MINNESOTA CHRONIC WASTING DISEASE SURVEILLANCE AND TESTING CWD TSE PRION UPDATE
CHRONIC WASTING DISEASE MANAGEMENT
Southeast Minnesota CWD
Surveillance
Due to continued discovery of new cases of Chronic Wasting Disease in deer
from northeast Iowa (Alamakee County) and western Wisconsin, the Minnesota DNR
will collect tissue samples from up to 3,600 deer harvested in 10 southeast
Minnesota permit areas (see map).
Hunters in these areas will need to check the DNR website this fall for
locations of registration stations where samples will be collected. For those
permit areas:
• Deer harvested in surveillance areas must be registered in person.
Hunters are strongly encouraged to allow staff to take tissue samples. Telephone
and internet registration options will be deactivated in these areas and will
remain off until sampling goals have been achieved.
• Submission of a sample is voluntary and there are no carcass movement
restrictions. This surveillance is being conducted because the disease was found
in close proximity to the Minnesota state line. The DNR’s CWD management plan
calls for surveillance when a new infection is discovered near Minnesota.
• A hunter will only be notified if a deer is found positive. Look for a
DNR news release for complete sampling results after the deer season ends.
• More information, including the stations where deer will be sampled, will
be posted on the DNR website this fall.
NEW FOR 2016
• The boundary of deer permit area 601 has been changed slightly. See
detail map on the back of the large fold-out map.
• Several fur registration stations have reduced hours in December. See **
in the table on page 56.
• The DNR will collect tissue samples from up to 3,600 deer in 10 southeast
permit areas as part of a CWD surveillance effort. See page 65 for locations and
details.
• It is likely that whole carcasses of deer, elk, moose and caribou
harvested in other states or provinces will not be allowed to be brought into
Minnesota to prevent the spread of chronic wasting disease. See page 62 for
details.
Chronic Wasting Disease
Chronic Wasting Disease occurs in deer, elk, and moose. It belongs to a
group of infectious diseases known as “transmissible spongiform
encephalopathies” (TSEs). It is caused by an abnormal protein, called a prion,
that affects the animal’s brain and is invariably fatal. Usually, months to
years pass from the time an animal is infected to when it shows signs of the
disease.
Typical signs of the disease include drooping head or ears, poor body
condition, tremors, stumbling, increased salivation, difficulty swallowing, or
excessive thirst or urination.
National CWD information can be found at www. cwd-info.org.
Carcass Import Restrictions
The increasing prevalence of chronic wasting disease (CWD) in North America
has prompted the Minnesota DNR to propose additional restrictions prohibiting
the importation of whole deer, elk, moose, and caribou carcasses into the state.
Previously this restriction applied only to deer, elk, moose and caribou
harvested in areas of North America where CWD has been known to occur.
Once the new rule is implemented, hunters may bring only the following
parts into Minnesota, regardless of where the animal was harvested outside of
the state:
• Meat that is boned out or that is cut and wrapped (either commercially or
privately).
• Quarters or other portions of meat with no part of the spinal column or
head attached.
• Hides and teeth.
• Antlers or clean (no brain tissue attached) skull plates with antlers
attached.
• Finished taxidermy mounts.
• Nonresidents transporting whole or partial carcasses on a direct route
through Minnesota are exempt from this restriction.
The Minnesota DNR will announce when these new restrictions are in place.
More information about chronic wasting disease is online at
mndnr.gov/hunting/deer/cwd
MINNESOTA STRATEGIC MANAGEMENT PLAN FOR ELK JANUARY 2016
Since then, CWD has been documented in five different captive deer or elk
herds in Minnesota, and in one free-ranging white-tailed deer in Olmsted County.
Through November 2014, 113 wild elk have been tested for CWD and none were
positive.
DISEASE MANAGEMENT
Elk are susceptible to a variety of known wildlife and domestic animal
diseases and parasites. Minnesota’s free-ranging elk populations are exposed to
both captive cervids and livestock (primarily beef cattle) operations, and the
potential movement of diseases between captive and wild animals is an ongoing
risk factor. Therefore, monitoring of Minnesota’s wild elk for a wide variety of
pathogens is important to maintaining the overall health of the
population.
