ALABAMA CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING PROGRAM?
Tuesday, March 29, 2016 ALABAMA CHRONIC WASTING DISEASE CWD TSE PRION
SURVEILLANCE AND TESTING PROGRAM?
ALABAMA CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM?
The Alabama Division of Wildlife and Freshwater Fisheries (WFF)
White-tailed Deer Program goal is to provide a quality white-tailed deer
population statewide and offer maximum outdoor recreational opportunity to the
public without negatively affecting the resource. Alabama"s deer population is
estimated to be approximately 1.5 million, with hunters harvesting in excess of
300,000 deer annually.
WFF biologists provide deer related technical assistance to managers on
private and public lands, conduct seminars, speak publicly, write articles for
professional publications, conduct statewide disease surveillance, and cooperate
with Auburn University deer research projects to ensure Alabama's deer resources
are managed in an appropriate manner.
The Deer Management Assistance Program (DMP) is a comprehensive deer
management program, consisting of data collection and cooperator education with
which the WFF tries to put the landowner/cooperator in a better position to
manage their lands for a healthy deer herd, while maintain habitat integrity.
Data from the program are used to develop site specific harvest recommendations,
and have prompted numerous research projects to help better understand deer
biology. Collecting harvest information including sex, age, weight, lactation
rates and other attributes should be a facet of an active deer management plan.
Chris Cook, Deer Project Study Leader, compiled instructions and developed data
sheets for hunting clubs to collect the necessary information to take an active
role in managing their white-tailed deer resources.
Instructions and Data Sheets for Data Collections
In addition to working with private landowners, WFF biologists also
provide technical assistance on various local, state, and federal public lands
across the state. Some of the assistance provided to the Wildlife Management
Area (WMA) program includes habitat modification recommendations, deer harvest
analysis, reproductive health evaluations, population surveys, deer disease
surveillance, and regulation recommendations.
WFF Deer Management Steering Committee Chris Cook, Deer Project Study
Leader PO Box 305 Northport, AL 35476 (205)339-5716
Kevin Pugh, Wildlife Biologist 21453 Harris Station Road Tanner, AL 35671
(256)353-2634
What is the Division of Wildlife and Freshwater Fisheries doing to keep
CWD from reaching our state?
The Division is currently taking several measures to help prevent CWD from
reaching our state. The State has had a regulation banning the importation of
all cervids (members of the deer family) into Alabama since 1973. Recently the
fines for violating this regulation were significantly increased. Investigations
have discovered animal movements among many of the 20 privately owned elk herds
(outside of Alabama) where CWD has been diagnosed. The movement of infected
animals very likely was the reason for the disease's spread. Halting the
movement of live captive deer and elk into and within Alabama is a major step in
preventing the disease from reaching our state.
The Division also started an active monitoring program for CWD during the
2001-02 hunting season. The number of Alabama deer tested for the presence of
CWD is as follows:
2001-02 90
2002-03 440
2003-04 768
2004-05 736
2005-06 779
2006-07 654
2007-08 627
2008-09 606
2009-10 308
2010-11 311
2011-12 304
2012-13 - no testing due to funding loss
2013-14 - no testing due to funding loss
2014-15 - testing has resumed
Total 5,623
None of those deer tested positive for the disease. Plans are to continue
this testing program during the 2011-2012 season.
*** 2012-13 - no testing due to funding loss
*** 2013-14 - no testing due to funding loss
*** 2014-15 - testing has resumed
???
TERRIBLE, simply terrible. overall sample survey too small in my opinion
as well. you don’t look, you don’t find, or, as with Texas, if you look in all
the wrong places for over a decade, you don’t find it either, but it was there
all along, spreading. ...tss
DCNR Wildlife Officials Keep Vigilant Watch on CWD By DAVID RAINER
Alabama Department of Conservation and Natural Resources
Deer hunters can rejoice that Chronic Wasting Disease (CWD) has not been
found in Alabama or any of the surrounding states. That, however, does not mean
we deer hunters can take that fact for granted.
