Chronic Wasting Disease (CWD)
Surveillance Update: April 12, 2016
We have completed testing all
heads received to date from the 2015/16 hunting seasons. In total we tested 4929
heads and detected CWD in 116 deer (2.4%). This is an increase in annual overall
prevalence from the 2.1% in the 4163 heads tested in the 2014 surveillance
program. The 116 cases in 2015 included 105 mule deer, 11 white-tailed deer; 84
males, 31 females, 1 of unknown gender). Majority of these cases (77 of 116;
66%) are mule deer bucks.
As in previous years, species-and
gender-specific differences are apparent in the surveillance data. In the 4798
heads that were suitable for determining disease status, CWD was detected
in:
- 3.8% of 2756 mule deer
- 0.8% of 1420 white-tailed deer
- 0 of 487 elk (primarily from CFB
Suffield)
- 0 of 135 moose (primarily from CFB
Wainwright).
In the 4033 deer for which gender/sex was
reported, CWD was detected in:
- 5.9% of 1310 male mule deer
- 2.0% of 1325 female mule deer
- 0.7% of 991 male whitetails
- 1.0% of 407 female whitetails.
The geographic distribution of CWD continues to
expand with the disease identified in the 2015/16 sample in 6 WMUs where CWD was
not previously known to occur. These include WMU 116 in southeast; 158, 166,
238, and 242 in eastcentral; and 500 in northeast Alberta. These cases are in
the Milk River, Red Deer River, Battle River, and North Saskatchewan River
watersheds.
The most remarkable new case is the outlier in
WMU 242 approximately 100 km further west than the closest known cases (in WMU
232 and 203). This was a mule deer buck harvested on the northern edge of the
Battle River watershed west of Miquelon Lake and approximately 30 km southeast
of Edmonton. Although we know CWD is well-established in the eastern reaches of
the Battle River, the case in WMU 242 significantly expands the known
distribution of CWD in central Alberta. Cumulatively we have tested 700 deer
heads from the Battle River watershed between WMU 242 and WMU 203/232 and all
were negative for CWD. Thus, until we have data to show otherwise, the case near
Miquelon Lake appears to be an outlier.
The 24-hr freezers are no longer
available. However, frozen heads can still be submitted at any Fish and Wildlife
office during their office hours. See page 14 of the 2015 Alberta Guide to
Hunting Regulations for office locations and phone numbers. Additional
information about preparing and submitting heads can be found at:
The success of the CWD surveillance program
relies heavily on participation by hunters, guides, and landowners to ensure a
successful harvest that provides heads to be tested. We gratefully acknowledge
the efforts of one and all.
The total number of CWD cases detected
in wild deer in Alberta since September 2005 is 413.
Note that hunters receive NEGATIVE test results
directly at the email address associated with their individual AlbertaRELM
account. Negative test results ARE NOT BEING POSTED to individual hunter
AlbertaRELM accounts. As such, the email process mentioned above is the only
notification hunters receive when their animal is NEGATIVE for CWD.
As in the past, hunters who harvest a CWD
POSITIVE deer are contacted directly by phone (see below).
Patterns of CWD in Alberta
There are significant overall patterns of
disease occurrence in Alberta. CWD continues to occur primarily in mule deer in
comparison to white-tailed deer despite testing large numbers of both species.
Similarly males are more likely to be infected than females.
Analyses of previous data determined the
weighted CWD occurrence in Alberta is:
- Mule Deer: male 1.00 female
0.4
- White-tailed Deer: male 0.3 female
0.1
Thus male mule deer are the most likely, and
female white-tailed deer the least likely to be infected with CWD.
The geographic distribution of CWD is clustered
in some WMUs but continues to expand westward.
The finding of CWD in a moose near the South
Saskatchewan River valley in 2012 is the first such case identified in
Canada.
Specific information about the CWD hunter
surveillance program is provided at:
Note that the freezer map in the 2015
Alberta Guide to Hunting Regulations contains freezer locations for 2014
(the guide is published before details for the fall are available). For 2015 the
freezers in Marwayne and Paradise Valley were removed and a few other freezers
changed location but stayed within the same town. Freezers were added in north
Edmonton, north Calgary, and Bassano.
The CWD Freezer Locations currently posted on
the Information for Hunters page has all the correct information for 2015.
However the freezers were removed in January and will not return until
prior to the 2016 rifle seasons. Current information is available from
any Fish and Wildlife office.
- CWD surveillance is focused on the
Alberta/Saskatchewan border; however, hunter-killed deer (and elk) are accepted
from anywhere in the province (as in all previous years).
- Ongoing NEGATIVE test results are posted to
AlbertaRELM and made available to individual hunters. When test results are
available the hunter also receives an email that provides the negative
result.
- Ongoing POSITIVE test results are provided by
phone directly to the hunter who harvested the infected deer.
2014 Fall CWD Surveillance Results
In 2014 we tested 4,163 heads and detected 86
cases of CWD (2.1%). CWD was confirmed in 74 mule deer (59 males, 15 females; 72
adults, 2 yearlings) and 12 white-tails (all males; 10 adults, 2 yearlings)
However in the 2014 data the extraordinarily
large number of elk heads tested (n= 909, all negative) many of which were
harvested in conjunction with hunting opportunities at Canadian Forces Base
Suffield in January and February 2015, provides a confounding factor in
comparison to previous years. Thus, to allow valid comparisons among years, the
proportion of infected animals is presented in the context of the number of
heads tested for each species.
In breaking down the identified 2014 sample, CWD
was detected in:
- 3.61% of 2048 mule deer
- 1.13% of 1062 white-tailed deer
- 0 of 131 moose
- 0 of 909 elk
An overview of the 2014 results reveals both
expected and unexpected patterns in the data. As in previous years, mule deer
remain the species at greatest risk of CWD (74 of 86 (86.0%) cases detected in
2014). However the ratio of infected males to females wherever CWD occurs
generally is ~2:1; but in 2014 the ratio in the Alberta sample was ~5:1 (71
males, 15 females). The reason for the unexpected increase in the proportion of
infected males is unknown, particularly since almost equal numbers of male and
female mule deer, the species at greatest risk, were tested in 2014 (n = 1040
and 1065, respectively).
Overall number (86 cases) and rate (2.1%) of CWD
positive deer in 2014 are significantly higher than in previous years. Similarly
the geographic distribution of CWD in eastern Alberta continues to expand. The
disease now occurs in local areas from the Battle River watershed in the north
to the Milk River in the south. We detected the first evidence of CWD in the
Hand Hills area northeast of Drumheller in WMU 160, first evidence of the
disease in the Bow River watershed (east of Lake Newell), and further evidence
of the disease in the vicinity of Canadian Forces Base (CFB) Suffield and the
Cypress Hills. However no CWD was found in elk harvested from CFB Suffield,
despite testing over 870 elk heads from WMU 732.
The disease remains well established in areas
directly adjacent to the Saskatchewan border and continues to expand into WMUs
further up the affected watersheds, primarily the Battle, Red Deer, and South
Saskatchewan rivers.
Hunters continue to support the program and are
providing a solid foundation on which we can monitor CWD as it becomes further
established in eastern deer populations.
To learn more about CWD Surveillance in Alberta,
see:
For past CWD surveillance results and a general
timeline of CWD in Alberta, see:
Attention
Hunters!
Submit deer heads for CWD testing at any Fish
and Wildlife office during their office hours or any of the forty-five 24 hr
freezers in Edmonton, Calgary, and across eastern Alberta during rifle seasons.
Submission of deer heads for CWD testing is
MANDATORY in eastern Alberta from Cold Lake south to the US border.
For more details, see:
CWD Map and Statistics
- Maps: Chronic Wasting Disease in Wild Deer and
Moose in Alberta since September 2005
Statistics: Chronic Wasting Disease
in Wild Deer and Moose in Alberta (2011-2015)- Apr 12, 2016 (7 pages, <1 mb="" span=""> 1>
Statistics: Chronic Wasting Disease
in Wild Deer in Alberta (2005 – 2010)- April 12, 2016 (1 page, <1 mb="" span=""> 1>
Time - and CWD - Marches On (overview
of Alberta CWD data patterns)- Oct 3, 2012 (1 page, <1 mb="" span=""> 1>
News Releases and Information
Bulletins
- Nineteen new cases of chronic wasting
disease in wild deer- Apr 1, 2011
- New cases of chronic wasting disease
found in wild deer-
Mar 19, 2010
- Eight new cases of chronic wasting
disease detected in wild deer- Mar 20, 2009
- Opportunities abound for Alberta
hunters in 2007 guide/Alberta continues program to manage chronic wasting
disease- Jul 16,
2007
- Testing completed for chronic wasting
disease winter program- May 8, 2007
- Expanded chronic wasting disease
testing discovers three more cases- Apr 5, 2007
- Alberta takes action on chronic
wasting disease in wild deer- Feb 22, 2007
- Three more cases of chronic wasting
disease found in wild deer- Dec 21, 2006
- Alberta hunters asked to assist with
CWD control efforts-
Sep 15, 2006
- Winter efforts to control CWD in wild
deer in Alberta wrap up- Apr 18, 2006
- Winter tests find one more case of
CWD in wild deer in Alberta- Mar 3, 2006
- Four more cases of CWD found in wild
deer in Alberta- Feb
17, 2006
- First case of CWD found in wild deer
killed by hunter in Alberta- Dec 9, 2005
- No chronic wasting disease found in
latest culled deer-
Nov 4, 2005
- Chronic wasting disease found in two
more wild deer in Alberta- Oct 3, 2005
- Chronic wasting disease found in a
wild deer in Alberta- Sep 2, 2005
Herds infected with Chronic Wasting Disease in Canada – 2016 The CFIA works
with provincial governments and industry to conduct regular Chronic Wasting
Disease (CWD) surveillance. Ongoing provincial surveillance for CWD varies with
each particular province's perceived threat and infection status. Testing is
mandatory in Manitoba, Saskatchewan, Alberta and the Yukon; it is voluntary
elsewhere.
