Texas Animal Health Commission (TAHC) is Now Accepting Comments on Rule Proposals for “Chronic Wasting Disease (CWD)”
Texas Animal Health Commission (TAHC)
Announcement
October 12, 2012 The Texas Animal Health Commission (TAHC) is Now Accepting
Comments on Rule Proposals
The Texas Animal Health Commission (TAHC) is now accepting public comments
on rules proposed at its September 18, 2012 Commission meeting.
Proposed rules to amend Chapter 40, entitled "Chronic Wasting Disease
(CWD)" have a 45-day comment period. To read the full news release with details
on the proposals to modify the CWD rules,visit
This specific rule proposal may be commented on until 5 p.m. on Monday,
November 26, 2012.
The Commission is also proposing amendments to the following:
Chapter, 33, Fees, CVI Fee (Moving from Chapter 59) Chapter 35,
Brucellosis, Identification Chapter 38, Trichomoniasis Chapter 51, Entry
Requirements, Cattle, Cervidae Chapter 59, E.D. Declaration for a Disease High
Risk Area or County *These proposals have a 30-day comment period. Comments must
be submitted by 5 p.m. on Monday, November 12, 2012.*
A detailed explanation of each rule proposal, including the CWD rule
proposal can be found on the TAHC web site at http://www.tahc.state.tx.us/regs/proposals.html.
The TAHC encourages and appreciates all comments. Comments on the TAHC's
proposed regulations must be submitted in writing to Carol Pivonka, Texas Animal
Health Commission, 2105 Kramer Lane, Austin, Texas 78758, by fax at (512)
719-0721 or by e-mail to comments@tahc.state.tx.us
Leisa Fletcher, Communications & Public Relations Assistant Texas
Animal Health Commission (TAHC)
www.tahc.state.tx.us
1-800-550-8242
www.Facebook.com/TexasAHC
FOR IMMEDIATE RELEASE
September 27, 2012
TAHC Proposes Modifications to Chronic Wasting Disease (CWD) Rules
AUSTIN – The Texas Animal Health Commission (TAHC) will soon be accepting
public comments on rules proposed at its September 18 meeting to amend Chapter
40, entitled “Chronic Wasting Disease (CWD)”. Publication of the proposed rules
is expected to be in mid-October with a 45 day comment period to follow.
The proposed rules revise numerous current requirements in an effort to
address recent developments involving CWD. This includes the diagnosis of CWD in
two mule deer near the New Mexico border and the addition of red deer and Sika
deer to the list of species susceptible to CWD. The amendments would also bring
Texas rules into alignment with the recently released Federal CWD interim final
rule, which sets the minimum standards for interstate movement of cervid
species.
The proposed TAHC rules apply to the non-indigenous cervid species of Texas
under its jurisdiction. The Texas Parks and Wildlife Department (TPWD) is also
in the process of evaluating its rules for the cervid species it regulates
(indigenous to Texas), including white-tailed deer and mule deer.
Below are key points of the proposed rules to Chapter 40:
• Require additional cervid species such as North American Elk or Wapiti,
red deer and Sika deer to participate in surveillance for CWD if they are being
moved or transported within the state.
• Provide enrollment requirements for the TAHC Complete Monitored Herd
Program for CWD, based in large part on the USDA interim final rule on CWD.
o Complete physical inventory of the herd every three years
o Fences must be 8 feet in height for herds enrolling after the rule is
effective
o Require 30 feet of separation between herds, with no shared working
facilities
o Requires reporting of all CWD suspicious animals and testing of all death
losses in animals 12 months of age or older (changed from 16 months).
• Delegates authority to the Executive Director to issue an order to
declare a CWD high risk area or county based on sound epidemiological principles
for disease detection, control and eradication.
“The rule proposals are written to meet the federal standards but they can
be adapted to recognize comments received,” Dr. Andy Schwartz, Assistant
Executive Director, said. “The TAHC is committed to hosting as many meetings as
necessary with the cervid industry and stakeholder groups to ensure that a
successful Texas specific program is created that matches the USDA interim final
rule. The TAHC’s ultimate goal is to enhance marketability.”
CWD has never been shown to affect people or domestic livestock. The
progressively fatal disease causes chronic weight loss and abnormal behavior
such as disorientation. Prions (the infectious agent of CWD), are present in the
body fluids of infected animals, and can be shed onto the soil where they may
remain infectious to other susceptible animals for many years. For this reason
the proposed TAHC rules apply to land, as well as cervids where CWD has been
found or is likely to be found.