Chronic Wasting Disease (CWD) has become a concern with deer and elk
populations nationwide and in some Canadian provinces in recent years. CWD has
been documented in wild white-tailed deer populations in the neighboring states
of Wisconsin, Iowa, and South Dakota, as well as Saskatchewan to the northwest.
The presence of CWD in wild deer in adjacent states prompted monitoring in wild
populations of deer in Minnesota beginning in 2002. Since then, CWD has been
documented in five different captive deer or elk herds in Minnesota, and in one
free-ranging white-tailed deer in Olmsted County. Through November 2014, 113
wild elk have been tested for CWD and none were positive.
CHRONIC WASTING DISEASE SURVEILLANCE IN MINNESOTA’S SOUTHEASTERN WILD DEER
HERD
created: 11/2/15
Erik Hildebrand1, Michelle Carstensen, Margaret Dexter, and Chris
Jennelle
SUMMARY OF FINDINGS
In fall 2014, the Minnesota Department of Natural Resources (MNDNR) sampled
411 hunter-harvested white-tailed deer (Odocoileus virginianus) for chronic
wasting disease (CWD) in southeastern Minnesota. The surveillance effort focused
on testing deer within deer permit areas (DPA) 348 and 349, in response to the
first detection of CWD in a free-ranging deer by the Iowa Department of Natural
Resources in Allamakee County. All deer were negative for the disease. MNDNR
also submitted samples from 69 deer from within DPA’s 236 and part of 601 (north
metro surveillance area) where a captive European red deer (Cervus elaphus) farm
was found positive for CWD in summer 2012. These deer were collected through
vehicle kills, special hunts, and depredation permits; all deer were negative
for CWD. In addition, MNDNR submitted samples from 18 cervids through targeted
surveillance, which included sick animals, escaped captive cervids, and
vehicle-kills; these were also all negative for CWD. Currently, MNDNR has
suspended efforts to test for CWD through hunter-harvested surveillance in the
state, but will continue with targeted surveillance efforts.
INTRODUCTION
Chronic wasting disease is a transmissible spongiform encephalopathy (TSE)
that affects elk (Cervus elaphus), mule deer (Odocoileus hemionus), white-tailed
deer, and moose (Alces alces). TSEs are infectious diseases that alter the
morphology of the central nervous system, resulting in a “sponge-like”
appearance of this tissue. The etiological agent of CWD is an infectious
protein, called a prion. Incubation time of the disease can range from 1.5 to
nearly 3 years, although infected animals have been shown to shed prions in
their feces up to a year before showing signs of illness (Tamguney et al. 2009,
Haley et al. 2011). Clinical signs are nonspecific and may include a loss of
body condition and weight, excessive salivation, ataxia, and behavioral changes.
There is no known treatment or vaccine for the disease and it is always fatal.
Experimental and circumstantial evidence suggest that transmission of the
disease is primarily through direct contact with infected animals or their
infective saliva or excrement (Mathiason et al. 2006, Safar et al. 2008).
However, persistence of prions in the environment and resulting indirect
transmission has been shown to occur (Miller et al. 2004, Johnson et al. 2007,
and Maluquer de Motes et al. 2008).
The Center for Disease Control (CDC) and other public health agencies have
concluded there is no known link between CWD and any neurological disease in
humans (MaWhinney et al. 2006, Sandberg et al. 2010). However, both the CDC and
the World Health Organization (WHO) recommend that no part of a known positive
animal should be consumed by humans. Additionally, there is no evidence that CWD
can be naturally transmitted to species other than deer, elk, or moose.
