WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Wisconsin Chronic Wasting Disease CWD TSE Prion
Wisconsin Farm-Raised Deer
As of 2015 there were 421 registered deer farms in Wisconsin. White-tailed
deer farming is regulated and licensed by the Wisconsin Department of
Agriculture, Trade and Consumer Protection (DATCP) [exit DNR]. However the
Department of Natural Resources (DNR) is responsible for regulating white-tailed
deer farm fencing. Before you can register your farm with DATCP you must have
your fence inspected and receive a deer farm fence certificate from the
DNR.
Wisconsin Deer Farm Map numbers at 458 Farms
Wisconsin Chronic Wasting Disease CWD TSE Prion Positives Map
CWD prevalence in Wisconsin
There appears to be two central areas of CWD infection in Wisconsin. One is
centered in western Dane and eastern Iowa counties. The other is located in
northern Illinois and extends into southeastern Wisconsin. Analyses of the
geographic distribution of disease show that the disease is not evenly
distributed throughout the affected area. Disease prevalence is much higher near
the centers of each infection and declines with increasing distance from the
center as would be expected with this introduced disease which is now endemic in
southern Wisconsin.
CWD prevalence has also changed over time. Since 2002, CWD prevalence
within our western monitoring area has shown an overall increasing trend in all
sex and age classes. During the past 14 years, the trend in prevalence in adult
males has risen from 8-10 percent to about 30 percent and in adult females from
about 3-4 percent to nearly 15 percent. During that same time, the prevalence
trend in yearling males has increased from about 2 percent to about 10 percent
and in yearling females from roughly 2 percent to about 8 percent.
Surveillance and result maps Wisconsin geographic distribution of disease
and the number of deer that have been tested.
The points on the map include prevalence graphs. The graphs for these study
area show estimates of trend curves for yearling and adult males (blue) and
females (yellow) during 2002-2015. These annual monitoring data are important
for Wisconsin's understanding of CWD distribution and prevalence.
Wisconsin's chronic wasting disease response plan The department developed
a plan as a tool for guidance with chronic wasting disease (CWD). This 15 year
plan is to be used from 2010-2025.
CWD response plan details After multiple years of CWD management in
Wisconsin, it is increasingly clear that controlling CWD in Wisconsin's
free-ranging white-tailed deer will be extremely challenging and will require a
commitment of human and financial resources over an extended period of time. The
department developed the following plan recognizing its public trust
responsibility for managing wildlife and ensuring the health of wildlife
populations in the state. However, waning public support and limited fiscal
resources have limited the department's ability to fully implement the plan.
Download the entire 15 year CWD Response Plan [PDF]
Wisconsin’s Chronic Wasting Disease Response Plan: 2010–2025
Wisconsin Captive wildlife regulations and licenses
”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.
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
J Vet Diagn Invest 20:698–703 (2008)
Chronic wasting disease in a Wisconsin white-tailed deer farm
Delwyn P. Keane,1 Daniel J. Barr, Philip N. Bochsler, S. Mark Hall, Thomas
Gidlewski, Katherine I. O’Rourke, Terry R. Spraker, Michael D. Samuel
Abstract.
In September 2002, chronic wasting disease (CWD), a prion disorder of
captive and wild cervids, was diagnosed in a white-tailed deer (Odocoileus
virginianus) from a captive farm in Wisconsin. The facility was subsequently
quarantined, and in January 2006 the remaining 76 deer were depopulated. Sixty
animals (79%) were found to be positive by immunohistochemical staining for the
abnormal prion protein (PrPCWD) in at least one tissue; the prevalence of
positive staining was high even in young deer. Although none of the deer
displayed clinical signs suggestive of CWD at depopulation, 49 deer had
considerable accumulation of the abnormal prion in the medulla at the level of
the obex. Extraneural accumulation of the abnormal protein was observed in 59
deer, with accumulation in the retropharyngeal lymph node in 58 of 59 (98%), in
the tonsil in 56 of 59 (95%), and in the rectal mucosal lymphoid tissue in 48 of
58 (83%). The retina was positive in 4 deer, all with marked accumulation of
prion in the obex. One deer was considered positive for PrPCWD in the brain but
not in the extraneural tissue, a novel observation in white-tailed deer. The
infection rate in captive deer was 20- fold higher than in wild deer. Although
weakly related to infection rates in extraneural tissues, prion genotype was
strongly linked to progression of prion accumulation in the obex. Antemortem
testing by biopsy of recto– anal mucosal-associated lymphoid tissue (or other
peripheral lymphoid tissue) may be a useful adjunct to tonsil biopsy for
surveillance in captive herds at risk for CWD infection.
Key words: Cervids; chronic wasting disease; prion; transmissible
spongiform encephalopathy.
WISCONSIN CHRONIC WASTING DISEASE CWD CASES OUT OF CONTROL
Wednesday, March 16, 2016
Wisconsin CWD sample survey 2015 confirms 290 cases of Chronic Wasting
Disease TSE Prion
Wednesday, February 10, 2016
*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD
***
Tuesday, January 19, 2016
Wisconsin Second CWD-positive deer found in Oneida County 5-year-old buck
shot at Three Lakes Trophy Ranch LLC agency received the CWD-positive report on
the animal Dec. 29
Friday, January 29, 2016
Wisconsin CWD-positive white-tailed deer found on Iowa County farm January
29, 2016
State pays farmer $298,000 for infected deer herd
Jan. 16, 2016 8:05 p.m.
The State of Wisconsin paid nearly $300,000 to the Eau Claire County farmer
whose deer herd was depopulated after it was found to be infected with chronic
wasting disease.
Rick Vojtik, owner of Fairchild Whitetails in Fairchild, received an
indemnity payment of $298,770 for 228 white-tailed deer killed on his farm,
according to officials with the Department of Agriculture, Trade and Consumer
Protection.
The money was taken from the agency's general program revenue funded by
Wisconsin taxpayers.
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
Monday, January 16, 2012
9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD
Friday, December 04, 2015
Wisconsin CWD-positive white-tailed deer found on Oneida County hunting
preserve December 3, 2015
Thursday, November 19, 2015
Wisconsin Eau Claire Co. deer herd two day round of depopulation CWD
testing shows 23 positive
Wednesday, December 16, 2015
Wisconsin Chronic wasting disease confirmed in Crawford County buck
harvested on private land
Friday, December 04, 2015
Wisconsin CWD-positive white-tailed deer found on Oneida County hunting
preserve December 3, 2015
Wednesday, September 16, 2015
WISCONSIN CAPTIVE CERVID INDUSTRY RUNNING WILD AND ON THE LOOSE RISKING
FURTHER SPREAD OF CWD
Wednesday, March 04, 2015
Disease sampling results provide current snapshot of CWD in Wisconsin
finding 324 positive detections statewide in 2014
Tuesday, October 07, 2014
*** Wisconsin white-tailed deer tested positive for CWD on a Richland
County breeding farm, and a case of CWD has been discovered on a Marathon County
hunting preserve
Friday, April 04, 2014
*** Wisconsin State officials kept silent on CWD discovery at game farm
Tuesday, February 11, 2014
Wisconsin tracks 81 deer from game farm with CWD buck to seven other states
Tuesday, December 17, 2013
Wisconsin Second CWD positive deer found in Grant County
Monday, December 02, 2013
WISCONSIN CHRONIC WASTING DISEASE CWD DISCOVERED MARATHON COUNTY HUNTING
PRESERVE
Sunday, November 03, 2013
Wisconsin Second CWD deer found in Portage County
Wisconsin : 436 Deer Have Escaped From Farms to Wild
Date: March 18, 2003 Source: Milwaukee Journal Sentinel snip...
Sunday, November 03, 2013
Wisconsin Second CWD deer found in Portage County
Second CWD deer found in Portage County
News Release
Published: November 1, 2013 by the Northwest Region Contact(s): Kris
Johansen, DNR area wildlife supervisor, 715-284-1430; Ed Culhane,
DNR communications, 715-781-1683 WISCONSIN RAPIDS – A deer harvested by a
bow hunter in southeast Portage County has tested positive for chronic wasting
disease, the state Department of Natural Resources reports. This is the second
CWD-positive wild deer found in the county. Wildlife biologists in central
Wisconsin now are asking bow hunters to assist with increased surveillance for
the disease in four separate areas where positives have been confirmed outside
the CWD management zone.
CWD is contagious and fatal for deer, elk and moose. “Last fall CWD was
discovered for the first time in three wild, white-tailed deer in Adams, Juneau
and Portage counties” said DNR area wildlife supervisor Kris Johansen. “Now we
have a second positive in a different area of Portage County. To better define
the geographic extent of CWD in central Wisconsin, we are focusing additional
surveillance around each of these four locations.”
The latest CWD positive deer was harvested Oct. 6 just northwest of Almond
in Portage County.
To view where the surveillance focus areas are located, hunters can go to
the DNR website and enter “CWD registration” in the key word search, then click
on “CWD registration and sampling.” On this page – http://dnr.wi.gov/topic/wildlifehabitat/registersample.html
– detailed maps show the precise location of these surveillance circles for the
first three positives, the ones in Adams and Juneau counties and the first find
in Portage County, located in the northwest corner of the county.
There is also a map showing the two Portage County locations. A new map,
showing the precise surveillance area for the fourth positive, in southeast
Portage County, will be added to the web page as soon as it is prepared. This
page also links to a list of cooperating taxidermists and meat processors where
samples can be collected.
The DNR is asking hunters to work with these cooperators to have head and
lymph node samples from adult deer – harvested within the four focus areas –
removed for testing. To have the sample removed, the hunter can bring the whole
deer to one of the listed cooperators or just remove the head with at least
three inches of neck attached and bring that in for sampling.
