Arkansas confirms second case of Chronic Wasting Disease CWD
Chronic wasting disease confirmed in deer at Ponca Date 03/09/2016
Description LITTLE ROCK – A white-tailed deer in Ponca recently tested positive
for chronic wasting disease, according to the Arkansas Game and Fish Commission.
The disease is fatal to deer and elk.
The positive CWD test from a deer comes on the heels of an elk near Pruitt,
about 12 miles east of Ponca, that was confirmed to have the disease Feb. 23.
Both areas are in northern Newton County.
The AGFC took tissue samples from the 2½-year-old female deer, which was
found dead. The U.S. Department of Agriculture’s National Veterinary Services
Laboratories in Ames, Iowa, confirmed the test today.
The 2½-year-old female elk was killed by a hunter Oct. 6 on the Buffalo
National River near Pruitt during elk hunting season. It was the first animal in
Arkansas confirmed to have CWD. The disease was confirmed on Feb. 23. The elk
was tested by the same labs that confirmed CWD in the deer from Ponca.
To determine the prevalence and distribution of the disease among deer, the
AGFC will begin taking samples Monday within a capsule-shaped area ranging from
5 miles west of Ponca to 5 miles east of Pruitt, and 5 miles across.
“We need to sample 300 deer to determine the prevalence and the spatial
distribution of CWD in the population with 95 percent confidence,” said Dick
Baxter, an assistant chief in the Wildlife Management Division.
Enough free-ranging deer have to be tested before there’s a strong
statistical chance of detecting CWD in 1 percent of the herd. This is a common
method to estimate CWD prevalence in deer populations. As results are analyzed,
wildlife biologists will adjust the strategy.
“The test area will expand as positive (CWD) tests warrant,” said Cory
Gray, AGFC deer program coordinator.
Wildlife biologists will not use the same tactics with the elk herd.
“We’re not going to determine the prevalence of CWD in elk at this point,
because it would require a large sample of the relatively small elk herd to be
valid statistically,” Baxter said. “We want to target sick elk throughout the
elk range to find the spatial distribution.”
The elk strategy changed when the deer at Ponca tested positive.
“When we thought CWD was confined to the area where the elk was killed at
Pruitt, we believed we could take the elk herd that was in close contact, maybe
30-40 animals,” Gray said.
The sampled deer and elk will be processed at a base camp staffed by AGFC
and National Park Service personnel. Meat from deer that don’t test positive for
CWD will be given to landowners where the deer were harvested or Arkansas
Hunters Feeding the Hungry. Since only unhealthy elk will be harvested, meat
from those animals will not be consumed. Everything that is not packaged for
consumption will be incinerated.
“Landowners have been very helpful in allowing us access to their
property,” Gray said. “Much of the land within the zone where we’ll be working
is privately owned. We need their help and help from anyone who sees a deer or
elk that appears to be ill.”
The public can report sick deer and elk by calling 800-482-9262, 24 hours a
day.
Although there are no confirmed cases of CWD transmission from cervids to
humans or to livestock, the Centers for Disease Control and Prevention, the
World Health Organization and the Arkansas Department of Health recommend that
people not consume meat from animals known to be infected with CWD.
CWD was first documented among captive mule deer in Colorado in 1967, and
has been detected in 24 states and two Canadian provinces. It’s been found in
the wild in 20 states and among captive cervids in 15 states. Biologists don’t
know how the disease reached northern Arkansas at this point. The Arkansas elk
herd began with 112 animals from Colorado and Nebraska, relocated during
1981-85.
The AGFC has taken several steps to prevent the disease from entering the
state. The Commission established a moratorium on the importation of live
cervids in 2002, and restricted the importation of cervid carcasses in 2005. It
also set moratoriums on permits for commercial hunting resorts and
breeder/dealer permits for cervid facilities in 2006, and on obtaining
hand-captured white-tailed deer in 2012.
According to the Chronic Wasting Disease Alliance (http://cwd-info.org), CWD affects only cervids
(members of the cervidae family such as deer, elk and moose). Research shows
that prions (abnormal cellular proteins) are transmitted through feces, urine
and saliva. The shortest period between infection and symptoms of the disease is
16 months, although the infectious agent can survive for years in organic matter
such as soil and plants.
