Wyoming Game and Fish Commission Alkali Creek Feedground #39126 Singeltary comment submission
Chronic Wasting Disease (CWD) -- a deadly disease for elk, deer, and other
wildlife -- is marching toward Yellowstone, and we need your help to stop it.
It is time to finally draw a line in the sagebrush and say no to the
unnatural feeding of elk in western Wyoming, starting at a place called Alkali
Creek.
The Bridger-Teton National Forest will consider a new 20-year permit for
feeding elk at Alkali Creek, and together we must voice opposition to this idea!
The unnaturally dense concentrations of elk at such feedgrounds have
resulted in diseased animals, ravaged habitat and the prospect of a CWD disaster
moving inexorably closer to the famed herds in Yellowstone National Park and
Jackson Hole.
As America's Voice for a Greater Yellowstone, we can restore and preserve
healthy herds by phasing out these feedgrounds and allowing elk to roam free.
Let’s make Alkali Creek the first domino to fall!
Take a few moments right now and tell the Bridger-Teton National Forest
that you oppose the re-permitting of this obsolete elk feedground in the Gros
Ventre.
Sincerely,
Caroline Byrd Executive Director
***********************************************
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Wyoming Game and Fish Commission Alkali Creek Feedground #39126
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Singeltary submission to Wyoming Game and Fish Commission Alkali Creek
Feedground #39126 ;
Greetings Wyoming Game and Fish Commission et al,
I would kindly like to comment on the Wyoming Game and Fish Commission
Alkali Creek Feedground #39126 and the unnatural feeding of elk.
Chronic Wasting Disease CWD of cervids is spreading, and there seems no
stopping it. It would seem prudent to use all your weapons and sources to stop
this agent from spreading, and this includes the enhancement of CWD by the
unnatural feeding of these cervids, thus causing the congregation of said
cervids, thus causing the surrounding environment becoming exposed and loaded up
with the CWD TSE prion. Once this is done, there is no going back. Once the soil
content is so loaded with the CWD TSE prion, you risk exposing every animal and
man that comes on that land. The land will then be rendered useless. just see
what happened to one state with one infected cwd farm ;
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 ???
? game farms in a state X $465,000., do all these game farms have insurance
to pay for this risk of infected the wild cervid herds, in each state ???
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.
Form 1100-001
(R 2/11)
NATURAL RESOURCES BOARD AGENDA ITEM
SUBJECT: Information Item: Almond Deer Farm Update
FOR: DECEMBER 2011 BOARD MEETING
TUESDAY
TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief
SUMMARY:
pens, pens, PENS !
*** 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.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
see more of these transmission studies later...
Generation of a new form of human PrPSc in vitro by inter-species
transmission from cervids prions
Marcelo A. Barria1, Glenn C. Telling2, Pierluigi Gambetti3, 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 77030, 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. Running Title: Conversion of human PrPC by cervid PrPSc
Keywords: Prion / transmissible spongiform encephalopathy / infectivity /
misfolded prion protein / prion strains * To whom correspondence should be
addressed. University of Texas Houston Medical School, 6431 Fannin St, Houston,
TX 77030. Tel 713-5007086; Fax 713-5000667; E-mail Claudio.Soto@uth.tmc.edu The
latest version is at
http://www.jbc.org/cgi/doi/10.1074/jbc.M110.198465
JBC Papers in Press.
Published on January 4, 2011 as Manuscript M110.198465 Copyright 2011 by
The American Society for Biochemistry and Molecular Biology, Inc. 5, Downloaded
from www.jbc.org by guest, on November 11, 2012 2
Prion diseases are infectious neurodegenerative disorders affecting humans
and animals that result from the conversion of normal prion protein (PrPC) into
the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion
disorder of increasing prevalence within the United States that affects a large
population of wild and captive deer and elk. Determining the risk of
transmission of CWD to humans is of utmost importance, considering that people
can be infected by animal prions, resulting in new fatal diseases. To study the
possibility that human PrPC can be converted into the misfolded 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 conversion of human PrPC, but only
after the CWD prion strain has been stabilized by successive passages in vitro
or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct
biochemical pattern that differs from any of the currently known forms of human
PrPSc. Our results also have profound implications for understanding the
mechanisms of prion species barrier and indicate that the transmission barrier
is a dynamic process that depend on the strain and moreover the degree of
adaptation of the strain. If our findings are corroborated by infectivity
assays, they will imply that CWD prions have the potential to infect humans, and
that this ability depends on CWD strain adaptation.
Various studies aimed to analyze the transmission of CWD to transgenic mice
expressing human PrP have consistently given negative results (9-11), indicating
a strong species barrier. This conclusion is consistent with our many failed
experiments to attempt converting human PrPC with natural CWD, even after
pushing the PMCA conditions (see figure 1). We found successful conversion only
after adaptation of the CWD prion strain by successive passages in vitro or in
cervid transgenic mice. We are not aware that in any of the transgenic mice
studies the inoculum used was a previously stabilized CWD strain. Although, it
has been shown that strain stabilization in vitro by PMCA (17;26) and in vivo
using experimental rodents (36) has similarities with the strain adaptation
process occurring in natural hosts, we cannot rule out that the type of CWD
strain adaptation that is required to produce strains transmissible to humans
may take much longer time in cervids or not occur at all. An important
experiment will be to study transmissibility to humanized transgenic mice of CWD
passed experimentally in deer several times. Besides the importance of our
results for public health in relation to the putative transmissibility of CWD to
humans, our data also illustrate a very important and novel scientific concept
related to the mechanism of prion transmission across species barriers. Today
the view is that species barrier is mostly controlled by the degree of
similarity on the sequence of the prion protein between the host and the
infectious material (4). In our study we show that the strain and moreover the
stabilization of the strain plays a major role in the inter-species
transmission. In our system there is no change on the protein sequence, but yet
strain adaptation results in a complete change on prion transmissibility with
potentially dramatic consequences. Therefore, our findings lead to a new view of
the species barrier that should not be seen as a static process, but rather a
dynamic biological phenomenon that can change over time when prion strains
mature and evolve. It remains to be investigated if other species barriers also
change upon progressive strain adaptation of other prion forms (e.g. the
sheep/human barrier).