“Please call ahead to set up an appointment,” Johansen said. “These are
private business operators who are helping us out, and we want to respect their
time and their schedules.” This list will be updated online as new cooperators
join the surveillance effort:
• Wisconsin River Meats, N5340 County HH, Mauston 608-847-7413
• A&B Butchering, 6971 Hwy 34, Rudolph 715-435-3893
• Strickly Wild Processing, 140 Buffalo St, Wisconsin Rapids 715-421-0587
• Hartnell's Wild Game Processing, 1925 Cypress Ave., Arkdale 608-339-7288
• Trevor Athens Taxidermy, 982 15th Ave., Arkdale 608-547-6117
• Tall Tines Taxidermy, N2621 Cassidy Road, Mauston 608-547-0818
• Todd's Wildlife Taxidermy, N2148 State 58, Mauston 608-847-7693
• Vollmer Taxidermy, 3631 Plover Road, Plover 715-345-1934
• Field and Stream Taxidermy, 217 S. Front St., Coloma 608-547-1565
• DNR Service Center, 473 Griffith Ave., Wisconsin Rapids 715-421-7813
• Mead Wildlife Area, S2148 County S, Milladore 715-457-6771
• Adams Ranger Station, 532 N. Adams St., Adams 608-339-4819
• Almond Market, 111 Main St., Almond 715-366-2002
Hunters may also have deer from any of the four focus areas tested for CWD
by contacting one of these DNR offices:
• Mead Wildlife Area headquarters, S2148 County S, Milladore – 715-457-6771
• WI Rapids Service Center, 473 Griffith Avenue, Wisconsin Rapids –
715-421-7813
• Adams-Friendship Ranger Station, 532 N. Main Street, Adams – 608-339-4819
On the weekends or during warm periods, hunters should remove the deer head
with at least three inches of neck attached, freeze the head and then contact
the DNR to arrange a drop off. DNR staff will also collect samples from
hunter-harvested deer on the opening weekend of the gun deer season. Collection
stations and hours will be published prior to the gun deer season. The CWD tests
are free to hunters. Each person who submits a head for testing will receive lab
results within three or four weeks. http://dnr.wi.gov/news/BreakingNews_Lookup.asp?id=2996
Monday, September 16, 2013
CWD Wisconsin Updated on 9-16-2013 : Item 3C3 - related to deer management,
hunting, and implementation of the 2012 White-tailed Deer Trustee’s Report
Thursday, June 13, 2013
WISCONSIN DEER FARMING Chronic Wasting Disease CWD DATCP
Thursday, April 04, 2013
Wisconsin DNR confirms second case of Chronic Wasting Disease in Waukesha
County
Monday, April 01, 2013
Dr. Deer/Dough from Texas on Wisconsin’s CWD implementation survey, is now
available
Wednesday, February 06, 2013
Wisconsin Deer tests positive for CWD in Waukesha County
Wednesday, January 02, 2013
Wisconsin First CWD-positive wild deer detected in Portage and Juneau
Counties
Friday, December 14, 2012 2:35 PM
Deer tests positive for CWD in Adams County
Tuesday, December 11, 2012
Wisconsin Receives Federal Approval for CWD Herd Certification Program for
Farm-raised Deer
Monday, December 03, 2012
WISCONSIN Deer from Racine County has tested positive for CWD
Monday, April 02, 2012
WISCONSIN Washburn County deer test positive for Chronic Wasting Disease
(CWD)
Saturday, February 04, 2012
*** Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
Monday, January 16, 2012
9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD
see full text and more here ;
2010 WISCONSIN CAPTIVE DEER ESCAPES
There were 26 reported escape incidents so far this year, this amounted to
20 actual confirmed escape incidents because 3 were previously reported, 2 were
confirmed as wild deer, and 1 incident was not confirmed. ... snip... C. &
D. Captive Cervid and Law Enforcement Update (11:10 AM)- Warden Pete Dunn gave
the captive cervid farm update. There were 26 reported escape incidents so far
this year, this amounted to 20 actual confirmed escape incidents because 3 were
previously reported, 2 were confirmed as wild deer, and 1 incident was not
confirmed. Approximately 30% of these escapes were caused by gates being left
open and the other 70% resulted from bad fencing or fence related issues. The 20
actual confirmed escape incidents amounted to 77 total animals. 50 of the
escaped animals were recovered or killed and 27 were not recovered and remain
unaccounted for. Last year the CWD Committee passed a resolution to require
double gates, but this has not gone into effect yet. Questions were raised by
the committee about double fencing requirements? Pete responded that double
fencing has not been practical or accepted by the industry. The DNR has the
authority to do fence inspections. ?If a fence fails to pass the inspection the
fencing certificate can be revoked and the farmer can be issued a citation. This
year three citations and one warning have been issued for escapes. Pete reviewed
the reporting requirements for escape incidents that these must be reported
within 24 hours. The farmer then has 72 hours to recover the animals or else it
will affect the farm’s herd status and ability to move animals. Davin proposed
in the 15 year CWD Plan that the DNR take total control and regulatory authority
over all deer farm fencing. Larry Gohlke asked Pete about the reliability for
reporting escapes? Pete said that the majority of escapes were reported by the
farmer, but it is very difficult to determine when an escape actually occurred.
Pete said that they are more concerned that an escape is reported and not that
it is reported at the exact time that it happened.
The Wisconsin DNR has issued a report on the results of an audit of the
deer farms in their state. This is a very interesting report and sheds light on
the operation of these facilities. A couple of interesting findings is that DNR
investigators documented the escape of 436 deer into the wild from game farms.
These escapes are from approximately 1/3 of the deer facilities in the state.
Additionally, several cash transactions were uncovered where the required
shipping tags were not used and record keeping ranged from very meticulous to
trying to rely on memory. At one facility, investigators found partially burnt
records in a trashcan. The complete report can be downloaded at: http://www.dnr.state.wi.us/org/es/enforcement/docs/DeerFarmAudit.pdf.
Attempts in the legislature of Montana to negate or change the citizen vote
to ban game farms continue. Previously, several bills to overturn the ban had
been introduced or discussed. Citizen response has been to maintain the ban.
Current efforts are to provide a buy out to the operators of the remaining
facilities. The latest bill, introduced by Representative Jim Peterson would
provide funds to pay farmers up to $6,000 per animal. The bill will be heard in
the Montana Agriculture Committee, which has been friendly to operators in the
past.
In brief, the audits revealed:
• The majority of whitetail deer farm fences were in compliance with state
laws;
however, 77 farms were found to be in violation of fence specifications. As
with any other problem, violations were handled on a case by case basis taking
into account all of the circumstances.
• Deer farms contained at least 16,070 deer.
• Most deer farmers reported they have not experienced problems with
escapes; however, 182 deer farmers reported escapes or intentional releases into
the wild.
• Deer farmers reported at least 436 escaped deer that had not been
recovered or returned to farms.
• Twenty-four deer farms were unlicensed.
• Records maintained by deer farm operators ranged from meticulous
documentation to relying on memory.
• Wardens discovered a variety of law violations during the course of the
audit and inspection process, some of which they did not have jurisdiction to
pursue.
• Tracking of individual deer without individual identification was almost
impossible.
• Over the past three years at least 1,222 deer died on deer farms due to
various reasons. Disease testing was not performed nor required on the majority
of deer.
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Terry S. Singeltary Sr. says:
August 21, 2015 at 1:23 PM
good ol boy system alive and well in the great state of Texas, protect the
industry at all cost, including human and animal health.
where is the official announcement of this 4th case (or more cases), by the
TAHC and or the TPWD? we’re still waiting.
why is the media having to do the TAHC and or the TPWD job, and reporting
this critical information to the public domain?
of course, it took 7+ months and an act of Congress to finally confirm and
announce to the public that last mad cow in Texas as well. political science as
usual in Texas.
IF the state of Texas does not get serious real fast with CWD, and test all
those deer, that 5 year plan is a ticking time bomb waiting to happen.
all cervid tested after slaughter, and test results must be released to the
public.
the tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a
mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment
Processes.
IN fact, you should also know that the TSE Prion agent will survive in the
environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of
protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple
autoclave will not kill this TSE prion agent.
TEXAS DEER CZAR SENT TO WISCONSIN TO SOLVE CWD CRISIS, WHILE ROME (TEXAS)
BURNS
Tuesday, August 11, 2015
Wisconsin doing what it does best, procrastinating about CWD yet again
thanks to Governor Walker
From: Terry S. Singeltary Sr. Sent: Friday, April 03, 2015 10:14 AM To:
BSE-L@LISTS.AEGEE.ORG Subject: [BSE-L] Wisconsin Did Walker Cave In to Hunting
Lobby? Chronic Wasting Disease in deer is at all-time high
Did Walker Cave In to Hunting Lobby?
Chronic Wasting Disease in deer is at all-time high because of changes in
how DNR handles it.
By Bill Lueders, Wisconsin Center for Investigative Journalism - Apr 2nd,
2015 10:14 am
Sign-up for the Urban Milwaukee daily email
Chronic Wasting Disease Prevalence. Chronic Wasting Disease
Prevalence.
Patrick Durkin, the Waupaca-based outdoor writer, had some fun with a
recent state Department of Natural Resources press release regarding chronic
wasting disease.
The release documenting the unmitigated spread of the always-fatal brain
disease among deer, was titled: “Disease sampling results provide current
snapshot of CWD in Wisconsin.” Durkin, in a column, jokingly suggested a
comparable headline for a report on the sinking Titanic: “Damage-control party
assesses condition of ship’s hull.”
Though fewer deer are being tested, the incidence of the disease is up. In
the 2014 season, which ended March 31, more than 6 percent of the roughly 5,400
deer tested were positive, a DNR tally shows. That’s an all-time high disease
rate; as recently as 2008, it was below 2 percent.
More alarming still, the disease rate among adult male deer has reached 40
percent in north-central Iowa County and around 25 percent in two other sectors.
And CWD is no longer found only in southern Wisconsin.
Tami Ryan, the DNR’s wildlife health section chief, calls these numbers
“not a good news scenario” but also not unexpected, given that the state is no
longer attempting to manage the disease but is instead just monitoring its
distribution and prevalence. Earlier attempts to employ more aggressive
strategies were abandoned amid intense public opposition.
Now, 13 years after CWD was first discovered in Wisconsin, Ryan says many
hunters “just want things to go back to normal.”
That’s not likely to happen. A far more plausible scenario is that the
disease will continue to spread, infecting and killing deer, until the number of
animals available for hunters is seriously depleted. And then, look out.