CWD is a neurological disease that’s part of a group of diseases called
transmissible spongiform encephalopathies. Once in a host’s body, prions
transform normal cellular protein into abnormal shapes that accumulate until the
cell ceases to function. As the brains of infected animals degenerate, they lose
weight, lose their appetite and develop an insatiable thirst. They tend to stay
away from herds, walk in patterns, carry their head low, salivate and grind
their teeth.
Two meetings have been scheduled in Ponca and Huntsville to discuss the
most recent finding of CWD.
The first meeting will be held in Ponca on Thursday, March 10. The meeting
will begin at 6 p.m. at the Ponca Fire Department on Arkansas Highway 43.
The second meeting will be held on Friday, March 11 at Carroll Electric,
5056 Highway 412B in Huntsville. This meeting will begin at 6 p.m.
Visit www.agfc.com/cwd for more information.
1st case cwd Arkansas
Tuesday, February 23, 2016
ARKANSAS Detects First Chronic Wasting Disease CWD in a wild elk
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
News Details All News Items
AGFC commission meeting Date 02/23/2016 Description You are hereby notified
that Commissioners of the Arkansas Game and Fish Commission will meet on the
following dates and times to consider any business that may be brought before
the Commission. Unless otherwise stated, meetings will be held at the AGFC
offices, 2 Natural Resources Drive in Little Rock.
Tuesday, Feb. 23 5:30 p.m. Meeting by conference call to discuss
confirmation of chronic wasting disease in a wild Arkansas elk.
Chronic Wasting Disease Found in Arkansas
An elk harvested near Pruitt on the Buffalo National River during the
October 2015 hunting season tested positive for chronic wasting disease.
This is the first time an animal in Arkansas has tested positive for the
disease, which is fatal to elk and white-tailed deer. According to the AGFC's
CWD response plan, created in 2006, samples from elk and deer in the area will
be taken to determine the prevalence of the disease and a future course of
action.
A multi-county CWD management zone will be established, and public meetings
in the area will be scheduled to discuss plans and answer questions.
Biologists don’t know how the disease reached northern Arkansas. The local
herd began with 112 elk from Colorado and Nebraska, relocated between
1981-85.
“(CWD) would have raised its ugly head a lot sooner than now,” said Don
White, a wildlife ecologist at the University of Arkansas Agriculture Experiment
Station in Monticello. “It's extremely unlikely that it came from those 112
elk.”
More than 200 elk harvested in Arkansas since 1997 have been tested for
CWD. The AGFC also routinely gathers samples from white-tailed deer across the
state to test for the disease.
??? One of the subjects confessed to taking a fourth deer in Texas, which
was wasted and dumped in Arkansas. ???
Wrong State of Mind
A Bowie County game warden received a call from Arkansas Game and Fish
officers in reference to a truck they had stopped that was traveling east on
Interstate 30 from Texas. The vehicle contained 10 whitetail deer, a bobcat and
a turkey breast that had all been harvested in Central Texas. It is illegal to
transport a deer with bones from a chronic wasting disease state into the state
of Arkansas. Since the wildlife officers in Arkansas were not entirely familiar
with Texas laws, they requested the Bowie County warden to inspect the subject’s
game for any Texas violations. The warden inspected the deer at the Arkansas
Game and Fish district office and wrote several citations for tagging
proof-of-sex violations. The state of Arkansas filed several cases for
transporting deer with bone still attached, seized all of the animals and parts
for their violations, and tested the deer for chronic wasting disease.
Don’t Mess With Texas... or Arkansas
A Gregg County game warden responded to a Longview Animal Control call
regarding a decaying doe hanging in a resident’s tree. When the warden located
the deer, he also discovered an additional untagged doe behind the property and
an untagged nine-point buck. Two of the four individuals interviewed claimed
they harvested the two deer in Arkansas. One of the subjects confessed to taking
a fourth deer in Texas, which was wasted and dumped in Arkansas. When questioned
about the discrepancy between their harvest dates versus the date printed on
their Arkansas hunting licenses, two of the subjects acknowledged hunting
without a license. The warden then contacted Arkansas Game and Fish Commission
wildlife officers who advised that they were pursuing more than $2,500 in
charges. They also said that two of the men face one year suspensions, while
another would receive a lifetime hunting license suspension in Arkansas. Civil
restitution and multiple charges were filed, including no hunting license;
hunting during closed season; failure to keep game in edible condition; untagged
deer; and no harvest log. Investigation is ongoing and cases pending.