Currently, the Alabama Wildlife and Freshwater Fisheries (WFF) Division is
revising the strategy that will help WFF officials respond quickly should CWD be
detected in Alabama in the future.
CWD is an insidious disease that affects the four members of the cervid
family of animals: white-tailed deer, mule deer, Shiras moose and Rocky Mountain
elk. The malady, similar to mad cow disease, is caused by a prion that affects
the brain, lymph and nervous systems. The disease is always fatal. The animals
basically waste away.
In states where CWD has been detected, “hot zones” have been established.
It is recommended that animals that come out of those zones be tested for CWD.
If the deer tests positive, the U.S. Centers for Disease Control advises that
the venison not be consumed. Captive animals where the disease has been detected
are destroyed and the carcasses are carefully disposed of.
Chuck Sykes, WFF Director, said just because Alabama doesn’t have any
cases of CWD right now, it’s not time to let our guard down. He has friends who
have been directly affected by the disease.
“I have a real good friend in Ohio who is having to deal with it right
now,” Sykes said. “It’s basically changed the way they’re having to do business.
Since other management duties were starting to suffer a bit on the Wildlife Area
due to the collection within the hot zone last year, they decided to hire
seasonal positions whose sole purpose is to collect samples from successful
sportsmen and women as well as from roadkills within the hot zone.”
“Texas has had confirmed cases in the past year as well.”
The first documented case of CWD was diagnosed in a captive mule deer herd
in Colorado way back in 1967. Since then, CWD has been confirmed in 20 states
and three Canadian provinces.
Alabama has 207 licensed game breeders, and as a precaution against CWD or
other diseases, each facility is required by law to test any deer over a year of
age that dies, according to Sykes.
“The vast majority of commercial breeders and hunting-enclosure operators
are law-abiding, conservation-minded citizens,” Sykes said. “Much of the
information received regarding alleged illegal imports has come from within the
industry.”
In addition to the game-breeder monitoring, WFF officials are taking
samples from about 300 wild deer per year from sites scattered throughout the
state. The sampling involves taking brain tissue and lymph nodes from the head
and neck of the deer and sending the samples to a certified lab for testing.
Alabama has had a ban on the importation of deer and other cervids since
the mid-1970s. Conservation Enforcement Officers are in charge of monitoring the
deer breeding facilities and licensed exhibitors to ensure compliance with
current laws and regulations. The Alabama law was recently changed to increase
the fine for violations of the importation law to $5,000 per incident.
A recent case illustrates how costly some violations can be. A man from
Georgia was prosecuted for importing deer from Ohio to his property in Florida.
He also attempted to import deer from Ohio into Georgia but was caught while the
deer were en route to Georgia.
The Georgia man pleaded guilty to the charges. He was assessed a fine and
required to pay restitution for a total of $1.6 million, a record for game-law
violations. He was sentenced to three years of probation and four months of home
confinement. His co-defendant pleaded guilty to 12 Lacey Act violations and was
sentenced to 21 months in prison with a $125,000 fine and 200 hours of community
service.
“This record fine shows all states are looking very carefully at these
type of violations and that penalties are very harsh,” Sykes said.
Four cases of CWD were recently confirmed in Texas, where officials are
scrambling to track the movements of the affected deer.
“We’re on the front end of this,” Sykes said. “We don’t really know how
CWD would impact our deer population. Thankfully, Texas has an accurate tracking
protocol of captive deer, so as soon as the first deer tested positive, they
could start tracing back where that deer had been and what facilities it had
been in. Now, they’re trying to test all of the places that had had contact with
the deer.
“Without that methodology in place and the ability to find out quickly and
trace all the tentacles of it, Texas would have been in bad shape. Now, they at
least know where those deer had been, what facilities they had been in, when the
deer had left those facilities and where they had gone. They at least know where
to test. Without that protocol, it would have taken years, if ever, to get that
information.”
Sykes said WFF officials are testing a system similar to the one in Texas
to keep track of Alabama captive deer herds and hope it will be in place soon.