At its September 18 meeting, the Commission also passed a rule proposed at
their previous meeting, establishing movement restriction zones in the
Trans-Pecos Region of far West Texas. This will allow a coordinated effort
between the TAHC and TPWD to control and contain CWD in the Hueco Mountains
where it was recently discovered. The two agencies are currently working on
plans for enhanced hunter kill surveillance and movement control enforcement for
the coming hunting season.
“The TAHC will continue to work closely with Texas Parks and Wildlife and
the CWD Task Force to ensure alignment of our rules and cooperation to protect
the health of the entire cervid population of Texas,” said Dr. Dee Ellis, State
Veterinarian and TAHC Executive Director.
A detailed explanation of the rule proposals will be available soon on the
TAHC web site at http://www.tahc.state.tx.us/regs/proposals.html
.
The TAHC rule proposals have a comment period of 45 days once they have
been published. The TAHC encourages and appreciates all comments.
Comments on the TAHC’s proposed regulations must be submitted in writing to
Carol Pivonka, Texas Animal Health Commission, 2105 Kramer Lane, Austin, Texas
78758, by fax at (512) 719-0721 or by e-mail to comments@tahc.state.tx.us .
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.
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Greetings TAHC, Carol Pivonka, et al,
I kindly wish to comment on the proposed rule making for “Chronic Wasting
Disease (CWD)”.
AS a layperson, and since the confirmed death of my mother to the
Heidenhain Variant of Creutzfeldt Jakob Disease, I have followed the mad cow
debacle/blunder, the CWD blunder, the scrapie blunder, and the human CJD
science, daily since that day December 14, 1997 MOM DOD hvCJD. I made a promise
to her about the fact I would not let this die with her. back then there was no
information, and I made a promise I would my best to find this information, make
it public, for everyone to know.
There is much science out there, updated peer review science, and
transmission studies, that dispute some of the things said by TAHC, and other
government agencies, I wish to kindly submit this science. I hope that my
submission is made available to the public, and especially the members of the
meeting that is to be held on September 18, 2012 meeting, to amend Chapter 40,
entitled “Chronic Wasting Disease (CWD)”.
My submission is as follows, and I will comment after each key point
separately ;
Below are key points of the proposed rules to Chapter 40:
• Require additional cervid species such as North American Elk or Wapiti,
red deer and Sika deer to participate in surveillance for CWD if they are being
moved or transported within the state.
• Provide enrollment requirements for the TAHC Complete Monitored Herd
Program for CWD, based in large part on the USDA interim final rule on CWD.
o Complete physical inventory of the herd every three years
o Fences must be 8 feet in height for herds enrolling after the rule is
effective
o Require 30 feet of separation between herds, with no shared working
facilities
o Requires reporting of all CWD suspicious animals and testing of all death
losses in animals 12 months of age or older (changed from 16 months).
• Delegates authority to the Executive Director to issue an order to
declare a CWD high risk area or county based on sound epidemiological principles
for disease detection, control and eradication.
>>> • Require additional cervid species such as North American Elk
or Wapiti, red deer and Sika deer to participate in surveillance for CWD if they
are being moved or transported within the state.
1st and foremost, any voluntary cwd program will fail.
BY only requiring this, ONLY ‘if these cervids are being moved or
transported within state’, and NOT in general, this is a mistake. Elk or Wapiti,
red deer and Sika that are not moved within state, will not be in the
surveillance program, and these animals could potentially risk CWD to other herd
mates, that might be transported within state.
ALSO, these same cervids, once traded within state, could potentially be
subclinically infected with CWD (considering cwd testing protocols, age limits
etc.), and once traded within state, could it not be possible to then trade them
out of state?
*** I propose this proposal should be that all cervids, should be in this
CWD surveillance program, and this program should be MANDATORY, if the state is
going to license ANY game farm or fenced in game farm/ranch. ...TSS
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)
Tuesday, June 19, 2012
Experimental Oral Transmission of Chronic Wasting Disease to Reindeer
(Rangifer tarandus tarandus)
====================================
>>> • Provide enrollment requirements for the TAHC Complete
Monitored Herd Program for CWD, based in large part on the USDA interim final
rule on CWD.
o Complete physical inventory of the herd every three years
o Fences must be 8 feet in height for herds enrolling after the rule is
effective
o Require 30 feet of separation between herds, with no shared working
facilities
o Requires reporting of all CWD suspicious animals and testing of all death
losses in animals 12 months of age or older (changed from 16 months).