Cervid Carcass Importation Restrictions In 2013, the AGFC adopted
regulations to prevent CWD from spreading into the state through mishandled
cervid carcasses. Cervids include any member of the Cervidae family, including
white-tailed deer, elk, moose, red deer, sika deer, fallow deer, mule deer and
caribou.
According to Code 05.26 of the Arkansas Game and Fish Commission Code Book,
it is unlawful to import, transport or possess any portion of a cervid carcass
originating from any area outside the boundaries of Arkansas, with the following
exceptions:
Meat that has been completely deboned. Antlers, antlers attached to cleaned
skull plates or cleaned skulls where no tissue is attached to the skull. Cleaned
teeth. Finished taxidermy and antler products. Hides and tanned products. Other
portions of deer originating from the land between the Mississippi River levees
in Tennessee and Mississippi.
Deer or elk harvested in commercial wildlife hunting resorts in Arkansas
may be transported or possessed only after a CWD sample is collected.
Carcass
I knew this was coming. I had sent out a warning to Arkansas on July 11,
2015. see;
From: Terry S. Singeltary Sr.
Sent: Saturday, July 11, 2015 5:26 PM
To: askAGFC@agfc.state.ar.us Cc: nledbetter@agfc.state.ar.us ;
kastephens@agfc.state.ar.us ; srwilson@agfc.state.ar.us ;
jfwilliams@agfc.state.ar.us
Subject: CHRONIC WASTING DISEASE CWD TSE PRION WARNING TO ARKANSAS
what you don’t know, and what they will not tell you about CWD...it’s not
pretty...terry
Longitudinal Detection of Prion Shedding in Saliva and Urine by
CWD-Infected Deer by RT-QuIC
Davin M. Henderson1, Nathaniel D. Denkers1, Clare E. Hoover1, Nina
Garbino1, Candace K. Mathiason1 and Edward A. Hoover1# + Author
Affiliations
1Prion Research Center, Department of Microbiology, Immunology, and
Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado
State University, Fort Collins, CO 80523 ABSTRACT Chronic Wasting Disease (CWD)
is an emergent, rapidly spreading prion disease of cervids. Shedding of
infectious prions in saliva and urine is thought to be an important factor in
CWD transmission. To help elucidate this issue, we applied an in vitro
amplification assay to determine the onset, duration, and magnitude of prion
shedding in longitudinally collected saliva and urine samples from CWD-exposed
white-tailed deer. We detected prion shedding as early as 3 months after CWD
exposure and sustained shedding throughout the disease course. We estimated that
a 50% lethal dose (LD50) for cervidized transgenic mice would be contained in 1
ml of infected deer saliva or 10 ml or urine. Given the average course of
infection and daily production of these body fluids, an infected deer would shed
thousands of prion infectious dosesover the course of CWD infection. The direct
and indirect environmental impact of this magnitude of prion shedding for cervid
and non-cervid species is surely significant.
Importance: Chronic wasting disease (CWD) is an emerging and uniformly
fatal prion disease affecting free ranging deer and elk and now recognized in 22
United States and 2 C anadian Provinces. It is unique among prion diseases in
that it is transmitted naturally though wild populations. A major hypothesis for
CWD's florid spread is that prions are shed in excreta and transmitted via
direct or indirect environmental contact. Here we use a rapid in vitro assay to
show that infectious doses of CWD prions are in fact shed throughout the
multi-year disease course in deer. This finding is an important advance in
assessing the risks posed by shed CWD prions to animals as well as humans.
FOOTNOTES
↵#To whom correspondence should be addressed: Edward A. Hoover, Prion
Research Center, Department of Microbiology, Immunology and Pathology, Colorado
State University, Fort Collins, Colorado, US Email: edward.hoover@colostate.edu
cwd environmental load factor in the land and surrounding plants and
objects.
transportation of cervids and HUMANS from cwd zone should be regarded as a
great risk factor, and environmental contamination.