“The research we’ve done shows the disease is in an accelerating pace,”
says Mike Samuel, a UW-Madison associate professor of wildlife ecology who
studies CWD. “It’s going to continue to rise at a rapid pace and it’s going to
continue to spread until the people decide we’ve had enough.”
And while Samuel sees no way to get rid of CWD, using currently available
strategies, he thinks it can be controlled through management practices. He
suggests killing more bucks, among whom the infection rate is highest, perhaps
by opening the gun hunting season earlier, when deer rut (mate).
But this, Samuel notes, is when bow hunters do their thing, and they are a
powerful lobby group. Past CWD-eradication strategies seen as detrimental to
herd size drew opposition from hunters and were axed by lawmakers and Gov. Scott
Walker. And Walker’s so-called “deer czar” recommended a more passive approach
to CWD.
“We have a lot of ways to manage the disease that are politically
unpopular,” Samuel says.
Michael Hansen, a senior staff scientist with the national Consumers Union
who has long tracked the spread of CWD and related diseases, is appalled by
what’s happening in Wisconsin.
“That’s horrendous news,” he says of the most recent numbers. “Do they not
care about an epidemic that is sweeping the state? The science doesn’t matter to
them?”
Hansen says the “proper response is to try and get rid of the epidemic,
rather than just give up and let it sweep through.” Otherwise, it’s only a
matter of time before “you’ve got such high rates that populations begin to
crash.”
Dave Clausen, a veterinarian who formerly served on the state’s Natural
Resources Board, shares this concern. “The current policy is inconsistent with a
long-term healthy deer herd,” he says, diplomatically. What is happening now is
exactly what he warned the DNR two years ago would happen, absent an aggressive
response: “CWD will continue to spread across the state and will increase in
prevalence where it is established.”
Now retired, Clausen calls the state’s willingness to essentially let this
happen “a political decision, not a scientific one.” If the scientists are
right, and Wisconsin’s deer hunt is devastated, will politicians get the
blame?
Bill Lueders is the Money and Politics Project director at the Wisconsin
Center for Investigative Journalism (www.WisconsinWatch.org). The Center
produces the project in partnership with MapLight. The Center collaborates with
Wisconsin Public Radio, Wisconsin Public Television, other news media and the
UW-Madison School of Journalism and Mass Communication. All works created,
published, posted or disseminated by the Center do not necessarily reflect the
views or opinions of UW-Madison or any of its affiliates.
> Did Walker Cave In to Hunting Lobby?
of course he did, in my opinion. it’s all about money and trade
folks.
see;
‘’It is interesting to note that, in 2001, the State of Texas shifted its
deer management strategies toward the same leanings that Kroll has suggested for
Wisconsin. In Texas, the change was brought about via heavy lobbying from the
high-fence deer ranching industry. This pressure helped convince the Texas Parks
and Wildlife to change their regulations and allow private landowners to select
the own deer biologists.’’
nothing like the wolf guarding the henhouse.
Texas just documented another case of CWD, I wonder what the Wisconsin’s
Deer Czar (from TEXAS), seems Dr. Dough’s passive approach on CWD is not working
out too well.
yep, while the Texas deer czar dr. dough was off to Wisconsin pushing the
privately owned shooting pen industry (livestock cervid industry), Texas fell to
CWD, and have now documented 7 cases of CWD to date.
IF Texas would test for CWD in the captive industry aggressively, I think
we would all be shocked as to what they would find.
for your information...
According to Wisconsin’s White-Tailed Deer Trustee Dr. James Kroll, people
who call for more public hunting opportunities are “pining for socialism.” He
further states, “(Public) Game management is the last bastion of
communism.”
“Game Management,” says James Kroll, driving to his high-fenced,
two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.”
Kroll, also known as Dr. Deer, is the director of the Forestry Resources
Institute of Texas at Stephen F. Austin State University, and the “management”
he is referring to is the sort practiced by the State of Texas. The 55-year-old
Kroll is the leading light in the field of private deer management as a means to
add value to the land. His belief is so absolute that some detractors refer to
him as Dr. Dough, implying that his eye is on the bottom line more than on the
natural world.
Kroll, who has been the foremost proponent of deer ranching in Texas for
more than thirty years, doesn’t mind the controversy and certainly doesn’t fade
in the heat. People who call for more public lands are “cocktail
conservationists,” he says, who are really pining for socialism. He calls
national parks “wildlife ghettos” and flatly accuses the government of gross
mismanagement. He argues that his relatively tiny acreage, marked by eight-foot
fences and posted signs warning off would-be poachers, is a better model for
keeping what’s natural natural while making money off the land.
Dr. Deer Wisconsin Report: Will High-Fence Bias Skew Final Plan?
Categories: Blogs, Daniel Schmidt's Whitetail Wisdom, Deer News, Featured
Tags: antler restricitons, dan schmidt, Dr. Deer, james kroll, James Kroll
Wisconsin, qdm, quality deer management, texas hunting, wisconsin deer hunting
March 29, 2012 According to Wisconsin’s White-Tailed Deer Trustee Dr. James
Kroll, people who call for more public hunting opportunities are “pining for
socialism.” He further states, “(Public) Game management is the last bastion of
communism.”
OPINION BLOG
These are just two insights into the man who has been asked to provide
analysis and recommended changes to Wisconsin’s deer management program. Kroll’s
insights are from an article entitled “Which Side of the Fence Are You On?” by
Joe Nick Patoski for a past edition of Texas Monthly. If nothing more, the
article gives an unabashed look into the mind-set that will be providing the
Wisconsin DNR with recommendations on how to change their deer management
practices. James Kroll (also known as “Deer Dr.”) was appointed to the Wisconsin
“deer czar” position last fall. He was hired by the Department of Administration
and instructed to complete a review of the state’s deer management program.
Here’s a sample of the article:
“Game Management,” says James Kroll, driving to his high-fenced,
two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.”
Kroll, also known as Dr. Deer, is the director of the Forestry Resources
Institute of Texas at Stephen F. Austin State University, and the “management”
he is referring to is the sort practiced by the State of Texas. The 55-year-old
Kroll is the leading light in the field of private deer management as a means to
add value to the land. His belief is so absolute that some detractors refer to
him as Dr. Dough, implying that his eye is on the bottom line more than on the
natural world.
Kroll, who has been the foremost proponent of deer ranching in Texas for
more than thirty years, doesn’t mind the controversy and certainly doesn’t fade
in the heat. People who call for more public lands are “cocktail
conservationists,” he says, who are really pining for socialism. He calls
national parks “wildlife ghettos” and flatly accuses the government of gross
mismanagement. He argues that his relatively tiny acreage, marked by eight-foot
fences and posted signs warning off would-be poachers, is a better model for
keeping what’s natural natural while making money off the land.
A trip to South Africa six years ago convinced Kroll that he was on the
right track. There he encountered areas of primitive, lush wildlife-rich
habitats called game ranches. They were privately owned, privately managed, and
enclosed by high fences. He noticed how most of the land outside those fences
had been grazed to the nub, used up. “Game ranches there derive their income
from these animals — viewing them, hunting them, selling their meat,” he says.
“There are no losers.” At his own ranch Kroll has set up a smaller version of
the same thing. His land is indeed lush, verdant, with pine groves, an abundance
of undergrowth, wild orchids, New Jersey tea, jack-in-the-pulpits, and other
native plants. He has also set up a full-scale breeding research center and is
one of twenty Texas deer breeders using artificial insemination to improve his
herd. “We balance sex and age ratio,” he says. “We manage habitat. We control
the population and manage for hunting. I want to leave the deer herd better than
it was before we came.”
It is interesting to note that, in 2001, the State of Texas shifted its
deer management strategies toward the same leanings that Kroll has suggested for
Wisconsin. In Texas, the change was brought about via heavy lobbying from the
high-fence deer ranching industry. This pressure helped convince the Texas Parks
and Wildlife to change their regulations and allow private landowners to select
the own deer biologists.
“That has given landowners more freedom,” Kroll told Texas Monthly.
“(However,) You still have to let the state on your land to get a
wildlife-management permit.” The key difference here is that 98 percent of Texas
is comprised of private land. Wisconsin, on the other hand, consists of
approximately 34.8 million acres of land, and 25.5 percent of the state’s
638,000 gun-hunters reported hunting on public land at some point during the
season (2010, Duey, Rees).
According to the Wisconsin Realtors Association, more than 5.7 million
acres of this land, or 16.5 percent, is publicly owned and used for parks,
forests, trails, and natural resource protection. [Note: these statistics do not
include the public land used for roads, government buildings, military bases,
and college/school campuses.] This 5.7 million acres of public land is owned as
follows:
Federal government owns approximately 1.5 million acres (4.4 percent of the
state’s land area). Almost all of the federal forestland in Wisconsin is located
in Chequamegon-Nicolet National Forest.
State government owns approximately 1.6 million acres (4.6 percent of the
state’s land area). The land is managed by two agencies, the Board of
Commissioners of Public Land (who manages lands granted by federal government)
and the DNR (managing land owned by the state).
County government owns approximately 2.6 million acres (7.5 percent of the
state’s land area).
Public land is located in 71 of Wisconsin’s 72 counties, with the most
public land located in Bayfield County (464,673 acres). [Note: Menominee County
does not have any public land, but 98 percent of the land is held in trust by
the Menominee Tribe.] Twenty counties have more than 100,000 acres of public
land, while only 12 counties have fewer than 10,000 acres.
What does this all mean? My initial reaction, which is one that I predicted
when Kroll was named to the state’s deer trustee position, is that his team’s
final recommendations — if implemented — will be heavily skewed toward the
state’s larger landowners (500+ acres) and folks who own small parcels in areas
comprised mostly of private land.
It is also my prediction that the final recommendations (again, if
implemented) will do little, if anything, to improve deer herds and deer hunting
on Wisconsin’s 5.7 million acres of public land.
Where does this leave the public-land hunter? “It will suck to be you,”
said one deer manager who asked to remain anonymous out of fear for his job.
“The resources and efforts will go toward improving the private land sector.
