Pennsylvania CWD DETECTED IN SIX MORE FREE-RANGING DEER Disease Management Area 2 again expanded due to new cases Release #030-15
Pennsylvania CWD DETECTED IN SIX MORE FREE-RANGING DEER Disease Management
Area 2 again expanded due to new cases Release #030-15
FOR IMMEDIATE RELEASE: May 05, 2015
Release #030-15
CWD UPDATE: DISEASE DETECTED IN SIX MORE FREE-RANGING DEER Disease
Management Area 2 again expanded due to new cases.
From the start of 2014 through the present, six additional cases of
chronic wasting disease have been documented in Pennsylvania, the Pennsylvania
Game Commission announced today. All six deer to test positive were killed on
highways within Disease Management Area 2 (DMA 2), the only area of the state
where chronic wasting disease (CWD) has been detected in free-ranging deer. None
of the samples collected from deer or elk harvested by hunters anywhere in the
state during the 2014-15 hunting seasons tested positive for CWD, and no
road-killed deer or elk from outside DMA 2 tested positive. Additionally, no new
cases have been detected in captive deer or elk outside the borders of an
established Disease Management Area (DMA). However, the boundary of DMA 2 again
has been expanded because CWD-positive deer detected within DMA 2 or in Maryland
were near previous boundaries. Pennsylvania’s CWD Response Plan requires a
10-mile buffer around sites associated with positive tests.
DMA 2 now encompasses parts of Bedford, Blair, Cambria, Huntington, Fulton
and Somerset counties.
CWD is not known to afflict humans, but is always fatal to the deer and
elk it infects.
Sampling in 2014-15
The Game Commission sampled 4,266 deer statewide during 2014. Of these,
1,701 were from DMAs.
DMA 1 (York and Adams counties) accounted for 520 samples, 938 samples
came from DMA 2, and there were 243 samples from DMA 3 (Clearfield, Indiana and
Jefferson counties).
Additionally, the Game Commission sampled 89 elk for CWD in 2014, and no
positives were detected.
In Pennsylvania, monitoring for CWD continues year-round and since the
start of 2015, 253 additional samples have been collected. One of these tested
positive, and is counted among the six additional positives within DMA 2.
The six additional CWD-positive deer brings the total to 11 free-ranging
CWD-positive deer detected in Pennsylvania. All of these have been within DMA 2.
Overall, the proportion of deer to test positive remains small.
Since 1998, the Game Commission has collected and submitted more than
52,000 wild deer and elk for CWD testing, with a total of 11 positive tests.
DMA 2 expands
While most of the six additional CWD cases were centralized within DMA 2,
two of the positive deer came from sites near what previously was DMA 2’s
western boundary.
One of them, an 18-month-old male deer, was struck and killed by a vehicle
on Route 220 in November in Bedford County. The other, a 30-month-old female,
was killed in March on state Route 56, also in Bedford County.
In response to those positives, and in accordance with Pennsylvania’s CWD
Response Plan, the boundary of DMA 2 again has been adjusted, and DMA 2 now
contains parts of Somerset County, in addition to other counties.
The new DMA 2 boundary is as follows: Beginning in the southeastern extent
of the DMA at the intersection of state Route 655 and the Maryland state line,
proceed north on Route 655 for approximately 57 miles to the intersection of
U.S. Route 22. The DMA boundary follows U.S. Route 22 west for 16.6 miles to
state Route 453, then south along state Route 453 for 9 miles to Tyrone. In
Tyrone, the boundary follows the western, southbound lane of Interstate 99 for
6.5 miles to state Route 865 at Bellwood. Follow state Route 865 west 2.75 miles
to Grandview Road (state Route 4015). Follow Grandview Road south 6.4 miles to
Juniata Gap Road in Altoona. Follow Juniata Gap Road 4 miles to Skyline Drive.
Follow Skyline Drive approximately 2 miles to state Route 36. Follow state Route
36 west 1.5 miles to Coupon-Gallitzin Road (state Route 1015). Follow
Coupon-Gallitzin Road south 5 ¼ miles to U.S. Route 22. Follow U.S. Route 22
west for approximately 4 miles to state Route 53. Follow state Route 53 south
9.3 miles to state Route 160. Follow state Route 160 south 45.4 miles to the
borough of Berlin, take Main Street (state Route 2030) west through downtown
Berlin for 0.44 miles, then south along state Route 219 for 20 miles to the
Maryland border.
A map of the newly expanded DMA 2 is available on the CWD Information page
at the Game Commission’s website, www.pgc.state.pa.us. Because the boundaries of
DMAs change in response to new positives being detected, the website is always
the best source for the most up-to-date DMA maps and descriptions.
DMA 2 Antlerless Deer Permits
The Game Commission in the 2015-16 license year again will issue special
permits for taking antlerless deer within DMA 2.
DMA 2 Antlerless Deer Permits will become available at the same time
antlerless licenses go on sale.
The DMA 2 permits were created as a way to direct hunting pressure to DMA
2. The permits seek to increase the antlerless deer harvest within DMA 2 by one
deer per square mile.
A total of 13,500 permits have been allocated and the permits can be used
only within DMA 2, which includes parts of Bedford, Blair, Huntingdon, Cambria,
Fulton and Somerset counties.
Hunters may apply for DMA 2 permits in addition regular antlerless deer
licenses. Obtaining one or more DMA 2 permits does not reduce the number of
antlerless deer licenses for which a hunter may apply.
