NEBRASKA CHRONIC WASTING DISEASE CWD TSE PRION DISEASE 2013-2014 UPDATE MIA ?
Greetings again Nebraska CWD officials et al,
I thought I should update you a bit on CWD TSE Prion. I hope you don’t
mind. it’s been a while, so I thought it was time. lot going on.
I am still banned from posting on http://www.nefga.org/
you can see a bit of history here, and in the full history of me being
banned in the link below in the post, there is another link.
NEFGA claims ;
CWD affects the central nervous system of mule deer, white-tailed deer and
elk in captive and wild populations. Research has found no evidence the disease
can be transmitted to humans, livestock or other wildlife. Researchers also
believe eating or handling meat from infected animals is safe...
I AM STUNNED BY THIS FALSE INFORMATION...STUNNED!!!
please see why and the latest studies on cwd transmission to other species,
including livestock, below...thank you, kindest regards, terry
CWD Test Results CWD Home To find results for your deer, please enter the
tag number below:
Please enter CWD test ID: Hunters were asked to assist Nebraska Game and
Parks Commission efforts to monitor and control Chronic Wasting Disease (CWD) in
Nebraska during this fall's deer hunting seasons by volunteering their deer
heads for testing, and using the unlimited, free antlerless-only bonus tags
offered in CWD control areas.
To address the spread of CWD in the wild population and to protect the
state's deer herds, the Commission has developed an expanded monitoring program
for this fall. As a result, hunters at all Panhandle check stations will be
asked to voluntarily submit the heads of deer they harvest for testing. In the
rest of Nebraska, 100 heads in each deer management unit will be collected.
Using the search tool above, hunters can find test results for the deer they
have harvested.
The control units include the Pine Ridge Control Area in the northwest
Panhandle and Season Choice Area 15 in portions of Kimball, Cheyenne and Deuel
counties in the southern Panhandle. Hunters in the control units can receive
unlimited, free antlerless-only bonus tags to help the Commission reduce deer
populations to help reduce and eliminate CWD in the wild deer population.
Hunters who do not participate in the monitoring program can have CWD testing
performed by three participating veterinary laboratories at their own
expense.
CWD affects the central nervous system of mule deer, white-tailed deer and
elk in captive and wild populations. Research has found no evidence the disease
can be transmitted to humans, livestock or other wildlife. Researchers also
believe eating or handling meat from infected animals is safe.
Additionally, recent research indicates that there may be pockets of
infection with very high rates of the CWD within the larger endemic area. Also,
mature bucks appear to be infected at a higher rate than other portions of the
population. Prevalence in the endemic area of Nebraska is generally less than 1
percent. However, there are portions of the Panhandle that approach 2 percent.
No wild elk in Nebraska have tested positive for the disease. The Commission has
tested over 33,000 deer from 1997 to 2007 with 133 deer testing positive for the
disease.
Disease Update April 2012 Chronic Wasting Disease
Due to a decrease in available funding the Chronic Wasting Disease
surveillance conducted during the 2011 firearm deer season concentrated in
management units through the center of the state, or along the leading edge of
the disease. In addition, sampling was conducted in the Pine Ridge Unit to
determine prevalence (6%). A total of 1,565 deer was tested, with 26 being
confirmed positive. Counties with new positives included Buffalo, Custer and
Holt. A similar surveillance effort is planned for this year. A total of 50 deer
exhibiting clinical symptoms was submitted to the UNL diagnostic laboratory for
CWD testing. One mule deer from Garden County tested positive.
This disease continues to slowly spread from west to east across the state
and increase in prevalence. There is nothing to indicate this is likely to
change in the foreseeable future. In all likelihood federal funding for
surveillance will be gone after this year. The following map is provided as a
summary of the disease’s spread.
Nebraska Domestic Cervid Facilities
The Nebraska Department of Agriculture (NDA) is responsible for licensing
and inspection of domestic cervid facilities. They have reported a third
facility testing positive for CWD. This latest facility is near Chadron
(Rocking Heart Ranch). The other two are at Oshkosh (Pollard) and Harrison
(Edwards). It is now the intention of the NDA to create management plans for
the facilities that test positive for CWD located within the endemic area. These
plans will allow them to continue operation. Plans include indefinite
quarantine, restrictions on movement in and out of pens, restrictions on the
purchase and sale of animals and additional testing requirements.