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
snip...
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentallyrelevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
Wednesday, June 10, 2015
Zoonotic Potential of CWD Prions
LATE-BREAKING ABSTRACTS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
Chronic wasting disease (CWD) is a widespread and expanding prion disease
in free-ranging and captive cervid species in North America. The zoonotic
potential of CWD prions is a serious public health concern. Current literature
generated with in vitro methods and in vivo animal models (transgenic mice,
macaques and squirrel monkeys) reports conflicting results. The susceptibility
of human CNS and peripheral organs to CWD prions remains largely unresolved. In
our earlier bioassay experiments using several humanized transgenic mouse lines,
we detected protease-resistant PrPSc in the spleen of two out of 140 mice that
were intracerebrally inoculated with natural CWD isolates, but PrPSc was not
detected in the brain of the same mice. Secondary passages with such
PrPSc-positive CWD-inoculated humanized mouse spleen tissues led to efficient
prion transmission with clear clinical and pathological signs in both humanized
and cervidized transgenic mice. Furthermore, a recent bioassay with natural CWD
isolates in a new humanized transgenic mouse line led to clinical prion
infection in 2 out of 20 mice. ***These results indicate that the CWD prion has
the potential to infect human CNS and peripheral lymphoid tissues and that there
might be asymptomatic human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
The propensity for trans-species prion transmission is related to the
structural characteristics of the enciphering and heterologous PrP, but the
exact mechanism remains mostly mysterious. Studies of the effects of primary or
tertiary prion protein structures on trans-species prion transmission have
relied primarily upon animal bioassays, making the influence of prion protein
structure vs. host co-factors (e.g. cellular constituents, trafficking, and
innate immune interactions) difficult to dissect. As an alternative strategy, we
used real-time quakinginduced conversion (RT-QuIC) to investigate trans-species
prion conversion.
To assess trans-species conversion in the RT-QuIC system, we compared
chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions,
as well as feline CWD (fCWD) and feline spongiform encephalopathy (FSE). Each
prion was seeded into each host recombinant PrP (full-length rPrP of
white-tailed deer, bovine or feline). We demonstrated that fCWD is a more
efficient seed for feline rPrP than for white-tailed deer rPrP, which suggests
adaptation to the new host.
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD. ***This insinuates that, at the level
of protein:protein interactions, the barrier preventing transmission of CWD to
humans is less robust than previously estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods. *** We recently observed
the direct transmission of a natural classical scrapie isolate to macaque after
a 10-year silent incubation period, ***with features similar to some reported
for human cases of sporadic CJD, albeit requiring fourfold longe incubation than
BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), ***is the
third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the
origin of human sporadic cases. We will present an updated panorama of our
different transmission studies and discuss the implications of such extended
incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases...TSS
===============
Friday, January 30, 2015
*** Scrapie: a particularly persistent pathogen ***
Tuesday, December 16, 2014
*** Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. ***The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. ***These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
see more 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
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...
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
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations 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.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***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.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C.
Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡,
Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure.
Friday, May 22, 2015
*** Chronic Wasting Disease and Program Updates - 2014 NEUSAHA Annual
Meeting 12-14 May 2014
Wednesday, July 01, 2015
TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Wednesday, July 01, 2015
*** DRAFT Virginia Deer Management Plan 2015-2024 (*** bans urine scents do
to CWD 2015) ***
Thursday, July 09, 2015
TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed
Herd with Testing of Exposed Animals
***Immediate and Ongoing Detection of Prions in the Blood of Hamsters and
Deer following Oral, Nasal, or Blood Inoculations
Alan M. Eldera, Davin M. Hendersona, Amy V. Nallsa, Edward A. Hoovera,
Anthony E. Kincaidb,c, Jason C. Bartzb and Candace K. Mathiasona aDepartment of
Microbiology, Immunology and Pathology, Colorado State University, Fort Collins,
Colorado, USA bMedical Microbiology and Immunology, Creighton University, Omaha,
Nebraska, USA cDepartment of Pharmacy Sciences, Creighton University, Omaha,
Nebraska, USA S. Perlman, Editor + Author Affiliations
2013
Strain characteristics of the in vitro-adapted rabbit and dog BSE agent
remained invariable with respect to the original cattle BSE prion, suggesting
that the naturally low susceptibility of rabbits and dogs to prion infections
should not alter their zoonotic potential if these animals became infected with
BSE.