To date, CWD has been diagnosed in 3 captive elk (Cervus canadensis) herds,
1 captive white-tailed deer herd, and 1 captive European red deer (Cervus
elaphus) herd in Minnesota. Two of the elk herds (Stearns and Aitkin counties)
were discovered in 2002 and depopulated; no additional CWD-positive animals were
found. In 2006, a captive white-tailed deer from a mixed deer/elk herd in Lac
Qui Parle County was infected with CWD and depopulated without additional
infection being detected. In 2009, another captive elk herd (Olmsted County) was
found infected
1 Corresponding author email: erik.hildebrand@state.mn.us 2014 Wildlife
Research Summaries Wildlife Health Research Group
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with CWD and, following depopulation of >600 animals, a total of 4 elk
were confirmed with the disease. The United States Department of Agriculture’s
(USDA) indemnification document noted there was an apparent longstanding
infection within this captive elk facility. In 2012, a captive European red deer
was found infected with CWD in a herd of approximately 400 animals in North
Oaks, MN. This marked the first time CWD was discovered in this species. This
red deer herd was depopulated in 2014; no additional infected animals were
found. According to the indemnity agreement, perimeter fences must remain intact
at this property until 2019, in an effort to keep wild deer from entering the
property to reduce disease transmission risks.
Currently, Minnesota has approximately 500 captive cervid facilities. As
the current statewide population estimate of wild deer approaches one million,
there is an element of inherent disease transmission risk between captive and
wild cervids. Overall, risk is difficult to quantify because deer populations
are unevenly distributed over the landscape ranging in densities from < 1-15
deer/km2 (i.e., 1–40 deer/mi2), facility fences vary in construction quality,
and direct/indirect contact rates between captive and wild cervids are unknown.
In addition, captive cervid facilities are sporadically distributed on the
landscape and are independent of wild deer densities.
In November 2010, MNDNR sampled 564 hunter-harvested deer focused on a
32.2-km (20-mi) radius around a CWD-positive captive elk facility near Pine
Island (Olmstead county), discovered in 2009. One free-ranging deer tested
positive for CWD, marking the first detection of the disease in Minnesota’s wild
deer population. In response to this disease detection, MNDNR conducted a
fixed-wing aerial deer survey in a 16.0-km (10-mi) radius of the index case in
late January 2011 and estimated 6,200 deer (7.3 deer/km2 or 19 deer/mi2). A
supplemental surveillance effort was conducted in February–March 2011; 752 adult
deer were sampled and all tested negative. To prevent further disease spread,
MNDNR banned recreational feeding of deer in a 4-county area in southeastern
Minnesota and created a CWD Management Zone DPA 602.
From 2011–2013, a total of 4,050 (n = 1,125, 1,195, and 978 for 2011, 2012,
and 2013, respectively) deer were sampled for CWD within DPA 602 with no further
infection detected. These data, in combination with historical data from
2002-2009 indicated >99% probability that disease prevalence was no greater
than 0.5% assuming independence between years and animals within year. These
results provide strong evidence that Minnesota was on the front end of a CWD
outbreak in wild deer. Our inability to detect any additional infected deer in
the immediate vicinity of the index case or in surrounding DPA’s or in DPA’s
bordering neighboring infected counties is encouraging. The data suggests CWD
was recently introduced on the southeastern MN landscape, with a high likelihood
that widespread wild cervid exposure has been minimal.
METHODS
Hunter-harvested surveillance during 2014 was conducted at deer
registration stations during the first two weekends of the regular firearm
hunting season in southeastern Minnesota. Selected stations were staffed with
MNDNR personnel and students (veterinary medicine and natural resources) trained
in lymph node collection. Stations were selected based on deer volume and
distribution throughout the surveillance zone to meet a sampling goal of 450
between DPAs 348 and 349 combined. Hunters were asked to voluntarily submit
medial retropharyngeal lymph node samples from deer ≥1.5 years of age to be
tested for CWD, and a front incisor was extracted from all deer visually
assessed to be ≥2.5 years old for aging by cementum annuli. To obtain access to
deer from the north metro surveillance area MNDNR worked with local contractors
and the Wildlife Science Center to collect vehicle-killed deer within a 10-mile
radius of the CWDinfected red deer farm in North Oaks. Additional deer were
obtained through special hunts in Ramsey and Anoka counties, as well as both
private and city depredation permits. All deer samples were inventoried, entered
into a database, and sent to Colorado State University (Fort Collins, CO) for
enzyme-linked immunosorbent assay (ELISA) testing. Any presumptive positive deer
from ELISA testing would be confirmed using immunohistochemistry (IHC) testing
at the National Veterinary Services Laboratory in Ames, Iowa.