There are some differences between the application process for a DMA 2
permit and that for an antlerless license.
Only residents and nonresidents ages 12 and older with valid general
hunting licenses may apply for permits. Participants in Mentored Youth and
Mentored Adult hunting programs are ineligible to apply, and the permits cannot
be transferred to participants in those programs.
Each permit costs $6.70, and payments must be made by credit card, check or
money order made payable to the “Pennsylvania Game Commission.”
Applications for DMA 2 permits will be accepted in two ways –
electronically through the Game Commission’s Outdoor Shop, http://www.theoutdoorshop.state.pa.us,
or by mail. Those wishing to send applications by mail can obtain an application
form at the Game Commission’s website, the agency’s Harrisburg headquarters or
any region office.
The application schedule is similar to that for antlerless deer licenses,
however, residents and nonresidents can apply on the same dates in all rounds.
Applications will be accepted beginning Monday, July 13. Each eligible
applicant may submit one application during this first round, which lasts three
weeks.
Beginning Aug. 3, a second round of application begins. Again in the second
round, each eligible applicant may submit one application. However, an applicant
who did not submit an application during the first round may submit two during
the second round.
A third round of applications will begin Aug. 17. Eligible applicants may
submit an unlimited number of applications during this round, and the round will
continue until all permits have been issued.
A DMA 2 permit can be used to harvest an antlerless deer during any deer
season, including the antlered deer season.
Those who are issued DMA 2 permits are required to submit reports,
regardless of whether they harvest a deer. Hunters who take a deer with a DMA 2
permit must report within 10 days; those who don’t must report by Feb. 2. Those
who fail to report as required are subject to criminal prosecution and may be
ineligible to apply for permits if the program is continued the following
year.
Through their reports, hunters provide valuable data that plays a crucial
role in the Game Commission’s management of CWD.
Rules within DMAs
Those who hunt or live within established Disease Management Areas need to
be aware of special rules that apply to the hunting, processing and feeding of
deer.
Hunters harvesting deer within any DMA are not permitted to remove from the
DMA any deer parts with a high risk of transmitting the disease. There are a few
exceptions to this rule, including taking a deer to an approved deer processor
or taxidermist outside the DMA, or traveling to an approved laboratory for
disease testing.
The possession of urine-based deer attractants also is prohibited within
any DMA, as is the direct or indirect feeding of deer. The feeding of elk is
unlawful everywhere in Pennsylvania.
A complete list of rules applying to DMAs can be found in a Game Commission
executive order, which also is available at the agency’s website.
The head and spinal column are among the identified high-risk parts that
cannot be removed from a DMA. Meat and antlers can be removed, so long as the
backbone is separated from the meat and left behind, and the skull plate
attached to the antlers is free of visible brain material.
A complete list of high-risk parts is available at the Game Commission’s
website.
Many hunters who harvest deer within DMAs take their deer to processors and
taxidermists within those DMAs in order to comply with the law. Those who do
their own processing may remove and safely dispose of high-risk parts in
dumpsters placed on game lands tracts within the DMA. Sites are identified prior
to hunting seasons.
CWD Information
While chronic wasting disease is relatively new to Pennsylvania, it is not
a new disease. CWD was discovered in 1967, and it has been researched in great
detail since then.
CWD affects members of the cervid, or deer family. It is spread from
animal to animal by direct and indirect contact.
There currently is no practical way to test live animals for CWD, nor is
there a vaccine. Clinical signs include poor posture, lowered head and ears,
uncoordinated movement, rough-hair coat, weight loss, increased thirst,
excessive drooling, and, ultimately death. Any animals suspected of having CWD
should be reported to the Game Commission.
There currently is no scientific evidence that CWD has or can spread to
humans, either through contact with infected animals or by eating the meat of
infected animals. As a precaution, however, people are advised not to consume
meat from animals infected with CWD.
Much more information on CWD, as well as a video instructing hunters on
how they can process venison for transport and consumption, is available at the
Game Commission’s website.
The deer from an infected Reynoldsville, Jefferson County farm tested
positive for Chronic Wasting Disease. Two other white-tailed deer died in April
on the farm and tested positive for the disease. This marks the 14th
white-tailed deer in the state to test positive for the disease since 2012.
snip
“This is an unprecedented level of infection in a captive deer herd,” said
Greig. “The department and deer farmers worked together to accommodate the
requests of these researchers. The more we know, the greater the chance we can
eradicate the disease.”
Sunday, July 13, 2014
Louisiana deer mystery unleashes litigation 6 does still missing from CWD
index herd in Pennsylvania Great Escape
Saturday, June 29, 2013
PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN
INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA
Tuesday, June 11, 2013
*** CWD GONE WILD, More cervid escapees from more shooting pens on the
loose in Pennsylvania
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd
Pennsylvania Update May 28, 2013
*** 6 doe from Pennsylvania CWD index herd still on the loose in
Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles
premises.
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
Wednesday, November 14, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO
LOUISIANA and INDIANA
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
Thursday, October 11, 2012
Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests
Positive
Monday, June 23, 2014
PRION 2014 CHRONIC WASTING DISEASE CWD
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s
the risk to humans and pets?