FIRST LET’S look at the USDA interim final rule on CWD and my submission ;
Comment from Terry Singeltary Document ID: APHIS-2011-0032-0002Document
Type: Public Submission This is comment on Notice: Agency Information Collection
Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd
Certification Program Docket ID: APHIS-2011-0032RIN: Topics: No Topics
associated with this document
View Document: Show Details
Document Subtype: Public Comment Status: Posted Received Date: January 24
2012, at 12:00 AM Eastern Standard Time Date Posted: January 25 2012, at 12:00
AM Eastern Standard Time Comment Start Date: January 24 2012, at 12:00 AM
Eastern Standard Time Comment Due Date: March 26 2012, at 11:59 PM Eastern
Daylight Time Tracking Number: 80fa2c68 First Name: Terry Middle Name: S. Last
Name: Singeltary City: Bacliff Country: United States State or Province: TX
Organization Name: LAYPERSON Submitter's Representative: CJD TSE PRION VICTIMS
Comment:
Agency Information Collection Activities; Proposals, Submissions, and
Approvals: Chronic Wasting Disease Herd Certification Program (Document ID
APHIS-2011-0032-0001) I believe that any voluntary program for CWD free herd
certification from game farms will be futile, as was the partial and voluntary
mad cow feed ban of August 4, 1997. That failed terribly, with some 10,000,000
of banned blood laced MBM being fed out in 2007, a decade post August 4, 1997
partial and voluntary ban. Game farms are a petri dish for CWD TSE Prion
disease, with Wisconsin having documented 9 CWD infected game farms, with one
having the highest CWD infection rate in the world, 80% CWD infection rate. I
believe that all game farms should be SHUT DOWN PERMANENTLY. CWD TSE prion
disease survives ashing to 600 degrees celsius, that’s around 1112 degrees
farenheit. you cannot cook the CWD TSE prion disease out of meat. you can take
the ash and mix it with saline and inject that ash into a mouse, and the mouse
will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still Infectious
after Biodiesel Production as well. the TSE prion agent also survives Simulated
Wastewater Treatment Processes. IN fact, you should also know that the CWD TSE
Prion agent will survive in the environment for years, if not decades. you can
bury it and it will not go away. CWD TSE agent is capable of infected your water
table i.e. Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area. it’s not your ordinary pathogen you can just cook it out and
be done with. that’s what’s so worrisome about Iatrogenic mode of transmission,
a simple autoclave will not kill this TSE prion agent.
Tuesday, December 20, 2011 CHRONIC WASTING DISEASE CWD WISCONSIN Almond
Deer (Buckhorn Flats) Farm Update DECEMBER 2011
additional data submission ;
Name: Terry S. Singeltary
Address: Bacliff, TX,
Submitter's Representative: CJD TSE PRION VICTIMS
Organization: LAYPERSON
--------------------------------------------------------------------------------
General Comment
Agency Information Collection Activities; Proposals, Submissions, and
Approvals: Chronic Wasting Disease Herd Certification Program (Document ID
APHIS-2011-0032-0001)
I believe that any voluntary program for CWD free herd certification from
game farms will be futile, as was the partial and voluntary mad cow feed ban of
August 4, 1997. That failed terribly, with some 10,000,000 of banned blood laced
MBM being fed out in 2007, a decade post August 4, 1997 partial and voluntary
ban.
Game farms are a petri dish for CWD TSE Prion disease, with Wisconsin
having documented 9 CWD infected game farms, with one having the highest CWD
infection rate in the world, 80% CWD infection rate.
I believe that all game farms should be SHUT DOWN PERMANENTLY.
CWD TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit.
you cannot cook the CWD TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a
mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the CWD TSE Prion agent will survive in
the environment for years, if not decades.
you can bury it and it will not go away.
CWD TSE agent is capable of infected your water table i.e. Detection of
protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple
autoclave will not kill this TSE prion agent.
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
=====================================
>>> o Complete physical inventory of the herd every three years
By only doing a physical inventory of the herd every three years, any
cervid escapee from any game farm will not be detected for 3 years. This will
allow 3 years for any potential CWD infected cervid that might escape to infect
the wild herds.
*** I propose a physical inventory of the herd should be done every year,
and this should be mandatory. ...TSS
Deer, elk continue to escape from state farms
Article by: DOUG SMITH , Star Tribune Updated: March 14, 2011 - 12:08 PM
Curbing chronic wasting disease remains a concern; officials are increasing
enforcement.
Almost 500 captive deer and elk have escaped from Minnesota farms over the
past five years, and 134 were never recaptured or killed.