Our results have far-reaching implications for human health, since they
indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc,
suggesting that CWD might be infectious to humans. Interestingly our findings
suggest that unstable strains from CWD affected animals might not be a problem
for humans, but upon strain stabilization by successive passages in the wild,
this disease might become progressively more transmissible to man.
Generation of a New Form of Human PrPScin Vitro by Interspecies
Transmission from Cervid Prions*
Marcelo A. Barria‡, Glenn C. Telling§, Pierluigi Gambetti¶, James A.
Mastrianni‖ and Claudio Soto‡,1 + Author Affiliations
From the ‡Mitchell Center for Alzheimer's Disease and Related Brain
Disorders, Department of Neurology, University of Texas Medical School at
Houston, Houston, Texas 77030, the §Departments of Microbiology, Immunology, and
Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of
Kentucky Medical Center, Lexington, Kentucky 40506, the ¶Institute of Pathology,
Case Western Reserve University, Cleveland, Ohio 44106, and the ‖Department of
Neurology, The University of Chicago, Chicago, Illinois 60637 1 To whom
correspondence should be addressed: University of Texas Medical School at
Houston, 6431 Fannin St., Houston, TX 77030. Tel.: 713-500-7086; Fax:
713-500-0667; E-mail: claudio.soto@uth.tmc.edu.
Abstract
Prion diseases are infectious neurodegenerative disorders that affect
humans and animals and that result from the conversion of normal prion protein
(PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD)
is a prion disorder of increasing prevalence within the United States that
affects a large population of wild and captive deer and elk. Determining the
risk of transmission of CWD to humans is of utmost importance, considering that
people can be infected by animal prions, resulting in new fatal diseases. To
study the possibility that human PrPC can be converted into the misfolded form
by CWD PrPSc, we performed experiments using the protein misfolding cyclic
amplification technique, which mimics in vitro the process of prion replication.
Our results show that cervid PrPSc can induce the conversion of human PrPC but
only after the CWD prion strain has been stabilized by successive passages in
vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a
distinct biochemical pattern that differs from that of any of the currently
known forms of human PrPSc. Our results also have profound implications for
understanding the mechanisms of the prion species barrier and indicate that the
transmission barrier is a dynamic process that depends on the strain and
moreover the degree of adaptation of the strain. If our findings are
corroborated by infectivity assays, they will imply that CWD prions have the
potential to infect humans and that this ability progressively increases with
CWD spreading.
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010
Tuesday, June 05, 2012
Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012
Legislative Session
Friday, August 31, 2012
COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a
review
Tuesday, April 16, 2013
*** Cervid Industry Unites To Set Direction for CWD Reform and seem to
ignore their ignorance and denial in their role in spreading Chronic Wasting
Disease
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
The overall diagnostic specificity was 99.8%. Selective use of antemortem
rectal biopsy sample testing would provide valuable information during disease
investigations of CWD-suspect deer herds.
Tuesday, April 09, 2013
EFFICACY OF ANTEMORTEM RECTAL BIOPSIES TO DIAGNOSE AND ESTIMATE PREVALENCE
OF CHRONIC WASTING DISEASE IN FREE-RANGING COW ELK (CERVUS ELAPHUS NELSONI)
Monday, March 18, 2013
PROCEEDINGS ONE HUNDRED AND FIFTEENTH ANNUAL MEETING of the UNITED STATES
ANIMAL HEALTH ASSOCIATION September 29 – October 5, 2011
see updated 2012 RESOLUTIONS
please see what the U.K. DEFRA recently said ;
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... see full text report here ;
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
Research Article
Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with
Lyophilized Chronic Wasting Disease Prion Particulate Complexed to
Montmorillonite Clay
Tracy A. Nichols mail, Terry R. Spraker, Tara D. Rigg, Crystal
Meyerett-Reid, Clare Hoover, Brady Michel, Jifeng Bian, Edward Hoover, Thomas
Gidlewski, Aru Balachandran, Katherine O'Rourke, Glenn C. Telling, Richard
Bowen, [ ... ], Kurt C. VerCauteren equal contributor
Abstract
Chronic wasting disease (CWD), the only known prion disease endemic in
wildlife, is a persistent problem in both wild and captive North American cervid
populations. This disease continues to spread and cases are found in new areas
each year. Indirect transmission can occur via the environment and is thought to
occur by the oral and/or intranasal route. Oral transmission has been
experimentally demonstrated and although intranasal transmission has been
postulated, it has not been tested in a natural host until recently. Prions have
been shown to adsorb strongly to clay particles and upon oral inoculation the
prion/clay combination exhibits increased infectivity in rodent models. Deer and
elk undoubtedly and chronically inhale dust particles routinely while living in
the landscape while foraging and rutting. We therefore hypothesized that dust
represents a viable vehicle for intranasal CWD prion exposure. To test this
hypothesis, CWD-positive brain homogenate was mixed with montmorillonite clay
(Mte), lyophilized, pulverized and inoculated intranasally into white-tailed
deer once a week for 6 weeks. Deer were euthanized at 95, 105, 120 and 175 days
post final inoculation and tissues examined for CWD-associated prion proteins by
immunohistochemistry. Our results demonstrate that CWD can be efficiently
transmitted utilizing Mte particles as a prion carrier and intranasal exposure.
snip...
The results of this study confirm that CWD can be successfully transmitted
IN as a lyophilized prion particulate adsorbed to Mte and that genotype at codon
96 affects the lymphoid distribution of CWD within the body. Additionally, two
novel intranasal tracking methods were employed that provided insight into CWD
translocation within the nasal cavity. The data collected in this study may also
shed light on why there is a higher prevalence of CWD in males, as males
participate in more behaviors that generate dust. We propose chronic, long-term
exposure to CWD prions adsorbed to dust particles to be a natural CWD infection
route in addition to chronic oral and nasal contact exposure.