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM
Tuesday, October 21, 2014
Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer
Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE
Thursday, October 23, 2014
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE
PRESERVE
Thursday, April 02, 2015
OHIO CONFIRMS SECOND POSTIVE CHRONIC WASTING DISEASE CWD on Yoder's
properties near Millersburg
Wednesday, February 11, 2015
World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with
two counts of tampering with evidence
CWD TO HUMANS, AND RISK FACTORS THERE FROM (see latest science)
Tuesday, November 04, 2014
*** Six-year follow-up of a point-source exposure to CWD contaminated
venison in an Upstate New York community: risk behaviours and health outcomes
2005–2011
PRION2015 CONFERENCE FORT COLLINS
May 2015
Wednesday May 27
14:45 Jean-Phillipe Deslys Atomic Energy Commission, France,
Transmission of prions to primates after extended silent incubation
periods: *** IMPLICATIONS FOR BSE AND SCRAPIE RISK ASSESSMENT IN HUMAN
POPULATIONS.
16:45
Quingzhong Kong Case Western Reserve University
***Zoonotic Potential of CWD Prions
Increased Infectivity of Anchorless Mouse Scrapie Prions in Transgenic Mice
Overexpressing Human Prion Protein
Brent Racea, Katie Phillipsa, Kimberly Meade-Whiteb, James Striebela and
Bruce Chesebroa aLaboratory of Persistent Viral Diseases, Rocky Mountain
Laboratories, National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Hamilton, Montana, USA bRocky Mountain Veterinary Branch,
Rocky Mountain Laboratories, National Institute of Allergy and Infectious
Diseases, National Institutes of Health, Hamilton, Montana, USA K. L. Beemon,
Editor + Author Affiliations
ABSTRACT
Prion protein (PrP) is found in all mammals, mostly as a glycoprotein
anchored to the plasma membrane by a C-terminal glycosylphosphatidylinositol
(GPI) linkage. Following prion infection, host protease-sensitive prion protein
(PrPsen or PrPC) is converted into an abnormal, disease-associated,
protease-resistant form (PrPres). Biochemical characteristics, such as the PrP
amino acid sequence, and posttranslational modifications, such as glycosylation
and GPI anchoring, can affect the transmissibility of prions as well as the
biochemical properties of the PrPres generated. Previous in vivo studies on the
effects of GPI anchoring on prion infectivity have not examined cross-species
transmission. In this study, we tested the effect of lack of GPI anchoring on a
species barrier model using mice expressing human PrP. In this model, anchorless
22L prions derived from tg44 mice were more infectious than 22L prions derived
from C57BL/10 mice when tested in tg66 transgenic mice, which expressed
wild-type anchored human PrP at 8- to 16-fold above normal. Thus, the lack of
the GPI anchor on the PrPres from tg44 mice appeared to reduce the effect of the
mouse-human PrP species barrier. In contrast, neither source of prions induced
disease in tgRM transgenic mice, which expressed human PrP at 2- to 4-fold above
normal.
IMPORTANCE Prion protein (PrP) is found in all mammals, usually attached to
cells by an anchor molecule called GPI. Following prion infection, PrP is
converted into a disease-associated form (PrPres). While most prion diseases are
species specific, this finding is not consistent, and species barriers differ in
strength. The amino acid sequence of PrP varies among species, and this
variability affects prion species barriers. However, other PrP modifications,
including glycosylation and GPI anchoring, may also influence cross-species
infectivity. We studied the effect of PrP GPI anchoring using a mouse-to-human
species barrier model. Experiments showed that prions produced by mice
expressing only anchorless PrP were more infectious than prions produced in mice
expressing anchored PrP. Thus, the lack of the GPI anchor on prions reduced the
effect of the mouse-human species barrier. Our results suggest that prion
diseases that produce higher levels of anchorless PrP may pose an increased risk
for cross-species infection.
FOOTNOTES Received 2 February 2015. Accepted 18 March 2015. Accepted
manuscript posted online 25 March 2015. Address correspondence to Brent Race,
raceb@niaid.nih.gov. Citation Race B, Phillips K, Meade-White K, Striebel J,
Chesebro B. 2015. Increased infectivity of anchorless mouse scrapie prions in
transgenic mice overexpressing human prion protein. J Virol 89:6022–6032.
doi:10.1128/JVI.00362-15.
Copyright © 2015, American Society for Microbiology. All Rights
Reserved.
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
Friday, January 30, 2015
*** Scrapie: a particularly persistent pathogen ***
Sunday, March 29, 2015
Uncommon prion disease induced in macaque ten years after scrapie
inoculation
Friday, April 24, 2015
The placenta shed from goats with classical scrapie is infectious to goat
kids and lambs
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01 Most doctors believe that sCJD is caused by a prion protein
deforming by chance into a killer. But Singeltary thinks otherwise. He is one of
a number of campaigners who say that some sCJD, like the variant CJD related to
BSE, is caused by eating meat from infected animals. Their suspicions have
focused on sheep carrying scrapie, a BSE-like disease that is widespread in
flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb...
2001
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01
Like lambs to the slaughter
31 March 2001
by Debora MacKenzie Magazine issue 2284.
FOUR years ago, Terry Singeltary watched his mother die horribly from a
degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary
was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded
an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number of
campaigners who say that some sCJD, like the variant CJD related to BSE, is
caused by eating meat from infected animals. Their suspicions have focused on
sheep carrying scrapie, a BSE-like disease that is widespread in flocks across
Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no
evidence that it poses a risk to human health. But if the French finding means
that scrapie can cause sCJD in people, countries around the world may have
overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD. They
injected the brains of macaque monkeys with brain from BSE cattle, and from
French and British vCJD patients. The brain damage and clinical symptoms in the
monkeys were the same for all three. Mice injected with the original sets of
brain tissue or with infected monkey brain also developed the same symptoms.