CHRONIC WASTING DISEASE MANAGEMENT IN NEBRASKA
INTRODUCTION
Wednesday, January 04, 2012
CWD NEBRASKA NGPC 26 DEER CARCASSES TESTED POSITIVE BUFFALO, CUSTER AND
HOLT COUNTIES DURING NOVEMBER HUNT
Tuesday, April 24, 2012
NEBRASKA CHRONIC WASTING DISEASE CWD SPREADING SLOWLY 2011 REPORT GAME FARM
RANCH UPDATE
There were 1,565 lymph node samples collected from deer taken during the
2011 November firearm deer season, with 26 samples testing positive for CWD. In
addition, samples were taken from 37 culled deer that showed clinical symptoms
for CWD, with one male mule deer from Garden County testing positive. Those
symptoms include a rough, emaciated appearance and a lack of fear of humans.
There were a record 51 positives from 3,645 samples in Nebraska in 2010.
However, the surveillance effort was reduced in 2011 due to a lack of funds. The
2011 effort focused on central Nebraska, the leading edge of the disease as it
spreads from west to east.
Wednesday, March 02, 2011
CWD IN NEBRASKA IS INCREASING WITH 51 POSITIVE CASES IN 2010
Wednesday, February 04, 2009
Nebraska reports 22 cases of CWD in deer
Tuesday, December 18, 2007
NEBRASKA CWD tested 3,400 deer, with 17 testing positive 2007
Wednesday, January 25, 2012
Nebraska Fish and Game Association Censors Singeltary from speaking about
Chronic Wasting Disease (CWD) again
snip...
2012
NOW, let me be perfectly clear. this time, it was the Nebraska Fish and
Game Association that allowed me back on board, to post about CWD, after I had
asked them to do so. what happened was, I got to speaking the truth about game
farms, and CWD spreading there from, and a certain few complained, and kept
complaining, they did not want anymore information (valid scientific peer review
journals) that might hurt their industry. SO, I thank NFGC again for giving me a
chance to try and educate hunters on CWD and the TSE prion disease. I think I
supplied enough information to help educate, the ones that wanted to be
educated, however, it’s the other folks I am concerned about. the ones that
don’t want to be educated on this CWD, the ones that don’t want to speak about
it, or learn about, and they don’t want others to either. these few folks are
the ones that will help continue the spread of CWD. these folks caused the
surpressing of CWD TSE prion information. to be good stewards of the woods and
hunt, you cannot stick your head in the sand. these few folks did, and in doing
so, they want everyone else’s head in the sand. and that’s been the problem all
along. ...good luck!
so much for freedom of speech. can’t say I did not try. ... TSS
snip...
CWD GAME FARMS AND RANCHES IN NEBRASKA and RISK FACTOR THERE FROM
Although the Game and Parks Commission's wildlife management areas and U.S.
Forest Service pastures in the Bordeaux and Hat Creek units provide some
opportunities for elk hunters, most elk taken in Nebraska are killed on private
land. Obtaining private land access to hunt elk is difficult, but not
impossible, and a growing number of Nebraska landowners charge fees for hunting
privileges.
2014 February 11th, 10:16pm
Terry, I found you on the CJD site and wanted to know if you'd consider
sharing some of your knowledge about CJD.
My husband passed away w sCJD last March. My 3 daughters and grandson and I
attended the CJD Conference in Washington DC last July in hopes of finding
answers.
We live in central Nebraska on a cattle ranch and our area had a large
death loss in the white tail deer due to CWD in 2012.
I know of 3 other cases in our area (very rural and remote).
In reading from the sites you have posted I think you are closer to voicing
the many questions we have had.
Do you believe there is a common denominator?
I'm very sure there are more unconfirmed cases of CJD.
SNIP...
Thank you XXXXX XXXXX
USDA ET AL are wrong on the science of BSE and risk factor there from from
young animals, especially with veal (*** see BSE Inquiry CJD report on veal and
BSE), and the department of justice missed the boat on the NSLP deadstock downer
cow program, where for 4 years, the NSLP fed deadstock downer cows to our
children all across the Nation, the most high risk cattle for mad cow disease
and other deadly pathogens, then hid this fact under a recall for animal
abuse...these are the sad facts as I have come to know them...who will watch our
children for the next 50 years $$$
============================================================================================================
*** Individuals reported to eat veal on average at least once a year appear
to be at 13 TIMES THE RISK of individuals who have never eaten veal.
*** There is, however, a very wide confidence interval around this
estimate. There is no strong evidence that eating veal less than once per year
is associated with increased risk of CJD (p = 0.51).