Hunters who spot or harvest a deer that is acting strangely or appears
diseased should contact the nearest district office to have a WFF wildlife
biologist examine the deer and collect samples, according to Sykes, who said
white-tailed deer can suffer from a variety of maladies that can affect behavior
and appearance, especially epizootic hemorrhagic disease (EHD).
“They need to call us and we can have somebody take it and have it
tested,” Sykes said. “It could be EHD or a whole host of things. The only way to
know is to test it. We see deer every year that have been killed in the state
that have evidence of having recovered from EHD. The thing about CWD is the deer
never come back from it. It’s 100-percent fatal.”
Hunting in Alabama has an economic impact of more than $1 billion, and
Sykes said WFF is doing everything possible to ensure that the deer hunting so
cherished in Alabama will not be impacted by CWD.
He is worried that Alabama hunters won’t take the threat seriously since
CWD is currently not in nearby states.
“This isn’t the time for the public to be apathetic because this disease
could affect more than just hunters,” Sykes said. “Everybody knows somebody who
deer hunts or works in an industry that supports deer hunting. It would have a
major economic impact, so don’t think it’s somebody else’s problem.”
The most effective defense against CWD or other potentially catastrophic
pathogens is a well-involved public who actively report information regarding
illegal movement of deer or other wildlife within the state. Rewards for
information leading to an arrest and conviction of game-law violators are
available through the Alabama Wildlife Federation. Call GAMEWATCH at
800-272-4263 to report such activity.
###
Advisory Board Considers Hunting Season Changes ... harvest strategy. In
the continuing effort to keep Chronic Wasting Disease (CWD) out of Alabama, WFF
proposed an amended regulation that ...
drainer - 02/25/2016 - 5:22pm
In the continuing effort to keep Chronic Wasting Disease (CWD) out of
Alabama, WFF proposed an amended regulation that would prohibit the importation
of certain deer parts. Only deboned meat, hides and antlers attached to a
cleaned skull plate could be brought into the state.
“This is mirrored in many, many other states,” Sykes said. “This
complements our existing CWD Response Plan that was instituted in 2012.”
Chronic Wasting Disease By Chris Nix, Wildlife Biologist, Division of
Wildlife and Freshwater Fisheries
Chronic Wasting Disease (CWD) is a contagious neurological disease
affecting the central nervous system of captive and free-ranging mule deer,
white-tailed deer, moose, and Rocky Mountain elk throughout various locations in
North America. This is a fatal and untreatable disease belonging to a group of
diseases known as transmissible spongiform encephalopathies and is similar to
mad cow disease in cattle and scrapie in sheep.
CWD can reduce the growth and size of wild deer and elk in areas where
populations are high, and is of increasing concern for wildlife managers across
North America. The disease had been long thought to be limited in the wild to a
relatively small area in northeastern Colorado, southeastern Wyoming and
southwestern Nebraska, but has recently been found in several new areas across
the North American continent.
To date there has been no case of CWD detected in Alabama or any other
southeastern state. Although that is good news, it is still of upmost importance
to prohibit the spread of CWD.
It is thought that a major method by which CWD is spread is through the
movement of live animals, most often for game farming or breeding operations.
Fortunately, the importation of any deer into Alabama has been prohibited since
1973. It is critical that this importation ban is strictly followed. Any
suspected violations should be reported to the nearest Wildlife and Freshwater
Fisheries office immediately.
In Alabama, annual samples from deer harvested throughout the state are
tested for CWD. This survey began during the 2001-2002 hunting season and
continues today. Collectively, throughout this study approximately 4,100 deer
have been tested for CWD. All tests were negative.
CWD is indicated by a variety of physical signs. Because the brain is the
primary organ affected by the disease, infected animals begin to lose bodily
functions and display abnormal behavior. In early stages of infection, animals
do not show any symptoms. The incubation period can range from about 12-18
months up to 3-5 years. In later stages, infected animals begin to display
abnormal behavior such as staggering or standing with very poor posture. Animals
may have an exaggerated wide posture or carry the head and ears lowered, and may
drool. Infected animals become emaciated (thus the name “wasting disease”) and
appear in very poor body condition. Clinical symptoms are typically not seen in
deer younger than 18 months of age. CWD symptoms may also be characteristic of
diseases other than CWD (e.g. deer with bacterial brain abscesses or chronic
hemorrhagic disease).