As a control experiment, the team also injected mice with brain tissue from
people and animals with other prion diseases: a French case of sCJD; a French
patient who caught sCJD from human-derived growth hormone; sheep with a French
strain of scrapie; and mice carrying a prion derived from an American scrapie
strain. As expected, they all affected the brain in a different way from BSE and
vCJD. But while the American strain of scrapie caused different damage from
sCJD, the French strain produced exactly the same pathology.
"The main evidence that scrapie does not affect humans has been
epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute
for Animal Health in Edinburgh, who was a member of the same team as Deslys.
"You see about the same incidence of the disease everywhere, whether or not
there are many sheep, and in countries such as New Zealand with no scrapie." In
the only previous comparisons of sCJD and scrapie in mice, Bruce found they were
dissimilar.
But there are more than 20 strains of scrapie, and six of sCJD. "You would
not necessarily see a relationship between the two with epidemiology if only
some strains affect only some people," says Deslys. Bruce is cautious about the
mouse results, but agrees they require further investigation. Other trials of
scrapie and sCJD in mice, she says, are in progress.
People can have three different genetic variations of the human prion
protein, and each type of protein can fold up two different ways. Kretschmar has
found that these six combinations correspond to six clinical types of sCJD: each
type of normal prion produces a particular pathology when it spontaneously
deforms to produce sCJD.
But if these proteins deform because of infection with a disease-causing
prion, the relationship between pathology and prion type should be different, as
it is in vCJD. "If we look at brain samples from sporadic CJD cases and find
some that do not fit the pattern," says Kretschmar, "that could mean they were
caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence
elsewhere. Singeltary and other US activists think that some of these people
died after eating contaminated meat or "nutritional" pills containing dried
animal brain. Governments will have a hard time facing activists like Singeltary
if it turns out that some sCJD isn't as spontaneous as doctors have insisted.
Deslys's work on macaques also provides further proof that the human
disease vCJD is caused by BSE. And the experiments showed that vCJD is much more
virulent to primates than BSE, even when injected into the bloodstream rather
than the brain. This, says Deslys, means that there is an even bigger risk than
we thought that vCJD can be passed from one patient to another through
contaminated blood transfusions and surgical instruments.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire).
*** 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.
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 ; http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
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
snip...
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.
*** We conclude that TSE infectivity is likely to survive burial for long
time periods with minimal loss of infectivity and limited movement from the
original burial site. However PMCA results have shown that there is the
potential for rainwater to elute TSE related material from soil which could lead
to the contamination of a wider area. These experiments reinforce the importance
of risk assessment when disposing of TSE risk materials.
*** The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
Sunday, December 21, 2014
Mucosal immunization with an attenuated Salmonella vaccine partially
protects white-tailed deer from chronic wasting disease
Friday, December 19, 2014
Pan-Provincial Vaccine Enterprise Inc. (PREVENT) Conducting a Chronic
Wasting Disease (CWD) Vaccine Efficacy Trial in Elk
CHRONIC WASTING DISEASE CWD TSE PRION, how much does it pay to find CWD
$$$
CWD, spreading it around...
for the game farm industry, and their constituents, to continue to believe
that they are _NOT_, and or insinuate that they have _NEVER_ been part of the
problem, will only continue to help spread cwd. the game farming industry, from
the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet
mills, shooting pens, to large ranches, are not the only problem, but it is
painfully obvious that they have been part of the problem for decades and
decades, just spreading it around, as with transportation and or exportation and
or importation of cervids from game farming industry, and have been proven to
spread cwd. no one need to look any further than South Korea blunder ;
===========================================
spreading cwd around...
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of
farmed elk in Saskatchewan in a single epidemic. All of these herds were
depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease
eradication program. Animals, primarily over 12 mo of age, were tested for the
presence CWD prions following euthanasia. Twenty-one of the herds were linked
through movements of live animals with latent CWD from a single infected source
herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily
infected herds.
***The source herd is believed to have become infected via importation of
animals from a game farm in South Dakota where CWD was subsequently diagnosed
(7,4). A wide range in herd prevalence of CWD at the time of herd depopulation
of these herds was observed. Within-herd transmission was observed on some
farms, while the disease remained confined to the introduced animals on other
farms.
spreading cwd around...
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim,
Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research
Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion
disease in native North America deer and Rocky mountain elks. The disease is a
unique member of the transmissible spongiform encephalopathies (TSEs), which
naturally affects only a few species. CWD had been limited to USA and Canada
until 2000.
On 28 December 2000, information from the Canadian government showed that a
total of 95 elk had been exported from farms with CWD to Korea. These consisted
of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72
elk in 1997, which had been held in pre export quarantine at the “source
farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD
surveillance program was initiated by the Ministry of Agriculture and Forestry
(MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994
were impossible to identify. CWD control measures included stamping out of all
animals in the affected farm, and thorough cleaning and disinfection of the
premises. In addition, nationwide clinical surveillance of Korean native
cervids, and improved measures to ensure reporting of CWD suspect cases were
implemented.
Total of 9 elks were found to be affected. CWD was designated as a
notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and
2005.