Citation: Nichols TA, Spraker TR, Rigg TD, Meyerett-Reid C, Hoover C, et
al. (2013) Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus)
with Lyophilized Chronic Wasting Disease Prion Particulate Complexed to
Montmorillonite Clay. PLoS ONE 8(5): e62455.
doi:10.1371/journal.pone.0062455
Editor: Anthony E. Kincaid, Creighton University, United States of America
Received: November 30, 2012; Accepted: March 21, 2013; Published: May 9,
2013
This is an open-access article, free of all copyright, and may be freely
reproduced, distributed, transmitted, modified, built upon, or otherwise used by
anyone for any lawful purpose. The work is made available under the Creative
Commons CC0 public domain dedication.
Funding: Funding was provided by U.S. Department of Agriculture, Animal and
Plant Health Inspection Service, Veterinary Services (VS). The funders had no
role in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
Competing interests: The authors have declared that no competing interests
exist.
see full text ;
Thanks again to PLOS et al for full text access to this scientific research
on the CWD TSE prion disease...tss
April/May/June 2012; © 2012 Landes Bioscience
PO-033: Replication efficiency of soil-bound prions varies with soil type
Shannon Bartelt-Hunt,1 Samuel Saunders,1 Ronald Shikiya,2 Katie
Langenfeld,2 Jason Bartz2 1University of Nebraska-Lincoln; Omaha, NE USA;
2Creighton University; Omaha, NE USA
Prion sorption to soil is thought to play an important role in the
transmission of scrapie and chronic wasting disease (CWD) via the environment.
Sorption of PrP to soil and soil minerals is influenced by the strain and
species of PrPSc and by soil characteristics. However, the ability of soil-bound
prions to convert PrPc to PrPSc under these wide-ranging conditions remains
poorly understood. We developed a semiquantitative protein misfolding cyclic
amplification (PMCA) protocol to evaluate replication efficiency of soil-bound
prions. Binding of the hyper (HY) strain of transmissible mink encephalopathy
(TME) (hamster) prions to a silty clay loam soil yielded a greater-than-1-log
decrease in PMCA replication efficiency with a corresponding 1.3-log reduction
in titer. The increased binding of PrPSc to soil over time corresponded with a
decrease in PMCA replication efficiency. The PMCA efficiency of bound prions
varied with soil type, where prions bound to clay and organic surfaces exhibited
significantly lower replication efficiencies while prions bound to sand
exhibited no apparent difference in replication efficiency compared to unbound
controls. PMCA results from hamster and CWD agent-infected elk prions yielded
similar findings. Given that PrPSc adsorption affinity varies with soil type,
the overall balance between prion adsorption affinity and replication efficiency
for the dominant soil types of an area may be a significant determinant in the
environmental transmission of prion diseases.
PO-248: TSE infectivity survives burial for five years with little
reduction in titer
Allister Smith, Robert Somerville, Karen Fernie The Roslin Institute and
R(D)SVS; University of Edinburgh; Edinburgh, UK
BSE infected animals, BSE-contaminated materials and other sources of TSE
(prion) infection, such as carcasses from scrapie infected sheep, CWD infected
deer and cadavers of individuals infected with CJD may all end up in the
environment through burial or other methods of disposal. They may continue to
act as a reservoir of TSE infectivity if cattle or other susceptible animals
were to be exposed to these sources in the future. In order to address these
concerns, we performed two large scale demonstration experiments under field
conditions which were designed to mimic some of the ways by which TSE infected
materials may have been disposed of. The project examined the fate of TSE
infectivity over a period of five years in two scenarios; when the infectivity
was contained within bovine heads and when the infectivity was buried without
any containment. Two soil types were compared: a sandy loam and a clay loam. We
used the 301V TSE strain which was derived by serial passage of BSE in VM
mice.
TSE infectivity was recovered from all the heads exhumed annually for five
years from both types of soil, with little reduction in the amount of
infectivity throughout the period of the experiment. Small amounts of
infectivity were found in the soil immediately surrounding the heads, but not in
samples remote from them. Similarly there was no evidence of significant lateral
movement of infectivity from the buried bolus. However large amounts of TSE
infectivity were recovered at the site of burial of both boluses. There was
limited vertical upward movement of infectivity from the bolus buried in clay
soil and downward movement from the bolus buried in sandy soil.
Now that these experiments are completed we conclude that TSE infectivity
is likely to survive burial for long periods of time with minimal loss of
infectivity and restricted movement from the site of burial. These experiments
emphasize that the environment is a viable reservoir for retaining large
quantities of TSE infectivity, and reinforce the importance of risk assessment
when disposing of this type of infectious material.
PRION 2011
Envt.16: Soil Properties as a Factor in CWD Spread in Western Canada
Alsu Kuznetsova,† Tariq Siddique and Judd Aiken
University of Alberta; Edmonton, AB Canada†Presenting author; Email:
alsu@ualberta.ca
Soil can serve as a stable reservoir for infectious prion proteins (PrPSc).
Soils are diverse and complex, varying in clay, silt, sand and organic
components. We have shown that PrPSc binds clay minerals avidly, an interaction
that considerably enhances prion infectivity. Conversely quartz sand bound PrPSc
less avidly. These studies would suggest that soils with lower clay and higher
sand content bind prions less avidly and do not enhance infectivity to the same
level as clay-rich soils. We hypothesize that clay content of a soil plays an
integral role in the spread of CWD. In this study, we present the soil
properties in the western Canada. Soils of the CWD-region generally are similar
in texture, clay mineralogy and soil organic matter content. In total these
soils can be characterized as clay loamy, montmorillonite (smectite) with 6–10 %
organic carbon. The major soils in the CWD-region are Chernozems, present in 60%
of total area. These soils have a humic horizon in which organic matter has
accumulated (1–17% organic C). Solonetzic soils are also common to Alberta and
Saskatchewan. We suggest that the greatest risk of CWD spread in western Canada
is restricted to clay loamy, montmorillonite soils with humus horizon. Such
soils are predominant in the southern region of Alberta, Saskatchewan and
Manitoba, but are less common in northern regions of the provinces.