=======================================
Neurobiology of Disease
Bovine Spongiform Encephalopathy Induces Misfolding of Alleged
Prion-Resistant Species Cellular Prion Protein without Altering Its
Pathobiological Features
Enric Vidal3, Natalia Fernández-Borges1, Belén Pintado4, Montserrat
Ordóñez3, Mercedes Márquez6, Dolors Fondevila5,6, Juan María Torres7, Martí
Pumarola5,6, and Joaquín Castilla1,2 + Author Affiliations
1CIC bioGUNE, 48160 Derio, Bizkaia, Spain,
2IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Bizkaia, Spain,
3Centre de Recerca en Sanitat Animal, Campus de la Universitat Autònoma de
Barcelona (UAB)-IRTA, 08193 Bellaterra, Barcelona, Spain,
4Centro Nacional de Biotecnología, Campus de Cantoblanco, 28049
Cantoblanco, Madrid, Spain,
5Department of Animal Medicine and Surgery, Veterinary Faculty, UAB, 08193
Bellaterra (Cerdanyola del Vallès), Barcelona, Spain,
6Murine Pathology Unit, Centre de Biotecnologia Animal i Teràpia Gènica,
UAB, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain, and
7Centro de Investigación en Sanidad Animal-Instituto Nacional de
Investigación y Tecnología Agraria y Alimentaria, 28130 Valdeolmos, Madrid,
Spain
Author contributions: E.V., N.F.-B., and J.C. designed research; E.V.,
N.F.-B., B.P., M.O., M.M., D.F., and J.C. performed research; E.V., N.F.-B.,
B.P., and J.C. contributed unpublished reagents/analytic tools; E.V., N.F.-B.,
B.P., M.O., M.M., D.F., J.M.T., M.P., and J.C. analyzed data; E.V. and J.C.
wrote the paper.
Abstract
Bovine spongiform encephalopathy (BSE) prions were responsible for an
unforeseen epizootic in cattle which had a vast social, economic, and public
health impact. This was primarily because BSE prions were found to be
transmissible to humans. Other species were also susceptible to BSE either by
natural infection (e.g., felids, caprids) or in experimental settings (e.g.,
sheep, mice). However, certain species closely related to humans, such as canids
and leporids, were apparently resistant to BSE. In vitro prion amplification
techniques (saPMCA) were used to successfully misfold the cellular prion protein
(PrPc) of these allegedly resistant species into a BSE-type prion protein. The
biochemical and biological properties of the new prions generated in vitro after
seeding rabbit and dog brain homogenates with classical BSE were studied.
Pathobiological features of the resultant prion strains were determined after
their inoculation into transgenic mice expressing bovine and human PrPC. Strain
characteristics of the in vitro-adapted rabbit and dog BSE agent remained
invariable with respect to the original cattle BSE prion, suggesting that the
naturally low susceptibility of rabbits and dogs to prion infections should not
alter their zoonotic potential if these animals became infected with BSE. This
study provides a sound basis for risk assessment regarding prion diseases in
purportedly resistant species.
Received January 18, 2013. Revision received March 7, 2013. Accepted March
23, 2013. Copyright © 2013 the authors 0270-6474/13/337778-09$15.00/0
2005
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904
6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN: FAX:
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long
delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform
Encephalopathy Advisory Committee (SEAC), the UK Government's independent
Advisory Committee on all aspects related to BSE-like disease, gave the hound
study detailed consideration at their meeting in January 1994. As a summary of
this meeting published in the BSE inquiry noted, the Committee were clearly
concerned about the work that had been carried out, concluding that there had
clearly been problems with it, particularly the control on the histology, and
that it was more or less inconclusive. However was agreed that there should be a
re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound
study to see if any useful results could be gained from it. The Chairman
concluded that there were varying opinions within the Committee on further work.