This is all about turning deer hunting away from the Public Land Doctrine and
more toward a European-style of management — like they have in Texas.”
I do, of course, hope these assumptions are wrong. As with all things in
life, we should maintain an open mind to change. Life is all about change.
However, change for the sake of change is usually a recipe for disaster.
Especially when that change is driven by something more than a sincere desire to
manage public resources for the greater good.
As noted yesterday (Dr. James Kroll Report: Is That All You Get For Your
Money), I will provide more of my opinions and interpretation on this important
issue in forthcoming installments of this blog. Read his full preliminary report
here.
snip...see full text ;
Thursday, March 29, 2012
TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT
CALLING KETTLE BLACK
Saturday, March 10, 2012
*** CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow
protein feed CUSTOM MADE for deer and elk
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Tuesday, July 10, 2012
Dr. James C. Kroll Texas deer czar final report on Wisconsin
Wednesday, March 18, 2015
Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18,
2015
Wednesday, March 25, 2015
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
Thursday, August 20, 2015
*** TEXAS TAHC DEER BREEDER CWD PERMIT RULES EMERGENCY ADOPTION PREAMBLE
***
Thursday, August 20, 2015
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks
and CWD
Wednesday, May 04, 2016
TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99
Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment
Submission
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, April 25, 2016
Arkansas AGFC Phase 2 sampling reveals CWD positive deer in Madison and
Pope counties
Tuesday, April 19, 2016
Arkansas First Phase of CWD sampling reveals 23 percent prevalence rate in
focal area With 82 Confirmed to Date
Saturday, April 02, 2016
TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER
BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Friday, February 05, 2016
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER
RELEASE SITE
Friday, April 22, 2016
*** COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM IS MINIMAL AND LIMITED ***
snip...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
22
Visits to Colorado State University, College of Veterinary Medicine and the
Wyoming Game and Fish Department, Sybille Wildlife Research and Conservation
Education Unit.
The main objective here was to obtain some understanding of CWD. A visit
was made to the University of wyoming Game and Fish Department, Sybille wildlife
Research and Conservation Education Unit where most of the cases of CWD have
occurred. The Sybille Wildlife facility is situated some 50 miles northeast of
Laramie, Wyoming through the Laramie Mountains. Here most of the hoofed big game
species of North America; Hule Deer (odocoileus hemionus), Whitetail Deer
(Odocoileus virginianus), Elk (Cervis canadensis) Mountain Goat (Oreamnos
americana), Bighorn Sheep (0vis canadensis** and Pronghorn (Antilocapra
americana) and some other wildlife species are kept in small numbers for
experimental use in the investigation of wildlife diseases.
A colony of the blackfooted ferret (Hustela nigripes) has been established
because of its imminent extinction. At present there are only 35 but it is
proposed to breed up to 200 and then, probably in 1991, re-introduce them into
the wild in a nation wide operation. Blackfooted ferret diet is mainly Prairie
Dog (Cynoms spp.) and it is thought that the elimination of this species from
large areas by poisoning campaigns in the past has been responsible for the
precipitous ferret decline.
The buildings and pens at the facility are entirely of wooden/log
construction with heavy duty wire mesh fences. Pen floors are bare earth. A long
race connecting many different areas within the facility enables movement of
deer and antelope between pens when necessary. There is provision for holding
deer of different sizes in a custom built crush for bleeding and
treatments.
23
The educational role of the unit includes school visits to provide
instruction in the work of the department and to promote conservation. I was
accompanied on this visit by Stuart Young and Beth Williams. on arrival I was
introduced to Hughie Dawson who has managed the facility for some 20
years.
CWD occurred principally in two locations, this one at Sybille and in a
similar facility at Fort Collins, Colorado, some 120 miles southwest. It was
estimated that in total probably 60-10 cases of CWD have occurred.
It was difficult to gain a clear account of incidence and temporal sequence
of events ( - this presumably is data awaiting publication - see below) but
during the period 1981-84, 10-15 cases occurred at the Sybille facility.
Recollections as to the relative total numbers of cases at each facility were
confusing. Beth Williams recalled that more cases had occurred in the Colorado
facility.
The morbidity amongst mule deer in the facilities ie. those of the natural
potentially exposed group has been about 90% with 100% mortality. the age
distribution of affected deer was very similar to that in ESE. The clinical
duration of cases was 6-8 weeks. Mortality in CWD cases was greatest in winter
months which can be very cold.
When the problem was fully appreciated both the Sybille and the Colorado
facilities were depopulated. All cervids were culled but Pronghorn, Bighorn
Sheep and Mountain goat, where present simultaneously in the facility, were
retained. There have been no cases of CWD in these non cervid species.
A few cases continue to occur at Sybille, the last was 4 months ago.
24
An account of the occurrence of CWD at the Colorado facility was obtained
from Terry spraker, Diagnostic Laboratory, CSU College of Veterinary Medicine,
Fort Collins. He examined tissues from cases of CWD at the Colorado facility
some time prior to Beth Williams's involvement and examination of brains which
resulted in the initial diagnosis. The deer holding facilities in Colorado
comprise the Colorado Division of Wildlife Research Pen, established 10 years
ago and some older deer pens at the Foot Hills Campus of CSU, close to Fort
Collins. Originally there were just 1-2 cases CWD/year and a total of 24 over
several years. In contrast to Beth Williams recollection Terry Spraker thought
more cases had‘ occurred at Sybille than in Colorado. The cull at the Colorado
facility involved 20-30 clinically normal deer. Early lesions in dorsal nucleus
of the vagus and olfactory cortex were found in (some) of these deer. At the
time of the cull here Pronghorn was the only other hoofed species present.
Bighorn sheep and Mountain Goat were introduced only one year after the cull and
occupied ground where CWD had occurred. Immediately after depopulation the
ground was ploughed and disinfection was carried out using ?1% NaOH. The
buildings/pens were not changed. There has been no recurrence of disease at the
Colorado facility since the cull.
25
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation and
compared with natural cases (‘’first passage by this route’’ MARKED OUT...TSS)
resulted in a more rapidly progressive clinical disease with repeated episodes
of synocopy ending in coma. one control animal became affected, it is J believed
through contamination of inoculum (?saline). Further CWD transmissions were
carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission
occurred in all of these species with the shortest incubation period in the
ferret.
Mouse and hamster transmissions were attempted at Wyoming State Diagnostic
Laboratory, Laramie and at CSU Fort Collins but were unsuccessful.
Also at the Wyoming State Diagnostic Laboratory, Laramie, transmission to
goats was attempted. In 1984 three goats were inoculated intracerebrally with a
10% CWD brain suspension. one goat, untreated, was placed in contact with the
CWD inoculated goats and three controls, housed separately, received saline
intracerebrally. To date these animals remain healthy.
Epidemiology of CWD
Descriptive epidemiological data has been collected from the two wildlife
facilities and a publication is in preparation.
The occurrence of CWD must be viewed against the context of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite its subsequent recognition as a
new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA viewed it as a wildlife problem and
consequently not their province! Thus
26
there have been no specific epidemiological studies, other than information
gained from noting the occurrence of cases. Because of the relatively short term
nature of the programmed research at the facilities it has not been possible to
keep Mule Deer under the appropriate experimental circumstances or for
sufficient periods to establish horizontal or maternal transmission. Beth
Williams is of the view that the occurrence of CWD at Sybille is entirely
related to propagative spread by contagion. Investigations have failed to
identify any common source of infection and the incident has presented a
protracted time course with sporadic cases throughout. There is no evidence that
wild born deer were responsible for introduction of the disease to the
facility.
I asked Hughie Dawson about the nutritional aspects of the deer kept at
Sybille. Mule Deer calves are reared on condensed milk and homogenised or
pasteurised domestic cow's milk from birth to 1 month or to 6 months. some would
be given "Lamb milk replacer" which has a higher butter fat content than either
of the former products, but is derived also from domestic cow's milk. It was
thought that at the Colorado facility calves would receive only "evaporated
milk". Calves are weaned on to a pelletted feed containing corn, wheat bran and
linseed meal with no crude mineral suppliment. Salt licks ("sulphur blocks")
which have a specific mineral composition are supplied.
CWD has occurred or is suspected to have occurred in establishments
supplied with Mule Deer from the Colorado facility. In some cases evidence for
this is tenuous. For example, it is understood that Denver zoo state that "they
have not had cases of CWD" and yet they have had cases of Mule Deer succumbing
to a chronic wasting disorder which was not diagnosed. A case of CWD occurred in
a Mule Deer in Toronto zoo in 1976. The animal in
27
question came from Denver zoo but was originally from the Colorado wildlife
facility.
Pathology of CWD
A paper (Williams et al) is in preparation on the distribution of brain
lesions in CWD. Vacuolar changes occur predominantly in the dorsal nucleus of
the vagus nerve (this nucleus is invariably affected), the hypothalamus and the
olfactory cortex with occasional vacuolation of the olfactory tract white
matter.
Cerebellar lesions are sometimes present but there are very few changes in
the spinal cord which probably accounts for the rarity of ataxia clinically. As
in sheep scrapie the hypothalamic lesions correlate with the common clinical
occurrence of polydipsia. Beth Williams is aware of occasional neuronal vacuoles
occurring in the red nucleus of clinically normal deer! Spraker has added that
he has experienced vacuoles in neurons of Gasserian ganglia and at the level of
the obex in normal deer.
It has never been reported but Pat Merz carried out SAF detection on CWD
brain material. Work may be undertaken with NIH on the immunohistological
demonstration of PrP in sections but to date there has been no PrP work.
Does CWD occur in free-living cervids?
There is some, mostly circumstantial, evidence that CWD occurs in
free-living cervids but to what extent, if at all, this represents an
established reservoir of infection in the wild is not known.
At Sybille two Mule Deer orphans (wild caught) and a White—tail Deer
(Odocoileus virginianus) hybrid developed clinical signs when only 2 1/2 years
of age.
28
An Elk (Cervus canadensis) wild caught as an adult, presumed 2 years old,
developed signs when 3-4 years old.