At the time when deer were sampled, hunter information was recorded,
including the hunter’s name, a telephone number, MNDNR number, and location of
harvest. Maps were provided to assist the hunters in identifying the location
(Township, Range, and Section) of the harvest site. Cooperating hunters were
given a cooperator’s patch. Across MN, MNDNR consistently samples any cervid
exhibiting clinical symptoms of CWD
2014 Wildlife Research Summaries Wildlife Health Research Group Page
156
infection (targeted surveillance). We have disseminated information to
wildlife staff regarding clinical signs of infection for symptomatic deer. We
also provided staff with the necessary equipment and training for lymph node
removal and data recording. The number of samples expected through targeted
statewide surveillance is estimated to be less than 100 animals annually, as few
reports of deer with clinical signs are received.
RESULTS AND DISCUSSION
MNDNR collected a total of 411 samples in southeastern Minnesota from
hunterharvested deer during fall 2014 (Figure 1). All samples were negative for
CWD. The sampling goal was 450 samples between DPA’s 348 and 349 combined, and
we achieved 91% of our surveillance goal in southeastern MN.
From July 2014 to June 2015, MNDNR collected a total of 18 samples from
targeted surveillance efforts. This included samples from 2 escaped captive
deer, and 16 free-ranging deer with clinical signs; all samples were negative
for CWD.
In the north metro surveillance area, 69 deer were tested in fall 2014.
From 2012 – 2014, a total of 350 (160, 121, and 69, respectively) deer were
tested for CWD through vehicle-kills (n=48), special hunts (n=163), and from a
city-contracted sharpshooting effort within the city of North Oaks (n=139), with
no detection of the disease (Figure 2).
Hunter-harvested deer was and remains the primary source for obtaining
adequate samples for continued monitoring and management of this disease since
the first discovery of CWD in MN in 2002. MNDNR remains concerned about CWD
spread in wild cervids, and has increased surveillance focus in southeastern
Minnesota with evidence of increasing CWD detections in wild deer in
southwestern Wisconsin and northeastern Iowa.
Future Surveillance Plans
Given there have been no CWD detections in hunter-harvested wild deer since
2010, and no detections via targeted surveillance efforts, MNDNR will not
conduct hunter-harvest surveillance in 2015. Targeted CWD surveillance of deer
exhibiting clinical signs of illness will continue statewide.
ACKNOWLEDGMENTS
We would like to thank all the MNDNR Wildlife and Enforcement staff, who
volunteered to assist with this disease surveillance project. We also wish to
thank the students and faculty from the University of Minnesota, Colleges of
Veterinary Medicine and Natural Resources, for assisting in our fall sampling
efforts. Special thanks to Julie Hines and Bob Wright for fulfilling our GIS
mapping needs. We appreciate the support of the USDA-Wildlife Services disease
biologist Paul Wolf.
LITERATURE CITED
Haley, N., C. K. Mathiason, S. Carver, M. Zabel, G. C. Telling, and E. A.
Hoover. 2011. Detection of Chronic Wasting Disease Prions in Salivary, Urinary,
and Intestinal Tissues of Deer: Potential Mechanisms of Prion Shedding and
Transmission. Journal of Virology 85(13): 6309-6318.
Johnson, C. J., J. A. Pederson, R. J. Chappell, D. McKenzie, and J. M.
Aiken. 2007. Oral transmissibility of prion disease is enhanced by binding to
soil particles. PLoS Pathogens 3:e93.
Maluquer de Motes, C., M. J. Cano, M. Pumarola, and R. Girones. 2008.
Detection and survival of prion agents in aquatic environments. Water Research
42:2465-2472.