So far this year, 17 deer have escaped, and officials are still searching
for many of those.
see ;
Friday, September 28, 2012
Stray elk renews concerns about deer farm security Minnesota
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
==================================
>>> o Fences must be 8 feet in height for herds enrolling after
the rule is effective
IT’s been documented that cervids can jump much higher than 8ft. This is a
fact. This 8 foot rule on single fence heights does not completely protect the
wild cervid herds from Chronic Wasting Disease CWD.
*** I propose that it should be mandatory for double fencing, with the
height of either fence not to be any lower than 12 feet, if these deer
farms/ranches are going to be in existence. WE MUST PROTECT OUR WILD HERDS.
...TSS
Oh deer! Animals escape from Todmorden farm after fence cut
Published on Saturday 7 April 2012 15:00
A STAG and six hinds are on the loose after a wire fence was cut at a
Todmorden deer farm.
The damage was carried out between Tuesday April 3 and 8am the following
day at East Hey Farm, Stone Cross Road.
The high-value animals are reported to have run in the direction of
Burnley.
Police and the owner are appealing for witnesses or anyone with information
to contact Sergeant Damon Walker on 101 or Crimestoppers, in confidence, on 0800
555 111.
Last year, only one deer was removed from the airport. It was unclear how
the deer got past the wildlife fence — there might have been a small opening in
the fence, or the deer might have simply jumped the 10 feet. Scherschligt said
wildlife studies indicate that deer can sometimes jump 12-foot-tall
obstructions, and the U.S. Department of Agriculture rates some whitetail deer
as capable of jumping 15 feet.
Jumping to a vertical height of at least eight feet, deer can scale over
barriers you may think are impossible. Watching a deer confronted with a
vertical, eight-foot tall, hight-tensile wire fence then
watching it leap over from a standing position makes a startling
impression. A frightened deer mhurdle a fence as high as 12 feet if given a
running start and enough adrenalin. Horizontally, a deer may leap 15 to 30 feet,
the longer distance only when frightened. In general, a deer may jump high or
long, but not both at the same time. Deer have also been known to crawl under
fences and through openings as small as 7.5 inches. The will of a deer to
penetrate a fence is dependent on the force of the motivation behind it.
Sauer (1984) reported white-tailed deer could jump a 2.1-m fence from a
standing start and could jump a 2.4-m fence from a running start. In
contradiction, Fitzwater (1972) indicates that a 2.4-m fence is sufficient to
prevent deer from jumping. Ludwig and Bremicker (1981) concluded that 2.4-m
fencing was effective at keeping deer out of roadways as long as the length of
the fence is extended well beyond the high-risk area for deer-vehicle
collisions.
===================================
>>> o Require 30 feet of separation between herds, with no shared
working facilities
IN my opinion, 30 feet is not enough separation between herds, considering
AEROSOL SPREAD of the CWD TSE prion agent via dirt. Also, the spreading of the
CWD TSE agent via rodents in the pens, from pen to pen, and any potential salvia
from any feed that may be transferred from pen to pen via said rodents, could be
a risk factor.
*** I propose that all pens should be double fenced as I proposed above,
and that the separation between herds, should be much, much, greater than the 30
feet proposed, and that risk factors for any potential AEROSOL SPREAD, DIRT,
RODENTS, WATER. ...TSS
Saturday, September 01, 2012
Resistance of Soil-Bound Prions to Rumen Digestion
Monday, September 17, 2012
Rapid Transepithelial Transport of Prions Following Inhalation
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
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 ;
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 ;
======================================
>>> o Requires reporting of all CWD suspicious animals and testing
of all death losses in animals 12 months of age or older (changed from 16
months).
Chronic Wasting Disease CWD, has been documented in many cervids (when
tested), much younger than the 12 month rule now proposed. AS I so much
appreciate the TAHC decreasing the age from 16 months to 12 months, I believe
this rule to still leave a risk factor, due to the fact fawns as young as 4 or 5
months old have been documented with CWD.
*** I propose that ALL farmed cervids should be tested for CWD. going into
a farm, leaving a farm, and or at death. ...TSS
Wisconsin : Six White-Tailed Deer Fawns Test Positive for CWD
Date: May 13, 2003 Source: Wisconsin Department of Natural Resources
Contacts: Julie Langenberg Wildlife Veterinarian 608-266-3143 Tom Hauge
Director, Bureau of Wildlife Management 608-266-2193
MADISON -- Six fawns in the area of south central Wisconsin where chronic
wasting disease has been found in white-tailed deer have tested positive for the
disease, according to Department of Natural Resources wildlife health officials.