If a suspicious animal is encountered, document the location of the animal
and immediately contact the Wildlife and Freshwater Fisheries office nearest
you. For more information on CWD, contact Chris Nix, Wildlife Biologist, Alabama
Department of Conservation and Natural Resources, Division of Wildlife and
Freshwater Fisheries, 30571 Five Rivers Blvd., Spanish Fort, AL 36527;
251-626-5474.
ALABAMA DIVISION OF WILDLIFE AND FRESHWATER FISHERIES CHRONIC WASTING
DISEASE RESPONSE PLAN
Chronic Wasting Disease - What you should know CWD is not known to be
transmissible to humans or domestic livestock.
CWD is a fatal disease of white-tailed deer, mule deer, and elk.
CWD is not known to exist in Alabama or any other southeastern state.
CWD will not likely be found in the Southeast unless it is transported
here.
It is illegal to import any deer or other cervid into Alabama.
The range expansion of chronic wasting disease (CWD) in wild deer has led
to unprecedented attention and concern during the past few years. Unfortunately,
many rumors and much misinformation about CWD have been spread to the public.
This page provides up-to-date facts on what is known about CWD and what is being
done in Alabama to help prevent the disease from reaching our state.
What is CWD?
Chronic wasting disease is a fatal disease affecting the central nervous
system of deer and elk. This disease belongs to a family of diseases known as
transmissible spongiform encephalopathies (TSE"s). The disease attacks the
brains of infected deer and elk and causes animals to become emaciated (skinny),
display abnormal behavior, lose bodily functions, and die. The disease has been
found in either captive or wild deer in twelve western and midwestern states and
two Canadian provinces.
Mule deer, white-tailed deer, and Rocky Mountain elk are the three species
of the deer family known to be naturally susceptible to CWD. One case of CWD has
been detected in a wild moose taken by a hunter in Colorado. Susceptibility of
other species of deer to CWD is not known. No cases linking any disease in
livestock or humans to CWD have been discovered. At this time it is thought that
transmission to domestic animals or humans is unlikely.
Where has CWD been found?
Chronic wasting disease was first recognized in the 1960s as a syndrome of
captive mule deer held in research facilities in Ft. Collins, Colorado. CWD was
originally believed to be a nutritional disorder and was not recognized as a TSE
until 1978. CWD was soon identified in captive deer and elk from other wildlife
research facilities in Colorado and Wyoming, as well as in at least two
zoological collections.
CWD since has been diagnosed in captive elk and/or deer herds in Colorado,
Kansas, Minnesota, Montana, Nebraska, New York, Oklahoma, South Dakota,
Wisconsin, Wyoming and the Canadian provinces of Alberta and Saskatchewan. CWD
was first found in wild deer and elk in northeastern Colorado and southeastern
Wyoming. The disease since has been found in wild deer and/or elk in Colorado,
Illinois, Iowa, Kansas, Maryland, Minnesota, Missouri, Nebraska, New Mexico,
North Dakota, New York, Pennsylvania, South Dakota, Texas, Utah, Virginia,
Wisconsin, Wyoming, West Virginia and the Canadian provinces of Alberta and
Saskatchewan. Many of the wild deer were discovered in areas surrounding captive
deer facilities with infected animals. No cases of CWD have been found in
Alabama or any other southeastern state.
What is the Division of Wildlife and Freshwater Fisheries doing to keep
CWD from reaching our state?
The Division is currently taking several measures to help prevent CWD from
reaching our state. The State has had a regulation banning the importation of
all cervids (members of the deer family) into Alabama since 1973. Recently the
fines for violating this regulation were significantly increased. Investigations
have discovered animal movements among many of the 20 privately owned elk herds
(outside of Alabama) where CWD has been diagnosed. The movement of infected
animals very likely was the reason for the disease's spread. Halting the
movement of live captive deer and elk into and within Alabama is a major step in
preventing the disease from reaching our state.