It did not suggest any further transmission studies and thought that the lack of
clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as
conducted. As a result it is likely that the authors felt that it would not
stand up to r~eer review and hence it was never published. As noted above, and
in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether
additional work should be performed to examine dogs for evidence of TSE
infection. Although the Committee had mixed views about the merits of conducting
further work, the Chairman noted that when the Southwood Committee made their
recommendation to complete an assessment of possible spongiform disease in dogs,
no TSEs had been identified in other species and hence dogs were perceived as a
high risk population and worthy of study. However subsequent to the original
recommendation, made in 1990, a number of other species had been identified with
TSE ( e.g. cats) so a study in hounds was less
critical. For more details see- http://www.bseinquiry,
gov.uk/files/yb/1995/06/21005001 .pdf
As this study remains unpublished, my understanding is that the ownership
of the data essentially remains with the original researchers. Thus
unfortunately, I am unable to help with your request to supply information on
the hound survey directly. My only suggestion is that you contact one of the
researchers originally involved in the project, such as Gerald Wells. He can be
contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone,
Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases
of spongiform encephalopathy in animals and poultry were made notifiable. Hence
since that date there has been a requirement for vets to report any suspect SE
in dogs for further investigation. To date there has never been positive
identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
======================================
HOUND SURVEY
I am sorry, but I really could have been a co-signatory of Gerald's
minute.
I do NOT think that we can justify devoting any resources to this study,
especially as larger and more important projects such as the pathogenesis study
will be quite demanding.
If there is a POLITICAL need to continue with the examination of hound
brains then it should be passed entirely to the VI Service.
J W WILESMITH Epidemiology Unit 18 October 1991
Mr. R Bradley
cc: Mr. G A H Wells
3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would
by the end of the year, indentify the three brains that were from the
''POSITIVE'' end of the lesion spectrum.
TSE in dogs have not been documented simply because OF THE ONLY STUDY,
those brain tissue samples were screwed up too. see my investigation of this
here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS
BRAIN TISSUE SAF's. ...TSS
TSE & HOUNDS
GAH WELLS (very important statement here...TSS)
HOUND STUDY
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to
other species will invariably present pathology typical of a scrapie-like
disease.
snip...
http://web.archive.org/web/20060307063542/http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
***
Posted by flounder on 03 Jul 2015 at 16:53 GMT
76 pages on hound study;
snip...
The spongiform changes were not pathognomonic (ie. conclusive proof) for
prion disease, as they were atypical, being largely present in white matter
rather than grey matter in the brain and spinal cord. However, Tony Scott, then
head of electron microscopy work on TSEs, had no doubt that these SAFs were
genuine and that these hounds therefore must have had a scrapie-like disease. I
reviewed all the sections myself (original notes appended) and although the
pathology was not typical, I could not exclude the possibility that this was a
scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian
degeneration was also present in the white matter of the hounds, another feature
of scrapie.
38.I reviewed the literature on hound neuropathology, and discovered that
micrographs and descriptive neuropathology from papers on 'hound ataxia'
mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer
(Cambridge) had done much of this work, and I obtained original sections from
hound ataxia cases from him. This enabled me provisionally to conclude that
Robert Higgins had in all probability detected hound ataxia, but also that hound
ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination
of single restricted microscopic fields that there was no distinction between
the white matter vacuolation present in BSE and scrapie cases, and that
occurring in hound ataxia and the hound survey cases.
39.Hound ataxia had reportedly been occurring since the 1930's, and a known
risk factor for its development was the feeding to hounds of downer cows, and
particularly bovine offal. Circumstantial evidence suggests that bovine offal
may also be causal in FSE, and TME in mink. Despite the inconclusive nature of
the neuropathology, it was clearly evident that this putative canine spongiform
encephalopathy merited further investigation.
40.The inconclusive results in hounds were never confirmed, nor was the
link with hound ataxia pursued. I telephoned Robert Higgins six years after he
first sent the slides to CVL. I was informed that despite his submitting a
yearly report to the CVO including the suggestion that the hound work be
continued, no further work had been done since 1991. This was surprising, to say
the very least.
41.The hound work could have provided valuable evidence that a scrapie-like
agent may have been present in cattle offal long before the BSE epidemic was
recognised. The MAFF hound survey remains unpublished.
Histopathological support to various other published MAFF experiments
42.These included neuropathological examination of material from
experiments studying the attempted transmission of BSE to chickens and pigs (CVL
1991) and to mice (RVC 1994).