These are the youngest wild white-tailed deer detected with chronic wasting
disease (CWD) to date.
Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of fawns
sampled were between the ages of 5 to 9 months, though some were as young as 1
month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of
the positive fawns were taken from the core area of the CWD eradication zone
where the highest numbers of positive deer have been identified.
"This is the first intensive sampling for CWD in fawns anywhere," said Dr.
Julie Langenberg, Department of Natural Resources wildlife veterinarian, "and we
are trying to learn as much as we can from these data".
"One noteworthy finding is simply the fact that we found positive fawns,"
Dr. Langenberg said. "These results do show us that CWD transmission can happen
at a very young age in wild white-tailed deer populations. However, we found
that the percentage of fawns infected with CWD is very low, in the area of 0.14
percent. If there was a higher rate of infection in fawns, then fawns dispersing
in the spring could be much more worrisome for disease spread."
Dr. Langenberg noted that while the youngest CWD-positive fawns had
evidence of disease-causing prions only in lymph node tissue, several of the
older CWD-positive fawns had evidence of CWD prions in both lymph node and brain
tissues -- suggesting further progression of the disease.
"Finding CWD prions in both lymph and brain tissues of deer this young is
slightly surprising," said Langenberg, "and provides information that CWD
infection and illness may progress more rapidly in a white-tailed deer than
previously suspected. Published literature suggests that CWD doesn't cause
illness in a deer until approximately 16 months of age. Our fawn data shows that
a few wild white-tailed deer may become sick from CWD or may transmit the
disease before they reach that age of 16 months."
One of the positive fawns was shot with a doe that was also CWD positive.
Information about these fawn cases combined with will help researchers who are
studying the age and routes of CWD transmission in wild deer populations. "More
data analysis and ongoing deer movement studies should give us an even better
understanding of how this disease moves across the landscape", said Langenberg.
"Thanks to eradication zone hunters who submitted deer of all ages for
sampling, we have a valuable set of fawn data that is contributing to our
state's and the nation's understanding about CWD," Langenberg said.
> > > Two of the six fawns with CWD detected were 5 to 6 months
old. < < <
Why doesn't the Wisconsin DNR want to routinely test fawns ?
The DNR highly discourages the testing of any fawns regardless of where
they were harvested. Of the more than 15,000 fawns from the CWD-MZ that have
been tested, only 23 were test positive, and most of those were nearly one year
old. It is exceedingly unlikely that a deer less than one year old would test
positive for CWD, even in the higher CWD prevalence areas of southern Wisconsin.
Few fawns will have been exposed to CWD, and because this disease spreads
through the deer's body very slowly, it is very rare in a fawn that the disease
has progressed to a level that is detectable. This means that testing a fawn
provides almost no information valuable to understanding CWD in Wisconsin's deer
herd and does not provide information of great value to the hunter in making a
decision about venison consumption.
> > > It is exceedingly unlikely that a deer less than one year
old would test positive for CWD < < < ???
Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm
and 15 of 22 fawns aged 6 to 9 months (68.2%) were positive.
specific susceptibility?
194. It is probable, based on age-class specific prevalence data from wild
cervids and epidemiological evidence from captive cervids in affected research
centres, that both adults and fawns may become infected with CWD (Miller, Wild
& Williams, 1998; Miller et al., 2000).
198. In Odocoileus virginianus – white tailed deer, out of 179 white-tailed
deer which had become enclosed by an elk farm fence, in Sioux County,
northwestern Nebraska, four fawns only eight months old were among the 50% of
CWD-positive animals; these fawns were not showing any clinical signs of CWD
(Davidson, 2002).
see full text ;
Saturday, February 04, 2012
Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
=================================
>>> • Delegates authority to the Executive Director to issue an
order to declare a CWD high risk area or county based on sound epidemiological
principles for disease detection, control and eradication.
IN my opinion, there has been no ‘sound epidemiological principles for
disease detection, control and eradication’ in Texas for CWD, or any other TSE.
It’s been just the opposite. NOT even speaking about all the risk factors from
the cervid game ranch farms in Texas over the years, and trading, and the lax
rules and enforcement of said rules there from, the fact that CWD infected deer
have been waltzing across Texas for the past decade, in the exact spot I tried
warning TAHC back in 2001-2002, i.e. the Texas, New Mexico border at the WSMR
area, the complete state of Texas is at risk for CWD, and has been at risk for
CWD for years.