The Division also started an active monitoring program for CWD during the
2001-02 hunting season. The number of Alabama deer tested for the presence of
CWD is as follows:
2001-02 90
2002-03 440
2003-04 768
2004-05 736
2005-06 779
2006-07 654
2007-08 627
2008-09 606
2009-10 308
2010-11 311
2011-12 304
2012-13 - no testing due to funding loss
2013-14 - no testing due to funding loss
2014-15 - testing has resumed
Total 5,623
None of those deer tested positive for the disease. Plans are to continue
this testing program during the 2011-2012 season.
What can the public do to help?
Citizens of Alabama can assist the Division of Wildlife and Freshwater
Fisheries with its CWD monitoring program. The first and most important way to
assist is to report any transport of live deer or elk on Alabama's roads and
highways. Please call the Operation Game Watch line immediately at
1-800-272-4263 if you see live deer or elk being transported in Alabama.
Contacting the Division immediately makes it more likely the deer or elk will be
intercepted before they can be released.
The public also can help the Division in their active monitoring program.
A CWD infected deer will behave abnormally, showing little of their normal
wariness or fear of humans. Infected animals also will become emaciated
(skinny). It is important to note that other diseases may exhibit similar
symptoms. Please call the Division of Wildlife and Freshwater Fisheries Office
nearest you or the Operation Game Watch line at 1-800-272-4263 if you spot a
deer that exhibits these clinical signs of CWD. Personnel with the Division of
Wildlife and Freshwater Fisheries will contact you to obtain additional
information.
The greatest single threat of introducing CWD into Alabama's deer herd is
from the illegal importation of deer or elk into the state. Cooperation from our
hunters and landowners is essential to keeping CWD out or Alabama. Prohibiting
the movement of deer and elk will greatly reduce the chances of an undetected
ease of CWD spreading to a greater number of uninfected animals. We need your
support to maintain our CWD free status - be informed, be vigilant, and be
responsible.
Chronic Wasting Disease Alliance
The Boone and Crockett Club, Rocky Mountain Elk Foundation and Mule Deer
Foundation formed the Chronic Wasting Disease Alliance in January 2002. The
organizations agreed to pool resources, share information, and collaborate on
ways to positively address the CWD issue. Other organizations have since joined
the alliance.
The mission of the CWD Alliance is to promote responsible and accurate
communications regarding CWD, and to support strategies that effectively control
CWD to minimize its impact on wild, free-ranging cervids including deer, elk,
and moose. The CWD Alliance webiste is an excellent resource for hunters to
obtain information regarding the latest CWD news and updates. Please click here
for the latest map of where CWD is known to occur.
Alabama's Chronic Wasting Disease Response Plan
Alabama Wildlife and Freshwater Fisheries formalized a revised Chronic
Wasting Disease Response Plan in January, 2013.
Madison County conservation enforcement officers kill escaped bull elk
By Jeff Dute, Press-Register
on November 04, 2011 at 10:30 AM, updated November 04, 2011 at 12:13 PM
MADISON COUNTY, Alabama -- Conservation enforcement officers in Madison
County killed a young red deer/elk hybrid bull earlier this week that had
wandered more than 80 miles north, then east from where it is suspected to have
escaped from an enclosure near Hanceville, said District I assistant supervising
wildlife biologist Mitchell Marks.
Marks said the estimated 450-pound bull's path to where it was killed
north of Huntsville was easy to track from the numerous phone calls the
department received over the last two weeks.
When no one claimed ownership, Marks said the decision to kill it was
based on concerns over the possible spread of the always-fatal deer malady
chronic wasting disease and for public safety reasons.
"It's not believed that this animal had CWD, but since we don't know
exactly where it came from, first we have to test to make sure it doesn't," he
said. "We don't want to jeopardize our deer herd at all. Second, people in
Alabama are not used to seeing an animal of this size on our state's roads.
Something that big could be a public hazard that we want to remove."
There is no CWD test for live animals, so once it was killed, the hybrid's
head was removed and sent for testing while the carcass was buried, Marks said.