*** The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
*** There is some evidence that risk of CJD INCREASES WITH INCREASING
FREQUENCY OF LAMB EATING (p = 0.02). *** In conclusion, an analysis of dietary
histories revealed statistical associations between various meats/animal
products and INCREASED RISK OF CJD. When some account was taken of possible
confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE
STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
=============================================================================================================
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely
unchanged when attention was restricted to pairs with data obtained from
relatives. ...
Table 9 presents the results of an analysis of these data.
*** There is STRONG evidence of an association between ‘’regular’’ veal
eating and risk of CJD (p = .0.01).
*** Individuals reported to eat veal on average at least once a year appear
to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Thursday, October 10, 2013
*** CJD REPORT 1994 increased risk for consumption of veal and venison and
lamb
*** CHRONIC WASTING DISEASE CWD TSE PRION UPDATE MARCH 17 2014 ***
Program Standards: Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose
*** DOCUMENT ID: APHIS-2006-0118-0411
Saturday, March 15, 2014
Potential role of soil properties in the spread of CWD in western Canada
Sunday, March 09, 2014
Lesion Profiling and Subcellular Prion Localization of Cervid Chronic
Wasting Disease in Domestic Cats
Sunday, March 09, 2014
ACA Council Reviews Comment Period Procedure, Border Closings, Iowa Legal
Case, & Committee Recommendations
Friday, March 07, 2014
37th Annual Southeast Deer Study Group Meeting in Athens, Georgia (CWD TSE
Prion abstracts)
Monday, March 03, 2014
APHIS to Offer Indemnity for CWD Positive Herds as Part of Its Cervid
Health Activities
Wednesday, March 05, 2014
Iowa Brakke Family Wins DNR Legal Case
Tuesday, February 25, 2014
Test results provide current snapshot of CWD in south-central Wisconsin
Dane and Eastern Iowa counties Prevalence has increased in all categories
how many states have $465,000., and can quarantine and purchase there from,
each cwd said infected farm, but how many states can afford this for all the cwd
infected cervid game ranch type farms ???
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
OLD HISTORY ON CWD AND GAME FARMS IN USA
Elk and Deer Use of Mineral Licks: Implications for Disease Transmission
Results from the mineral analyses combined with camera data revealed that
visitation was highest at sodium-rich mineral licks. Mineral licks may play a
role in disease transmission by acting as sites of increased interaction as well
as reservoirs for deposition, accumulation, and ingestion of disease agents.
Friday, October 26, 2012
CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT
PRODUCTS, BAITING, AND MINERAL LICKS
Sunday, September 01, 2013
hunting over gut piles and CWD TSE prion disease
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and
behavioural changes that can span weeks or months (Williams, 2005). In addition,
signs might include excessive salivation, behavioural alterations including a
fixed stare and changes in interaction with other animals in the herd, and an
altered stance (Williams, 2005). These signs are indistinguishable from cervids
experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB,
for example, infected deer populations would need to be tested to differentiate
if they were infected with CWD or BSE to minimise the risk of BSE entering the
human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
*** 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. ...
also, see where even decades back, the USDA had the same thought as they do
today with CWD, not their problem...see page 27 below as well, where USDA stated
back then, the same thing they stated in the state of Pennsylvania, not their
damn business, once they escape, and they said the same thing about CWD in
general back then ;
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
sound familiar $$$
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
Wednesday, September 04, 2013
*** cwd - cervid captive livestock escapes, loose and on the run in the
wild
now, decades later, the obvious is visible...tss
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
snip...
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.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)
Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National
Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie
and CWD in inoculated deer. Interspecies transmission studies afford the
opportunity
After a natural route of exposure, 100% of white-tailed deer 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 scrapie by IHC and WB. Tissues with PrPSc immunoreactivity
included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node,
Peyer’s patches, and spleen. While two WB patterns have been detected in brain
regions of deer inoculated by the natural route, unlike the IC inoculated deer,
the pattern similar to the scrapie inoculum predominates.
2011 Annual Report
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit 2011 Annual Report
In Objective 1, Assess cross-species transmissibility of transmissible
spongiform encephalopathies (TSEs) in livestock and wildlife, numerous
experiments assessing the susceptibility of various TSEs in different host
species were conducted. Most notable is deer inoculated with scrapie, which
exhibits similarities to chronic wasting disease (CWD) in deer suggestive of
sheep scrapie as an origin of CWD.
snip...