In addition, CWD is a reportable disease under the Health of Animals
Regulations. This means that all suspected cases must be reported to the
CFIA.
Current as of: 2016-07-31
Domestic cervid herds confirmed to be infected with CWD in Canada in 2016
Date confirmed Location Animal type infected February 18 Saskatchewan Deer March
21 Saskatchewan Deer May 18 Saskatchewan Elk July 21 Saskatchewan Elk
CANADA
Herds infected with Chronic Wasting Disease in Canada – 2016 The CFIA
works with provincial governments and industry to conduct regular Chronic
Wasting Disease (CWD) surveillance. Ongoing provincial surveillance for CWD
varies with each particular province's perceived threat and infection status.
Testing is mandatory in Manitoba, Saskatchewan, Alberta and the Yukon; it is
voluntary elsewhere.
In addition, CWD is a reportable disease under the Health of Animals
Regulations. This means that all suspected cases must be reported to the CFIA.
Current as of: 2016-06-30
Domestic cervid herds confirmed to be infected with CWD in Canada in 2016
Date confirmed Location Animal type infected February 18 Saskatchewan Deer March
21 Saskatchewan Deer May 18 Saskatchewan Elk
Additional Information Main page - Chronic wasting disease Federally
Reportable Diseases in Canada - 2016 Federally Reportable Diseases in Canada -
2015 Federally Reportable Diseases in Canada - 2014 Federally Reportable
Diseases in Canada - 2013
Hunters Reminded About CWD Testing Released on December 16, 2015
As the 2015-16 hunting season winds down, the Ministry of Environment is
reminding hunters that free chronic wasting disease (CWD) testing is available
for harvested deer, elk and moose.
The ministry is currently monitoring the distribution of CWD in
Saskatchewan to determine how widespread the issue is and results of this
testing will be made available in 2016. Hunters are encouraged to drop off deer
and elk heads at ministry offices throughout the province. Moose heads can be
dropped off at the Canadian Wildlife Health Co-operative at the University of
Saskatchewan in Saskatoon.
CWD is a disease that affects the nervous system of deer, elk and moose,
and can be fatal for those animals. When healthy animals come in contact with
the bodily fluids of an infected animal or a contaminated environment, they can
become infected.
There is currently 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; however, hunters are encouraged not to consume meat from
animals that have tested positive for CWD.
CWD was first detected in Saskatchewan in the fall of 2000 in a wild mule
deer. It has since spread to wild white-tailed deer and elk populations in
several locations. There is no evidence that CWD-affected deer and elk can
transmit the disease to other species such as cattle.
Hunters should also take certain precautions when field dressing,
transporting and processing animals. Hunters can help slow the spread of CWD by
not introducing the disease to new areas of the province through disposal of
deer carcass waste. Avoid transporting a deer carcass from the area where it was
taken, especially from areas where CWD has been detected. If the carcass is
transported, dispose of carcass waste by double-bagging it and taking it to a
landfill.
Visit the Ministry of Environment’s website at
www.environment.gov.sk.ca/Default.aspx?DN=0e02165a-9ef2-440f-81f7-d6a0fd1e1ee7
for more information about chronic wasting disease.
-30-
For more information, contact:
Michele McEachern Environment Regina Phone: 306-787-0412 Email:
michele.mceachern@gov.sk.ca
Saskatchewan Wildlife Management Report 2013-14;
In 2013 and 2014, targeted collection of heads from sick and dying cervids
was used to test for Chronic Wasting Disease.
Chronic Wasting Disease
Chronic wasting disease (CWD) is a fatal prion disease that affects the
nervous system of deer, elk and moose. CWD belongs to a group of diseases known
as transmissible spongiform encephalopathies (TSEs) similar to BSE (mad cow
disease) in cattle and scrapie in sheep. CWD was introduced into Saskatchewan
from infected elk imported from the United States in the 1980s. The disease was
first detected in a wild mule deer in the fall of 2000. As of 2014, CWD has
spread to wild white-tailed deer, mule deer and elk populations, and has been
detected in 20 wildlife management zones within Saskatchewan.
The disease is caused by infectious proteins, called prions, which are
resistant to breakdown by the animal and the environment. Infectious prions
begin to accumulate in the nervous tissue of the animal and eventually cause
holes to a form in the brain. The disease can take close to two years for
infected 23 animals to show symptoms and therefore the disease can remain
unnoticed in wild populations for many years. Symptoms include excessive
salivation, exhaustion, poor coordination, trembling and drooping head and ears.
CWD is transmitted between animals through contaminated saliva feces, and urine.
Animals become infected by eating and drinking from shared food, water sources,
and indirectly by soils that have become contaminated by prions from the bodily
fluids of CWD infected animals. It is unknown exactly how long CWD-infected
material can persist in the soil, but it is known to be longer than 3 years.
CWD is invariably fatal. Population models and empirical evidence from
areas other jurisdictions of high prevalence indicate that CWD will result in a
younger age structure, lower recruitment, and lower numbers of deer and elk
(Bollinger, pers. com., Miller et al. 2008, Dulberger et al. 2010, Edmonds 2013,
Monello et al. 2014). Saskatchewan operated a CWD surveillance program from 1997
- 2012. Samples after 2012 include targeted samples collected by conservation
officers and collar-marked research animals. Cervids that tested positive for
CWD (2001-2014) include: 334 (of 28,281 tested) mule deer, 78 (of 15,597)
white-tailed deer, 9 (of 1,541) elk, and 0 (of 131) moose.
In 2014, at the request of stakeholders, the ministry established a CWD
working group to help development of a long-range strategic plan to outline
Saskatchewan’s response to CWD. Although there is currently no known risk to
humans, the World Health Organization continues to recommend that CWD infected
meat not be consumed. The CWD Working Group encourages the public to report sick
or dead animals to your local conservation officer.
=============
As of 2014, CWD has spread to wild white-tailed deer, mule deer and elk
populations, and has been detected in 20 wildlife management zones within
Saskatchewan.
Population models and empirical evidence from areas other jurisdictions of
high prevalence indicate that CWD will result in a younger age structure, lower
recruitment, and lower numbers of deer and elk (Bollinger, pers. com., Miller et
al. 2008, Dulberger et al. 2010, Edmonds 2013, Monello et al. 2014).
Saskatchewan operated a CWD surveillance program from 1997 - 2012. Samples after
2012 include targeted samples collected by conservation officers and
collar-marked research animals. Cervids that tested positive for CWD (2001-2014)
include: 334 (of 28,281 tested) mule deer, 78 (of 15,597) white-tailed deer, 9
(of 1,541) elk, and 0 (of 131) moose.
=================
Saskatchewan Hunters and Trappers Guide 2016
Chronic Wasting Disease
Chronic wasting disease (CWD) is a fatal disease that affects the nervous
system of deer, elk and moose. CWD was introduced into Saskatchewan in the late
1980s. It has since spread to wild white-tailed deer, mule deer, elk and moose
in Saskatchewan.
The ministry and several stakeholder groups are renewing CWD management
efforts in the province to better understand the impact of CWD on wildlife
populations. A CWD working group has been established consisting of
organizations representing government, conservation, agricultural and wildlife
health interests to help direct the development of a long-range strategic plan
to outline Saskatchewan's response to CWD. The CWD working group asks you to
report sick big game animals to your local conservation officer. The working
group is reviewing options for research, surveillance and long-term options for
managing wild populations that may reduce or stabilize CWD prevalence. The
Saskatchewan Ministry of Health, Health Canada and the World Health Organization
continue to recommend that CWD-infected meat not be consumed. If you are
interested in CWD testing, the province will pay for testing at no cost to the
hunter. Hunters can drop off head samples at any ministry field office for
results in four to six weeks, or at Prairie Diagnostic Services (PDS)/Canadian
Wildlife Health Cooperative (CWHC) Western College of Veterinary Medicine, 52
Campus Dr., Saskatoon for results in about five to 10 days.
Head samples must be accompanied by a submission form located at:
cwhc-rcsf.ca under the heading "report and submit".
Saskatchewan Hunters and Trappers Guide 2015
Chronic Wasting Disease
Chronic wasting disease (CWD) is a fatal disease that affects deer, elk and
moose. CWD was introduced into the province from infected farmed elk, imported
from the United States in the 1980s. This disease was first detected in a wild
mule deer in the fall of 2000. As of 2014, CWD has spread to whitetailed deer,
mule deer and elk populations, and has been detected in 20 WMZs within
Saskatchewan.
The province is resuming CWD testing this fall and will provide no-cost
analysis of hunter-killed deer and elk. Hunters can drop off head samples at all
ministry field offices or at the Prairie Diagnostic Services laboratory on the
University of Saskatchewan Campus in Saskatoon. See page 10 for more
information.
Chronic Wasting Disease
Chronic wasting disease (CWD) is a fatal disease that affects the nervous
system of deer, elk and moose. CWD is a protein-caused disease, similar to BSE
(mad cow disease) in cattle and scrapie in sheep. CWD was introduced into
Saskatchewan from infected farmed elk, imported from the United States in the
1980s. CWD was first detected in a wild mule deer in the fall of 2000. As of
2014, CWD has spread to white-tailed deer, mule deer and elk populations, and
has been detected in 20 wildlife management zones within Saskatchewan. The
ministry and several stakeholder groups are renewing CWD management efforts in
the province to better understand the impact of CWD on wildlife populations. A
CWD working group has been established consisting of organizations representing
government, conservation, agricultural and wildlife health interests to help
direct the development of a long-range strategic plan to outline Saskatchewan's
response to CWD.