Mathiason, C. K., J. G. Powers, S. J. Dahmes, D. A. Osborn, K. V. Miller,
R. J. Warren, G. L. Mason, S. A. Hays, J. Hayes-Klug, D. M. Seelig, M. A. Wild,
L. L. Wolfe, T. R. Spraker, M. W. Miller, C. J. Sigurdson, G. C. Telling, and E.
A. Hoover. 2006. Infectious prion in the saliva and blood of deer with chronic
wasting disease. Science 314:133-136. MaWhinney, S., W. J. Pape, J. E. Forster,
C. A. Anderson, P. Bosque, and M. W. Miller. 2006. Human prion disease and
relative risk associated with chronic wasting disease.
2014 Wildlife Research Summaries Wildlife Health Research Group Page
157
Emerging Infectious Diseases 12:1527-1535. Miller, M.W., E. S. Williams, N.
T. Hobbs, and L. L. Wolfe. 2004. Environmental sources of prion transmission in
mule deer. Emerging Infectious Diseases 10:1003–1006.
Tamguney, G., M. W. Miller, L. L. Wolfe, T. M. Sirochmann, D. V. Glidden,
C. Palmer, A. Lemus, S. J. DeArmond, and S. B. Prusiner. 2009. Asymptomatic deer
excrete infectious prions in feces. Nature 461:529–532.
Safar, J. G., P. Lessard, G. Tamguney, and Y. Freyman. 2008. Transmission
and detection of prions in feces. Journal of Infectious Diseases 198:81-89.
Sandberg, M. K., H. Al-Doujaily, C. J. Sigurdson, M. Glatzel, C. O’Malley, C.
Powell, E. A. Asante, J. M. Linehan, S. Brandner, J. D. F. Wadsworth1 and J.
Collinge. 2010.
Chronic wasting disease prions are not transmissible to transgenic mice
overexpressing human prion protein. Journal of General Virology 91: 2651–2657.
Figure 1. Samples collected from deer (n=411) for chronic wasting disease
(CWD) testing in
southeastern Minnesota during fall 2014.
Figure 2. Samples collected from deer (n=350) for chronic wasting disease
(CWD) testing in the
north metro surveillance area, in relation to the location of CWD-positive
European red deer farm,
2012 through fall 2014.
*** Table 1. Serological results from harvested elk in northwestern
Minnesota, 2004 - 2014. ***
Disease n Apparent prevalence %
Chronic Wasting Disease 115 0
Thursday, September 19, 2013
Chronic Wasting Disease CWD surveillance, deer feeding ban continues in
southeastern Minnesota
Friday, September 28, 2012
Stray elk renews concerns about deer farm security Minnesota
Friday, May 25, 2012
Chronic Wasting Disease CWD found in a farmed red deer from Ramsey County
Minnesota
Saturday, March 17, 2012
Minnesota CWD DNR, Can chronic wasting disease jump from deer to humans?
yes, maybe some day YOUTUBE
Tuesday, January 25, 2011
Minnesota, National Veterinary Services Laboratory in Ames, Iowa, has
confirmed CWD case near Pine Island
Friday, January 21, 2011
MINNESOTA HIGHLY SUSPECT CWD POSITIVE WILD DEER FOUND NEAR PINE ISLAND
Saturday, October 31, 2009
Elk from Olmsted County herd depopulated to control CWD Three additional
elk from the 558-head herd tested positive
Tuesday, January 27, 2009
Chronic Wasting Disease found in a farmed elk from Olmsted County ST. PAUL,
Minn.
CHRONIC WASTING DISEASE UPDATE September 6, 2002
Minnesota has announced the finding of CWD in a captive elk in Aitkin
County. The animal was a five-year-old male. It had been purchased from a
captive facility in Stearns County in August of 2000. The herd where the elk was
found has been placed under quarantine as has two additional facilities where
the infected elk had resided prior to it coming to the farm in Aitkin County.