Since February of 2005, when slaughtered elks were found to be positive,
all slaughtered cervid for human consumption at abattoirs were designated as
target of the CWD surveillance program. Currently, CWD laboratory testing is
only conducted by National Reference Laboratory on CWD, which is the Foreign
Animal Disease Division (FADD) of National Veterinary Research and Quarantine
Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the
human consumption was confirmed as positive. Consequently, all cervid – 54 elks,
41 Sika deer and 5 Albino deer – were culled and one elk was found to be
positive. Epidemiological investigations were conducted by Veterinary
Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary
services.
Epidemiologically related farms were found as 3 farms and all cervid at
these farms were culled and subjected to CWD diagnosis. Three elks and 5
crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and
confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were
linked to the importation of elks from Canada in 1994 based on circumstantial
evidences.
In December 2010, one elk was confirmed as positive at Farm 5.
Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer –
were culled and one Manchurian Sika deer and seven Sika deer were found to be
positive. This is the first report of CWD in these sub-species of deer.
Epidemiological investigations found that the owner of the Farm 2 in CWD
outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced
from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed
(species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as
negative.
IN CONFIDENCE
reference...
RB3.20
TRANSMISSION TO CHIMPANZEES
1. Kuru and CJD have been successfully transmitted to chimpanzees but
scrapie and TME have not.
2. We cannot say that scrapie will not transmit to chimpanzees. There are
several scrapie strains and I am not aware that all have been tried (that would
have to be from mouse passaged material). Nor has a wide enough range of field
isolates subsequently strain typed in mice been inoculated by the appropriate
routes (i/c, ilp and i/v) :
3. I believe the proposed experiment to determine transmissibility, if
conducted, would only show the susceptibility or resistance of the chimpanzee to
infection/disease by the routes used and the result could not be interpreted for
the predictability of the susceptibility for man. Proposals for prolonged oral
exposure of chimpanzees to milk from cattle were suggested a long while ago and
rejected.
4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments
(enclosed) are pertinent. I have yet to receive a direct communication from Dr
Schellekers but before any collaboration or provision of material we should
identify the Gibbs' proposals and objectives.
5. A positive result from a chimpanzee challenged severely would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
6. A negative result would take a lifetime to determine but that would be a
shorter period than might be available for human exposure and it would still not
answer the question regarding mans' susceptibility. In the meantime no doubt the
negativity would be used defensively. It would however be counterproductive if
the experiment finally became positive. We may learn more about public reactions
following next Monday' s meeting.
R. Bradley
23 September 1990
CVO (+Mr Wells' comments)
Dr T W A Little
Dr B J Shreeve
90/9.23/1.1.
IN CONFIDENCE CHIMPANZEES
CODE 18-77 Reference RB3.46
Some further information that may assist in decision making has been gained
by discussion with Dr Rosalind Ridley.
She says that careful study of Gajdusek's work shows no increased
susceptibility of chimpanzees over New World Monkeys such as Squirrel Monkeys.
She does not think it would tell you anything about the susceptibility to man.
Also Gajdusek did not, she believes, challenge chimpanzees with scrapie as
severely as we did pigs and we know little of that source of scrapie.
Comparisons would be difficult. She also would not expect the Home Office to
sanction such experiments here unless there was a very clear and important
objective that would be important for human health protection. She doubted such
a case could be made. If this is the case she thought it would be unethical to
do an experiment abroad because we could not do it in our own country.
Retrospectively she feels they should have put up more marmosets than they
did. They all remain healthy. They would normally regard the transmission as
negative if no disease resulted in five years.
We are not being asked for a decision but I think that before we made one
we should gain as much knowledge as we can. If we decided to proceed we would
have to bear any criticisms for many years if there was an adverse view by
scientists ormedia. This should not be undertaken lightly. There is already
some adverse comment here, I gather, on the pig experiment though that will
subside.
The Gibbs' (as' distinct from Schellekers') study is somewhat different. We
are merely supplying material for comparative studies in a laboratory with the
greatest experience of human SEs in the world and it has been sanctioned by USDA
(though we do not know for certain yet if chimpanzees specifically will be
used). This would keep it at a lower profile than if we conducted such an
experiment in the UK or Europe.
I consider we must have very powerful and defendable objectives to go
beyond Gibbs' proposed experiments and should not initiate others just because
an offer has been made.
Scientists have a responsibility to seek other methods of investigative
research other than animal experimentation. At present no objective has
convinced me we need to do research using Chimpanzees - a species in need of
protection. Resisting such proposals would enable us to communicate that
information to the scientist and the public should the need arise. A line would
have been drawn.
CVO cc Dr T Dr B W A Little Dr B J Shreeve
R Bradley
26 September 1990
90/9.26/3.2
I AM NOT AN ADVOCATE FOR EXPERIMENTAL USE OF CHIMPANZEES AS TEST VICTIMS.
However, I would be an advocate for (and i have said this before over the
years), of death row inmates being used. Their families could be compensated
with a monetary award, and the death row inmates could do one final thing for
the good of humanity. There going to die anyway. just my opinion. ...TSS-2011
POLICY - RESTRICTED
CREUTZFELDT-JAKOB DISEASE: 3RD ANNUAL REPORT OF THE UK SURVEILLANCE
UNIT
1. This submission, which has been agreed with colleagues in HEF(M). alerts
PS(L) to the contents of the forthcoming annual report of the CJD Surveillance
Unit and presents options for publication. It also highlights concern over the
presentation of results which could be misrepresented by the media and others as
evidence of a lilnk between CJD and the consumption of veal. ...