Envt.28:
High Survival Rates of TSE Infectivity Buried in Two Soil
Types Allister J. Smith The Roslin Insitute; Roslin, UK Email:
allister.smith@roslin.ed.ac.uk
Two field experiments nearing completion are investigating the migration
and/or persistence of TSE infectivity in the soil environment, either buried
within bovine heads or buried without containment. In the first experiment five
pairs of bovine heads, spiked with mouse-passaged BSE (301V) macerate, were
buried within lysimeters containing either clay or sandy soil. A pair of
unspiked bovine heads was also buried to act as controls. Pairs of heads have
been exhumed annually during which a corer is used to take soil samples above,
surrounding and below the head. Any brain material within the head is recovered
during dissection. The soil samples have undergone protein extraction, and the
extracts along with the brain material have been assayed for infectivity by
bioassay in VM mice. Bioassay results from the first experiment show that for
all four years most of the intracranial brain samples have been positive for TSE
infectivity in both the clay and sandy soil. There is little change in the
survival curves between years 1 and 4 indicating little reduction in the amounts
of infectivity over time. There has been very limited infectivity found in
samples surrounding the heads buried in the sandy soil, but infectivity has been
found in the soil samples surrounding the clay heads and the levels increase
slightly from years one to four, presumably as the heads have decomposed. In a
parallel experiment a bolus of infectivity (301V) was placed in the centre of
two large lysimeters, containing either clay or sandy soil. Over the course of
four years, core samples have been taken at eight time points, on the vertical
and at 3 distances from the centre. These samples have been assayed for
infectivity and to date only one sample from the sandy soil has produced
pathological evidence of TSE disease in one mouse. In order to ascertain whether
any of the bolus remained at the end of the experiment, we collected a much
larger central core (d = 16 cm) and extracted samples for bioassay,
concentrating on the core portions that correlated to the original bolus
location. The samples from these core portions caused disease in a high
proportion of mice (bioassay still in progress), with apparently higher
infectivity levels in the clay soil, so far. This result indicates that there
has been very little migration of TSE infectivity without containment in either
clay or sandy soil and that there has been little reduction in titre with time.
Envt.29:
Time-Dependent Decline in PrPTSE Desorption from Soil
Particles Christen B. Smith,1,† Clarissa J. Booth,2 Kartik Kumar2 and Joel
A. Pedersen1–3 1Environmental Chemistry and Technology Program; 2Molecular and
Environmental Toxicology Center; 3Department of Soil Science, University of
Wisconsin; Madison, WI USA †Presenting author, Email: cmbell@wisc.edu
Environmental routes of transmission are implicated in epizootics of sheep
scrapie and chronic wasting disease in deer, elk, and moose. Strong evidence
suggests that soil may serve as an environmental reservoir of prions, which can
persist in the environment for years. The disease-associated form of the prion
protein (PrPTSE) readily attaches to soil particle surfaces. Prior studies
reported reduced PrPTSE recovery from experimentally spiked soils after longer
contact times, which in some cases has been interpreted as degradation of
PrPTSE. Here, we investigate PrPTSE desorption from sterilized and untreated
soil particles as a function of protein-soil contact time. Soil particles were
sterilized by autoclaving or g-irradiation. Desorption of PrPTSE from whole
soils, montmorillonite clay, and quartz sand was analyzed by immunoblotting
following 1-, 7-, and 14-day contact times. We found that PrPTSE recovery from
both sterile and untreated soil samples declined significantly with contact time
suggesting the strengthening of protein-particle interactions over time.
Recovery of PrPTSE from whole soils declined to a larger extent than did that
from montmorillonite and quartz sand possibly reflecting t he contribution of
particle-associated natural organic matter to the mechanisms of PrPTSE
attachment. The influence of PrPTSE-soil particle attachment on oral disease
transmission warrants investigation.
PRION
Soil clay content underlies prion infection odds
W. David Walter 1 , * , Daniel P. Walsh 2 , * , Matthew L. Farnsworth 3 ,
Dana L. Winkelman 1 & Michael W. Miller 2
1 United States Department of the Interior, United States Geological
Survey, Colorado Cooperative Fish and Wildlife Research Unit , Fort Collins ,
Colorado
80523-1484, USA. 2 Colorado Division of Wildlife, Wildlife Research Center,
Fort Collins, Colorado 80526-2097, USA. 3 United States Department
of Agriculture, Animal and Plant Health Inspection Services, Veterinary
Services, Centers for Epidemiology and Animal Health , Fort Collins ,
Colorado
80526-8117 , USA . * These authors contributed equally to this work.
Correspondence and requests for materials should be addressed to M.W.M.
(email: mike.miller@state.co.us ) .
Received 6 Sep 2010 | Accepted 19 Jan 2011 | Published 15 Feb 2011 DOI:
10.1038/ncomms1203
Environmental factors — especially soil properties — have been suggested as
potentially important in the transmission of infectious prion diseases. Because
binding to montmorillonite (an aluminosilicate clay mineral) or clay-enriched
soils had been shown to enhance experimental prion transmissibility, we
hypothesized that prion transmission among mule deer might also be enhanced in
ranges with relatively high soil clay content. In this study, we report apparent
influences of soil clay content on the odds of prion infection in free-ranging
deer. Analysis of data from prion-infected deer herds in northern Colorado, USA,
revealed that a 1 % increase in the clay-sized particle content in soils within
the approximate home range of an individual deer increased its odds of infection
by up to 8.9 % . Our findings suggest that soil clay content and related
environmental properties deserve greater attention in assessing risks of prion
disease outbreaks and prospects for their control in both natural and production
settings.
snip....