It was thought likely that at least some, and probably all, of the cases in
zoo animals were caused by the BSE agent. Strong support for this hypothesis
came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A.,
McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of
bovine spongiform encephalopathy and scrapie to mice: strain variation and
species barrier. Philosophical Transactions of the Royal Society B 343, 405-411:
J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation
period and lesion profile in six strains of mice inoculated with brain
homogenates from an affected kudu and the nyala, was similar to that seen when
this panel of mouse strains was inoculated with brain from cattle with BSE. The
affected zoo bovids were all from herds that were exposed to feeds that were
likely to have contained contaminated ruminant-derived protein and the zoo
felids had been exposed, if only occasionally in some cases, to tissues from
cattle unfit for human consumption.
snip...
NEW URL ;
Friday, March 8, 2013
Dogs may have been used to make Petfood and animal feed
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
***
Posted by flounder on 03 Jul 2015 at 16:53 GMT
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A.
Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel
J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary
Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI
53706, USA 2US Geological Survey, National Wildlife Health Center, 6006
Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural
Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary
Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author
email: cjohnson@svm.vetmed.wisc.edu
We intracerebrally challenged four species of native North American rodents
that inhabit locations undergoing cervid chronic wasting disease (CWD)
epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed
mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles
(Myodes gapperi). The inocula were prepared from the brains of hunter-harvested
white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles
proved to be most susceptible, with a median incubation period of 272 days.
Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the
brains of all challenged meadow voles. Subsequent passages in meadow voles lead
to a significant reduction in incubation period. The disease progression in
red-backed voles, which are very closely related to the European bank vole (M.
glareolus) which have been demonstrated to be sensitive to a number of TSEs, was
slower than in meadow voles with a median incubation period of 351 days. We
sequenced the meadow vole and red-backed vole Prnp genes and found three amino
acid (AA) differences outside of the signal and GPI anchor sequences. Of these
differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is
particularly intriguing due its postulated involvement in "rigid loop" structure
and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5
years post-inoculation, but appear to be exhibiting a high degree of disease
penetrance. White-footed mice have an even longer incubation period but are also
showing high penetrance. Second passage experiments show significant shortening
of incubation periods. Meadow voles in particular appear to be interesting lab
models for CWD. These rodents scavenge carrion, and are an important food source
for many predator species. Furthermore, these rodents enter human and domestic
livestock food chains by accidental inclusion in grain and forage. Further
investigation of these species as potential hosts, bridge species, and
reservoirs of CWD is required.
Veterinary Pathology Onlinevet.sagepub.com Published online before print
February 27, 2014, doi: 10.1177/0300985814524798 Veterinary Pathology February
27, 2014 0300985814524798
Lesion Profiling and Subcellular Prion Localization of Cervid Chronic
Wasting Disease in Domestic Cats
D. M. Seelig1⇑ A. V. Nalls1 M. Flasik2 V. Frank1 S. Eaton2 C. K. Mathiason1
E. A. Hoover1 1Department of Microbiology, Immunology, and Pathology, Colorado
State University, Fort Collins, CO, USA 2Department of Biomedical Sciences,
Colorado State University, Fort Collins, CO, USA D. M. Seelig, University of
Minnesota, Department of Veterinary Clinical Sciences, Room 339 VetMedCtrS,
6192A (Campus Delivery Code), 1352 Boyd Ave, St Paul, MN 55108, USA. Email
address: dseelig@umn.edu
Abstract
Chronic wasting disease (CWD) is an efficiently transmitted, fatal, and
progressive prion disease of cervids with an as yet to be fully clarified host
range. While outbred domestic cats (Felis catus) have recently been shown to be
susceptible to experimental CWD infection, the neuropathologic features of the
infection are lacking. Such information is vital to provide diagnostic power in
the event of natural interspecies transmission and insights into host and strain
interactions in interspecies prion infection. Using light microscopy and
immunohistochemistry, we detail the topographic pattern of neural spongiosis
(the “lesion profile”) and the distribution of misfolded prion protein in the
primary and secondary passage of feline CWD (FelCWD). We also evaluated cellular
and subcellular associations between misfolded prion protein (PrPD) and central
nervous system neurons and glial cell populations. From these studies, we (1)
describe the novel neuropathologic profile of FelCWD, which is distinct from
either cervid CWD or feline spongiform encephalopathy (FSE), and (2) provide
evidence of serial passage-associated interspecies prion adaptation. In
addition, we demonstrate through confocal analysis the successful
co-localization of PrPD with neurons, astrocytes, microglia, lysosomes, and
synaptophysin, which, in part, implicates each of these in the neuropathology of
FelCWD. In conclusion, this work illustrates the simultaneous role of both host
and strain in the development of a unique FelCWD neuropathologic profile and
that such a profile can be used to discriminate between FelCWD and FSE.