RECOMMENDATION
2. PS(L) is invited to agree the recommendation at para 13.
PROBLEM
7. The main findings in the case-control study were STATISTICALLY
SIGNIFICANT ASSOCIATIONS BETWEEN CONSUMPTION OF VEAL OR VENISON AND THE
DEVELOPMENT OF CJD (INCREASED RISKS OF 2-13x). There was also evidence of a
dose-response relationship between dietary exposure and development of the
disease. (Last year's findings showed an apparent association between eating
black pudding and risk of CJD which was neither statistically significant nor
biologically plausible - interestingly, this has not been (replicated was marked
out with something i cannot read), and then this complete sentence was marked
through to be replaced ;
THIS YEAR'S FINDINGS SHOW A NUMBER OF ASSOCIATIONS BUT THE STRONGEST IS FOR
VEAL.
IP PS(L) wishes to probe this further we think it best to explain the
matter VERBALLY. The problem is how to present the findings in this year's
annual report in a way which avoids unnecessary public alarm and limits the
scope for media scare stores. (or the facts...TSS)
This is of considerable concern given recent development. In particular
Ministers will be particularly concerned about the European dimension given the
recent troubles with the Germans.
9. DH doctors advise - and we understand Dr Wills agrees - that the
association the study found between the developments of CJD and veal consumption
cannot be regarded as demonstrating a causal relationship or give any reason to
change the advice that eating beef and veal is safe. IF PS(L) wishes to probe
this further we think it best to explain the matter verbally. The problem is how
to present the findings in this year's annual report in a way which avoids
unnecessary public alarm and limits the scope for media scare stories.
Next steps ...
snip... full text ;
PROBLEM
7. The main findings in the case-control study were STATISTICALLY
SIGNIFICANT ASSOCIATIONS BETWEEN CONSUMPTION OF VEAL OR VENISON AND THE
DEVELOPMENT OF CJD (INCREASED RISKS OF 2-13x). There was also evidence of a
dose-response relationship between dietary exposure and development of the
disease. (Last year's findings showed an apparent association between eating
black pudding and risk of CJD which was neither statistically significant nor
biologically plausible - interestingly, this has not been (replicated was marked
out with something i cannot read), and then this complete sentence was marked
through to be replaced ;
see watered down report here ;
http://web.archive.org/web/20030511211625/http://www.bseinquiry.gov.uk/files/yb/1994/10/00004001.pdf
Lessons from BSE
4. In retrospect, a problem of scrapie transmission in feedstuffs was
perhaps predictable.
IN CONFIDENCE
NOT FOR PUBLICATION
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
snip...
To minimise the risk of farmers' claims for compensation from feed
compounders.
To minimise the potential damage to compound feed markets through adverse
publicity.
To maximise freedom of action for feed compounders, notably by maintaining
the availability of meat and bone meal as a raw material in animal feeds, and
ensuring time is available to make any changes which may be required.
snip...
THE FUTURE
4..........
MAFF remains under pressure in Brussels and is not skilled at handling
potentially explosive issues.
5. Tests _may_ show that ruminant feeds have been sold which contain
illegal traces of ruminant protein. More likely, a few positive test results
will turn up but proof that a particular feed mill knowingly supplied it to a
particular farm will be difficult if not impossible.
6. The threat remains real and it will be some years before feed
compounders are free of it. The longer we can avoid any direct linkage between
feed milling _practices_ and actual BSE cases, the more likely it is that
serious damage can be avoided. ...
Differentiation of ruminant transmissible spongiform encephalopathy isolate
types, including bovine spongiform encephalopathy and CH1641 scrapie
J. G. Jacobs1, M. Sauer2, L. J. M. van Keulen1, Y. Tang2, A. Bossers1 and
J. P. M. Langeveld1
1 Department of Infection Biology, Central Veterinary Institute of
Wageningen UR, PO Box 65, 8200 AB Lelystad, The Netherlands 2 Department of
Molecular Pathogenesis and Genetics, Veterinary Laboratories Agency-Weybridge,
Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK
Correspondence J. P. M. Langeveld jan.langeveld@wur.nl
With increased awareness of the diversity of transmissible spongiform
encephalopathy (TSE) strains in the ruminant population, comes an appreciation
of the need for improved methods of differential diagnosis. Exposure to bovine
spongiform encephalopathy (BSE) has been associated with the human TSE, variant
Creutzfeldt–Jakob disease, emphasizing the necessity in distinguishing low-risk
TSE types from BSE. TSE type discrimination in ruminants such as cattle, sheep,
goats and deer, requires the application of several prion protein (PrP)-specific
antibodies in parallel immunochemical tests on brain homogenates or tissue
sections from infected animals. This study uses in a single incubation step,
three PrP-specific antibodies and fluorescent Alexa dye-labelled anti-mouse Fabs
on a Western blot. The usual amount of brain tissue needed is 0.5 mg. This
multiplex application of antibodies directed towards three different PrP
epitopes enabled differential diagnosis of all established main features of
classical scrapie, BSE and Nor98-like scrapie in sheep and goats, as well as the
currently known BSE types C, H and L in cattle. Moreover, due to an
antibody-dependent dual PrP-banding pattern, for the first time CH1641 scrapie
of sheep can be reliably discriminated from the other TSE isolate types in
sheep.
----- Original Message -----
From: "BioMed Central Comments"
To:
Sent: Wednesday, February 16, 2011 4:13 AM
Subject: Your comment on BMC Veterinary Research 2011, 7:7
Your discussion posting "Scrapie cases Goats from same herd USA Michigan"
has been rejected by the moderator as not being appropriate for inclusion on the
site.