The capacity of clay minerals and clay-laden soils to capture and enhance
infectivity of shed or deposited prions 19,20,25 – 27 and the common tendency of
ruminants to ingest soil both deliberately and incidentally in the course of
foraging and grooming 12,44,45 provide an elegantly simple hypothetical
mechanism for indirect prion transmission, as follows: infected individuals
propagate infectious prions in mucosa-associated lymphoid tissues and shed
prions into ingesta and saliva; ingested and environmental soil microparticles
with a high phyllosilicate (especially smectite) content bind to, sequester and
enhance infectivity of prions both before and after leaving the host;
microparticle-bound prions are incorporated into surface soil; susceptible
individuals consume contaminated soil and some become infected. (Also see
Supplementary Figure S1 .) This mechanism may underlie the apparent importance
of indirect transmission in explaining observed patterns of prion infection
among captive mule deer 10,11 , and perhaps among sheep 3,4,6,7 . In light of
these and others ’ findings, soil clay content and related environmental
properties deserve greater attention in assessing local and regional risks of
prion disease outbreaks and prospects for their control in natural and
production settings.
Friday, February 25, 2011
Soil clay content underlies prion infection odds
Thursday, February 17, 2011
Environmental Sources of Scrapie Prions
PRION 2010
International Prion Congress: From agent to disease September 8–11, 2010
Salzburg, Austria
snip...
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute
and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental
routes, and there are also concerns about BSE infection remaining in the
environment after carcass burial or waste 3disposal. In two demonstration
experiments we are determining survival and migration of TSE infectivity when
buried for up to five years, as an uncontained point source or within bovine
heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters
containing either sandy or clay soil. Migration from the boluses is being
assessed from soil cores taken over time. With the exception of a very small
amount of infectivity found 25 cm from the bolus in sandy soil after 12 months,
no other infectivity has been detected up to three years. Secondly, ten bovine
heads were spiked with TSE infected mouse brain and buried in the two soil
types. Pairs of heads have been exhumed annually and assessed for infectivity
within and around them. After one year and after two years, infectivity was
detected in most intracranial samples and in some of the soil samples taken from
immediately surrounding the heads. The infectivity assays for the samples in and
around the heads exhumed at years three and four are underway. These data show
that TSE infectivity can survive burial for long periods but migrates slowly.
Risk assessments should take into account the likely long survival rate when
infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD
2009 CWD SYMPOSIUM UTAH
Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic
Area
65
Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic
Area
Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal
Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and
M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of
Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort
Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services,
United States Department of Agriculture, Fort Collins, Colorado, 80521, USA
3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA
4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory,
University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology,
Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging,
University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author-
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 ;
PO-248: TSE infectivity survives burial for five years with little
reduction in titer
Allister Smith, Robert Somerville, Karen Fernie The Roslin Institute and
R(D)SVS; University of Edinburgh; Edinburgh, UK
BSE infected animals, BSE-contaminated materials and other sources of TSE
(prion) infection, such as carcasses from scrapie infected sheep, CWD infected
deer and cadavers of individuals infected with CJD may all end up in the
environment through burial or other methods of disposal. They may continue to
act as a reservoir of TSE infectivity if cattle or other susceptible animals
were to be exposed to these sources in the future. In order to address these
concerns, we performed two large scale demonstration experiments under field
conditions which were designed to mimic some of the ways by which TSE infected
materials may have been disposed of. The project examined the fate of TSE
infectivity over a period of five years in two scenarios; when the infectivity
was contained within bovine heads and when the infectivity was buried without
any containment. Two soil types were compared: a sandy loam and a clay loam. We
used the 301V TSE strain which was derived by serial passage of BSE in VM mice.
TSE infectivity was recovered from all the heads exhumed annually for five
years from both types of soil, with little reduction in the amount of
infectivity throughout the period of the experiment. Small amounts of
infectivity were found in the soil immediately surrounding the heads, but not in
samples remote from them. Similarly there was no evidence of significant lateral
movement of infectivity from the buried bolus. However large amounts of TSE
infectivity were recovered at the site of burial of both boluses. There was
limited vertical upward movement of infectivity from the bolus buried in clay
soil and downward movement from the bolus buried in sandy soil. Now that these
experiments are completed we conclude that TSE infectivity is likely to survive
burial for long periods of time with minimal loss of infectivity and restricted
movement from the site of burial. These experiments emphasize that the
environment is a viable reservoir for retaining large quantities of TSE
infectivity, and reinforce the importance of risk assessment when disposing of
this type of infectious material.
Monday, November 26, 2012
Aerosol Transmission of Chronic Wasting Disease in White-tailed Deer
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
Thursday, December 29, 2011
Aerosols An underestimated vehicle for transmission of prion diseases?
PRION www.landesbioscience.com
please see more on Aerosols and TSE prion disease here ;
Friday, February 25, 2011
Soil clay content underlies prion infection odds
Monday, January 17, 2011
Aerosols Transmit Prions to Immunocompetent and Immunodeficient Mice
Wednesday, January 07, 2009
CWD to tighten taxidermy rules Hunters need to understand regulations
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
pens, pens, PENS ???