The CWD working group asks you to report sick animals to your local
conservation officer. The working group is reviewing options for research,
surveillance, management of game-farmed animals and long-term options for
managing wild populations that may reduce or stabilize CWD prevalence. Although
there is currently no known risk to humans, the World Health Organization
continues to recommend that CWD-infected meat not be consumed. For hunters
interested in CWD testing, the province will pay for testing at no cost to the
hunter. Hunters can drop off head samples at any ministry field office, in
person at the Prairie Diagnostic Services (University of Saskatchewan, Vet
College) If heads are dropped off at a ministry office, expect up to 4-6 weeks
for results. Hunters interested in obtaining results sooner can drop heads off
directly at CWHC/Prairie Diagnostics Services (PDS) at 52
10
Campus Dr, Saskatoon. Results for heads dropped off directly at CWHC will
take about 5-10 business days. Heads are being accepted at:
Canadian Wildlife Health Cooperative (CWHC) / Prairie Diagnostics Services
(PDS) 52 Campus Drive Saskatoon, SK S7N 5B4
A submission form to include the location where the animal was harvested
must accompany heads destined for CWD testing. A submission form to include the
location where the animal was harvested must accompany heads destined for CWD
testing. The submission form can be found online at:
http://www.cwhc-rcsf.ca/ under the heading
"report and submit". Canadian Wildlife Health Cooperative at cwhc-rcsf.ca
Tuesday, February 10, 2015
Alberta Canada First case of chronic wasting disease found in farm elk
since 2002
Saturday, February 14, 2015
Canadian Food Inspection Agency Confirms Bovine Spongiform Encephalopathy
(BSE) in Alberta
Monday, April 07, 2014
Saskatchewan’s first chronic wasting disease case of the year has been
confirmed 2014
Saturday, October 18, 2014
Chronic wasting disease threatens Canadian agriculture, Alberta MLA says
Sunday, May 27, 2012
CANADA PLANS TO IMPRISON ANYONE SPEAKING ABOUT MAD COW or ANY OTHER DISEASE
OUTBREAK, CENSORSHIP IS A TERRIBLE THING
Management of CWD in Canada: Past Practices, Current Conditions, Current
Science, Future Risks and Options
Thursday, December 22, 2011
Chronic Wasting Disease discovered on game farm Saskatchewan Wednesday Dec.
21, 2011
Wednesday, June 18, 2008
CHRONIC WASTING DISEASE FOUND IN 24 MORE DEER IN ALBERTA
First-Ever Case of Chronic Wasting Disease in Wild Elk Found in
Saskatchewan
Thursday, 15 May 2008 00:00
Animals found dead in early-April near Nipawin in province’s east-central
region
The first-ever cases of chronic wasting disease (CWD) in wild elk have been
discovered in Saskatchewan, but the provincial government hasn’t been very
public about it.
The animals were found dead west of Nipawin in early April, close to Fort a
la Corne in the province’s east-central region. An “announcement” was posted May
6 on the Ministry of Environment website but not on the government’s main page
or distributed as a news release.
“We want to understand the significance of it before we take any radical
action,” said Rick Ashton, director of resource allocation at the fish and
wildlife branch of the ministry. “They were found in an area highly infected
with CWD in white-tailed deer. It’s just another species. It’s not a significant
event at this point.”
“These are the first cases in wild elk. It’s out there now, so how long
before it moves into even more species,” said SWF executive director Darrell
Crabbe. “We know moose can contract the disease and there’s a good possibility
from there it could jump to caribou.”
The elk were both female cows, aged 11/2 and 31/2 years. The younger one
was found dead in a pea field near a road and exhibited severe trauma consistent
with being hit by a vehicle. The older animal was found in a field and appeared
to have been dead for three or four days, according to the government. Only the
head of the latter was submitted, so confirmation of the cause of death was not
possible.
Although both animals tested positive for CWD, it was believed they were in
the early stages of the disease and did not die from that, the announcement
states. The disease is a form of transmissible spongiform encephalopathy,
attacking the brains and nervous systems of cervid (deer family) animals.
The Ministry of Environment is planning to meet with a CWD committee –
comprised of wildlife groups, hunter organizations, stock growers, rural
municipalities and First Nations – to discuss the findings and develop a
management plan.
The SWF doesn’t have a lot of faith in the government management policies.
An inventory program intended to monitor the number of animals in game farms is
“a joke,” said Crabbe, who blames game farms for CWD in the province by setting
less valuable animals in the wild.
Hunt farms bring in a lot of money for farmers and ranchers who have
suffered from reduced incomes during the years. Wealthy hunters from the United
States will pay thousands of dollars for a day’s hunt, and they want to return
with something to show for it, said Crabbe, who is skeptical the diseased
Saskatchewan elk were wild animals.
“I find it very coincidental, too coincidental, to find two cows, so close
in age, both testing positive in that area,” he said, noting cows are less
valuable than elk bulls to hunters.
The ministry’s wildlife disease specialist, Dr. Yeen Ten Hwang, said there
is no evidence the elk were originally domestic.
“There were no ear tags and the pathologist saw no hair loss or ripping
where the tags might have been,” she said.
Asked why the findings weren’t publicized to the media, she said, “I don’t
know. We’ve had a lot of CWD in the deer and it was only a matter of time until
it was transferred to elk. We sort of expected it.”
The first cases of CWD in Canada were traced to a Lloydminster-area farm
that imported animals from South Dakota in the 1980s. How CWD is transmitted is
not yet completely understood, though it is believed to occur if animals are in
close proximity, likely through the saliva, feces or urine.
An outbreak of CWD in the 1990s devastated the herds and livelihoods of
many producers. There is no way to confirm the presence of the disease until the
brain can be examined. As a result, tens of thousands of animals have been
killed to contain the spread of CWD. The vast majority have tested
negative.
“We certainly weren’t trying to keep it quiet,” Ashton said of the dead
elk. “We let the important folks who needed to know about it know. We did
suppress it until we could tell our key and critical stakeholders because if
something like this gets out, it will spread fast and it is important to
carefully manage our communications. Then we put it on the website, which is
very public.”
New CWD Cases Found
Friday, 26 October 2007 00:00
The Canadian Food Inspection Agency has confirmed animals in a white-tail
deer herd and two elk hunt operations in Saskatchewan have tested positive for
chronic wasting disease (CWD).
As a result, the CFIA has quarantined a white-tail deer herd and an elk
hunt operation in the Prince Albert area along with an elk hunt farm in the
Moose Jaw area, an agency spokeswoman said.
The most recent case was confirmed Tuesday in a farmed elk herd in the
Prince Albert area. However, the agency spokeswoman said the quarantine would
likely have been imposed while awaiting the test results. Saskatchewan’s first
suspected case of CWD this year was diagnosed earlier in the month.
Chronic wasting disease is a progressive, fatal disease of the nervous
system of cervids such as mule deer, white-tailed deer and elk. Black-tail deer
and moose have also become infected naturally, according to the CFIA Web site.
The CFIA is also tracing the movement of animals on and off the premises, the
agency spokeswoman said, noting at this time no herds have been culled.
The findings of CWD is not unexpected, she said. There have been periodic
findings of the disease in the deer and elk population in the province over the
last 10 years.
Deer Infected With Chronic Wasting Disease Discovered Near Nipawin
Wednesday, 13 July 2005 00:00
A white tailed deer found near Nipawin, has tested positive for Chronic
Wasting Disease.
CWD is a contagious neurological disease affecting deer and elk.
It causes a degeneration of the brains of infected animals and is in the
same family of prion diseases as BSE.
“We don’t want to put out an alarm situation. This is one case out there,”
said Marvin Hlady, a wildlife specialist with Sask Environment.
This is the first deer diagnosed with CWD in northeast Saskatchewan. Since
a wild animal was found with CWD in 2000, there have been 68 reported cases in
Saskatchewan, with the majority of cases in Sask Landing Park, north of Swift
Current.
Hlady emphasized that deer meat is still safe to eat. “Right now there is
no evidence that people can get CWD.”
On May 19 Albert Swan discovered a dead deer inside a shed on his property
– five miles south of Love adjacent to the White Fox River.
On May 20, conservation officers from the Sask Environment office in
Nipawin picked up the animal and sent it to the Canadian Cooperative Wildlife
Health Centre at the University of Saskatchewan for testing. The results came
back positive and in late June, a Canadian Food Inspection Agency lab in Ontario
confirmed the diagnosis.
“We will be using this information… as part of our CWD management program,”
Hlady said.
Scientists are not certain how CWD is spread, but it may be passed on via
feces, saliva or urine. It is also believed that a high deer population
increases the risk of a CWD epidemic.
“A recognized way to reduce spread is to reduce deer numbers,” Hlady
said.
Sask Environment has no plans for a deer cull in the northeast, but they
will hold a public meeting in the region.
“We have started making preparations to answer any questions in a public
forum,” said Rick Douslin, Compliance manager at the Nipawin office for Sask
Environment. Douslin expects the public meeting will be in early August.
EC 1471/2004 of 18 August 2004 Amendment of EC 999/2001 – introducing
requirements for the import of cervid products from Canada and the United
States. This regulation imposes the removal of Specific Risk Materials (SRM)
from all cervid meats exported to the EU and limits exports of wild game to
areas free of Chronic Wasting Disease (CWD) from January 1, 2005.
CHRONIC WASTING DISEASE HITS THIRD SPECIES: Canadian animal health
officials are concerned after a farmed white-tailed deer in Alberta was recently
confirmed positive for chronic wasting DISEASE (CWD) a progressive, fatal,
degenerative DISEASE of the brain affecting elk, mule deer and white-tailed
deer. Formerly, the DISEASE in Canada had been found only in wild mule deer and
elk. CWD has been diagnosed in wild deer, elk and farmed elk throughout western
Canada and the United States. Alberta has had a moratorium on the import of elk
and deer since 1988, as well as a voluntary CWD surveillance program since
October 1996. In recent years, the Canadian Food Inspection Agency has ordered
the slaughter of thousands of farmed elk on Saskatchewan farms in attempt to
stop the spread of CWD. Compensation has run into the tens of millions of
dollars.