prion chronic wasting disease immunohistochemistry interspecies cat feline
spongiform encephalopathy transmissible spongiform encephalopathy adaptation
species barrier
Monday, August 8, 2011 Susceptibility of Domestic Cats to CWD Infection
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M.
Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K.
Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness.
*** Two of these cats have developed rear limb ataxia. Although the limited
data from this ongoing study must be considered preliminary, they raise the
potential for cervid-to-feline transmission in nature.
AD.63:
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado
State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN
USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to
the domestic cat, thus raising the issue of potential cervid-to- feline
transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
FELINE SPONGIFORM ENCEPHALOPATHY FSE
Wednesday, October 17, 2012
Prion Remains Infectious after Passage through Digestive System of American
Crows (Corvus brachyrhynchos)
HUMANS
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb**************
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.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Thursday, October 10, 2013
*** CJD REPORT 1994 increased risk for consumption of veal and venison and
lamb
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER
AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease
Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic
Association Volume 111, Issue 6 , Pages 858-863, June 2011.
NOR IS THE FDA recalling this CWD positive elk meat for the well being of
the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat
derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS
AND FIELD CORRECTIONS: FOODS CLASS II
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net) Subject: CWD aka MAD DEER/ELK TO
HUMANS ???
Date: September 30, 2002 at 7:06 am PST From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic
wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
Wednesday, July 01, 2015
*** DRAFT Virginia Deer Management Plan 2015-2024 (*** bans urine scents do
to CWD 2015) ***
Thursday, July 09, 2015
TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed
Herd with Testing of Exposed Animals
Wednesday, March 18, 2015
Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18,
2015
Wednesday, March 25, 2015
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
Thursday, May 02, 2013
*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY
TEXTING
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West
Texas
***for anyone interested, here is some history of CWD along the Texas, New
Mexico border, and my attempt to keep up with it...terry
snip...
see history CWD Texas, New Mexico Border ;
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER
Sunday, October 04, 2009
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009 2009 Summary of Chronic
Wasting Disease in New Mexico New Mexico Department of Game and Fish
Friday, May 22, 2015
*** Chronic Wasting Disease and Program Updates - 2014 NEUSAHA Annual
Meeting 12-14 May 2014
Wednesday, July 01, 2015
TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Posted by flounder on 03 Jul 2015 at 16:53 GMT
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
Singeltary comment ;
Singeltary said he became convinced that BSE is here as he watched his
mother, Barbara Poulter of Crystal Beach, dying of sporadic Creutzfeldt-Jakob
Disease. The rare, fatal brain disease is sometimes accompanied by severe
jerking.
"She would jerk so bad at times, it would take three of us to hold her
down," Singeltary said. "They can call it whatever they want, but I know what I
saw, and what she went through. `Sporadic' simply means they don't know."
just made a promise to mom (confirmed hvCJD DOD 12/14/97), never forget,
and never let them forget...
Terry S. Singeltary Sr.
Wednesday, February 10, 2016
*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD
***
Tuesday, February 23, 2016
Parks and Wildlife begins reducing deer population at Texas Mountain Ranch
Chronic Wasting Disease CWD TSE Prion Update
*** I kindly would like to comment on a few statements from the TPWD et al
;
Tuesday, February 23, 2016
ARKANSAS Detects First Chronic Wasting Disease CWD in a wild elk
Tuesday, March 08, 2016
Oklahoma Chronic Wasting Disease CWD of Deer and Elk Surveillance, Testing,
and Preparedness
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
3:14 PM
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