*** 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.
now, decades later ;
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. The purpose
of these experiments was to determine susceptibility of white-tailed deer (WTD)
to scrapie and to compare the resultant clinical signs, lesions, and molecular
profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD
intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral
and intranasal (IN); n = 5) with a US scrapie isolate. All deer were inoculated
with a 10% (wt/vol) brain homogenate from sheep with scrapie (1ml IC, 1 ml IN,
30 ml oral). All deer inoculated by the intracranial route had evidence of PrPSc
accumulation. PrPSc was detected in lymphoid tissues as early as 7
months-post-inoculation (PI) and a single deer that was necropsied at 15.6
months had widespread distribution of PrPSc highlighting that PrPSc is widely
distributed in the CNS and lymphoid tissues prior to the onset of clinical
signs. IC inoculated deer necropsied after 20 months PI (3/5) had clinical
signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural
and lymphoid tissues. The results of this study suggest that there are many
similarities in the manifestation of CWD and scrapie in WTD after IC inoculation
including early and widespread presence of PrPSc in lymphoid tissues, clinical
signs of depression and weight loss progressing to wasting, and an incubation
time of 21-23 months. Moreover, western blots (WB) done on brain material from
the obex region have a molecular profile similar to CWD and distinct from
tissues of the cerebrum or the scrapie inoculum. However, results of microscopic
and IHC examination indicate that there are differences between the lesions
expected in CWD and those that occur in deer with scrapie: amyloid plaques were
not noted in any sections of brain examined from these deer and the pattern of
immunoreactivity by IHC was diffuse rather than plaque-like. After a natural
route of exposure, 100% of WTD were susceptible to scrapie. Deer developed
clinical signs of wasting and mental depression and were necropsied from 28 to
33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB.
Similar to IC inoculated deer, samples from these deer exhibited two different
molecular profiles: samples from obex resembled CWD whereas those from cerebrum
were similar to the original scrapie inoculum. On further examination by WB
using a panel of antibodies, the tissues from deer with scrapie exhibit
properties differing from tissues either from sheep with scrapie or WTD with
CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive
when probed with mAb P4, however, samples from WTD with scrapie are only weakly
immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from
sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from
WTD with scrapie are strongly positive. This work demonstrates that WTD are
highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is
differentiable from CWD.
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 to better understand the potential host range and origins of prion
diseases. We inoculated white-tailed deer intracranially (IC) and by a natural
route of exposure (concurrent oral and intranasal inoculation) with a US scrapie
isolate. All deer inoculated by the intracranial route had evidence of PrPSc
accumulation and those necropsied after 20 months post-inoculation (PI) (3/5)
had clinical signs, spongiform encephalopathy, and widespread distribution of
PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6
months PI did not have clinical signs, but had widespread distribution of PrPSc.
This highlights the facts that 1) prior to the onset of clinical signs PrPSc is
widely distributed in the CNS and lymphoid tissues and 2) currently used
diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical
signs. The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in white-tailed deer 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 consistent with 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 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.
Committee Business:
The Committee discussed and approved three resolutions regarding CWD. They
can be found in the report of the Reswolutions Committee. Essentially the
resolutions urged USDA-APHIS-VS to:
Continue to provide funding for CWD testing of captive cervids
Finalize and publish the national CWD rule for Herd Certification and
Interstate Movement
Evaluate live animal test, including rectal mucosal biopsy, for CWD in
cervids
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
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 ;
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 ???
? game farms in a state X $465,000., do all these game farms have insurance
to pay for this risk of infected the wild cervid herds, in each state ???
how many game farms, are too many game farms ?
when you have states handing out shooting pen permits like candy on
halloween, just to advance their coffers, then other states wanting to do the
same thing, with most all of them ignoring the science on shooting pens and cwd,
what do you expect is going to happen.
when is enough, enough ?
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.
Form 1100-001
(R 2/11)
NATURAL RESOURCES BOARD AGENDA ITEM
SUBJECT: Information Item: Almond Deer Farm Update
FOR: DECEMBER 2011 BOARD MEETING
TUESDAY
TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief
SUMMARY:
SEE MORE USAHA REPORTS HERE, 2012 NOT PUBLISHED YET...TSS
Wednesday, November 14, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO
LOUISIANA and INDIANA
Pennsylvania CWD number of deer exposed and farms there from much greater
than first thought
Published: Wednesday, October 17, 2012, 10:44 PM Updated: Wednesday,
October 17, 2012, 11:33 PM
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
HERE, we see why these shooting pen owners some much like the USDA
oversight of these game farms ;
USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.”
problem solved $$$...TSS
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.”
what happened to the PA deer from the CWD index heard that went to
Louisiana ???
Monday, April 15, 2013
Deer farmers in the state of Louisiana are under a quarantine due to
Chronic Wasting Disease CWD
Friday, September 28, 2012
Stray elk renews concerns about deer farm security Minnesota
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
Friday, October 12, 2012
Texas Animal Health Commission (TAHC) is Now Accepting Comments on Rule
Proposals for “Chronic Wasting Disease (CWD)”
TO: comments@tahc.state.tx.us;
Texas Animal Health Commission (TAHC)
please note, I do not know how much of this 125 TONS of banned mad cow
protein was part of the ;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
bbbut, this was about 10 years post mad cow feed ban from 1997. 10 years
later, and still feeding banned mad cow protein to cervids???
considering that .005 gram is lethal to several bovines, and we know that
the oral consumption of CWD tainted products is very efficient mode of
transmission of CWD.
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall #
V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
***e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50
lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%,
Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to
20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall #
V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall #
V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email
and visit on June 9, 2006. FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
10,000,000 lbs banned blood laced meat and bone meal mbm 2007
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material
From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 –0500
From: "Terry S. Singeltary Sr."
To:
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000096/!x-usc:mailto:fdadockets@oc.fda.gov
Greetings FDA,
i would kindly like to comment on; Docket 03D-0186FDA Issues Draft Guidance
on Use of Material From Deer and Elk in Animal Feed; Availability Several
factors on this apparent voluntary proposal disturbs me greatly, please allow me
to point them out;
snip...
Oral transmission and early lymphoid tropism of chronic wasting
diseasePrPres in mule deer fawns (Odocoileus hemionus ) These results indicate
that CWD PrP res can be detected in lymphoid tissues draining the alimentary
tract within a few weeks after oral exposure to infectious prions and may
reflect the initial pathway of CWD infection in deer. The rapid infection of
deer fawns following exposure by the most plausible natural route is consistent
with the efficient horizontal transmission of CWD in nature and enables
accelerated studies of transmission and pathogenesis in the native
species.
snip...
now, just what is in that deer feed? _ANIMAL PROTEIN_
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr."