Dear Mr Singeltary,
Thank you for submitting your comment on BMC Veterinary Research article
(2011, 7:7). We have read your comment with interest but we feel that only the
authors of the article can answer your question about further investigation of
the route of infection of the five goats in Michigan. We advise that you contact
the authors directly rather than post a comment on the article.
With best wishes,
Maria
Maria Kowalczuk, PhD Deputy Biology Editor BMC-series Journals
BioMed Central 236 Gray's Inn Road London, WC1X 8HB
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======end=======
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Technical Abstract:
Prion strains may vary in their ability to transmit to humans and animals.
Few experimental studies have been done to provide evidence of differences
between U.S. strains of scrapie, which can be distinguished by incubation times
in inbred mice, microscopic lesions, immunoreactivity to various antibodies, or
molecular profile (electrophoretic mobility and glycoform ratio). Recent work on
two U.S. isolates of sheep scrapie supports that at least two distinct strains
exist based on differences in incubation time and genotype of sheep affected.
One isolate (No. 13-7) inoculated intracerebrally caused scrapie in sheep AA at
codon 136 (AA136) and QQ at codon 171 (QQ171) of the prion protein in an average
of 19 months post-inoculation (PI) whereas a second isolate (No. x124) caused
disease in less than 12 months after oral inoculation in AV136/QQ171 sheep.
Striking differences were evident when further strain analysis was done in R111,
VM, C57Bl6, and C57Bl6xVM (F1) mice. No. 13-7 did not induce disease in any
mouse strain at any time post-inoculation (PI) nor were brain tissues positive
by western blot (WB). Positive WB results were obtained from mice inoculated
with isolate No. x124 starting at day 380 PI. Incubation times averaged 508,
559, 601, and 633 days PI for RIII, C57Bl6, VM, and F1 mice, respectively.
Further passage will be required to characterize these scrapie strains in mice.
This work provides evidence that multiple scrapie strains exist in U.S.
sheep.
One of these isolates (TR316211) behaved like the CH1641 isolate, with
PrPres features in mice similar to those in the sheep brain. From two other
isolates (O100 and O104), two distinct PrPres phenotypes were identified in
mouse brains, with either high (h-type) or low (l-type) apparent molecular
masses of unglycosylated PrPres, the latter being similar to that observed with
CH1641, TR316211, or BSE. Both phenotypes could be found in variable proportions
in the brains of the individual mice. In contrast with BSE, l-type PrPres from
"CH1641-like" isolates showed lower levels of diglycosylated PrPres. From one of
these cases (O104), a second passage in mice was performed for two mice with
distinct PrPres profiles. This showed a partial selection of the l-type
phenotype in mice infected with a mouse brain with predominant l-type PrPres,
and it was accompanied by a significant increase in the proportions of the
diglycosylated band. These results are discussed in relation to the diversity of
scrapie and BSE strains.
In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q
(AAQQ) and the disease phenotype is similar to that seen with experimental
strain CH1641.
4.2.9 A further hypothesis to explain the occurrence of BSE is the
emergence or selection of a strain or strains of the scrapie agent pathogenic
for cattle. Mutations of the scrapie agent. which can occur after a single
passage in mice. have been well documented (9). This phenomenon cannot be
dismissed for BSE. but given the form of the epidemic and the geographically
widespread occurrence of BSE, such a hypothesis" would require the emergence of
a mutant scrapie strain simultaneously in a large . number of sheep flocks, or
cattle. throughout the country. Also. if it resulted "from a localised chance
transmission of the scrapie strain from sheep to cattle giving rise , . to a
mutant. a different pattern of disease would have been expected: its range would
'. have increased with time. Thus the evidence from Britain is against the
disease being due to a new strain of the agent, but we note that in the United
States from 1984 to 1988 outbreaks of scrapie in sheep flocks are reported to
have Increased markedly. now being nearly 3 times as high as during any previous
period (18).
If the scrapie agent is generated from ovine DNA and thence causes disease
in other species, then perhaps, bearing in mind the possible role of scrapie in
CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the
notifiable disease. ...
EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE
This is provided by the statistically significant increase in the incidence
of sheep scrape from 1985, as determined from analyses of the submissions made
to VI Centres, and from individual case and flock incident studies.
........
RISK OF BSE TO SHEEP VIA FEED
Marion Simmons communicated surprising evidence for oral transmissibility
of Nor98/atypical scrapie in neonatal sheep and although bioassay is ongoing,
infectivity of the distal ileum of 12 and 24 month infected sheep is positive in
Tg338 mice.
SUMMARY REPORTS OF MAFF BSE TRANSMISSION STUDIES AT THE CVL ;
THE RISK TO HUMANS FROM SHEEP;
EXPERIMENTAL TRANSMISSION OF BSE TO SHEEP
SHEEP AND BSE
PERSONAL AND CONFIDENTIAL
SHEEP AND BSE
A. The experimental transmission of BSE to sheep.
Studies have shown that the ''negative'' line NPU flock of Cheviots can be
experimentally infected with BSE by intracerebral (ic) or oral challenge (the
latter being equivalent to 0.5 gram of a pool of four cow brains from animals
confirmed to have BSE).
RB264
BSE - TRANSMISSION STUDIES
P.5.21 Parallels between different forms of sheep scrapie and types of
Creutzfeldt-Jakob disease (CJD)
Wiebke M. Wemheuer1, Sylvie L. Benestad2, Arne Wrede1, Wilhelm E.
