://www.surefed.com/deer.htm
================================
animal sterol????????????????TSS
Ingredients
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.
http://www.bodefeed.com/prod3.htm
=================================
[MORE ANIMAL PROTEIN PRODUCTS.....tss]
BODE'S GAME FEED SUPPLEMENT #400
A RATION FOR DEER
NET WEIGHT 50
POUNDS
22.6 KG.
GUARANTEED ANALYSIS
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%
Ingredients
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.
Ration
CORN 666.67 LBS
PEAS 666.67 LBS
F# 3153 666.67 LBS
FEEDING DIRECTIONS
Feed Free Choice
http://www.bodefeed.com/prod7.htm
===================================
[MORE ANIMAL PROTEIN...TSS]
Ingredients
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.
http://www.bodefeed.com/prod6.htm
===================================
MORE ANIMAL PROTEIN PRODUCTS FOR DEER
Bode's #1 Game Pellets
A RATION FOR DEER
F3153
GUARANTEED ANALYSIS
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%
Ingredients
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.
FEEDING DIRECTIONS
Feed as Creep Feed with Normal Diet
http://www.bodefeed.com/prod8.htm
[PROBABLY MORE HERE, JUST FOLLOW THE
''NEXT BUTTON PRODUCTS''...TSS]
=================
[MORE ANIMAL PROTEIN
DEER FEED...TSS]
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
nutrients
* 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.
PROFILE
Deer Builder Pellets
GUARANTEED ANALYSIS
Crude Protein, Not
less
than......................................................................................................20.0
%
Crude Fat, Not
less
than................................................................................................................2.0
%
Crude Fiber, Not
more
than........................................................................................................18.0
%
Calcium (Ca), Not
less
than.........................................................................................................1.0
%
Calcium (Ca), Not
more
than........................................................................................................1.5
%
Phosphorus (P), Not
less
than..................................................................................................0.95
%
Salt (NaCl), Not
less
than..............................................................................................................0.1
%
Salt (NaCl), Not
more
than............................................................................................................0.6
%
Potassium (K), Not
less
than.......................................................................................................1.0
%
Selenium (Se), ppm, Not
less
than..................................................................................................0.6
Copper
(Cu), ppm, Not
less
than......................................................................................................20
Zinc
(Zn), ppm, Not
less
than...........................................................................................................250
Vitamin
A, I.U./lb, Not
less
than..................................................................................................10,000
Vitamin
D3, I.U./lb, Not
less
than.....................................................................................................600
Vitamin
E, I.U./lb, Not
less
than..........................................................................................................70
INGREDIENTS
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
DIRECTIONS FOR USE
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.
http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html
[OR HOW ABOUT SOME ANIMAL FAT FOR YOUR ELK...TSS]
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.
PROFILE
Elk Lactation Cow Gest
GUARANTEED ANALYSIS
Crude Protein, Not
less
than.......................................................................................................16.0%
Crude
Fat, Not
less
than.................................................................................................................3.0%
Crude
Fiber, Not
more
than.........................................................................................................20.0%
Calcium
(Ca), Not
less
than..........................................................................................................1.0%
Phosphorus
(P), Not
less
than......................................................................................................0.4%
Salt
(NaCl), Not
less
than...............................................................................................................0.1%
Salt
(NaCl), Not
more
than.............................................................................................................0.6%
Potassium
(K), Not
less
than........................................................................................................1.1%
Magnesium
(Mg), Not
less
than....................................................................................................0.3%
Zinc
(Zn), ppm, Not
less
than...........................................................................................................190
Copper
(Cu), ppm, Not
less
than......................................................................................................50
Selenium
(Se), ppm, Not
less
than..................................................................................................0.5
Vitamin
A, I.U./lb, Not
less
than..................................................................................................15,000
Vitamin
D3, I.U./lb, Not
less
than.................................................................................................4,000
Vitamin
E, I.U./lb, Not
less
than..........................................................................................................75
INGREDIENTS
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
DIRECTIONS FOR USE
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
http://www.profilenutrition.com/Products/Specialty/elk_lactationcowgest.html
===================================================
considering 1/2 to 1 gram of TSE material is lethal;
DEPARTMENT OF HEALTH & HUMAN SERVICES
PUBLIC HEALTH SERVICE
FOOD
AND DRUG ADMINISTRATION
April 9, 2001 WARNING LETTER
01-PHI-12
CERTIFIED MAIL
RETURN RECEIPT REQUESTED
Brian J. Raymond, Owner
Sandy Lake Mills
26 Mill Street
P.O. Box
117
Sandy Lake, PA 16145
PHILADELPHIA DISTRICT
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
distinguished
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...