KOREA BANS CANADIAN ELK IMPORTS: According to the Calgary Sun, Korea has
moved to ban imports of Canadian deer and elk products (antlers and antler
velvet) due to the outbreak of Chronic Wasting Disease (CWD) in Saskatchewan elk
herds. Late last year, the Canadian Food Inspection Agency (CFIA) ordered the
slaughter of 1,700 domesticated elk at six Saskatchewan farms in attempt to stop
the spread of CWD (see CA 0206). The disease has not been detected in any other
province. Canada's elk population is estimated at 53,000 head and is raised
primarily for antler velvet. Canada is the fourth-largest antler velvet producer
in the world, behind New Zealand, China and Russia. Most of Canadian antler
velvet is exported to Asia where it is sold for medicinal purposes and as an
aphrodisiac.
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
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.
Canadian Policy June 19, 1998
What does the Canadian Food Inspection Agency (CFIA) do to prevent CWD from
entering or becoming established in Canada? Under the Health of Animals Act, the
CFIA has the power to act when a suspect case of CWD is found. This may include
quarantine and destruction of all exposed animals.
The CFIA routinely monitors for CWD. Each herd is tested every three years
for tuberculosis, and at that time agency inspectors examine each animal for
signs of neurological disease. In addition, all deer and elk sent to provincial
laboratories for post mortem are screened for CWD as part of an ongoing
surveillance program.
In 1988 a Captive Ungulate Program was created because the health status of
game farmed deer, elk and bison was not well known, and they posed a potential
health risk for the spread of tuberculosis and brucellosis to Canadian cattle.
In 1990 it became mandatory for a permit to be issued in order to move an
animal, thus allowing for the monitoring of all movement of these species.
Since 1990 there has been a ban on the importation of deer and elk from the
United States.
Are products like venison or powdered antler velvet from animals that have
been exposed to CWD safe?
According to Health Canada there are no studies available on the safety of
tissues from elk with CWD. In studies using mice experimentally infected with
scrapie, another TSE, muscle and skin tissues were not found to be infectious,
at any detectable level.
However, we have to be very cautious in using these results to predict the
safety of products from infected or exposed elk, since test results from one
species do not necessarily apply to another.
1 May 1996 Steve Sullivan, Agriculture and Agri-Food Canada, writes:
"In early 1996, Agriculture and Agri-Food Canada (AAFC) confirmed a case of
Chronic Wasting Disease (CWD) in a single elk located on a small game farm
facility in southern Saskatchewan. The affected animal was imported as a
yearling, in 1989, as part of a small shipment of elk originating from the U.S.
The game farm in question is not located near other (alternative or
conventional) livestock operations. No animals on this farm have died, nor have
any animals moved off the premises, for any reason, since the elk herd was
established.
Following the confirmation of CWD, the carcass of the affected elk was
incinerated and the following actions took place:
1) AAFC carried out an inventory of all elk on the farm;
2) no 'movement permits' for the elk were issued to the owner; (All captive
ungulates in Canada require numbered permits to allow their movement anywhere
within the country, including farm-to-farm)
3) all animals that were part of the original shipment from the U.S. were
traced and located; and
4) the affected herd was put in isolation.
Chronic Wasting Disease is not a "reportable disease", and the Office
International des ?pizooties (OIE) (the organization that establishes
international animal health guidelines), does not require notification its
presence."
2016
UW Research Finds First-Ever Evidence of White-Tailed Deer Declines from
CWD
man working with blindfolded deer David Edmunds, recent UW Ph.D. graduate,
performs a tonsil biopsy on a white-tailed deer to test for chronic wasting
disease. He and other UW researchers have documented the first conclusive
evidence that CWD found at high prevalence leads directly to population declines
in free-ranging deer populations. (Todd Cornish Photo)
September 2, 2016 — Chronic wasting disease has caused significant declines
in east-central Wyoming white-tailed deer populations, according to new research
published this week by University of Wyoming scientists.
Chronic wasting disease (CWD) is a prion disease of deer, elk and moose
found in 24 states and two Canadian provinces.
The research, led by recent UW Ph.D. graduate David Edmunds, under the
direction of Associate Professor Todd Cornish in the Department of Veterinary
Sciences, is the first conclusive evidence that CWD found at high prevalence
leads directly to population declines in free-ranging deer populations.
The findings, published in the scientific journal PLOS ONE this week,
provide new information that could influence management of this continually
expanding disease.
“Chronic wasting disease has likely been present in southeast Wyoming deer
and elk populations for approximately 50 years,” Edmunds says. “It has been
steadily increasing to the point that some hunt areas are seeing populations
with as many as 30 percent to almost 50 percent of harvested deer testing
positive for this disease.”
For eight years, he and his colleagues tracked white-tailed deer east of
Casper to determine if CWD itself can cause population numbers to decline by
increasing mortality of deer annually.
“We found that CWD drastically reduced annual survival rates in the deer
population, especially in females,” Edmunds says.
Working as a graduate student under Cornish in the Wyoming
Wildlife/Livestock Health Center in the Department of Veterinary Sciences,
Edmunds and colleagues captured both female and male fawns on their winter
ranges to test whether they had CWD; pregnancy tested females; and marked all
deer with radio transmitters attached to collars for tracking purposes.
two men and a woman in wooded area with binoculars, gps tracking gear and
papers
From left, Associate Professor Todd Cornish, graduate student David Edmunds
and graduate student Melia DeVivo use telemetry to find radio-collared deer in a
chronic wasting disease study. (Todd Cornish Photo)
Deer were tracked throughout the year and captured annually to retest for
CWD. A variety of data were collected, including survival and pregnancy rates,
number of fawns seen alongside does in late summer, and CWD prevalence. All of
these were used to determine the population growth rate -- which is by how much
the population size varies from one year to the next.
The researchers found that over the study period from 2003-10, the
population declined 10 percent annually, which they say could lead to localized
extinctions in less than 50 years.
“The decline was caused directly by CWD lowering annual survival of female
deer, which have the biggest impact on population growth rates,” Edmunds says.
“This was because CWD-positive deer died both directly from the disease and were
more likely to be killed by hunters than CWD-negative deer.”
Cornish says the findings highlight the importance of preventing CWD from
spreading into new deer and elk populations.
“We really do not have any effective strategies currently to manage CWD
once it becomes established in landscapes and in populations,” he says. “Now
that we know CWD causes populations to decline once the disease reaches
significant levels in deer, this is a disease to be taken very seriously, with
more research on control and prevention strategies warranted.”
Edmunds and Cornish are two of the co-authors of the report published
Tuesday -- along with a collaborative team of researchers from the Wyoming
Cooperative Fish and Wildlife Research Unit, the Wyoming Game and Fish
Department, UW’s College of Agriculture and Natural Resources, and Texas A&M
University.
To read the article summarizing the research in PLOS ONE, go to
bit.ly/cwddeer.
Friday, September 02, 2016
*** Chronic Wasting Disease Drives Population Decline of White-Tailed
Deer
*** WDA 2016 NEW YORK ***
We found that CWD adapts to a new host more readily than BSE and that human
PrP was unexpectedly prone to misfolding by CWD prions. In addition, we
investigated the role of specific regions of the bovine, deer and human PrP
protein in resistance to conversion by prions from another species. We have
concluded that the human protein has a region that confers unusual
susceptibility to conversion by CWD prions.
Student Presentations Session 2
The species barriers and public health threat of CWD and BSE prions
Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr.
Edward Hoover1 1Colorado State University
Chronic wasting disease (CWD) is spreading rapidly through cervid
populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease)
arose in the 1980s because cattle were fed recycled animal protein. These and
other prion diseases are caused by abnormal folding of the normal prion protein
(PrP) into a disease causing form (PrPd), which is pathogenic to nervous system
cells and can cause subsequent PrP to misfold. CWD spreads among cervids very
efficiently, but it has not yet infected humans. On the other hand, BSE was
spread only when cattle consumed infected bovine or ovine tissue, but did infect
humans and other species. The objective of this research is to understand the
role of PrP structure in cross-species infection by CWD and BSE. To study the
propensity of each species’ PrP to be induced to misfold by the presence of PrPd
from verious species, we have used an in vitro system that permits detection of
PrPd in real-time. We measured the conversion efficiency of various combinations
of PrPd seeds and PrP substrate combinations. We observed the cross-species
behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found
that CWD adapts to a new host more readily than BSE and that human PrP was
unexpectedly prone to misfolding by CWD prions. In addition, we investigated the
role of specific regions of the bovine, deer and human PrP protein in resistance
to conversion by prions from another species. We have concluded that the human
protein has a region that confers unusual susceptibility to conversion by CWD
prions. CWD is unique among prion diseases in its rapid spread in natural
populations. BSE prions are essentially unaltered upon passage to a new species,
while CWD adapts to the new species. This adaptation has consequences for
surveillance of humans exposed to CWD.
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust
Administration Exploring perceptions about chronic wasting disease risks among
wildlife and agriculture professionals and stakeholders
Ms. Alyssa Wetterau1, Dr. Krysten Schuler1, Dr. Elizabeth Bunting1, Dr.