Another group of elk, wild caught 400 miles from the facility, with an age
range 2-8 years, old subsequently developed the disease in the facility (?period
of captivity). The location of capture relative to the facility did not
apparently rule out that they may have at some time had fence-line nose contact
with animals in the facility!
Cases have also occurred in Mule Deer that were obtained from the wild
within one hour of birth but these were never kept completely isolated through
to maturity.
Also at Sybille there has been one case of CWD diagnosed in a free ranging
Elk. It was killed in Sybille Canyon 3 miles from the facility. It could have
had fence-line contact with captive Mule Deer in the facility.
Similar incidents had occurred in Colorado. In 1985 a free-ranging affected
Elk was caught in the Rocky Mountain National Park within a 2 mile radius of the
Colorado Division of Wildlife Research Pen. In 1986 and again in 1987 a single
affected Mule Deer on each occasion was caught within a 5 mile radius of the
Pen. These latter cases occurred within 2 years of the -cervid cull at the Pen
(?1985). Brain tissue from the free—ranging Elk brain was inoculated into mice
but for some reason these were kept for only 6 months and then the experiment
was abandoned.
A specific exercise has been carried out by Beth Williams with the Wyoming
State Diagnostic Laboratory and Fish Department to sample the brains of healthy
wild Mule Deer for histological examination. On two separate occasions the first
in 1985 and again in 1987 a total of 150 Mule Deer
29
brains were collected from areas of, and ajacent to, Sybille Canyon. These
deer would have been shot under a game permit by local hunters. As they were
brought down from the hills to the Game station for the mandatory registration
of the kill the heads were removed and ages estimated. Most were 2-5 year old
with a few 6 year old. For obvious reasons hunters were reluctant to give up
stag heads. Thus, but for 15-20 brains from stags, examinations were on brains
from females. No evidence of CWD lesions was found in any of these brains.
However, it was considered that sporadic cases of CWD, should they occur in the
wild population, would soon become separated from the herd and fall prey to
coyotes (Canis latrans).
The possibility of any reservoir of infection in wild cervids originating
from scrapie in domestic sheep flocks seems remote. Scrapie has been recorded in
only three flocks in Wyoming since 1947 and Beth Williams could recall only one
previous occurrence in 1966. This had involved a Suffolk flock close to the
border with Nebraska. However, there has been one new confirmed and a suspected
affected flock this year in Wyoming. In the latter a ewe bought—in from an
Illinois flock is incriminated.
Spraker suggested an interesting explanation for the occurrence of CWD. The
deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr Bob
Davis. At or about that time, allegedly, some" scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep. Whether they were scrapie infected sheep or
not is unclear. There were domestic sheep and goats present in the facility also
in the 1960's but there is no evidence that these animals developed scrapie.
During the 60's hybridization studies between the Bighorn and domestic sheep
were carried
30
out, again, without evidence of scrapie. Domestic goats were also kept at
Sybille in the 1960's.
Spraker considers that the nasal route is responsible for transmission of
CWD through nose to nose contact, which may well occur also between captive and
free—living individuals.
In domestic cattle of which about 15-20 adults were necropsied per year at
the Diagnostic Laboratory, CSU., Spraker had not encountered any lesions
suggesting BSE. Polioencephalomalacia (PEM) and Encephalic Listeriosis were the
most common morphologic neuropathological diagnoses. No bovine rabies was
seen.
31
Appendix I
VISIT TO USA - OR A E WRATHALL — INFO ON BSE AND SCRAPIE
Dr Clark lately of the Scrapie Research Unit, Mission Texas has I
successfully transmitted ovine and caprine Scrapie to cattle. The experimental
results have not been published but there are plans to do this. This work was
initiated in 1978. A summary of it is:-
Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a
2nd Suffolk scrapie passage:- i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.
1/6 went down after 48 months with a scrapie/BS2-like disease.
Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus
2/6 went down similarly after 36 months.
Expt C Mice inoculated from brains of calves/cattle in expts A & B were
resistant, only 1/20 going down with scrapie and this was the reason given for
not publishing.
Diagnosis in A, B, C was by histopath. No reports on SAF were given.
2. Dr Warren Foote indicated success so far in eliminating scrapie in
offspring from experimentally— (and naturally) infected sheep by ET. He had
found difficulty in obtaining embryos from naturally infected sheep (cf
SPA).
3. Prof. A Robertson gave a brief accout of BSE. The us approach was
to
32
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. BSE was not reported in
USA.
4. Scrapie incidents (ie affected flocks) have shown a dramatic increase
since 1978. In 1953 when the National Control scheme was started there were
10-14 incidents, in 1978 - 1 and in 1988 so far 60.
5. Scrapie agent was reported to have been isolated from a solitary fetus.
6. A western blotting diagnostic technique (? on PrP) shows some
promise.
7. Results of a questionnaire sent to 33 states on" the subject of the
national sheep scrapie programme survey indicated
17/33 wished to drop it
6/33 wished to develop it
8/33 had few sheep and were neutral
Information obtained from Dr Wrathall‘s notes of a meeting of the U.S.
Animal Health Association at Little Rock, Arkansas Nov. 1988.
33
snip...see full text ;
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. ...
snip...see full text ;
Colorado CWD
SEE CWD HIGH INFECTION RATE MAPS FOR COLORADO !
Thursday, February 09, 2012
Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
Wednesday, April 27, 2016
WYOMING GAME AND FISH DEPARTMENT CHRONIC WASTING DISEASE MANAGEMENT PLAN
APRIL 22, 2016
Friday, April 22, 2016
Missouri MDC finds seven new cases of ChronicWasting Disease CWD during
past‐season testing
Wednesday, April 20, 2016
UTAH CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM 70 mule deer and two elk have tested positive
KANSAS CWD CASES ALARMING
Wednesday, March 02, 2016 Kansas Chronic Wasting Disease CWD TSE Prion 52
cases 2015 updated report 'ALARMING'
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive for CWD in the Oswego
zone of Kendall County
SEE UPDATE ON CWD OUTBREAK IN OTHER STATES USA
Thursday, March 31, 2016
*** Chronic Wasting Disease CWD TSE Prion Roundup USA 2016 ***
Tuesday, April 12, 2016
*** The first detection of Chronic Wasting Disease (CWD) in Europe
***
Friday, April 22, 2016
Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in
a Mule Deer
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 Prion
2016 Tokyo
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Monday, May 02, 2016
Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo
Thursday, April 07, 2016
*** What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016 ***
Sheep and cattle may be exposed to CWD via common grazing areas with
affected deer but so far, appear to be poorly susceptible to mule deer CWD
(Sigurdson, 2008).
***In contrast, cattle are highly susceptible to white-tailed deer CWD and
mule deer CWD in experimental conditions but no natural CWD infections in cattle
have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how
susceptible humans are to CWD but given that the prion can be present in muscle,
it is likely that humans have been exposed to the agent via consumption of
venison (Sigurdson, 2008). Initial experimental research, however, suggests that
human susceptibility to CWD is low and there may be a robust species barrier for
CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD
is affecting wild and farmed cervid populations in endemic areas with some deer
populations decreasing as a result.
snip...
For the purpose of the qualitative risk assessment developed here it is
necessary to estimate the probability that a 30-ml bottle of lure contains urine
from an infected deer. This requires an estimate of the proportion of deer herds
in the USA which are infected with CWD together with the within herd
prevalence.
The distribution map of CWD in US shows it is present mainly in central
states (Figure 1). However, Virginia in the east of the country has recorded
seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take
steps to prevent urine being taken from infected animals eg by sourcing from
farms where the deer are randomly tested for CWD (Anon 2015a). However, if
disease is already present and testing is not carried out regularly, captive
populations are not necessarily disease free (Strausser 2014). Urine-based deer
lures have been known to be collected from domestic white-tailed deer herds and
therefore there is a recognised risk. This is reflected by 6 US States which
have
14
banned the use of natural deer urine for lures, as the deer urine may be
sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For
example, the US State of Virginia is banning the use of urine-based deer lures
on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska
banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned
urine-based deer lures and acknowledged that there is no way to detect their use
(Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it
appears that up to 50% of deer herds can be infected with 80-90% of animals
infected within some herds.
*** It is therefore assumed that probability that a 30-ml bottle of deer
urine lure imported from the USA is sources from an infected deer is
medium.
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 cannot be determined, however, as it is not specified in TRACES. It may
constitute a small percentage of the very low tonnage of non-fish origin
processed animal proteins that were imported from US into GB.
*** Overall, therefore, it is considered there is a greater than negligible
risk that (non-ruminant) 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...
Summary and MORE HERE ;
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Tuesday, April 12, 2016
*** The first detection of Chronic Wasting Disease (CWD) in Europe
***
WISCONSIN TRANSMISSIBLE MINK ENCEPHALOPATHY TME TSE PRION DISEASE AND FEED
SOURCES
In Confidence
Perceptions of unconventional slow virus diseases of animals in the
USA
G A H wells
REPORT OF A VISIT TO THE USA
APRIL—HAY 1989
snip...
Visit to Dept of Veterinary Science, University of Wisconsin -
Madison
1—3.5.89
The University is celebrating its Centenary this year. The Department of
Veterinary science has been established seventy years and currently comprises 13
faculty members and 98 graduate students. The Veterinary School (Dept of
Veterinary Medicine) is separate, was established 10 years ago and currently has
78 faculty.
After presenting a seminar on BSE it was arranged that we lunch with Dr G R
Hartsough. A brief but necessarily incomplete history of TME was recounted by
Hartsough:-
1947 1st outbreak in Wisconsin occurred in October in mink born the
previous May. Pathological material from this incident was sent to AFIP
Washington DC but no diagnosis was established. one hundred females that were
transferred from the farm to Minnesota also became affected but their kits
remained free of disease.
1952 2nd outbreak in Wisconsin. only 5-10% affected (ie markedly reduced
incidence from original outbreak).
1963 ‘Hayward’ outbreak in Wisconsin. This was discovered in May in females
nursing kits. In the following December (pelting season) 10 males were sold off
and these subsequently became affected. Hartsough recognised that in this
outbreak the clinical signs were similar to those of sheep scrapie and at this
time Hadlow was consulted. He concurred that clinically it was “just like
scrapie in mink" and confirmed the nature of the encephalopathy.