Minnesota DNR officials will test wild deer in the area to determine if there is
any sign of CWD in the free-ranging population. This is the first case of CWD in
either captive or freeranging cervids in Minnesota. Several more states have
passed bans on the importation of deer and elk carcasses from states where CWD
has been found in wild animals. Previously the states of Colorado, Illinois and
Iowa and the province of Manitoba had passed such bans. The states of Vermont,
Oregon and Missouri have enacted similar bans. Numerous states have issue
voluntary advisories to their out-of-state hunters encouraging them not to bring
the carcass or carcass parts of deer and elk into their state. The bans do
permit the importation of boned out meat, hides or cape with no meat attached,
clean skull cap with antler attached, finished taxidermy heads or the ivories of
elk. The state of Georgia has recently banned the importation of live cervids
into that state also. Some citizens of Colorado have formed a new political
action group called Colorado Wildlife Defense (just happens that the acronym is
CWD). The stated goal of this group are; Elimination of big game diseases,
especially CWD; promotion of healthy wildlife habitat; promotion of
scientifically sound wildlife research; promotion of a discussion of the ethics
of hunting and wildlife management; education of the hunting and non hunting
public. Their action plan calls for; requiring double fencing of all game farms
at owners expense; all game farmers provide annual proof of bonding; prohibit
new licenses for deer and elk farms; prohibit expansion in acreage of existing
game farms; prohibit the transfer of game farm licenses; prohibit charging for
hunting behind high wire; prohibit blocking of traditional migratory paths by
high fences; requiring game farms to maintain environmental controls and
prohibit the escape of contaminated water or soil; requiring immediate reporting
of missing deer or elk from game farms; and requiring all game farm deer and elk
to be tested for brucellosis and TB. Wisconsin has announced that 7 more
free-ranging deer have tested positive for CWD. They have expanded their
eradication zone by an additional 15 square miles to cover these findings. The
total number of free-ranging CWD positive in Wisconsin is now 31 white-tail
deer.
In 2000, a elk farmer in Wisconsin received elk from a CWD exposed herd in
Colorado. At that time, the farmer advised the Wisconsin Department of
Agriculture that both animals from the exposed herd in Colorado were dead. He
has now advised Wisconsin Ag. that he was mistaken and that one of the animals
is still alive in his herd. The second draft of the implementation documents for
the National CWD Plan was distributed to committee members and others on Friday,
August 30. The final documents are due to APHIS and USFWS on Friday, September
13. The herd of captive elk in Oklahoma that had been exposed to CWD will be
destroyed this week. This herd had an elk test positive for CWD in 1997 but the
depopulation of the herd was not agreed to by the owners and federal
representatives until this week. Since the discovery of CWD in the herd, the
remaining animals have been under quarantine, however, in the meantime the herd
has dropped from 150 animals to 74. Due to a lack of communication, not all of
the 76 animals that died in the interim were tested for CWD. All remaining
animals will be tested but the true degree of infection rate of the herd will
never be known.
The owners of the facility will not be permitted to restock the area with
cervids for a period of five years. A New York based organization, BioTech
Research Fund I LLC has committed a $1 million line of credit to fund
commercialization of tests for brain-wasting disorders and production of various
vaccines to Gene-Thera of Wheat Ridge, Colorado. Gene-Thera has spent three
years developing new ways not only to diagnose CWD, but create vaccines for mad
cow disease, E. coli contaminants and foot-and-mouth disease. Its tests for CWD
have been successful in more than 100 samples from Colorado and Wisconsin
according to company officials. Gene-Thera plans to license and market some o
fits disease test kits by the end of the year, then begin volume distribution by
mid-2003. The abstracts of the presentations from the CWD Conference in Denver
August 6 and 7 have been posted on the Colorado Division of Wildlife web site.
You will need adobe acrobat reader to read them.
The Division web site is: http://wildlife.state.co.us/CWD/Symposium_booklet.pdf
Minnesota: Second case in a game farmed elk discovered in Stearns Co.
This is a trace forward from the previously affected game farm in Aitkins
Co. An additional game farm in Benton Co is under quarantine.
snip...