Hussni Mohammed1 1Cornell University
Chronic wasting disease (CWD) is a fatal disease of North American
Cervidae. New York State (NYS, USA) successfully managed an outbreak of CWD in
2005 in both captive and wild white-tailed deer (Odocoileus virginianus) with no
reoccurrence of the disease as of 2015. To attain maximum compliance and
efficacy of management actions for prevention of CWD entry, understanding the
varied risk perceptions will allow for targeted, proactive communication efforts
to address divergences between expert-derived risk assessments and stakeholder
risk perceptions. We examined perceived risks associated with CWD introduction
and exposure among agricultural and wildlife agency professionals within and
outside of NYS, as well as stakeholder groups (e.g., hunters and captive cervid
owners). We measured perceived risk using a risk assessment questionnaire online
via Qualtrics survey software and evaluated similarities within, as well as
differences in, perception among participant groups. New York State biologists
employed by the Department of Environmental Conservation and independent non-NYS
wildlife and agricultural professionals thought CWD risks associated with
captive cervids were high; captive cervid owners thought risks for wild and
captive cervids were low. Agriculture and wildlife professional groups agreed on
general risk perceptions. We ranked 15 individual risk hazards into high and low
medium categories based on all responses. Differences between groups were most
evident in hypothetical disease pathways. Any pathway involving inter-state
import of live cervids received high ranking for all groups except captive
cervid owners. Comparatively low risk perceptions by captive cervid operators
may stem from misinformation, lack of understanding of testing programs, and
indemnity payments for animal depopulation. Communication and education directed
at areas of disagreement may facilitate effective disease prevention and
management.
* No evaluation of determination of CWD risk is required for alternative
livestock or captive wildlife shipped directly to slaughter or to a biosecure
facility approved by the Division and the Dept. of Agriculture.
*** We found that CWD adapts to a new host more readily than BSE and that
human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we
investigated the role of specific regions of the bovine, deer and human PrP
protein in resistance to conversion by prions from another species. We have
concluded that the human protein has a region that confers unusual
susceptibility to conversion by CWD prions. CWD is unique among prion diseases
in its rapid spread in natural populations. BSE prions are essentially unaltered
upon passage to a new species, while CWD adapts to the new species. This
adaptation has consequences for surveillance of humans exposed to CWD. ***
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Prion 2016
Purchase options Price * Issue Purchase USD 198.00
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting
disease (CWD) is the prion disease affecting deer, elk and moose, and it is a
widespread and expanding epidemic affecting 22 US States and 2 Canadian
provinces so far. CWD poses the most serious zoonotic prion transmission risks
in North America because of huge venison consumption (>6 million deer/elk
hunted and consumed annually in the USA alone), significant prion infectivity in
muscles and other tissues/fluids from CWD-affected cervids, and usually high
levels of individual exposure to CWD resulting from consumption of the affected
animal among often just family and friends. However, we still do not know
whether CWD prions can infect humans in the brain or peripheral tissues or
whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no
essays to reliably detect CWD infection in humans. We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) CWD transmission to humans has already occurred. We will test these
hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in
vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain
or peripheral lymphoid tissues at low levels by conducting systemic bioassays in
a set of "humanized" Tg mouse lines expressing common human PrP variants using a
number of CWD isolates at varying doses and routes. Experimental "human CWD"
samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission
barrier is dependent on prion strain and influenced by the host (human) PrP
sequence by examining and comparing the transmission efficiency and phenotypes
of several atypical/unusual CWD isolates/strains as well as a few prion strains
from other species that have adapted to cervid PrP sequence, utilizing the same
panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD
infection in humans by examining in details the clinical, pathological,
biochemical and in vitro seeding properties of existing and future experimental
"human CWD" samples generated from Aims 1-2 and compare them with those of
common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining
a significant number of brain samples from prion-affected human subjects in the
USA and Canada who have consumed venison from CWD-endemic areas utilizing the
criteria and essays established in Aim 3. The findings from this proposal will
greatly advance our understandings on the potential and characteristics of
cervid prion transmission in humans, establish reliable essays for CWD zoonosis
and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure
to cervid prions because chronic wasting disease (CWD, a widespread and highly
infectious prion disease among deer and elk in North America) continues
spreading and consumption of venison remains popular, but our understanding on
cervid-to-human prion transmission is still very limited, raising public health
concerns. This proposal aims to define the zoonotic risks of cervid prions and
set up and apply essays to detect CWD zoonosis using mouse models and in vitro
methods. The findings will greatly expand our knowledge on the potentials and
characteristics of cervid prion transmission in humans, establish reliable
essays for such infections and may discover the first case(s) of CWD infection
in humans.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 1R01NS088604-01A1
Application # 9037884
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2015-09-30
Budget End 2016-07-31
Support Year 1
Fiscal Year 2015
Total Cost $337,507
Indirect Cost $118,756
Institution
Name Case Western Reserve University
Department Pathology
Type Schools of Medicine
DUNS # 077758407
City Cleveland
State OH
Country United States
Zip Code 44106
===========================================================
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) *** CWD transmission to humans has already occurred. *** We will test
these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary
in vitro approaches.
============================================================
Key Molecular Mechanisms of TSEs
Zabel, Mark D.
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs),
are fatal neurodegenerative diseases affecting humans, cervids, bovids, and
ovids. The absolute requirement of PrPC expression to generate prion diseases
and the lack of instructional nucleic acid define prions as unique infectious
agents. Prions exhibit species-specific tropism, inferring that unique prion
strains exist that preferentially infct certain host species and confront
transmission barriers to heterologous host species. However, transmission
barriers are not absolute. Scientific consensus agrees that the sheep TSE
scrapie probably breached the transmission barrier to cattle causing bovine
spongiform encephalopathy that subsequently breached the human transmission
barrier and likely caused several hundred deaths by a new-variant form of the
human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human
health, emotion and economies can still be felt in areas like farming, blood and
organ donations and the threat of a latent TSE epidemic. This precedent raises
the real possibility of other TSEs, like chronic wasting disease of cervids,
overcoming similar human transmission barriers. A groundbreaking discovery made
last year revealed that mice infected with heterologous prion strains facing
significant transmission barriers replicated prions far more readily in spleens
than brains6. Furthermore, these splenic prions exhibited weakened transmission
barriers and expanded host ranges compared to neurogenic prions. These data
question conventional wisdom of avoiding neural tissue to avoid prion
xenotransmission, when more promiscuous prions may lurk in extraneural tissues.
Data derived from work previously funded by NIH demonstrate that Complement
receptors CD21/35 bind prions and high density PrPC and differentially impact
prion disease depending on the prion isolate or strain used. Recent advances in
live animal and whole organ imaging have led us to generate preliminary data to
support novel, innovative approaches to assessing prion capture and transport.
We plan to test our unifying hypothesis for this proposal that CD21/35 control
the processes of peripheral prion capture, transport, strain selection and
xenotransmission in the following specific aims. 1. Assess the role of CD21/35
in splenic prion strain selection and host range expansion. 2. Determine whether
CD21/35 and C1q differentially bind distinct prion strains 3. Monitor the
effects of CD21/35 on prion trafficking in real time and space 4. Assess the
role of CD21/35 in incunabular prion trafficking
Public Health Relevance Transmissible spongiform encephalopathies, or prion
diseases, are devastating illnesses that greatly impact public health,
agriculture and wildlife in North America and around the world. The impact to
human health, emotion and economies can still be felt in areas like farming,
blood and organ donations and the threat of a latent TSE epidemic. This
precedent raises the real possibility of other TSEs, like chronic wasting
disease (CWD) of cervids, overcoming similar human transmission barriers. Early
this year Canada reported its first case of BSE in over a decade audits first
case of CWD in farmed elk in three years, underscoring the need for continued
vigilance and research. Identifying mechanisms of transmission and zoonoses
remains an extremely important and intense area of research that will benefit
human and other animal populations.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Allergy and Infectious Diseases (NIAID)
Type High Priority, Short Term Project Award (R56)
Project # 1R56AI122273-01A1
Application # 9211114
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Beisel, Christopher E
Project Start 2016-02-16
Project End 2017-01-31
Budget Start 2016-02-16
Budget End 2017-01-31
Support Year 1
Fiscal Year 2016
Total Cost
Indirect Cost Institution Name Colorado State University-Fort Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
PMCA Detection of CWD Infection in Cervid and Non-Cervid Species
Hoover, Edward Arthur
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Chronic wasting disease (CWD) of deer and elk is an emerging highly
transmissible prion disease now recognized in 18 States, 2 Canadian provinces,
and Korea. We have shown that Infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces, and in the tissues
generating those body fluids and excreta, thereby leading to facile transmission
by direct contact and environmental contamination. We have also shown that CWD
can infect some non-cervid species, thus the potential risk CWD represents to
domestic animal species and to humans remains unknown. Whether prions borne in
blood, saliva, nasal fluids, milk, or excreta are generated or modified in the
proximate peripheral tissue sites, may differ in subtle ways from those
generated in brain, or may be adapted for mucosal infection remain open
questions. The increasing parallels in the pathogenesis between prion diseases
and human neurodegenerative conditions, such as Alzheimer's and Parkinson's
diseases, add relevance to CWD as a transmissible protein misfolding disease.
The overall goal of this work is to elucidate the process of CWD prion
transmission from mucosal secretory and excretory tissue sites by addressing
these questions: (a) What are the kinetics and magnitude of CWD prion shedding
post-exposure? (b) Are excreted prions biochemically distinct, or not, from
those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the
source of excreted prions? and (d) Are excreted prions adapted for horizontal
transmission via natural/trans-mucosal routes? The specific aims of this
proposal are: (1) To determine the onset and consistency of CWD prion shedding
in deer and cervidized mice; (2); To compare the biochemical and biophysical
properties of excretory vs. CNS prions; (3) To determine the capacity of
peripheral tissues to support replication of CWD prions; (4) To determine the
protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To
compare the mucosal infectivity of excretory vs. CNS prions. Understanding the
mechanisms that enable efficient prion dissemination and shedding will help
elucidate how horizontally transmissible prions evolve and succeed, and is the
basis of this proposal. Understanding how infectious misfolded proteins (prions)
are generated, trafficked, shed, and transmitted will aid in preventing,
treating, and managing the risks associated with these agents and the diseases
they cause.