Wemheuer3, Tatjana Pfander1, Bjørn Bratberg2, Bertram Brenig3,Walter J.
Schulz-Schaeffer1 1University Medical Center Goettingen, Germany; 2Institute of
Veterinary Medicine Oslo, Norway; 3Institute of Veterinary Medicine Goettingen,
Germany
Background: Scrapie in sheep and goats is often regarded as the archetype
of prion diseases. In 1998, a new form of scrapie - atypical/Nor98 scrapie - was
described that differed from classical scrapie in terms of epidemiology, Western
blot profile, the distribution of pathological prion protein (PrPSc) in the body
and its stability against proteinase K. In a similar way, distinct disease types
exist in sporadic Creutzfeldt-Jakob disease (CJD). They differ with regard to
their clinical outcome, Western blot profile and PrPSc deposition pattern in the
central nervous system (CNS).
Objectives: The comparison of PrPSc deposits in sheep scrapie and human
sporadic CJD. Methods: Tissues of the CNS of sheep with classical scrapie, sheep
with atypical/Nor98 scrapie and 20 patients with sporadic CJD were examined
using the sensitive Paraffin Embedded Tissue (PET) blot method. The results were
compared with those obtained by immunohistochemistry. With the objective of
gaining information on the protein conformation, the PrPSc of classical and
atypical/Nor98 sheep scrapie and sporadic CJD was tested for its stability
against denaturation with guanidine hydrochloride (GdnHCl) using a Membrane
Adsorption Assay.
Results: The PrPSc of atypical/Nor98 scrapie cases and of CJD prion type 1
patients exhibits a mainly reticular/synaptic deposition pattern in the brain
and is relatively sensitive to denaturation with GdnHCl. In contrast classical
scrapie cases and CJD prion type 2 patients have a more complex PrPSc deposition
pattern in common that consists of larger PrPSc aggregates and the PrPSc itself
is comparatively stable against denaturation. Discussion: The similarity between
CJD types and scrapie types indicates that at least two comparable forms of the
misfolded prion protein exist beyond species barriers and can elicit prion
diseases. It seems therefore reasonable to classify classical and atypical/Nor98
scrapie - in analogy to the existing CJD types - as different scrapie types.
Monday, December 1, 2008
When Atypical Scrapie cross species barriers
Thursday, December 20, 2012
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED, WISHES TO
CONTINUE SPREADING IT AROUND THE GLOBE
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH
CODE, DOES NOT SURPRISE ME $
Wednesday, December 4, 2013
Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine
Products; Final Rule Federal Register / Vol. 78 , No. 233 / Wednesday, December
4, 2013
TO ALL IMPORTING COUNTRIES THAT IMPORTS FROM THE USA, BE WARNED, NEW MAD
COW BSE REGULATIONS USDA, AND OIE, not worth the paper the regulations were
wrote on, kind of like the mad cow feed ban of August 1997, nothing but ink on
paper $$$
full text ;
Sunday, April 12, 2015
*** Research Project: Transmission, Differentiation, and Pathobiology of
Transmissible Spongiform Encephalopathies 2014 Annual Report ***
http://transmissiblespongiformencephalopathy.blogspot.com/2015/04/research-project-transmission.html
Wednesday, April 15, 2015
KURU Transmissible Spongiform Encephalopthy TSE Prion Disease
for anyone interested, see more here ;
Sunday, May 3, 2015
PRION2015 FORT COLLINS
Tuesday, April 21, 2015
*** Transmissible Spongiform Encephalopathy Advisory Committee TSEAC
MEETING SCHEDULED FOR June 1, 2015 ***
Comment from Terry Singeltary This is a Comment on the Food and Drug
Administration (FDA) Notice: Draft Guidance for Industry on Ensuring Safety of
Animal Feed Maintained and Fed On-Farm; Availability
For related information, Open Docket Folder Docket folder icon
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Comment View document:
Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed
On-Farm Draft Guidance FDA-2014-D-1180 Singeltary Comment
Greetings FDA et al,
I wish to comment on Guidance for Industry Ensuring Safety of Animal Feed
Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180.
Once again, I wish to kindly bring up the failed attempt of the FDA and the
ruminant to ruminant mad cow feed ban of August 4, 1997. This feed ban is still
failing today, as we speak. Even more worrisome, is the fact it is still legal
to feed cervids to cervids in the USA, in fact, the FDA only _recommends_ that
deer and elk considered to be of _high_ risk for CWD do not enter the animal
food chain, but there is NO law, its only voluntary, a recipe for a TSE prion
disaster, as we have seen with the ruminant to ruminant feed ban for cattle,
where in 2007, one decade post August 1997 mad cow feed ban, where in 2007
10,000,000 POUNDS OF BANNED BLOOD LACED MEAT AND BONE MEAL WHEN OUT INTO
COMMERCE, TO BE FED OUT. Since 2007, these BSE feed ban rules have been breached
time and time again. tons and tons of mad cow feed went out in Alabama as well,
where one of the mad cows were documented, just the year before in 2006, and in
2013 and 2014, breaches so bad (OAI) Official Action Indicated were issued.
those are like the one issued where 10 million pounds of banned blood laced meat
and bone meal were fed out.
What is the use of having a Guidance for Industry Ensuring Safety of Animal
Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180, if it cannot be
enforced, as we have seen with a mandatory ruminant to ruminant feed ban?
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
TSS
posted by Terry S. Singeltary Sr. at
11:08 PM
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