*** I propose that Texas, and the Executive Director, should take that
authority, and declare the complete state of Texas (not just a high risk area,
where the State of New Mexico finally forced Texas to finally test, and finally
embarrassed Texas enough to finally do CWD testing where it should have been
done 10 years ago), but I believe the complete state of Texas should be declared
a high risk area for CWD, until proper testing (in sufficient numbers, in all
geographical regions), and tested 100% of all farmed cervids. ...TSS
2001 - 2002
TEXAS OLD STATISTICS BELOW FOR PAST CWD TESTING;
Subject: CWD testing in Texas
Date: Sun, 25 Aug 2002 19:45:14 –0500
From: Kenneth Waldrup
To: flounder@wt.net
Dear Dr. Singletary,
In Fiscal Year 2001, seven deer from Texas were tested by the National
Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed
deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer).
During these two years, an additional six elk and one white-tailed deer were
tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal
Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least
eight other white-tailed deer have been tested at TVMDL. One elk has been tested
at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke
of the Texas Parks and Wildlife Department also has records of 601 clinically
ill white-tailed deer which were necropsied at Texas A&M during the late
1960's and early 1970's, and no spongiform encepalopathies were noted.
Thank you for your consideration.
Ken Waldrup, DVM, PhD Texas Animal Health Commission
========================
TEXAS CWD STATUS
Captive Cervids
There have been no reported CWD infections of captive elk or deer in Texas.
There is currently no mandatory surveillance program for susceptible cervids
kept on game farms, although, there has been voluntary surveillance since 1999,
which requires owners of participating herds to maintain an annual herd
inventory and submit samples for all mortalities of animals over 16 months of
age.
snip...
SO, i thought i would just see where these Ecoregions were, and just how
the CWD testing was distributed. YOU would think that with the cluster of CWD
bordering TEXAS at the WPMR in NM, you would have thought this would be where
the major CWD testing samples were to have been taken? wrong! let's have a look
at the sample testing. here is map of CWD in NM WPMR bordering TEXAS;
NEW MEXICO 7 POSITIVE CWD WHITE SANDS MISSILE RANGE MAP
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging
Cervids and see where the CWD cluster in NM WSMR borders TEXAS;
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
Ecoregions of TEXAS
IF you look at the area around the NM WSMR where the CWD cluster was and
where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my
Geography and my Ciphering is correct ;-) that region only tested 55% of it's
goal. THE most important area on the MAP and they only test some 96 samples,
this in an area that has found some 7 positive animals? NOW if we look at the
only other border where these deer from NM could cross the border into TEXAS,
this area is called the High Plains ecoregion, and again, we find that the
sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD
sampling was met, only 16 samples were tested from some 175 that were suppose to
be sampled.
AS i said before;
> SADLY, they have not tested enough from the total population to
> know if CWD is in Texas or not.
BUT now, I will go one step further and state categorically that they are
not trying to find it. just the opposite it seems, they are waiting for CWD to
find them, as with BSE/TSE in cattle, and it will eventually...
snip...see full text ;
Thursday, September 27, 2012
TAHC Proposes Modifications to Chronic Wasting Disease (CWD) Rules
September 27, 2012
NEWS RELEASE
Texas Animal Health Commission
Wednesday, September 26, 2012
TPWD Gearing Up for CWD Response during Deer Season
Monday, September 17, 2012
New Mexico DGF EXPANDS CHRONIC WASTING DISEASE CONTROL AREAS, while Texas
flounders
Friday, September 07, 2012
Texas Wildlife Officials Considering New Deer Movement Rules in Response to
CWD
Saturday, July 07, 2012
TEXAS Animal Health Commission Accepting Comments on Chronic Wasting
Disease Rule Proposal
Considering the seemingly high CWD prevalence rate in the Sacramento and
Hueco Mountains of New Mexico, CWD may be well established in the population and
in the environment in Texas at this time.
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West
Texas
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILS FROM TEXAS BORDER
Saturday, June 09, 2012
USDA Establishes a Herd Certification Program for Chronic Wasting Disease
in the United States
Wednesday, June 13, 2012
TAHC Modifies Entry Requirements Effective Immediately for Cervids DUE TO
CWD
FOR IMMEDIATE RELEASE
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
key word here is _considering_. so consider this, CWD still spreading in
Texas. ...TSS
Friday, September 07, 2012
Texas Wildlife Officials Considering New Deer Movement Rules in Response to
CWD
Friday, August 31, 2012
COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a
review
Friday, June 01, 2012
TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Friday, August 24, 2012
Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting
disease within white-tailed deer (Odocoileus virginianus) herds in North America
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation,
although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This
finding raised concerns that CWD prions might be transmitted to cattle grazing
in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight,
revealed abnormal clinical signs, and were euthanatized. Laboratory tests
revealed the presence of a unique pattern of the disease agent in tissues of
these animals. These findings demonstrate that when CWD is directly inoculated
into the brain of cattle, 86% of inoculated cattle develop clinical signs of the
disease.