14
1963 Outbreak in Blackfoot, Idaho.
1985 The Stetsonville outbreak (farmer's name: Brecke). In addition to the
downer cows and horses Brecke's mink received a cereal supplement. Hartsough's
view was that this would contain bone meal and would be from a commercial
source. If this were so and it was contaminated with a TME agent why were there
no other ranches affected?
Many mink ranches now feed a commercial pelleted diet. ’Brecke was equipped
to process large carcasses using a crusher/mixer which could accommodate a whole
cow!
Idaho is the only US state other than Wisconsin in which primary outbreaks
of TME have been recorded.
The largest mink farms in the USA are in Wisconsin, Utah and Minnesota but
several other states, including Georgia have smaller units.
Finland, Norway and Denmark are major producers of mink and feed only fish
and poultry proteins. Denmark has a mink population of 14 million.
Utah mink ranches feed out of a large cooperative mixer-of poultry and fish
sources (but no beef sources) mainly originating in California.
Dead mink go for rendering but are used only in poultry feed.
Scrapie was first recognised in Wisconsin in the 1970's. A state indemnity
is paid but, unlike in Michigan, where payment is based on full value of flocks,
only partial value is paid.
15
Recently, USDA has invited comment from experts in the field on the
proposals to abandon the national scrapie control programme with the result that
there is now a move toward reconsideration. An adjudicating council has been
formed to decide future policy, especially against the background of knowledge
of BSE. (A draft document: Report of the Scientific Advisory Subcommittee to the
scrapie Task Force of the Sheep Industry Development Program, was passed to me
by Dick Harsh for comment].
Transmissions from the Brecke (stetsonville) THE outbreak to date are:-
(All i/c unless stated otherwise).
(snip...see chart in url...tss)
A visit was made (2.5.89) to the Universities experimental animal resource
facility, specifically the Mink Unit which presently houses 50 breeding females.
In an adjacent building clinical stages of scrapie (263k) in hamsters were
observed. A clinical evaluation system for hamster scrapie was described and
demonstrated.
16
A commercial mink ranch was visited. This was Johny Werth‘s, Capitol Fur
Farm comprising 1400 breeding females. The feed is bought in from a commercial
supplier in the form of frozen packs of "poultry", "fish", "dried egg" or
"tripe". A commercial mink cereal supplement is used and contains "animal meat
meal" which was said to contain material mainly from poultry or fish origin but
occasionally from beef sources. the partially thawed packs were tipped into an
augur mixer which has a fully loaded capacity of 6000lb and this would feed
approximately 15000 mink per day.
In the fall at pelting time the skinned carcasses of the mink are placed in
large barrels which are left in the open to freeze. when full, a renderer
collects "for use in poultry feeds“.
Sections from the brains of the two Brecke THE inoculated cattle were
examined and Marsh provided all the blocks from the 2nd steer for study at CVL
and comparison with BSE. In general the vacuolar changes were more severe than
in most cases of BSE but very similar in distribution. Unfortunately material
taken for histopathology from those animals omitted representation of most of
the brain stem. PrP has been extracted from both steer brains. About 25g of
cerebral cortex is required to obtain 100ug PrP. (The yield would almost
certainly be greater from brain stem)
The Central Animal Health Laboratory (the State Diagnostic Laboratory)
Wisconsin Department of Agriculture - Trade and Consumer Protection, was visited
and a seminar presented on BSE. This laboratory is responsible for diagnosis of
only a very small proportion of the bovine suspected rabies cases, most go to
the State Hygiene Laboratory. It was thought that only 5-10% of bovine suspect
rabies case proved positive. In Wisconsin bovine rabies usually occurred as the
‘dumb’ form with somnolence as the major feature but occasionally also occurence
of coarse bellowing. Clinical
17
duration was only a few days. Confusion with BSE on the basis of what
Department staff had seen on the videotape was, they considered, unlikely. The
question of red nucleus neuronal vacuolation as an incidental finding in bovine
brains was raised with Lynne Siegfried, Director and Peter Schmidt a recently
appointed veterinary pathologist with an interest in neuropathology but they did
not know if it occurred in submissions to the laboratory. It was apparent that
routine coronal slicing of brains was not followed and that the midbrain was
seldom specifically examined. It was agreed that in conjunction with proposed
surveillance for BSE this question would be addressed.
With regard to scrapie in Wisconsin, there were no clinical cases to date
this year.
18
snip...see full text ;
In Confidence
Perceptions of unconventional slow virus diseases of animals in the
USA
G A H wells
REPORT OF A VISIT TO THE USA
APRIL—HAY 1989
It is clear that the designing scientists must also have shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
*** 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...
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al, I would kindly like to comment
on ; Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
#158
Guidance for Industry
Use of Material from Deer and Elk in Animal Feed
This version of the guidance replaces the version made available
September15, 2003.
This document has been revised to update the docket number, contact
information, and standard disclosures. Submit comments on this guidance at any
time.
Submit electronic comments to http://www.regulations.gov. Submit written
comments to the Division of Dockets Management (HFA-305), Food and Drug
Administration, 5630 Fishers Lane, Rm. 1061, Rockville, MD 20852. All comments
should be identified with the Docket No. FDA-2003-D-0432 (formerly 03D-0186).
For further information regarding this guidance, contact Burt Pritchett,
Center for Veterinary Medicine (HFV-222), Food and Drug Administration, 7519
Standish Place, Rockville, MD 20855, 240-402-6276, E-mail:
burt.pritchett@fda.hhs.gov.
Additional copies of this guidance document may be requested from the
Policy and Regulations Staff (HFV-6), Center for Veterinary Medicine, Food and
Drug Administration, 7519 Standish Place, Rockville, MD 20855, and may be viewed
on the Internet at either http://www.fda.gov/AnimalVeterinary/default.htm
or http://www.regulations.gov.
U.S. Department of Health and Human Services Food and Drug Administration
Center for Veterinary Medicine March 2016
Contains Nonbinding Recommendations
2
Guidance for Industry Use of Material from Deer and Elk in Animal Feed
This guidance represents the current thinking of the Food and Drug
Administration (FDA or Agency) on this topic. It does not establish any rights
for any person and is not binding on FDA or the public. You can use an
alternative approach if it satisfies the requirements of the applicable statutes
and regulations. To discuss an alternative approach, contact the FDA office
responsible for this guidance as listed on the title page.
I. Introduction
Under FDA’s BSE feed regulation (21 CFR 589.2000) most material from deer
and elk is prohibited for use in feed for ruminant animals. This guidance
document describes FDA’s recommendations regarding the use in all animal feed of
all material from deer and elk that are positive for Chronic Wasting Disease
(CWD) or are considered at high risk for CWD. The potential risks from CWD to
humans or non-cervid animals such as poultry and swine are not well understood.
However, because of recent recognition that CWD is spreading rapidly in
white-tailed deer, and because CWD’s route of transmission is poorly understood,
FDA is making recommendations regarding the use in animal feed of rendered
materials from deer and elk that are CWD-positive or that are at high risk for
CWD.
In general, FDA’s guidance documents do not establish legally enforceable
responsibilities. Instead, guidances describe the Agency’s current thinking on a
topic and should be viewed only as recommendations, unless specific regulatory
or statutory requirements are cited. The use of the word should in Agency
guidances means that something is suggested or recommended, but not required.
II. Background
CWD is a neurological (brain) disease of farmed and wild deer and elk that
belong in the animal family cervidae (cervids). Only deer and elk are known to
be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer, white-tailed deer, North American elk, and in farmed
black-tailed deer. CWD belongs to a family of animal and human diseases called
transmissible spongiform encephalopathies (TSEs). These include bovine
spongiform encephalopathy (BSE or “mad cow” disease) in cattle; scrapie in sheep
and goats; and classical and variant Creutzfeldt-Jakob diseases (CJD and vCJD)
in humans. There is no known treatment for these diseases, and there is no
vaccine to prevent them. In addition, although validated postmortem diagnostic
tests are available, there are no validated diagnostic tests for CWD that can be
used to test for the disease in live animals.
Contains Nonbinding Recommendations
III. Use in animal feed of material from CWD-positive deer and elk
Material from CWD-positive animals may not be used in any animal feed or
feed ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and
Cosmetic Act, animal feed and feed ingredients containing material from a
CWD-positive animal would be considered adulterated. FDA recommends that any
such adulterated feed or feed ingredients be recalled or otherwise removed from
the marketplace.
IV. Use in animal feed of material from deer and elk considered at high
risk for CWD Deer and elk considered at high risk for CWD include:
(1) animals from areas declared by State officials 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 immediately
before the time of slaughter were in a captive herd that contained a
CWD-positive animal.
FDA recommends that materials from deer and elk considered at high risk for
CWD no longer be entered into the animal feed system. Under present
circumstances, FDA is not recommending that feed made from deer and elk from a
non-endemic area be recalled if a State later declares the area endemic for CWD
or a CWD eradication zone. In addition, at this time, FDA is not recommending
that feed made from deer and elk believed to be from a captive herd that
contained no CWD-positive animals be recalled if that herd is subsequently found
to contain a CWD-positive animal.
V. Use in animal feed of material from deer and elk NOT considered at high
risk for CWD FDA continues to consider materials from deer and elk NOT
considered at high risk for CWD to be acceptable for use in NON-RUMINANT animal
feeds in accordance with current agency regulations, 21 CFR 589.2000. Deer and
elk not considered at high risk include:
(1) deer and elk from areas not declared by State officials to be endemic
for CWD and/or to be CWD eradication zones; and
(2) deer and elk that were not at some time during the 60-month period
immediately before the time of slaughter in a captive herd that contained a
CWD-positive animal.
3
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al,
MY comments and source reference of sound science on this very important
issue are as follows ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
I kindly wish to once again submit to Docket No. FDA-2003-D-0432 (formerly
03D-0186) Use of Material from Deer and Elk in Animal Feed.