Kevin Dodd, Alabama's assistant chief of enforcement said since state
regulations only mention deer in regard to seasons and bag limits, hunters who
happen to encounter a non-native species such as the sika deer shot by a
bowhunter in Jackson County on Monday or even an elk are within their rights to
legally kill it.
"If they happen to see a sika or an elk, it's fair game as far as the
law's concerned," Dodd said. "Shoot it, drag it to the truck and have it
packaged at the processor."
As an example, Dodd said a hunter legally killed what he thought was the
biggest whitetail doe of his life near Tuscaloosa last year. The animal turned
out to be a cow elk that had escaped from an eclosure and that was twice as big
as the average whitetail female.
Alabama : Elk Escape From Killen Farm to Greenhill
Date: December 05, 2003 Source: The Associated Press
Contacts: The Associated Press
A small herd of elk escaped a game farm in Killen and made its way to
Greenhill, giving local hunters a rare chance to hunt the animal close to home.
Residents had reported seeing animals that looked like deer but were
bigger, but wildlife officials were unable to track down any of the creatures.
It wasn't until residents began hunting Tuesday that authorities realized the
animals were elk.
Wildlife officials initially were puzzled about where the animals came
from - the Smoky Mountains in eastern Tennessee is the area closest to the
Shoals where elk are known to roam freely.
Authorities seized and buried three elk shot in a field off U.S. 43 by a
hunter who did not have the landowner's permission to hunt there.
Capt. Johnny Johnson of the Division of Wildlife and Freshwater Fisheries
said elk hunted in the Greenhill area would be tested for chronic wasting
disease. The disease has been spotted in several Western states and Wisconsin,
but not in Alabama.
Wildlife and Freshwater Fisheries enforcement officer Richard Wallace
warned hunters not to eat any meat from the elk until the tests are complete.
snip...see more here ;
2012
10-29-2012, 10:49 AM
Alabama captive cervid farming, testing and regulations for CWD, recipe
for disaster ?
10-29-2012, 10:49 AM
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*** Chronic Wasting Disease CWD TSE Prion Roundup March 30, 2016 ***
============================================================
Chronic Wasting Disease CWD TSE Prion Roundup
Tuesday, March 29, 2016
Maryland Department of Natural Resources Five Deer Test Positive for
Chronic Wasting Disease ONE OUTSIDE CWD MANAGEMENT ZONE
Thursday, March 24, 2016
ARKANSAS FIRST BATCH OF TARGET TESTS REVEALS 19 ADDITIONAL CWD-POSITIVE
CERVIDS
Friday, March 18, 2016
Michigan confirms additional CWD-positive free-ranging, white-tailed deer,
bringing the total to seven
Wednesday, March 16, 2016
Wisconsin CWD sample survey 2015 confirms 290 cases of Chronic Wasting
Disease TSE Prion
Tuesday, March 08, 2016
Oklahoma Chronic Wasting Disease CWD of Deer and Elk Surveillance,
Testing, and Preparedness ???
Sunday, March 06, 2016
Missouri 2015-2016 CWD Surveillance Summary to Date, with confirmed cases
mounting
TEXAS CWD TESTING TOTAL FIGURES ??? anyone’s guess to date. TAHC et al
should take up Arkansas reporting of test results to the public and open
discussion. ...
Friday, February 05, 2016
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER
RELEASE SITE
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Thursday, March 10, 2016
WYOMING RIDE EM COWBOY HELICOPTER WRANGLING RAMBO STYLE DEER BULLDOGGING
RODEO FOR CWD VIDEO
CHRONIC WASTING DISEASE: The Final Epidemic
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
Friday, February 26, 2016
Pennsylvania Monitoring the Growing Threat of Chronic Wasting Disease CWD
TSE Prion
Friday, February 05, 2016
IOWA Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee
County
Friday, January 29, 2016
NEBRASKA Three Positives for CWD Found in Recent Testing of Deer
Friday, November 20, 2015
ODNR Takes Action to Monitor Chronic Wasting Disease in Ohio's Deer Herd
Friday, October 23, 2015
Ohio Wildlife Council Passes Rule to Help Monitor CWD
Wednesday, August 05, 2015
Ohio confirms to me Chronic Wasting Disease CWD Spreads 19 confirmed cases
to date
Thursday, October 23, 2014
*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE
PRESERVE
Wednesday, February 11, 2015
World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with
two counts of tampering with evidence
Thursday, October 23, 2014
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE
PRESERVE
Monday, June 11, 2012
*** OHIO Captive deer escapees and non-reporting ***
Saturday, February 6, 2016
*** Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission ***
Friday, February 05, 2016
Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids, as well as non-ruminants such as cats and dogs as
well, as soon as possible for the following reasons...