4.Accomplishments 1. Deer inoculated with domestic isolates of sheep
scrapie. Scrapie-affected deer exhibit 2 different patterns of disease
associated prion protein. In some regions of the brain the pattern is much like
that observed for scrapie, while in others it is more like chronic wasting
disease (CWD), the transmissible spongiform encephalopathy typically associated
with deer. This work conducted by ARS scientists at the National Animal Disease
Center, Ames, IA suggests that an interspecies transmission of sheep scrapie to
deer may have been the origin of CWD. This is important for husbandry practices
with both captive deer, elk and sheep for farmers and ranchers attempting to
keep their herds and flocks free of CWD and scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
snip...
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 ;
----- 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.
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
Thursday, November 21, 2013
*** Assessing the susceptibility of transgenic mice over-expressing deer
prion protein to bovine spongiform encephalopathy
The present study was designed to assess the susceptibility of the
prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy
(BSE) prions, which have the ability to overcome species barriers.
Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a
90-100% attack rates, BSE from cattle failed to transmit, indicating agent
adaptation in the deer.
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population CWD TSE Prion
disease Singeltary submission to Scottish Parliament
Thursday, October 10, 2013
*** CJD REPORT 1994 increased risk for consumption of veal and venison and
lamb
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
The chances of a person or domestic animal contracting CWD are “extremely
remote,” Richards said. The possibility can’t be ruled out, however. “One could
look at it like a game of chance,” he explained. “The odds (of infection)
increase over time because of repeated exposure. That’s one of the downsides of
having CWD in free-ranging herds: We’ve got this infectious agent out there that
we can never say never to in terms of (infecting) people and domestic
livestock.”
P35
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A
WISCONSIN STRAIN OF CWD
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of
Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2
Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary
Research Institute, 4.Center for Prions and Protein Folding Diseases, 5
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
T6G 2P5
The identification and characterization of prion strains is increasingly
important for the diagnosis and biological definition of these infectious
pathogens. Although well-established in scrapie and, more recently, in BSE,
comparatively little is known about the possibility of prion strains in chronic
wasting disease (CWD), a disease affecting free ranging and captive cervids,
primarily in North America. We have identified prion protein variants in the
white-tailed deer population and demonstrated that Prnp genotype affects the
susceptibility/disease progression of white-tailed deer to CWD agent. The
existence of cervid prion protein variants raises the likelihood of distinct CWD
strains. Small rodent models are a useful means of identifying prion strains. We
intracerebrally inoculated hamsters with brain homogenates and phosphotungstate
concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD
endemic area) and experimentally infected deer of known Prnp genotypes. These
transmission studies resulted in clinical presentation in primary passage of
concentrated CWD prions. Subclinical infection was established with the other
primary passages based on the detection of PrPCWD in the brains of hamsters and
the successful disease transmission upon second passage. Second and third
passage data, when compared to transmission studies using different CWD inocula
(Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin
white-tailed deer population is different than the strain(s) present in elk,
mule-deer and white-tailed deer from the western United States endemic region.
PPo3-7:
Prion Transmission from Cervids to Humans is Strain-dependent
Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi
Gambetti and Liuting Qing Department of Pathology; Case western Reserve
University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial
Sloan-Kettering Cancer Center; New York, NY USA
Key words: CWD, strain, human transmission
Chronic wasting disease (CWD) is a widespread prion disease in cervids
(deer and elk) in North America where significant human exposure to CWD is
likely and zoonotic transmission of CWD is a concern. Current evidence indicates
a strong barrier for transmission of the classical CWD strain to humans with the
PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD
strains. What remain unknown is whether individuals with the PrP-129VV/MV
genotypes are also resistant to the classical CWD strain and whether humans are
resistant to all natural or adapted cervid prion strains. Here we report that a
human prion strain that had adopted the cervid prion protein (PrP) sequence
through passage in cervidized transgenic mice efficiently infected transgenic
mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion
strain-dependent and humans can be vulnerable to novel cervid prion strains.
Preliminary results on CWD transmission in transgenic mice expressing human
PrP-129V will also be discussed.
Acknowledgement Supported by NINDS NS052319 and NIA AG14359.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A.
Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and
related Brain disorders; Dept of Neurology; University of Texas Houston Medical
School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular
Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky
Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve
University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago;
Chicago, IL USA
Prion diseases are infectious neurodegenerative disorders affecting humans
and animals that result from the conversion of normal prion protein (PrPC) into
the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of
cervids is a prion disorder of increasing prevalence within the United States
that affects a large population of wild and captive deer and elk. CWD is highly
contagious and its origin, mechanism of transmission and exact prevalence are
currently unclear. The risk of transmission of CWD to humans is unknown.