" although the infection rate was low (4 of 13 animals [Hamir et al.
2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly
as possible all updates/comments that contribute substantially to the topic
under discussion.
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author
Affiliations
1Institute for Neurodegenerative Diseases, University of California, San
Francisco, San Francisco, California 94143 2Department of Neurology, University
of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As
the only prion disease identified in free-ranging animals, CWD appears to be far
more communicable than other forms of prion disease. CWD was first described in
1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of
histopathology of the brain. Originally detected in the American West, CWD has
spread across much of North America and has been reported also in South Korea.
In captive populations, up to 90% of mule deer have been reported to be positive
for prions (Williams and Young 1980). The incidence of CWD in cervids living in
the wild has been estimated to be as high as 15% (Miller et al. 2000). The
development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible
to CWD, has enhanced detection of CWD and the estimation of prion titers
(Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces,
even in presymptomatic deer, has been identified as a likely source of infection
for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD
has been transmitted to cattle after intracerebral inoculation, although the
infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding
raised concerns that CWD prions might be transmitted to cattle grazing in
contaminated pastures.
snip...
----- Original Message -----
From: David Colby To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor
Department of Chemical Engineering University of Delaware
===========END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION
CONGRESS SEPTEMBER 8-11 2010
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN,
AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY
PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF
FILE...TSS)
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. The purpose
of these experiments was to determine susceptibility of white-tailed deer (WTD)
to scrapie and to compare the resultant clinical signs, lesions, and molecular
profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD
intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral
and intranasal (IN); n = 5) with a US scrapie isolate.
All deer were inoculated with a 10% (wt/vol) brain homogenate from sheep
with scrapie (1ml IC, 1 ml IN, 30 ml oral). All deer inoculated by the
intracranial route had evidence of PrPSc accumulation. PrPSc was detected in
lymphoid tissues as early as 7 months-post-inoculation (PI) and a single deer
that was necropsied at 15.6 months had widespread distribution of PrPSc
highlighting that PrPSc is widely distributed in the CNS and lymphoid tissues
prior to the onset of clinical signs. IC inoculated deer necropsied after 20
months PI (3/5) had clinical signs, spongiform encephalopathy, and widespread
distribution of PrPSc in neural and lymphoid tissues.
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
After a natural route of exposure, 100% of WTD were susceptible to scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive.
This work demonstrates that WTD are highly susceptible to sheep scrapie,
but on first passage, scrapie in WTD is differentiable from CWD.
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
CHRONIC WASTING DISEASE CWD RISK FACTORS FOR TRANSMISSION TO HUMANS
Envt.06:
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2
Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6
and Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food
Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS
USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa,
ON Canada
†Presenting author; Email: emmanuel.comoy@cea.fr
The constant increase of chronic wasting disease (CWD) incidence in North
America raises a question about their zoonotic potential. A recent publication
showed their transmissibility to new-world monkeys, but no transmission to
old-world monkeys, which are phylogenetically closer to humans, has so far been
reported. Moreover, several studies have failed to transmit CWD to transgenic
mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the
only animal prion disease for which a zoonotic potential has been proven. We
described the transmission of the atypical BSE-L strain of BSE to cynomolgus
monkeys, suggesting a weak cattle-to-primate species barrier. We observed the
same phenomenon with a cattleadapted strain of TME (Transmissible Mink
Encephalopathy). Since cattle experimentally exposed to CWD strains have also
developed spongiform encephalopathies, we inoculated brain tissue from
CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice
overexpressing bovine or human PrP. Since CWD prion strains are highly
lymphotropic, suggesting an adaptation of these agents after peripheral
exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid
brains using the oral route. Nearly four years post-exposure, monkeys exposed to
CWD-related prion strains remain asymptomatic. In contrast, bovinized and
humanized transgenic mice showed signs of infection, suggesting that CWD-related
prion strains may be capable of crossing the cattle-to-primate species barrier.