http://www.fda.gov/foi/warning_letters/g1115d.pdf
===================================================
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.
http://www.gamecalls.net/huntingproducts/deerlures.html
ELK SCENT/SPRAY BOTTLE
*
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
http://www.elkinc.com/Scent.asp
prions in urine?
[PDF] A URINE TEST FOR THE IN-VIVO DIAGNOSIS OF PRION DISEASES
http://www.sigov.si/vurs/PDF/diagnoastika-bse-urin.pdf
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
Scotland.
Ronald B. Caffey
Assistant to the Deputy Administrator
Plant Protection
and Quarantine
http://www.aphis.usda.gov/ppq/manuals/PPQ_BB/Update%20APM%20120299.htm
TO: ALL PPQ PORT OFFICES
(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
http://www.aphis.usda.gov/ppq/manuals/PPQ_BB/Update%20APM%20060500.htm
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
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
############
######## 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 ceverett@tahc.state.tx.us
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."
---30---
TSS
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Mad cow disease: Could it be here? / Man's
stubborn crusade attracts experts' notice
CAROL CHRISTIAN Staff
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:
FOR IMMEDIATE RELEASE
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, www.tpwd.state.tx.us/CWD or at the Chronic Wasting Disease Alliance
website, www.cwd-info.org.
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
LANCET INFECTIOUS DISEASE JOURNAL
Volume 3, Number 8 01 August 2003
Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
My name is Terry S Singeltary Sr, and I live in
Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been
searching for answers ever since. What I have found is that we have not been
told the truth. CWD in deer and elk is a small portion of a much bigger problem.
49-year-old Singeltary is one of a number of people
who have remained largely unsatisfied after being told that a close relative
died from a rapidly progressive dementia compatible with spontaneous
Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents
on transmissible spongiform encephalopathies (TSE) and realised that if Britons
could get variant CJD from bovine spongiform encephalopathy (BSE), Americans
might get a similar disorder from chronic wasting disease (CWD)the relative of
mad cow disease seen among deer and elk in the USA. Although his feverish search
did not lead him to the smoking gun linking CWD to a similar disease in North
American people, it did uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few
attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states
have made CJD reportable. Human and animal TSEs should be reportable nationwide
and internationally, he complained in a letter to the Journal of the American
Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue
to expect us to still believe that the 85% plus of all CJD cases which are
sporadic are all spontaneous, without route or source.
Until recently, CWD was thought to be confined to the
wild in a small region in Colorado. But since early 2002, it has been reported
in other areas, including Wisconsin, South Dakota, and the Canadian province of
Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic
previously increased concern about a widespread outbreak and possible
transmission to people and cattle.
To date, experimental studies have proven that the
CWD agent can be transmitted to cattle by intracerebral inoculation and that it
can cross the mucous membranes of the digestive tract to initiate infection in
lymphoid tissue before invasion of the central nervous system. Yet the
plausibility of CWD spreading to people has remained elusive.
Getting data on TSEs in the USA from the government
is like pulling teeth, Singeltary argues. You get it when they want you to have
it, and only what they want you to have.
SNIP...FULL TEXT ;
now, a few things to ponder about those said double fences that will
supposedly stop those deer from escaping.
what about water that drains from any of these game farms. surrounding
water tables etc., are the double fences going to stop the water from becoming
contaminated? where does it drain? who's drinking it?
Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic
Area
65
Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal
Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and
M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of
Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort
Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services,
United States Department of Agriculture, Fort Collins, Colorado, 80521, USA
3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA
4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory,
University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology,
Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging,
University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author-
tracy.a.nichols@aphis.usda.gov
Chronic wasting disease (CWD) is the only known transmissible spongiform
encephalopathy affecting free-ranging wildlife. Experimental and epidemiological
data indicate that CWD can be transmitted horizontally and via blood and saliva,
although the exact mode of natural transmission remains unknown. Substantial
evidence suggests that prions can persist in the environment, implicating it as
a potential prion reservoir and transmission vehicle. CWD- positive animals can
contribute to environmental prion load via biological materials including
saliva, blood, urine and feces, shedding several times their body weight in
possibly infectious excreta in their lifetime, as well as through decomposing
carcasses. Sensitivity limitations of conventional assays hamper evaluation of
environmental prion loads in water. Here we show the ability of serial protein
misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions
in spiked water samples at a 1:1 x106 , and protease-resistant prions in
environmental and municipal-processing water samples from a CWD endemic area.
Detection of CWD prions correlated with increased total organic carbon in water
runoff from melting winter snowpack. These data suggest prolonged persistence
and accumulation of prions in the environment that may promote CWD transmission.
snip...
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
snip...end...full text at ;
what about rodents there from? 4 American rodents are susceptible to CWD to
date. are those double fences going to stop these rodents from escaping these
game farms once becoming exposed to CWD?
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A.
Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel
J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary
Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI
53706, USA 2US Geological Survey, National Wildlife Health Center, 6006
Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural
Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary
Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author
email: cjohnson@svm.vetmed.wisc.edu
We intracerebrally challenged four species of native North American rodents
that inhabit locations undergoing cervid chronic wasting disease (CWD)
epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed
mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles
(Myodes gapperi). The inocula were prepared from the brains of hunter-harvested
white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles
proved to be most susceptible, with a median incubation period of 272 days.
Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the
brains of all challenged meadow voles. Subsequent passages in meadow voles lead
to a significant reduction in incubation period. The disease progression in
red-backed voles, which are very closely related to the European bank vole (M.
glareolus) which have been demonstrated to be sensitive to a number of TSEs, was
slower than in meadow voles with a median incubation period of 351 days. We
sequenced the meadow vole and red-backed vole Prnp genes and found three amino
acid (AA) differences outside of the signal and GPI anchor sequences. Of these
differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is
particularly intriguing due its postulated involvement in "rigid loop" structure
and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5
years post-inoculation, but appear to be exhibiting a high degree of disease
penetrance. White-footed mice have an even longer incubation period but are also
showing high penetrance. Second passage experiments show significant shortening
of incubation periods. Meadow voles in particular appear to be interesting lab
models for CWD. These rodents scavenge carrion, and are an important food source
for many predator species. Furthermore, these rodents enter human and domestic
livestock food chains by accidental inclusion in grain and forage. Further
investigation of these species as potential hosts, bridge species, and
reservoirs of CWD is required.
please see ;
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M.
Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness. Two of these cats have
developed rear limb ataxia. Although the limited data from this ongoing study
must be considered preliminary, they raise the potential for cervid-to-feline
transmission in nature.
www.landesbioscience.com Prion
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
----- 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
====================END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
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)
http://chronic-wasting-disease.blogspot.com/2012/06/natural-cases-of-cwd-in-eight-sika-deer.html
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).
SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5).
PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B).
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Wednesday, April 25,
2012
USA MAD COW DISEASE AND CJD THERE FROM
SINGELTARY ET AL 1999 – 2012
Tuesday, July 29, 2008
Heidenhain Variant Creutzfeldt Jakob Disease Case Report
FINAL AUTOPSY DIAGNOSIS
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,
terry
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