Public Health Relevance Chronic wasting disease (CWD) of deer and elk is an
emergent highly transmissible prion disease now recognized throughout the USA as
well as in Canada and Korea. We have shown that infected deer harbor and shed
high levels of infectious prions in saliva, blood, urine, and feces thereby
leading to transmission by direct contact and environmental contamination. In
that our studies have also shown that CWD can infect some non-cervid species,
the potential risk CWD may represents to domestic animal species and humans
remains unknown. The increasing parallels in the development of major human
neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and
prion diseases add relevance to CWD as a model of a transmissible protein
misfolding disease. Understanding how infectious misfolded proteins (prions) are
generated and transmitted will aid in interrupting, treating, and managing the
risks associated with these agents and the diseases they cause.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 4R01NS061902-07
Application # 9010980
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May Project Start 2009-09-30
Project End 2018-02-28
Budget Start 2016-03-01
Budget End 2017-02-28
Support Year 7
Fiscal Year 2016
Total Cost $409,868
Indirect Cost $134,234 Institution Name Colorado State University-Fort
Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** 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).***
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** 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
*** 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
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.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** 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.
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
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.
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid
prion protein (PrP) sequence through passage in cervidized transgenic mice
efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion
strain-dependent and humans can be vulnerable to novel cervid prion strains.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on the
existence of different CWD strains.
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.
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
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.
Yet, it has to be noted that our assessments of PrPTSE levels in skeletal
muscles were based on findings in presumably pre- or subclinically infected
animals. Therefore, the concentration of PrPTSE in skeletal muscles of WTD with
clinically manifest CWD may possibly exceed our estimate which refers to
clinically inconspicuous animals that are more likely to enter the human food
chain. Our tissue blot findings in skeletal muscles from CWD-infected WTD would
be consistent with an anterograde spread of CWD prions via motor nerve fibres to
muscle tissue (figure 4A). Similar neural spreading pathways of muscle infection
were previously found in hamsters orally challenged with scrapie [28] and
suggested by the detection of PrPTSE in muscle fibres and muscle-associated
nerve fascicles of clinically-ill non-human primates challenged with BSE prions
[29]. Whether the absence of detectable PrPTSE in myofibers observed in our
study is a specific feature of CWD in WTD, or was due to a pre- or subclinical
stage of infection in the examined animals, remains to be established. In any
case, our observations support previous findings suggesting the precautionary
prevention of muscle tissue from CWD-infected WTD in the human diet, and
highlight the need to comprehensively elucidate of whether CWD may be
transmissible to humans. While the understanding of TSEs in cervids has made
substantial progress during the past few years, the assessment and management of
risks possibly emanating from prions in skeletal muscles of CWD-infected cervids
requires further research.
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,§ + Author
Affiliations
1 Department of Microbiology, Immunology and Molecular Genetics, University
of Kentucky, Lexington, KY 40536, USA. 2 Sanders Brown Center on Aging,
University of Kentucky, Lexington, KY 40536, USA. 3 Department of Neurology,
University of Kentucky, Lexington, KY 40536, USA. 4 Department of Microbiology,
Immunology and Pathology, Colorado State University, Fort Collins, CO 80523,
USA. 5 Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO
80526, USA. ↵§ To whom correspondence should be addressed. E-mail:
gtell2@uky.edu ↵* These authors contributed equally to this work.
↵† Present address: Department of Infectology, Scripps Research Institute,
5353 Parkside Drive, RF-2, Jupiter, FL 33458, USA.
↵‡ Present address: Institute of Neuropathology, University of Zurich,
Schmelzbergstrasse 12, 8091 Zurich, Switzerland.
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.
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin
Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic
Wasting Disease
Contact: Exotic Meats USA 1-800-680-4375
FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San
Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may
contain meat derived from an elk confirmed to have Chronic Wasting Disease
(CWD). The meat with production dates of December 29, 30 and 31, 2008 was
purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk
Farm LLC in Pine Island, MN and was among animals slaughtered and processed at
USDA facility Noah’s Ark Processors LLC.
Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease
found in elk and deer. The disease is caused by an abnormally shaped protein
called a prion, which can damage the brain and nerves of animals in the deer
family. Currently, it is believed that the prion responsible for causing CWD in
deer and elk is not capable of infecting humans who eat deer or elk contaminated
with the prion, but the observation of animal-to-human transmission of other
prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has
raised a theoretical concern regarding the transmission of CWD from deer or elk
to humans. At the present time, FDA believes the risk of becoming ill from
eating CWD-positive elk or deer meat is remote. However, FDA strongly advises
consumers to return the product to the place of purchase, rather than disposing
of it themselves, due to environmental concerns.
Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The
Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was
packaged in individual vacuum packs weighing approximately 3 pounds each. A
total of six packs of the Elk Tenderloins were sold to the public at the Exotic
Meats USA retail store. Consumers who still have the Elk Tenderloins should
return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX
78209. Customers with concerns or questions about the Voluntary Elk Recall can
call 1-800-680-4375. The safety of our customer has always been and always will
be our number one priority.
Exotic Meats USA requests that for those customers who have products with
the production dates in question, do not consume or sell them and return them to
the point of purchase. Customers should return the product to the vendor. The
vendor should return it to the distributor and the distributor should work with
the state to decide upon how best to dispose. If the consumer is disposing of
the product he/she should consult with the local state EPA office.
#
COLORADO: Farmer's market meat recalled after testing positive for
CWD
24.dec.08 9News.com Jeffrey Wolf
Elk meat that was sold at a farmer's market is being recalled because tests
show it was infected with chronic wasting disease. The Boulder County Health
Department and Colorado Department of Public Health and Environment issued the
recall Wednesday after the meat was sold at the Boulder County Fairgrounds on
Dec. 13. Although there isn't any human health risk connected with CWD, the
recalled was issued as a precaution. About 15 elk were bought from a commercial
ranch in Colorado in early December and processed at a licensed plant. All 15
were tested for CWD and one came up positive. The labeling on the product would
have the following information: *Seller: High Wire Ranch *The type of cut:
"chuck roast," "arm roast," "flat iron," "ribeye steak," "New York steak,"
"tenderloin," "sirloin tip roast," "medallions" or "ground meat." *Processor:
Cedaredge Processing *The USDA triangle containing the number "34645" People
with questions about this meat can contact John Pape, epidemiologist at the
Colorado Department of Public Health and Environment at 303-692-2628.
COULD NOT FIND any warning or recalls on these two sites confirming their
recall of CWD infected meat. ...TSS
Wednesday, April 06, 2011
Presence and Seeding Activity of Pathological Prion Protein (PrPTSE) in
Skeletal Muscles of White-Tailed Deer Infected with Chronic Wasting Disease
Prion Infectivity in Fat of Deer with Chronic Wasting Disease
Brent Race,# Kimberly Meade-White,# Richard Race, and Bruce Chesebro* Rocky
Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840
Received 2 June 2009/ Accepted 24 June 2009
ABSTRACT Top ABSTRACT TEXT REFERENCES
Chronic wasting disease (CWD) is a neurodegenerative prion disease of
cervids. Some animal prion diseases, such as bovine spongiform encephalopathy,
can infect humans; however, human susceptibility to CWD is unknown. In
ruminants, prion infectivity is found in central nervous system and lymphoid
tissues, with smaller amounts in intestine and muscle. In mice, prion
infectivity was recently detected in fat. Since ruminant fat is consumed by
humans and fed to animals, we determined infectivity titers in fat from two
CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD
infectivity and might be a risk factor for prion infection of other
species.
snip...
The highest risk of human contact with CWD might be through exposure to
high-titer CNS tissue through accidental skin cuts or corneal contact at the
time of harvest and butchering. However, the likelihood of a human consuming fat
infected with a low titer of the CWD agent is much higher. It is impossible to
remove all the fat present within muscle tissue, and fat consumption is
inevitable when eating meat. Of additional concern is the fact that meat from an
individual deer harvested by a hunter is typically consumed over multiple meals
by the same group of people. These individuals would thus have multiple
exposures to the CWD agent over time, which might increase the chance for
transfer of infection.
In the Rocky Mountain region of North America, wild deer are subject to
predation by wolves, coyotes, bears, and mountain lions. Although canines such
as wolves and coyotes are not known to be susceptible to prion diseases, felines
definitely are susceptible to BSE (9) and might also be infected by the CWD
agent. Deer infected with the CWD agent are more likely to be killed by
predators such as mountain lions (11). Peripheral tissues, including lymph
nodes, muscle, and fat, which harbor prion infectivity are more accessible for
consumption than CNS tissue, which has the highest level of infectivity late in
disease. Therefore, infectivity in these peripheral tissues may be important in
potential cross-species CWD transmissions in the wild.
The present finding of CWD infectivity in deer fat tissue raises the
possibility that prion infectivity might also be found in fat tissue of other
infected ruminants, such as sheep and cattle, whose fat and muscle tissues are
more widely distributed in both the human and domestic-animal food chains.
Although the infectivity in fat tissues is low compared to that in the CNS,
there may be significant differences among species and between prion strains.
Two fat samples from BSE agent-infected cattle were reported to be negative by
bioassay in nontransgenic RIII mice (3, 6). However, RIII mice are
10,000-fold-less sensitive to BSE agent infection than transgenic mice
expressing bovine PrP (4). It would be prudent to carry out additional
infectivity assays on fat from BSE agent-infected cattle and scrapie
agent-infected sheep using appropriate transgenic mice or homologous species to
determine the risk from these sources.