Thank you kindly for allowing me to comment again, ...and again...and
again, on a topic so important, why it is ‘NON-BINDING’ is beyond me. this
should have been finalized and made ‘BINDING’ or MANDATORY OVER A DECADE AGO.
but here lay the problem, once made ‘BINDING’ or ‘MANDATORY’, it is still
nothing but ink on paper. we have had a mad cow feed ban in place since August
1997, and since then, literally 100s of millions of pounds BANNED MAD COW FEED
has been sent out to commerce and fed out (see reference materials). ENFORCEMENT
OF SAID BINDING REGULATIONS HAS FAILED US TOO MANY TIMES.
so, in my opinion, any non-binding or voluntary regulations will not work,
and to state further, ‘BINDING’ or MANDATORY regulations will not work unless
enforced. with that said, we know that Chronic Wasting Disease CWD TSE Prion
easily transmits to other cervid through the oral route. the old transmission
studies of BSE TSE floored scientist once they figured out what they had, and
please don’t forget about those mink that were fed 95%+ dead stock downer cow,
that all came down with TME.
please see ; It is clear that the designing scientists must also have
shared Mr Bradleys surprise at the results because all the dose levels right
down to 1 gram triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
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...
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016 Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use
of Material from Deer and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary
Submission
Sunday, March 20, 2016
UPDATED MARCH 2016 URGENT Docket No. FDA-2003-D-0432 (formerly 03D-0186)
Use of Material from Deer and Elk in Animal Feed Singeltary Submission
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards
Singeltary Comment Submission
Sunday, March 20, 2016
*** UPDATED MARCH 2016 URGENT Docket No. FDA-2003-D-0432 (formerly
03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21
CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from
deer and elk is prohibited for use in feed for ruminant animals. With regards to
feed for non-ruminant animals, under FDA law, CWD positive deer may not be used
for any animal feed or feed ingredients. For elk and deer considered at high
risk for CWD, the FDA recommends that these animals do not enter the animal feed
system.
***However, this recommendation is guidance and not a requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated
feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
see page 176 of 201 pages...tss
Monday, April 04, 2016
*** Limited amplification of chronic wasting disease prions in the
peripheral tissues of intracerebrally inoculated cattle ***
Prion 6:2, 1-10; April/May/June 2012; © 2012 Landes Bioscience review
REVIEW Introduction *Correspondence to: Stacie J. Robinson; Email:
stacie.j.robinson@gmail.com Submitted: 10/19/11; Revised: 02/02/12; Accepted:
02/06/12 http://dx.doi.org/10.4161/pri.6.2.19640
Chronic wasting disease (CWD) is a major concern for the management of
North American cervid populations.
This fatal prion disease has led to declines in populations which have high
CWD prevalence and areas with both high and low infection rates have experienced
economic losses in wildlife recreation and fears of potential spill-over into
livestock or humans. Research from human and veterinary medicine has established
that the prion protein gene (Prnp) encodes the protein responsible for
transmissible spongiform encephalopathies (TSEs). Polymorphisms in the Prnp gene
can lead to different prion forms that moderate individual susceptibility to and
progression of TSE infection. Prnp genes have been sequenced in a number of
cervid species including those currently infected by CWD (elk, mule deer,
white-tailed deer, moose) and those for which susceptibility is not yet
determined (caribou, fallow deer, sika deer). Over thousands of sequences
examined, the Prnp gene is remarkably conserved within the family Cervidae; only
16 amino acid polymorphisms have been reported within the 256 amino acid open
reading frame in the third exon of the Prnp gene. Some of these polymorphisms
have been associated with lower rates of CWD infection and slower progression of
clinical CWD. Here we review the body of research on Prnp genetics of North
American cervids. Specifically, we focus on known polymorphisms in the Prnp
gene, observed genotypic differences in CWD infection rates and clinical
progression, mechanisms for genetic TSE resistance related to both the cervid
host and the prion agent and potential for natural selection for CWD-resistance.
We also identify gaps in our knowledge that require future research.
The role of genetics in chronic wasting disease of North American
cervids
The greatest number of Prnp alleles and amino acid substitution occurs in
white-tailed deer, red deer, caribou and mule deer (Table 1). So far, research
has demonstrated that Prnp coding variations in elk, white-tailed deer and mule
deer are associated with the rate of CWD infection or disease progression, with
no evidence for a completely resistant genotype (references in Table 1).
Research Article
Modeling Routes of Chronic Wasting Disease Transmission: Environmental
Prion Persistence Promotes Deer Population Decline and Extinction Emily S.
Almberg , * E-mail: esa5046@psu.edu
Affiliations: Northern Rocky Mountain Science Center, United States
Geological Survey, Bozeman, Montana, United States of America, The Huck
Institutes of the Life Sciences, Pennsylvania State University, University Park,
Pennsylvania, United States of America
⨯ Paul C. Cross, Affiliation: Northern Rocky Mountain Science Center,
United States Geological Survey, Bozeman, Montana, United States of America
⨯ Christopher J. Johnson, Affiliation: Prion Research Laboratory, National
Wildlife Health Center, United States Geological Survey, Madison, Wisconsin,
United States of America
⨯ Dennis M. Heisey, Affiliation: Prion Research Laboratory, National
Wildlife Health Center, United States Geological Survey, Madison, Wisconsin,
United States of America
⨯ Bryan J. Richards Affiliation: National Wildlife Health Center, United
States Geological Survey, Madison, Wisconsin, United States of America
⨯ Modeling Routes of Chronic Wasting Disease Transmission: Environmental
Prion Persistence Promotes Deer Population Decline and Extinction Emily S.
Almberg, Paul C. Cross, Christopher J. Johnson, Dennis M. Heisey, Bryan J.
Richards PLOS x Published: May 13, 2011 http://dx.doi.org/10.1371/journal.pone.0019896
OLD HISTORY ON CWD AND GAME FARMS IN USA
THE YEAR 2000
Stop the madness: CWD threatens Wisconsin's elk, deer and, ultimately,
people.
15 July 00
The Isthmus magazine By BRIAN McCOMBIE
Imagine a disease worse than AIDS rippling through Wisconsin's deer herd.
One that's always fatal, cannot be tested for in live animals, and has the
chance of spreading to anyone who eats the infected venison. Sound like the
premise for Michael Crichton's next apocalyptic thriller?
Unfortunately, such a disease already exists in epidemic levels in the
wilds of Colorado and Wyoming. It's infected some game farms, too, and Wisconsin
game farmers have imported more than 350 elk with the potential for this
disease, including elk from farms known to be infected.
"If most people knew what kind of risk this disease poses to free-ranging
deer in the state, they'd be very concerned," says Dr. Sarah Hurley, Lands
Division administrator for the Department of Natural Resources. The DNR is now
testing free-ranging deer around these game farms for the disease: "We're
focusing our energies on those areas where we think there's the greatest
possibility of transmission."
The malady the DNR's looking for is chronic wasting disease (CWD)--better
known, to the extent it is known at all, as mad elk disease. It's a form of the
mad cow disease that devastated Britain's cattle industry in the 1980s, scared
the bejesus out of the populace, and is believed to have killed at least 70
people to date. An elk or deer with CWD can be listless, may walk in circles,
will lose weight and interact progressively less with fellow animals.
The corresponding human affliction is called Creutzfeldt-Jakob disease
(pronounced Croytz-feld Yawkob) or CJD. People with CJD experience symptoms
similar to Alzheimer's, including memory loss and depression, followed by
rapidly progressive dementia and death, usually within one year. While CJD is
rare (literally one in a million odds of getting it), over the last few years at
least three deer hunters have died of it. There is no proof either way whether
they contracted the disease from CWD-infected venison, but new research says it
is possible.
All three varieties--mad cow, mad elk and CJD--belong to a family of
diseases called transmissible spongiform encephalopathy. These diseases alter
the conformation of proteins in the brain called prions; after-death brain
samples usually show a series of microscopic holes in and around brain cells.
No one is exactly sure how mad elk disease spreads. At first, transmittal
through blood seemed likely, as from mother to fawn. But CWD has moved between
adult animals at game farms, leading scientists to conclude that it can be
spread through saliva or simple contact. Also, the rates of transmission are
higher in areas where animals have the most opportunities for contact.
Wisconsin's concentrated population of 1.7 million deer interact freely with
each other, and scientific modeling suggests CWD could tear through our deer
herd devastatingly fast. Despite the danger, Wisconsin and other states are
relying on only sporadic testing and a system of voluntary compliance. It's a
system that some say has more holes in it than a CWD-infected brain.
At present, Wisconsin game farm owners, even those harboring elk and deer
brought in from farms with known cases of CWD, do not have to call a
veterinarian if a deer or elk suddenly dies or acts strange. They're also not
required to inform the state Department of Natural Resources (DNR) or the
Department of Agriculture, Trade and Consumer Protection (DATCP) if animals
escape into the wild.
"The lax attitude is pretty shocking," says John Stauber, a Madison
activist and co-author of Mad Cow U.S.A. To protect people and deer, Stauber
argues for an immediate importation ban for game farms, plus programs of testing
and surveillance. He suggests both DATCP and DNR aren't taking such measures
because, as the regulators in charge, they don't want to find the CWD he thinks
is likely already in state. "It's in their bureaucratic interest to not
[actively] look for CWD in the game farms," says Stauber. "Because if they find
it, who's to blame?"
In the wild and especially out west, chronic wasting disease is spreading
fast. Northeastern Colorado documented its first case in 1981. By the mid-1990s,
samplings of mule deer brains showed 3% to 4% testing positive for CWD. Within a
few years, the rate was 8%, and now Larimer County, the center of the endemic
area, has a 15% rate of infection among mule deer. It's also being found in deer
and elk in Wyoming.
"Fifteen percent of a wild population of animals with this disease is
staggering," says Dr. Thomas Pringle, who tracks CWD-type diseases for the
Sperling Biomedical Foundation in Eugene, Ore. "It's basically unheard of. This
appears to be an unusually virulent strain. with highly efficient horizontal
transmission mechanisms."
CWD could eventually spread to Wisconsin on its own, animal to animal. But
that would take decades. Game farms, though, provide a mechanism to cut through
all that time and distance and drop CWD smack in the middle of the state.