Reply-To: BSE-LTo: BSE-L
8420-20.5% Antler DeveloperFor Deer and Game in the wildGuaranteed Analysis
Ingredients / Products Feeding Directions
snip...
_animal protein_
snip...
DEPARTMENT OF HEALTH & HUMAN SERVICESPUBLIC HEALTH SERVICEFOOD AND DRUG
ADMINISTRATIONApril 9, 2001 WARNING LETTER01-PHI-12CERTIFIED MAILRETURN RECEIPT
REQUESTED
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy
Lake, PA 16145
PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:Food and Drug Administration Investigator Gregory E.
Beichner conducted an inspection of your animal feed manufacturing operation,
located in Sandy Lake, Pennsylvania, on March 23,2001, and determined that your
firm manufactures animal feeds including feeds containing prohibited materials.
The inspection found significant deviations from the requirements set forth in
Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins
Prohibited in Ruminant Feed. The regulation is intended to prevent the
establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such
deviations cause products being manufactured at this facility to be misbranded
within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic
Act (the Act).Our investigation found failure to label your swine feed with the
required cautionary statement "Do Not Feed to cattleor other Ruminants" The FDA
suggests that the statement be distinguished by different type-size or color or
other means of highlighting the statement so that it is easily noticed by a
purchaser.
In addition, we note that you are using approximately 140 pounds of cracked
corn to flush your mixer used in the manufacture of animal feeds containing
prohibited material. This flushed material is fed to wild game including deer, a
ruminant animal.Feed material which may potentially contain prohibited material
should not be fed to ruminant animals which may become part of the food
chain.The above is not intended to be an all-inclusive list of deviations
fromthe regulations. As a manufacturer of materials intended for animalfeed use,
you are responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance withthe law. We have enclosed a
copy of FDA's Small Entity Compliance Guideto assist you with complying with the
regulation... blah, blah, blah...
snip...end...full text ;
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In
Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #: 1
see my full text submission here ;
Sunday, April 21, 2013
Politicians ignore alarming CWD spike in Wyoming valley Wisconsin
Tuesday, April 16, 2013
Cervid Industry Unites To Set Direction for CWD Reform and seem to ignore
their ignorance and denial in their role in spreading Chronic Wasting
Disease
Thursday, May 02, 2013
Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TEXTING
what about human exposure to CWD and friendly fire (iatrogenic) pass it
forward mode of transmission i.e. 2nd hand exposure via surgical, medical,
blood, tissue, dental, to humans ???
Monday, May 23, 2011
CDC Assesses Potential Human Exposure to Prion Diseases Travel
Warning
Public release date: 23-May-2011
Contact: Francesca Costanzo
adajmedia@elsevier.com 215-239-3249
Elsevier Health Sciences
CDC assesses potential human exposure to prion diseases Study results
reported in the Journal of the American Dietetic Association Philadelphia, PA,
May 23, 2011 – Researchers from the Centers for Disease Control and Prevention
(CDC) have examined the potential for human exposure to prion diseases, looking
at hunting, venison consumption, and travel to areas in which prion diseases
have been reported in animals. Three prion diseases in particular – bovine
spongiform encephalopathy (BSE or "Mad Cow Disease"), variant Creutzfeldt-Jakob
disease (vCJD), and chronic wasting disease (CWD) – were specified in the
investigation. The results of this investigation are published in the June issue
of the Journal of the American Dietetic Association.
"While prion diseases are rare, they are generally fatal for anyone who
becomes infected. More than anything else, the results of this study support the
need for continued surveillance of prion diseases," commented lead investigator
Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious
Diseases, CDC, Atlanta."But it's also important that people know the facts about
these diseases, especially since this study shows that a good number of people
have participated in activities that may expose them to infection-causing
agents."
Although rare, human prion diseases such as CJD may be related to BSE.
Prion (proteinaceous infectious particles) diseases are a group of rare brain
diseases that affect humans and animals. When a person gets a prion disease,
brain function is impaired. This causes memory and personality changes,
dementia, and problems with movement. All of these worsen over time. These
diseases are invariably fatal. Since these diseases may take years to manifest,
knowing the extent of human exposure to possible prion diseases could become
important in the event of an outbreak.
CDC investigators evaluated the results of the 2006-2007 population survey
conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This
survey collects information on food consumption practices, health outcomes, and
demographic characteristics of residents of the participating Emerging
Infections Program sites. The survey was conducted in Connecticut, Georgia,
Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties
in the San Francisco Bay area, seven counties in the Greater Denver area, and 34
counties in western and northeastern New York.
Survey participants were asked about behaviors that could be associated
with exposure to the agents causing BSE and CWD, including travel to the nine
countries considered to be BSE-endemic (United Kingdom, Republic of Ireland,
France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the
cumulative length of stay in each of those countries. Respondents were asked if
they ever had hunted for deer or elk, and if that hunting had taken place in
areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming
or southwestern Nebraska). They were also asked if they had ever consumed
venison, the frequency of consumption, and whether the meat came from the
wild.
The proportion of survey respondents who reported travel to at least one of
the nine BSE endemic countries since 1980 was 29.5%. Travel to the United
Kingdom was reported by 19.4% of respondents, higher than to any other
BSE-endemic country. Among those who traveled, the median duration of travel to
the United Kingdom (14 days) was longer than that of any other BSE-endemic
country. Travelers to the UK were more likely to have spent at least 30 days in
the country (24.9%) compared to travelers to any other BSE endemic country. The
prevalence and extent of travel to the UK indicate that health concerns in the
UK may also become issues for US residents.
The proportion of survey respondents reporting having hunted for deer or
elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic
areas. Venison consumption was reported by 67.4% of FoodNet respondents, and
88.6% of those reporting venison consumption had obtained all of their meat from
the wild. These findings reinforce the importance of CWD surveillance and
control programs for wild deer and elk to reduce human exposure to the CWD
agent. Hunters in CWD-endemic areas are advised to take simple precautions such
as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or
spinal cord tissues, minimizing the handling of brain and spinal cord tissues,
and wearing gloves when field-dressing carcasses.