0C7.04
North American Cervids Harbor Two Distinct CWD Strains
Authors
Angers, R. Seward, T, Napier, D., Browning, S., Miller, M., Balachandran
A., McKenzie, D., Hoover, E., Telling, G. 'University of Kentucky; Colorado
Division of Wildlife, Canadian Food Inspection Agency; University Of Wisconsin;
Colorado State University.
Content
Despite the increasing geographic distribution and host range of CWD,
little is known about the prion strain(s) responsible for distinct outbreaks of
the disease. To address this we inoculated CWD-susceptible Tg(CerPrP)1536+/·
mice with 29 individual prion samples from various geographic locations in North
America. Upon serial passage, intrastudy incubation periods consistently
diverged and clustered into two main groups with means around 210 and 290 days,
with corresponding differences in neuropathology. Prion strain designations were
utilized to distinguish between the two groups: Type I CWD mice succumbed to
disease in the 200 day range and displayed a symmetrical pattern of vacuolation
and PrPSc deposition, whereas Type II CWD mice succumbed to disease near 300
days and displayed a strikingly different pattern characterized by large local
accumulations of florid plaques distributed asymmetrically. Type II CWD bears a
striking resemblance to unstable parental scrapie strains such as 87A which give
rise to stable, short incubation period strains such as ME7 under certain
passage conditions. In agreement, the only groups of CWD-inoculated mice with
unwavering incubation periods were those with Type I CWD. Additionally,
following endpoint titration of a CWD sample, Type I CWD could be recovered only
at the lowest dilution tested (10-1), whereas Type II CWD was detected in mice
inoculated with all dilutions resulting in disease. Although strain properties
are believed to be encoded in the tertiary structure of the infectious prion
protein, we found no biochemical differences between Type I and Type II CWD. Our
data confirm the co·existence of two distinct prion strains in CWD-infected
cervids and suggest that Type II CWD is the parent strain of Type I CWD.
see page 29, and see other CWD studies ;
Sunday, November 23, 2008
PRION October 8th - 10th 2008 Book of Abstracts
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A
WISCONSIN STRAIN OF CWD
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of
Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2
Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary
Research Institute, 4.Center for Prions and Protein Folding Diseases, 5
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
T6G 2P5
The identification and characterization of prion strains is increasingly
important for the diagnosis and biological definition of these infectious
pathogens. Although well-established in scrapie and, more recently, in BSE,
comparatively little is known about the possibility of prion strains in chronic
wasting disease (CWD), a disease affecting free ranging and captive cervids,
primarily in North America. We have identified prion protein variants in the
white-tailed deer population and demonstrated that Prnp genotype affects the
susceptibility/disease progression of white-tailed deer to CWD agent. The
existence of cervid prion protein variants raises the likelihood of distinct CWD
strains. Small rodent models are a useful means of identifying prion strains. We
intracerebrally inoculated hamsters with brain homogenates and phosphotungstate
concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD
endemic area) and experimentally infected deer of known Prnp genotypes. These
transmission studies resulted in clinical presentation in primary passage of
concentrated CWD prions. Subclinical infection was established with the other
primary passages based on the detection of PrPCWD in the brains of hamsters and
the successful disease transmission upon second passage. Second and third
passage data, when compared to transmission studies using different CWD inocula
(Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin
white-tailed deer population is different than the strain(s) present in elk,
mule-deer and white-tailed deer from the western United States endemic
region.
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
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated.
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains.
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
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
1978 SCRAPIE IN CONFIDENCE SCJD
1979
SILENCE ON CJD AND SCRAPIE
1980
SILENCE ON CJD AND SCRAPIE
*** 1981 NOVEMBER
Thursday, August 04, 2016
*** MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL
SCJD
2016
SCRAPIE AND CWD ZOONOSIS
PRION 2016 CONFERENCE TOKYO
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Transmission of scrapie prions to primate after an extended silent
incubation period
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
Transmission of scrapie prions to primate after an extended silent
incubation period
Emmanuel E. Comoy , Jacqueline Mikol , Sophie Luccantoni-Freire , Evelyne
Correia , Nathalie Lescoutra-Etchegaray , Valérie Durand , Capucine Dehen ,
Olivier Andreoletti , Cristina Casalone , Juergen A. Richt , Justin J. Greenlee
, Thierry Baron , Sylvie L. Benestad , Paul Brown & Jean-Philippe Deslys
Abstract
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion
disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD)
in humans and having guided protective measures for animal and human health
against animal prion diseases. Recently, partial transmissions to humanized mice
showed that the zoonotic potential of scrapie might be similar to c-BSE. We here
report the direct transmission of a natural classical scrapie isolate to
cynomolgus macaque, a highly relevant model for human prion diseases, after a
10-year silent incubation period, with features similar to those reported for
human cases of sporadic CJD. Scrapie is thus actually transmissible to primates
with incubation periods compatible with their life expectancy, although fourfold
longer than BSE. Long-term experimental transmission studies are necessary to
better assess the zoonotic potential of other prion diseases with high
prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98
scrapie.
snip...
In addition to previous studies on scrapie transmission to primate1,8,9 and
the recently published study on transgenic humanized mice13, our results
constitute new evidence for recommending that the potential risk of scrapie for
human health should not be dismissed. Indeed, human PrP transgenic mice and
primates are the most relevant models for investigating the human transmission
barrier. To what extent such models are informative for measuring the zoonotic
potential of an animal TSE under field exposure conditions is unknown. During
the past decades, many protective measures have been successfully implemented to
protect cattle from the spread of c-BSE, and some of these measures have been
extended to sheep and goats to protect from scrapie according to the principle
of precaution. Since cases of c-BSE have greatly reduced in number, those
protective measures are currently being challenged and relaxed in the absence of
other known zoonotic animal prion disease. We recommend that risk managers
should be aware of the long term potential risk to human health of at least
certain scrapie isolates, notably for lymphotropic strains like the classical
scrapie strain used in the current study. Relatively high amounts of infectivity
in peripheral lymphoid organs in animals infected with these strains could lead
to contamination of food products produced for human consumption. Efforts should
also be maintained to further assess the zoonotic potential of other animal
prion strains in long-term studies, notably lymphotropic strains with high
prevalence like CWD, which is spreading across North America, and atypical/Nor98
scrapie (Nor98)50 that was first detected in the past two decades and now
represents approximately half of all reported cases of prion diseases in small
ruminants worldwide, including territories previously considered as scrapie
free. Even if the prevailing view is that sporadic CJD is due to the spontaneous
formation of CJD prions, it remains possible that its apparent sporadic nature
may, at least in part, result from our limited capacity to identify an
environmental origin.
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
2015
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, Valerie 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 long 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***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Summary
The previous assessment concentrated on the incursion of disease from North
America through the imports of animal feed or the movement of contaminated
clothing, footwear and equipment. The results suggested that import of pet feed
was a non-negligible risk, but given the unlikely contact of resident deer in GB
with such non-ruminant feed, this was considered overall a negligible to very
low risk. The movement of contaminated clothing, footwear or equipment
(particularly hunting equipment) could pose a very low risk, although the volume
of contaminated soil which would need to be ingested to give rise to an
infection is likely to be higher than would be present. There is a variable
level uncertainty in all these assessments.
The new assessment focuses on an additional potential route of entry: the
importation of natural deer urine lures. The main conclusions from this
assessment are:
In areas of North America where CWD has been reported, given that CWD is
excreted in faeces, saliva, urine and blood, and survives in the environment for
several years there is a medium probability that the deer urine in North America
contains CWD (high uncertainty; depends on the source of deer used for
production).
The risk of a deer in GB being infected per 30 ml bottle of urine
imported from the USA is very low, albeit with high uncertainty. Overall it is
concluded that the risk of at least one infection of deer in the UK with CWD per
year from deer urine lures imported from the USA is medium. This assumes a high
number of 30 ml bottles imported per year from all areas of the USA.
None of the species affected by CWD in North America are present in GB.
For a British species to become infected with CWD following exposure, the dose
and inherent susceptibility of the species will be important. Based on current
scientific evidence Red deer (Cervus elaphus elaphus) are susceptible to CWD,
Fallow deer (Dama dama) are likely to be less susceptible and Roe deer
(Capreolus capreolus) have a gene conferring susceptibility. Therefore, it is
likely that given exposure to an infectious dose of CWD, deer in GB could become
infected with CWD.
Overall, the probability of importing CWD into GB from North America and
causing infection in British deer is uncertain but likely to be negligible to
very low via movement of deer hunters, other tourists and British servicemen and
very low via imported (non-
2
ruminant) animal feed and medium for the use of lures. However, if it was
imported and (a) deer did become infected with CWD, the consequences would be
severe as eradication of the disease is impossible, it is clinically
indistinguishable from BSE infection in deer (Dalgleish et al., 2008) and
populations of wild and farmed deer would be under threat.
The USA has implemented a Herd Certification Programme for farmed and
captive cervids. So far, 29 States are approved for HCP status (APHIS, 2015).
The list includes States such as Colorado, where CWD is present, therefore it is
recommended that any sourcing of such natural urine lures should be not only
from States with an HCP programme, but also from a herd which is registered as
being regularly tested free of CWD.
Animal urine is not considered a commodity which is subject to animal
by-products legislation for imports. Internet sales are common and although a
license would be required, there are no conditions for the safe sourcing of such
products. Deer urine lures are also available in Europe and may be produced from
carcases of hunted deer. The use of deer urine produced from a species not
present in Europe (such as white tailed deer) is questioned for its value with
native GB deer according to the British Deer Society survey.
Background
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
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...
What is the risk of chronic wasting disease 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 well as non-ruminants such as cats and dogs as
well, as soon as possible for the following reasons...