An open-records search by Isthmus reveals that the first shipment of farm
elk from areas with CWD in the wild occurred in 1992, with 66 Colorado elk going
to a game farm in Plymouth. In April 1998, DATCP was informed that a Bloomer
game farm had purchased one elk from a Nebraska farm later found to be
CWD-infected. This prompted a Sept. 15, 1998, memo from Steven Miller, head of
the DNR's Lands Division, to Secretary George Meyer, with copies to DATCP chief
Ben Brancel and Gov. Tommy Thompson. In it, Miller recommends that Wisconsin
follow the lead of Montana (which found CWD on two game farms) and place "a
moratorium on the importation of all game farm animals.... At present it appears
the only way to help assure the disease does not spread into Wisconsin."
But the moratorium was never put in place, so it's possible that even more
elk potentially carrying CWD are now in state.
Instead of a moratorium, Wisconsin has opted for testing. It is among 12
states and two Canadian provinces that currently test deer for CWD. Last year,
the Wisconsin DNR began testing road- and hunter-killed deer in 1999 within a
five-mile radius of game farms that have brought in elk from CWD-infected areas.
Test areas include all or part of Fond du Lac, Dodge, Jefferson, Sheboygan and
Washington counties. All of the approximately 250 brains examined in 1999 came
back negative; this year, 500 to 600 deer will be tested.
Meanwhile, DATCP is asking owners of game farms that have animals from
herds known to have cases of CWD infection to voluntarily enter a surveillance
program. The agency's top veterinarian, Dr. Clarence Siroky, argues that
voluntary compliance makes more sense than a moratorium because, ban or no ban,
game farm operators "are going to find a way to bring these animals into the
state. We don't have police patrols and impregnable borders to keep anything in
or out."
With voluntary compliance, Siroky says, at least there are records of
animals entering the state. So if CWD or other diseases are discovered, the
animals can be traced back to their original herds and other farms they may have
been at. "It's better to know where the animals are coming in from," he insists.
Siroky may be right that an importation ban would result in some game farms
smuggling in animals. But currently, game farmers can bring in any deer or elk,
even those from known CWD-infected areas, so long as they can produce a health
certificate showing the animal's been tested. The problem is that no test exists
to find CWD in live animals. Animals can carry CWD for years and still look
healthy, so some of the 370 elk shipped into Wisconsin between 1996 and 1999
from CWD areas could have the disease. The odds are even higher for animals
purchased from farms later found to have CWD.
Wisconsin has approximately 100 deer or elk farms and they're big business.
On the Internet, prices for elk calves start at $1,500, and breeding bulls go
for up to $20,000. Some farms sell venison and the velvet that peels from new
elk antlers (considered an aphrodisiac in Asia). Others offer "hunts" costing
between $1,000 and $5,000 for trophy deer, to more than $10,000 for bull elk
with massive antlers.
Given these economics, it's reasonable to question why anyone with a
suspicion of CWD in his or her herd would call in state regulators or a vet. A
farm with a proven CWD case, confirms Dr. Robert Ehlenfeldt, DATCP's director of
Animal Disease Control, would be shut down indefinitely.
And if a problem develops on a Wisconsin game farm, there's no guarantee
that's where it will stay. Dr. Hurley says even fenced-in animals have easy
nose-to-nose contact with wild and other farmed animals. Besides, as the DNR's
chief of special operations Thomas Solin has documented, many game farms are not
secure. Gates are sometimes left open. Fences rust and break, rot and topple,
get crushed by fallen trees. Even if game farm animals don't escape, such
breaches allow wild deer to get in, mingle with the farmed deer and elk, then
leave.
Unlike other diseases, there's no test for CWD in living animals because it
doesn't create an immune system counter-response, detectable through blood
analysis. You can't kill CWD and related diseases by cooking the meat. One test
Stauber recounts in Mad Cow U.S.A. found that scrapie, a sheep form of CWD,
stayed viable after a full hour at 680 degrees Fahrenheit. Most disinfectants
don't kill these diseases, either, and they can exist in the soil for years.
And while diseases like mad cow and mad elk do have some trouble jumping
from species to species, it can happen. This May, Byron Caughey of the National
Institutes of Health announced that he had converted human brain materials with
mad-elk-contaminated brain matter at rates roughly equal to the transfer between
mad cow and humans.
Says Dr. Pringle, referring to Caughey's work, "CWD may not transmit that
easily, but the rate isn't zero." Pringle notes that the test Caughey used has
been a very reliable proxy in the past in determining transmission possibilities
for other diseases, including mad cow.
Once they jump the species barrier, transmissible spongiform encephalopathy
diseases adapt to fit the new host and are then passed on rather easily within
that species. Unfortunately, says Pringle, no one is trying to determine if CWD
has jumped into people as Creutzfeldt-Jakob disease. Making matters more
difficult is the fact that the disease can incubate for decades before symptoms
are seen.
In states with CWD-infected deer, thousands of people have undoubtedly been
exposed to CWD-infected venison. A February 1998 Denver Post article tells of
one hunter who's venison tested positive for CWD. By the time he was notified,
his meat had already been ground up and mixed with meat from hundreds of other
deer for venison sausage.
With AIDS, Pringle notes, there was a definite overreaction, with people
initially afraid to even shake hands with people infected with the virus.
Looking at the CWD situation in Colorado, he says there's been complete
underreaction. "It's like, oh, what the hell. Nobody's died yet--so keep eating
the venison!'" Pringle worries that if the disease is found in humans, it will
be so only after years of spreading through the human community.
Looking over documents obtained by Isthmus through its open-records
request, Stauber says DATCP is behaving more like a lobbyist for the game farm
industry than an agency bent on protecting Wisconsin's people from CWD. He
points to DATCP's Cervidae Advisory Committee as a prime example. In a Nov. 11,
1998, memo from Siroky to DATCP secretary Ben Brancel, Siroky notes that the
committee is needed to "obtain information from the public concerning disease
regulation" of farmed deer and elk, and "to help formulate action plans for
importation requirements, prevention and control" of CWD. But of the 12 people
Siroky nominates, one's a DNR warden, one's a DATCP employee, and the other 10
are game farm owners. And two of these owners were among those DATCP knew had
purchased elk from farms at high risk of having CWD.
"There's no significant input from anyone else," says Stauber. "Farmers,
deer hunters and consumers are all left out. Meanwhile, the government's failing
to take all necessary precautions to alert the public to this potential health
threat."
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild ***
the CWD LOTTO ENTITLEMENT of captive game farms where the states pays game
farms for CWD MUST BE STOPPED. if the cwd infected farm does not buy insurance
for any and all loss from CWD for them and any party that does business with
them, and or any loss to the state, and or any products there from, that’s to
bad, they should never be allowed to be permitted. in fact, for any state that
does allow game farming, urine mills, sperm mills, antler mills, velvet mills,
big high fence ranch, little low fence farm, in my opinion, it’s that states
responsibility to protect that state, thus, any states that allow these farms
and business there from, it should be mandatory before any permit is allowed,
that game farm must have enough personal insurance that would cover that farm,
any farm that does business with them, and or any products there from, and the
state, before such permit is issued. personally, I am sick and tired of all the
big ag entitlement programs, and that’s all cwd indemnity is. in fact, the USDA
CWD INDEMNITY PROGRAM, should read, THE USDA CWD ENTITLEMENT PROGRAM.
we cannot, and must not, let the industry regulate itself, especially with
the junk science they try to use. it’s just not working, and it’s been going on
long enough.
if they are not going to be science based, they must be banned.
science has told us for 3 decade or longer, that these are the things that
_might_ work, yet thanks to the industry, and government catering to industry,
regulations there from have failed, because of catering to the industry, and the
cwd tse prion agent has continued to spread during this time. a fine example is
Texas. ...
snip...see full text submission ;
Saturday, February 6, 2016
*** Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission ***
spontaneous TSE PRION IN HUMANS AND ANIMALS
SPORADIC CJD SIMPLY MEANS CJD FROM UNKNOWN ROUTE AND SOURCE, AND IT COULD
VERY WELL BE ZOONOTIC...TSS
for one, spontaneous TSE under natural field conditions, have ever been
documented as spontaneous. in fact ;
***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.***
***********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.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
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 TOKYO CONFERENCE
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.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary: The transmissible spongiform encephalopathies (also
called prion diseases) are fatal neurodegenerative diseases that affect animals
and humans. The agent of prion diseases is a misfolded form of the prion protein
that is resistant to breakdown by the host cells. Since all mammals express
prion protein on the surface of various cells such as neurons, all mammals are,
in theory, capable of replicating prion diseases. One example of a prion
disease, bovine spongiform encephalopathy (BSE; also called mad cow disease),
has been shown to infect cattle, sheep, exotic undulates, cats, non-human
primates, and humans when the new host is exposed to feeds or foods contaminated
with the disease agent. The purpose of this study was to test whether non-human
primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.
After an incubation period of approximately 10 years a macaque developed
progressive clinical signs suggestive of neurologic disease. Upon postmortem
examination and microscopic examination of tissues, there was a widespread
distribution of lesions consistent with a transmissible spongiform
encephalopathy. This information will have a scientific impact since it is the
first study that demonstrates the transmission of scrapie to a non-human primate
with a close genetic relationship to humans. This information is especially
useful to regulatory officials and those involved with risk assessment of the
potential transmission of animal prion diseases to humans. Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease
that also causes variant Creutzfeldt-Jakob disease in humans. Over the past
decades, c-BSE's zoonotic potential has been the driving force in establishing
extensive protective measures for animal and human health.
*** 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.
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 online
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.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J.
Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§
snip...
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure.
Wednesday, November 16, 2011
Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
*** 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 ***
*** 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.
Friday, August 09, 2013
CWD TSE prion, plants, vegetables, and the potential for environmental
contamination
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
Sunday, May 1, 2016
Center for Biologics Evaluation and Research 25th Meeting of: The
Transmissible Spongiform Encephalopathies Advisory Committee June 1, 2015
Transcript
AND DRUG ADMINISTRATION
2001
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
2:53 PM
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