Defining that risk is of utmost importance, considering that people have been
infected by animal prions, resulting in new fatal diseases. To study the
possibility that human PrPC can be converted into the infectious form by CWD
PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification
(PMCA) technique, which mimic in vitro the process of prion replication. Our
results show that cervid PrPSc can induce the pathological conversion of human
PrPC, but only after the CWD prion strain has been stabilized by successive
passages in vitro or in vivo. Interestingly, this newly generated human PrPSc
exhibits a distinct biochemical pattern that differs from any of the currently
known forms of human PrPSc, indicating that it corresponds to a novel human
prion strain.
*** Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD
Isolates
Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin,
Germany
Key words: CWD, strains, FT-IR, AFM
Chronic wasting disease (CWD) is one of three naturally occurring forms of
prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie
in sheep. CWD is contagious and affects captive as well as free ranging cervids.
As long as there is no definite answer of whether CWD can breach the species
barrier to humans precautionary measures especially for the protection of
consumers need to be considered.
*** In principle, different strains of CWD may be associated with different
risks of transmission to humans. Sophisticated strain differentiation as
accomplished for other prion diseases has not yet been established for CWD.
However, several different findings indicate that there exists more than one
strain of CWD agent in cervids. We have analysed a set of CWD isolates from
white-tailed deer and could detect at least two biochemically different forms of
disease-associated prion protein PrPTSE. Limited proteolysis with different
concentrations of proteinase K and/or after exposure of PrPTSE to different
pH-values or concentrations of Guanidinium hydrochloride resulted in distinct
isolate-specific digestion patterns. Our CWD isolates were also examined in
protein misfolding cyclic amplification studies. This showed different
conversion activities for those isolates that had displayed significantly
different sensitivities to limited proteolysis by PK in the biochemical
experiments described above. We further applied Fourier transform infrared
spectroscopy in combination with atomic force microscopy. This confirmed
structural differences in the PrPTSE of at least two disinct CWD isolates. The
data presented here substantiate and expand previous reports on the existence of
different CWD strains.
2012
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.
HD.13: CWD infection in the spleen of humanized transgenic mice
Liuting Qing and Qingzhong Kong
Case Western Reserve University; Cleveland, OH USA
Chronic wasting disease (CWD) is a widespread prion disease in free-ranging
and captive cervid species in North America, and there is evidence suggesting
the existence of multiple CWD strains. The susceptibility of human CNS and
peripheral organs to the various CWD prion strains remains largely unclear.
Current literature suggests that the classical CWD strain is unlikely to infect
human brain, but the potential for peripheral infection by CWD in humans is
unknown. We detected protease-resistant PrpSc in the spleens of a few humanized
transgenic mice that were intracerebrally inoculated with natural CWD isolates,
but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our
ongoing bioassays in humanized Tg mice indicate that intracerebral challenge
with such PrpSc-positive humanized mouse spleen already led to prion disease in
most animals.
*** These results indicate that the CWD prion may have the potential to
infect human peripheral lymphoid tissues.
=====
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of
the ability of sheep, cattle and deer prion disease isolates to convert normal
human prion protein to its pathological isoform in a cell-free system
Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki
Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and
Mark W. Head1
1National CJD Research and Surveillance Unit; Centre for Clinical Brain
Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh,
UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food
Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious
Pathogen Research Section; Central Research Laboratory; Japan Blood Products
Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku
University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division;
The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush;
Midlothian; Edinburgh, UK
Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic
prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans.
In contrast, classical scrapie in sheep is thought to offer little or no danger
to human health. However, a widening range of prion diseases have been
recognized in cattle, sheep and deer. The risks posed by individual animal prion
diseases to human health cannot be determined a priori and are difficult to
assess empirically. The fundamemal event in prion disease pathogenesis is
thought to be the seeded conversion of normal prion protein (PrPC) to its
pathological isoform (PrPSc). Here we report the use of a rapid molecular
conversion assay to test whether brain specimens from different animal prion
diseases are capable of seeding the conversion of human PrPC ro PrPSc.
Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE,
classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain
homogenates were tested for their ability to seed conversion of human PrPC to
PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed
human PrPSc was detected by protease digestion and western blotting using the
antibody 3F4.