Comparisons with transmission results and incubation periods obtained after
exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted
TME) will also be presented, in order to evaluate the respective risks of each
strain.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2
Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch
Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and
Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany
†Presenting author; Email: dausm@rki.de
Chronic wasting disease (CWD) is a contagious, rapidly spreading
transmissible spongiform encephalopathy (TSE) occurring in cervids in North
America. Despite efficient horizontal transmission of CWD among cervids natural
transmission of the disease to other species has not yet been observed. Here, we
report a direct biochemical demonstration of pathological prion protein PrPTSE
and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected
cervids. The presence of PrPTSE was detected by Western- and postfixed frozen
tissue blotting, while the seeding activity of PrPTSE was revealed by protein
misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal
muscles of CWD-infected WTD was estimated to be approximately 2000- to
10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE
was located in muscle- associated nerve fascicles but not, in detectable
amounts, in myocytes. The presence and seeding activity of PrPTSE in skeletal
muscle from CWD-infected cervids suggests prevention of such tissue in the human
diet as a precautionary measure for food safety, pending on further
clarification of whether CWD may be transmissible to humans.
Volume 18, Number 3—March 2012
Samuel E. Saunders1, Shannon L. Bartelt-Hunt, and Jason C. Bartz
Author affiliations: University of Nebraska-Lincoln, Omaha, Nebraska, USA
(S.E. Saunders, S.L. Bartelt-Hunt); Creighton University, Omaha (J.C. Bartz)
Synopsis
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
snip...
Most epidemiologic studies and experimental work have suggested that the
potential for CWD transmission to humans is low, and such transmission has not
been documented through ongoing surveillance (2,3). In vitro prion replication
assays report a relatively low efficiency of CWD PrPSc-directed conversion of
human PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are
resistant to CWD infection (31); these findings indicate low zoonotic potential.
However, squirrel monkeys are susceptible to CWD by intracerebral and oral
inoculation (32). Cynomolgus macaques, which are evolutionarily closer to humans
than squirrel monkeys, are resistant to CWD infection (32). Regardless, the
finding that a primate is orally susceptible to CWD is of concern...
snip...
Reasons for Caution There are several reasons for caution with respect to
zoonotic and interspecies CWD transmission. First, there is strong evidence that
distinct CWD strains exist (36). Prion strains are distinguished by varied
incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc
depositions (3,32). Strains have been identified in other natural prion
diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies
transmission of prions from CWD-positive deer and elk isolates resulted in
identification of >2 strains of CWD in rodent models (36), indicating that
CWD strains likely exist in cervids. However, nothing is currently known about
natural distribution and prevalence of CWD strains. Currently, host range and
pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of
CWD may also vary with CWD strain. In addition, diversity in host (cervid) and
target (e.g., human) genotypes further complicates definitive findings of
zoonotic and interspecies transmission potentials of CWD.
Intraspecies and interspecies passage of the CWD agent may also increase
the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial
passage naturally as the disease continues to emerge. In vitro and in vivo
intraspecies transmission of the CWD agent yields PrPSc with an increased
capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission
can alter CWD host range (38) and yield multiple novel prion strains (3,28). The
potential for interspecies CWD transmission (by cohabitating mammals) will only
increase as the disease spreads and CWD prions continue to be shed into the
environment. This environmental passage itself may alter CWD prions or exert
selective pressures on CWD strain mixtures by interactions with soil, which are
known to vary with prion strain (25), or exposure to environmental or gut
degradation.
Given that prion disease in humans can be difficult to diagnose and the
asymptomatic incubation period can last decades, continued research,
epidemiologic surveillance, and caution in handling risky material remain
prudent as CWD continues to spread and the opportunity for interspecies
transmission increases. Otherwise, similar to what occurred in the United
Kingdom after detection of variant CJD and its subsequent link to BSE, years of
prevention could be lost if zoonotic transmission of CWD is subsequently
identified,...
snip...
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER
AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease
Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages
858-863, June 2011.
NOR IS THE FDA recalling this CWD positive elk meat for the well being of
the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat
derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS
AND FIELD CORRECTIONS: FOODS CLASS II
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD
transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article
and call me if you have questions or need more clarification (phone:
404-639-3091). Also, we do not claim that "no-one has ever been infected with
prion disease from eating venison." Our conclusion stating that we found no
strong evidence of CWD transmission to humans in the article you quoted or in
any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip...
full text ;
CWD ongoing experiment on humans, long term $$$
Monday, November 14, 2011
WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Wednesday, November 16, 2011
Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Sunday, November 13, 2011
COLORADO CWD CJD TSE PRION REPORTING 2011
*** Saturday, October 6, 2012 ***
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM
ENCEPHALOPATHIES 2011 Annual Report
MOM DOD 12/14/97 hvCJD confirmed. ...TSS
layperson
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
4:10 PM
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