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
*** 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
Monday, March 28, 2016
National Scrapie Eradication Program February 2016 Monthly Report
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
http://www.regulations.gov/#!documentDetail;D=APHIS-2007-0127-0032
http://scrapie-usa.blogspot.com/2015/11/docket-no-aphis-2007-0127-scrapie-in.html
Friday, March 18, 2016 CFSAN
Constituent Update: FDA Announces Final Rule on Bovine Spongiform
Encephalopathy BSE MAD COW TSE PRION Center for Food Safety and Applied
Nutrition - Constituent Update
Tuesday, March 15, 2016
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information Singeltary Submission
Saturday, February 6, 2016
Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission
Friday, August 14, 2015
*** Susceptibility of cattle to the agent of chronic wasting disease from
elk after intracranial inoculation
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.
***********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
*** 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).***
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
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.
***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.
***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.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
”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.
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. ...
MAD COW DISEASE HAS BEEN IN THE USA FOR DECADES, AND I BELIEVE IT WAS IN
THE USA FIRST, PLEASE SEE ;
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...
PL1
Using in vitro prion replication for high sensitive detection of prions
and prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
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 ;
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 ***
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.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease
Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in
white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in
white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
PPo3-22:
Detection of Environmentally Associated PrPSc on a Farm with Endemic
Scrapie
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh
Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of
Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories
Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University
of Nottingham; Sutton Bonington, Loughborough UK
Key words: scrapie, evironmental persistence, sPMCA
Ovine scrapie shows considerable horizontal transmission, yet the routes
of transmission and specifically the role of fomites in transmission remain
poorly defined. Here we present biochemical data demonstrating that on a
scrapie-affected sheep farm, scrapie prion contamination is widespread. It was
anticipated at the outset that if prions contaminate the environment that they
would be there at extremely low levels, as such the most sensitive method
available for the detection of PrPSc, serial Protein Misfolding Cyclic
Amplification (sPMCA), was used in this study. We investigated the distribution
of environmental scrapie prions by applying ovine sPMCA to samples taken from a
range of surfaces that were accessible to animals and could be collected by use
of a wetted foam swab. Prion was amplified by sPMCA from a number of these
environmental swab samples including those taken from metal, plastic and wooden
surfaces, both in the indoor and outdoor environment. At the time of sampling
there had been no sheep contact with these areas for at least 20 days prior to
sampling indicating that prions persist for at least this duration in the
environment. These data implicate inanimate objects as environmental reservoirs
of prion infectivity which are likely to contribute to disease transmission.
Veterinary Pathology Onlinevet.sagepub.com Published online before print
February 27, 2014, doi: 10.1177/0300985814524798 Veterinary Pathology February
27, 2014 0300985814524798
Lesion Profiling and Subcellular Prion Localization of Cervid Chronic
Wasting Disease in Domestic Cats
D. M. Seelig1⇑ A. V. Nalls1 M. Flasik2 V. Frank1 S. Eaton2 C. K.
Mathiason1 E. A. Hoover1 1Department of Microbiology, Immunology, and Pathology,
Colorado State University, Fort Collins, CO, USA 2Department of Biomedical
Sciences, Colorado State University, Fort Collins, CO, USA D. M. Seelig,
University of Minnesota, Department of Veterinary Clinical Sciences, Room 339
VetMedCtrS, 6192A (Campus Delivery Code), 1352 Boyd Ave, St Paul, MN 55108, USA.