Results. C-type BSE and vCJD were found to efficiently convert PrPC to
PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion
diseases tested only chronic wasting disease appeared to have the capability ro
convert human PrPC to PrPSc. The results were consistent whether the human PrPC
came from human brain, humanised transgenic mouse brain or from cultured human
cells and the effect was more pronounced for PrPC with methionine at codon 129
compared with that with valine.
Conclusion. Our results show that none of the tested animal prion disease
isolates are as efficient as C-type BSE and vCJD in converting human prion
protein in this in vitro assay.
*** However, they also show that there is no absolute barrier ro conversion
of human prion protein in the case of chronic wasting disease.
=====
AD.06: Detecting prions in the brain and blood of TSE-infected deer and
hamsters
Alan Elder,1 Davin Henderson,1 Anca Selariu,1 Amy Nalls,1 Byron Caughey,2
Richard Bessen,1 Jason Bartz3 and Candace Mathiason1
1Colorado State University; Fort Collins, CO USA; 2NIH Rocky Mountain
Laboratories; Hamilton, MT USA; 3Creighton University; Omaha, NE USA
While large quantities of protease resistant prion protein (PrPres) can be
demonstrated by western blot or IHC in lymphoid biopsies or post-mortem brain
tissues harvested from prion-infected animals, these conventional assays are
less reliable as means to detect the small quantities of prions thought to be
present in bodily fluids or associated with early and asymptomatic phases of TSE
disease. The Real Time-Quaking Induced Conversion (RT-QuIC) assay is capable of
detecting prions at concentrations below the level of sensitivity of
conventional assays and provides a real-time fluorescent readout negating the
use of proteases. We have made modifications to the RT-QuIC assay to utilize it
for the detection of PrPres in brain and blood harvested from various species
infected with prions. In this study, we analyzed CWD-infected deer and
CWD/TME-infected hamster whole blood to determine the effect of:
(1) various anticoagulants,
(2) freezing and
(3) NaPTA precipitation.
Brain tissue and blood collected from naive deer and hamsters served as
negative controls.
We were able to demonstrate amplifiable prions in
(1) brain and blood samples harvested from CWD/TME-infected animals,
(2) heparinized blood,
(3) frozen vs. fresh blood and
(4) NaPTA treated samples.
The RT-QuIC assay is able to detect PrPres in various species of animals
and shows promise as an antemortem diagnostic tool for blood-borne TSEs.
=====
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood,
and mother to offspring transmission
Sunday, July 21, 2013
*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for
humans?
SEE MORE USAHA REPORTS HERE, 2012 NOT PUBLISHED YET...TSS
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
The chances of a person or domestic animal contracting CWD are “extremely
remote,” Richards said. The possibility can’t be ruled out, however. “One could
look at it like a game of chance,” he explained. “The odds (of infection)
increase over time because of repeated exposure. That’s one of the downsides of
having CWD in free-ranging herds: We’ve got this infectious agent out there that
we can never say never to in terms of (infecting) people and domestic
livestock.”
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
November 2012
Friday, December 14, 2012
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005
- December 14, 2012
Saturday, March 09, 2013
Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest
Incubation Time Model for Prion Diseases
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
WHAT about the sporadic CJD TSE proteins ?
WE now know that some cases of sporadic CJD are linked to atypical BSE and
atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all
it’s sub-types $$$
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010 ***
Sunday, October 13, 2013
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
Friday, February 14, 2014
Creutzfeldt-Jakob disease (CJD) biannual update (February 2014), with
briefing on novel human prion disease National CJD Research and Surveillance
Unit NCJDRSU
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
http://download.thelancet.com/pdfs/journals/laninf/PIIS1473309903007151.pdf?id=baa1CkXPkhI3Ih_Vlh6ru
Tuesday, March 11, 2014
Science and Technology Committee Oral evidence: Blood, tissue and organ
screening, HC 990 Wednesday 5 March 2014 SPORADIC CJD
Actually, it is nearer 2 per million per year of the population will
develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about
1 in 30,000. So that has not really changed. When people talk about 1 per
million, often they interpret that as thinking it is incredibly rare. They think
they have a 1-in-a-million chance of developing this disease. You haven’t.
You’ve got about a 1-in-30,000 chance of developing it.
Sunday, March 09, 2014
*** A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of
Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease
FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
Thursday, February 20, 2014
*** Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS
Dr. Linda Detwiler 2014
Wednesday, December 11, 2013
*** Detection of Infectivity in Blood of Persons with Variant and Sporadic
Creutzfeldt-Jakob Disease ***
kind regards,
terry
posted by Terry S. Singeltary Sr. at
1:21 PM
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