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Terry Singeltary Sr. comment ;
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards
Singeltary Comment Submission
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
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.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***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 environmentally relevant 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.
see ;
with CWD TSE Prions, I am not sure there is any absolute yet, other than
what we know with transmission studies, and we know tse prion kill, and tse
prion are bad. science shows to date, that indeed soil, dirt, some better than
others, can act as a carrier. same with objects, farm furniture. take it with
how ever many grains of salt you wish, or not. if load factor plays a role in
the end formula, then everything should be on the table, in my opinion. see
;
***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 environmentally relevant 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.
see ;
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil
Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable
neurological diseases likely caused by a misfolded form of the prion protein.
TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’
disease) in cattle, chronic wasting disease in deer and elk, and
Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are
unique among TSEs because they can be transmitted between animals, and the
disease agents appear to persist in environments previously inhabited by
infected animals. Soil has been hypothesized to act as a reservoir of
infectivity and to bind the infectious agent. In the current study, we orally
dosed experimental animals with a common clay mineral, montmorillonite, or whole
soils laden with infectious prions, and compared the transmissibility to unbound
agent. We found that prions bound to montmorillonite and whole soils remained
orally infectious, and, in most cases, increased the oral transmission of
disease compared to the unbound agent. The results presented in this study
suggest that soil may contribute to environmental spread of TSEs by increasing
the transmissibility of small amounts of infectious agent in the
environment.
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
>>>Particle-associated PrPTSE molecules may migrate from locations
of deposition via transport processes affecting soil particles, including
entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several
years. Significant interest remains in developing methods that could be applied
to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests
that serine proteases and the microbial consortia in stimulated soils and
compost may partially degrade PrPTSE. Transition metal oxides in soil (viz.
manganese oxide) may also mediate prion inactivation. Overall, the effect of
prion attachment to soil particles on its persistence in the environment is not
well understood, and additional study is needed to determine its implications on
the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding,
inferring a durable environmental reservoir, and an efficient mechanism for
indirect horizontal CWD transmission.
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600°C. It has been assumed, without proof, that incineration totally inactivates
the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Histochemical analysis of hamster brains inoculated with the solid residue
showed typical spongiform degeneration and vacuolation. Re-inoculation of these
brains into a new cohort of hamsters led to onset of clinical scrapie symptoms
within 75 days, suggesting that the specific infectivity of the prion protein
was not changed during the biodiesel process. The biodiesel reaction cannot be
considered a viable prion decontamination method for MBM, although we observed
increased survival time of hamsters and reduced infectivity greater than 6 log
orders in the solid MBM residue. Furthermore, results from our study compare for
the first time prion detection by Western Blot versus an infectivity bioassay
for analysis of biodiesel reaction products. We could show that biochemical
analysis alone is insufficient for detection of prion infectivity after a
biodiesel process.
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative
assessment is described that estimates the amount of TSE infectivity that is
present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for
cattle and classical/atypical scrapie for sheep and lambs) and the amounts that
subsequently fall to the floor during processing at facilities that handle
specified risk material (SRM). BSE in cattle was found to contain the most oral
doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to
a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep
infected with classical and atypical scrapie, respectively. Lambs contained the
least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie
and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity
falling to the floor and entering the drains from slaughtering a whole carcass
at SRM facilities were found to be from cattle infected with BSE at rendering
and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate
plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and
collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains
are from lambs infected with classical and atypical scrapie at intermediate
plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO
ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key
inputs for the model in the companion paper published here.
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
Tuesday, July 12, 2016
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE,
TSE, Prion Zoonosis Science History
see history of NIH may destroy human brain collection
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild ***
Sunday, July 17, 2016
*** CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
***
***at present, no cervid PrP allele conferring absolute resistance to prion
infection has been identified.
P-145 Estimating chronic wasting disease resistance in cervids using real
time quaking- induced conversion
Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David
Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2
1 Department of Microbiology and Immunology, Midwestern University, United
States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State
University; 3Prion Research Center; Colorado State University; 4U.S. Geological
Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural
Research Service, United States Department of Agriculture; 6Canadian Food
Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWO
In mammalian species, the susceptibility to prion diseases is affected, in
part, by the sequence of the host's prion protein (PrP). In sheep, a gradation
from scrapie susceptible to resistant has been established both in vivo and in
vitro based on the amino acids present at PrP positions 136, 154, and 171, which
has led to global breeding programs to reduce the prevalence of scrapie in
domestic sheep. In cervids, resistance is commonly characterized as a delayed
progression of chronic wasting disease (CWD); at present, no cervid PrP allele
conferring absolute resistance to prion infection has been identified. To model
the susceptibility of various naturally-occurring and hypothetical cervid PrP
alleles in vitro, we compared the amplification rates and efficiency of various
CWD isolates in recombinant PrPC using real time quaking-induced conversion. We
hypothesized that amplification metrics of these isolates in cervid PrP
substrates would correlate to in vivo susceptibility - allowing susceptibility
prediction for alleles found at 10 frequency in nature, and that there would be
an additive effect of multiple resistant codons in hypothetical alleles. Our
studies demonstrate that in vitro amplification metrics predict in vivo
susceptibility, and that alleles with multiple codons, each influencing
resistance independently, do not necessarily contribute additively to
resistance. Importantly, we found that the white-tailed deer 226K substrate
exhibited the slowest amplification rate among those evaluated, suggesting that
further investigation of this allele and its resistance in vivo are warranted to
determine if absolute resistance to CWD is possible.
***at present, no cervid PrP allele conferring absolute resistance to prion
infection has been identified.
PRION 2016 CONFERENCE TOKYO
Tuesday, August 9, 2016
*** Concurrence with OIE Risk Designations for Bovine Spongiform
Encephalopathy [Docket No. APHIS-2015-0055]
Saturday, July 23, 2016
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING,
AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Tuesday, July 26, 2016
*** Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY
2016
Saturday, July 16, 2016
*** Importation of Sheep, Goats, and Certain Other Ruminants [Docket No.
APHIS-2009-0095]RIN 0579-AD10
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS,
are working to further legalize the trading of Transmissible Spongiform
Encephalopathy TSE Pion disease around the globe.
THIS is absolutely insane. it’s USDA INC.
Thursday, October 22, 2015
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk
mad cow disease USDA and what really happened those mad cows in Texas ***
Monday, June 20, 2016
*** Specified Risk Materials SRMs BSE TSE Prion Program ***
Thursday, April 14, 2016
Arizona 22 year old diagnosed with Creutzfeldt Jakob Disease CJD
Thursday, January 15, 2015
41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE
Prion: Case Report
Saturday, January 17, 2015
*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed
with the extremely rare Creutzfeldt-Jakob disease
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
Sunday, August 21, 2016
Kay Ellen Roedl Schwister Deceased August 7, 2016 at the age of 53 with
Creutzfeldt-Jakob disease CJD TSE Prion spontaneous sporadic, zoonosis, or
iatrogenic?
Monday, August 22, 2016
CREUTZFELDT JAKOB DISEASE USA 2015 SPORADIC CJD TOTAL FIGURES REACHES
HIGHEST ANNUAL COUNT TO DATE AT 239 CONFIRMED CASES
*** Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle ***
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
”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.
Sunday, August 28, 2016
CONFIDENTIAL
Transmissible Spongiform Encephalopathy TSE Prion and how Politics and
Greed by the Industry spread madcow type diseases from species to species and
around the globe
TSE PRIONS AKA MAD COW TYPE DISEASE, LIONS AND TIGERS AND BEARS, OH MY!
Texas Intrastate – within state movement of all Cervid or Trucking Chronic
Wasting Disease CWD TSE Prion Moratorium
Monday, July 18, 2016
Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers
Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster
*** TEXAS Thirteen new cases of chronic wasting disease (CWD) were
confirmed at a Medina County captive white-tailed deer breeding facility on June
29, 2016***
*** How Did CWD Get Way Down In Medina County, Texas?
DISCUSSION Observations of natural outbreaks of scrapie indicated that the
disease spread from flock to flock by the movement of infected, but apparently
normal, sheep which were incubating the disease.
There was no evidence that the disease spread to adjacent flocks in the
absent of such movements or that vectors or other host species were involved in
the spread of scrapie to sheep or goats; however, these possibilities should be
kept open...
Tuesday, August 02, 2016
TEXAS TPWD Sets Public Hearings on Deer Movement Rule Proposals in Areas
with CWD Rule Terry S. Singeltary Sr. comment submission
Thursday, August 25, 2016
TPWD Action Disease Detection and Response – Chronic Wasting Disease TPW
Commission Adopts New CWD Zones, Deer Movement Rules August 25, 2016
This map shows the recently imposed Surveillance Zone for CWD in portions
of Bandera, Medina and Uvalde counties.
Arkansas Chronic Wasting Disease CWD TSE Prion Potentially Trucked in from
Missouri, what about Florida and ?
Wednesday, July 27, 2016
Arkansas CWD 101 positive cases documented to date, Biologists to take
additional samples in in southern Pope County, Aug. 1-5
Tuesday, May 03, 2016
Arkansas Chronic Wasting Disease CWD TSE Prion and Elk Restoration Project
and Hunkering Down in the BSE Situation Room USDA 1998
Monday, August 29, 2016
*** NWHC USGS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE ***
Thursday, August 18, 2016
*** PROCEEDINGS ONE HUNDRED AND Nineteenth ANNUAL MEETING of the USAHA BSE,
CWD, SCRAPIE, PORCINE TSE PRION October 22 28, 2015 ***
Friday, August 26, 2016
Journal Journal of Toxicology and Environmental Health, Part A Volume 79,
2016 - Issue 16-17 Prion Research in Perspective IV
*** CANADA BSE CWD SCRAPIE CJD TSE Prion Disease ***
Monday, August 22, 2016
CREUTZFELDT JAKOB DISEASE USA 2015 SPORADIC CJD TOTAL FIGURES REACHES
HIGHEST ANNUAL COUNT TO DATE AT 239 CONFIRMED CASES
Terry S. Singeltary Sr.
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