Email address: dseelig@umn.edu
Abstract
Chronic wasting disease (CWD) is an efficiently transmitted, fatal, and
progressive prion disease of cervids with an as yet to be fully clarified host
range. While outbred domestic cats (Felis catus) have recently been shown to be
susceptible to experimental CWD infection, the neuropathologic features of the
infection are lacking. Such information is vital to provide diagnostic power in
the event of natural interspecies transmission and insights into host and strain
interactions in interspecies prion infection. Using light microscopy and
immunohistochemistry, we detail the topographic pattern of neural spongiosis
(the “lesion profile”) and the distribution of misfolded prion protein in the
primary and secondary passage of feline CWD (FelCWD). We also evaluated cellular
and subcellular associations between misfolded prion protein (PrPD) and central
nervous system neurons and glial cell populations. From these studies, we (1)
describe the novel neuropathologic profile of FelCWD, which is distinct from
either cervid CWD or feline spongiform encephalopathy (FSE), and (2) provide
evidence of serial passage-associated interspecies prion adaptation. In
addition, we demonstrate through confocal analysis the successful
co-localization of PrPD with neurons, astrocytes, microglia, lysosomes, and
synaptophysin, which, in part, implicates each of these in the neuropathology of
FelCWD. In conclusion, this work illustrates the simultaneous role of both host
and strain in the development of a unique FelCWD neuropathologic profile and
that such a profile can be used to discriminate between FelCWD and FSE.
prion chronic wasting disease immunohistochemistry interspecies cat feline
spongiform encephalopathy transmissible spongiform encephalopathy adaptation
species barrier
Monday, August 8, 2011 Susceptibility of Domestic Cats to CWD Infection
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis
M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K.
Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness.
*** Two of these cats have developed rear limb ataxia. Although the
limited data from this ongoing study must be considered preliminary, they raise
the potential for cervid-to-feline transmission in nature.
AD.63:
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado
State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN
USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to
the domestic cat, thus raising the issue of potential cervid-to- feline
transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
FELINE SPONGIFORM ENCEPHALOPATHY FSE
Wednesday, October 17, 2012
Prion Remains Infectious after Passage through Digestive System of
American Crows (Corvus brachyrhynchos)
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A.
Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel
J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary
Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI
53706, USA 2US Geological Survey, National Wildlife Health Center, 6006
Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural
Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary
Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author
email: cjohnson@svm.vetmed.wisc.edu
We intracerebrally challenged four species of native North American
rodents that inhabit locations undergoing cervid chronic wasting disease (CWD)
epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed
mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles
(Myodes gapperi). The inocula were prepared from the brains of hunter-harvested
white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles
proved to be most susceptible, with a median incubation period of 272 days.
Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the
brains of all challenged meadow voles. Subsequent passages in meadow voles lead
to a significant reduction in incubation period. The disease progression in
red-backed voles, which are very closely related to the European bank vole (M.
glareolus) which have been demonstrated to be sensitive to a number of TSEs, was
slower than in meadow voles with a median incubation period of 351 days. We
sequenced the meadow vole and red-backed vole Prnp genes and found three amino
acid (AA) differences outside of the signal and GPI anchor sequences. Of these
differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is
particularly intriguing due its postulated involvement in "rigid loop" structure
and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5
years post-inoculation, but appear to be exhibiting a high degree of disease
penetrance. White-footed mice have an even longer incubation period but are also
showing high penetrance. Second passage experiments show significant shortening
of incubation periods. Meadow voles in particular appear to be interesting lab
models for CWD. These rodents scavenge carrion, and are an important food source
for many predator species. Furthermore, these rodents enter human and domestic
livestock food chains by accidental inclusion in grain and forage. Further
investigation of these species as potential hosts, bridge species, and
reservoirs of CWD is required.
please see ;
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being
introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids, as well as non-ruminants such as cats and dogs as
well, as soon as possible for the following reasons...
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
*** 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
ALABAMA CWD TSE PRION ???
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
5:24 PM
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