According to Abrams, "The 2006-2007 FoodNet population survey provides
useful information should foodborne prion infection become an increasing public
health concern in the future. The data presented describe the prevalence of
important behaviors and their associations with demographic characteristics.
Surveillance of BSE, CWD, and human prion diseases are critical aspects of
addressing the burden of these diseases in animal populations and how that may
relate to human health."
###
The article is "Travel history, hunting, and venison consumption related to
prion disease exposure, 2006-2007 FoodNet population survey" by Joseph Y.
Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger,
MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic
Association, Volume 111, Issue 6 (June 2011) published by Elsevier.
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.
Travel History, Hunting, and Venison Consumption Related to Prion Disease
Exposure, 2006-2007 FoodNet Population Survey
Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH ,
Lawrence B. Schonberger, MD , Ermias D. Belay, MD
Accepted 15 November 2010. Abstract Full Text PDF References .
Abstract
The transmission of bovine spongiform encephalopathy (BSE) to human beings
and the spread of chronic wasting disease (CWD) among cervids have prompted
concerns about zoonotic transmission of prion diseases. Travel to the United
Kingdom and other European countries, hunting for deer or elk, and venison
consumption could result in the exposure of US residents to the agents that
cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007
population survey was used to assess the prevalence of these behaviors among
residents of 10 catchment areas across the United States. Of 17,372 survey
respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5%
reported travel to any of the nine European countries considered to be
BSE-endemic since 1980. The proportion of respondents who had ever hunted deer
or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More
than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents
who traveled spent more time in the United Kingdom (median 14 days) than in any
other BSE-endemic country. Of the 11,635 respondents who had consumed venison,
59.8% ate venison at most one to two times during their year of highest
consumption, and 88.6% had obtained all of their meat from the wild. The survey
results were useful in determining the prevalence and frequency of behaviors
that could be important factors for foodborne prion transmission.
CDC
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting
Disease
CDC Volume 18, Number 3—March 2012
SNIP...
Interspecies transmission of CWD to noncervids has not been observed under
natural conditions. CWD infection of carcass scavengers such as raccoons,
opossums, and coyotes was not observed in a recent study in Wisconsin (22). In
addition, natural transmission of CWD to cattle has not been observed in
experimentally controlled natural exposure studies or targeted surveillance (2).
However, CWD has been experimentally transmitted to cattle, sheep, goats, mink,
ferrets, voles, and mice by intracerebral inoculation (2,29,33).
CWD is likely transmitted among mule, white-tailed deer, and elk without a
major species barrier (1), and other members of the cervid family, including
reindeer, caribou, and other species of deer worldwide, may be vulnerable to CWD
infection. Black-tailed deer (a subspecies of mule deer) and European red deer
(Cervus elaphus) are susceptible to CWD by natural routes of infection (1,34).
Fallow deer (Dama dama) are susceptible to CWD by intracerebral inoculation
(35). Continued study of CWD susceptibility in other cervids is of considerable
interest.
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, CWD will likely continue to emerge in North America. ...
SNIP...
Generation of a new form of human PrPSc in vitro by inter-species
transmission from cervids prions
Our results have far-reaching implications for human health, since they
indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc,
suggesting that CWD might be infectious to humans. Interestingly our findings
suggest that unstable strains from CWD affected animals might not be a problem
for humans, but upon strain stabilization by successive passages in the wild,
this disease might become progressively more transmissible to man.
Our results also have profound implications for understanding the
mechanisms of the prion species barrier and indicate that the transmission
barrier is a dynamic process that depends on the strain and moreover the degree
of adaptation of the strain. If our findings are corroborated by infectivity
assays, they will imply that CWD prions have the potential to infect humans and
that this ability progressively increases with CWD spreading.
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.
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
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”
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 ;
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
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
*** 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
___________________________________
PRODUCT
a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each
package is approximately 2 lbs., and each case is approximately 16 lbs.; Item
number 755125, Recall # F-129-9;
b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;
c) Elk Meat, French Rack, Chilled. Item number 755132, Recall #
F-131-9;
d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;
e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall #
F-133-9;
f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall #
F-134-9;
CODE
Elk Meats with production dates of December 29, 30, and 31
RECALLING FIRM/MANUFACTURER
Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009
and press release on February 9, 2009.
Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is
ongoing.
REASON
Elk products contain meat derived from an elk confirmed to have Chronic
Wasting Disease (CWD).
VOLUME OF PRODUCT IN COMMERCE
Unknown
DISTRIBUTION
NV, CA, TX, CO, NY, UT, FL, OK
___________________________________
Monday, February 09, 2009
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin
Because It May Contain Meat Derived From An Elk Confirmed To Have CWD
snip...
Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a
new prion strain
Date: August 25, 2007 at 12:42 pm PST
our results raise the possibility that CJD cases classified as VV1 may
include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne
infection by type 1 prions from animals, e.g., chronic wasting disease prions in
cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have
been reported (40, 41). The results of the present study emphasize the need for
traceback studies and careful re-examination of the biochemical properties of
sCJD-VV1 prions.
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
Tuesday, March 05, 2013
Chronic Wasting Disease Management Plan/Environmental Impact Statement,
Shenandoah National Park Virginia
Monday, April 15, 2013
Dr. Stephen B. Thacker Director Centers for Disease Control and
Prevention's Office of Science, Epidemiology and Laboratory Services (OSELS)
dies from Creutzfeldt Jakob Disease CJD
Thursday, May 02, 2013
Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TEXTING
Wednesday, May 15, 2013
Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with
Lyophilized Chronic Wasting Disease Prion Particulate Complexed to
Montmorillonite Clay
Research Article
Friday, November 16, 2012
Yellowstone elk herds feeding grounds, or future killing grounds from CWD
Sunday, April 21, 2013
Politicians ignore alarming CWD spike in Wyoming valley Wisconsin
layperson
MOM DOD 12/14/97 confirmed hvCJD