Supporting Documents: Colorado: CWD-Exposed Elk Used in 1990 Study-
Wildlife officials call W. Slope move a mistake Date: January 17, 2003 Source:
Denver Post Contacts: Theo Stein Environment Writer
The Colorado Division of Wildlife knowingly used a herd of captive elk
exposed to chronic wasting disease in a grazing study on the Western Slope in
January 1990, possibly introducing the disease to the elk-rich area. "It was a
bad call," said Jeff Ver Steeg, the division's top game manager. "I can't deny
it." About 150 wild elk were allowed to graze in the same pens near Maybell
after the research herd was removed and may have picked up the abnormal protein
that causes the disease from the feces and urine left by the captive elk. While
the Division of Wildlife has expressed concern before that its animals might
have helped spread CWD, this is the first time the agency has acknowledged it
knowingly moved elk exposed to CWD deep into an area where the disease was not
known to already exist. Studies that could help determine the source of CWD on
the Western Slope are incomplete, and officials say what data that do exist are
so new and so spotty they may not provide all the answers. So far, it appears
that less than 1 percent of deer and elk in the area are infected, compared with
as much as 15 to 20 percent in hotspots in northeastern Colorado. But as
wildlife officials grapple with CWD's appearance in northwestern Colorado,
officials now admit the decision to continue the grazing study over the
objections of some biologists was an error. At the time, biologists wanted to
see whether elk grazing on winter range depleted forage that ranchers wanted for
fattening cattle in spring. "I think in hindsight a lot of good people probably
did some dumb things, myself included," said Bruce Gill, a retired wildlife
manager who oversaw research efforts and remembers the debate over the project.
"Had we known CWD would explode into such a potentially volatile ecologic and
economic issue, we wouldn't have done it." Elk ranchers, who have been blamed
for exporting the disease from its stronghold on the Colorado and Wyoming plains
to seven states and two Canadian provinces, say the agency's belated disclosure
smacks of a coverup. "It's pure negligence," said Jerry Perkins, a Delta banker
and rancher who is now demanding a legislative inquiry. "If I'd have moved
animals I knew to be infected around like that, I'd be in jail." Grand Junction
veterinarian and sportsman Dick Steele said he faults the agency for not
disclosing information about CWD-exposed research animals before October, when
information was posted on the Division of Wildlife website. "This went way
beyond poor judgment," he said. "My main concern is that this has been hidden
for the last 12 years. It would have been real important to our decision-making
process on how to deal with CWD." While the Maybell information is new, Perkins
and other ranchers have long suspected Division of Wildlife research facilities
near Meeker and Kremmling, which temporarily housed mule deer kept in heavily
infected pens at the Fort Collins facility, have leaked CWD to the wild. Fear of
an outbreak led the agency to sample 450 deer around the Meeker and Kremmling
facilities. None tested positive, but the sample size was only large enough to
detect cases if the infection rate was greater than 1 percent. This fall, tests
on 23,000 deer and elk submitted by hunters statewide have revealed 48 CWD cases
north of Interstate 70 and west of the Continental Divide. Biologists believe
the infection rate in that area, which includes the Maybell, Meeker and
Kremmling sites, is still well below 1 percent. But CWD has never been contained
in a wild population, so experts fear the problem will grow worse.
The Division of Wildlife says it will be months before a statistical
analysis of the fall's sampling results can be completed, an exercise that may
shed light on the disease's origin on the Western Slope. "We're just not going
to speculate at this point," said Ver Steeg of the possible Maybell connection.
"This is one possibility, but certainly not the only possibility." Some
biologists think a defunct elk ranch near Pagoda, which had dozens of
unexplained deaths in the mid-'90s, is another, a suggestion Perkins rejects.
"It may be inconclusive to them," said Perkins. "It isn't inconclusive to us."
To date, 19 CWD-positive animals have been found on six Wisconsin farms.
All have been white-tailed deer except for one elk imported from a Minnesota
herd later found to be infected. More than 8,000 farm-raised deer and elk have
been tested in Wisconsin, and about 540 herds are enrolled in the CWD monitoring
program.
CWD disease detected on Lac qui Parle County cervid farm southwestern
Minnesota (2006-03-15)
Date: March 15, 2006 at 12:36 pm PST
Chronic wasting disease detected on Lac qui Parle County cervid farm
(2006-03-15) The Board of Animal Health announced today that chronic wasting
disease (CWD) has been detected in one domestic white-tailed deer on a cervid
farm in Lac qui Parle County, which is located in southwestern Minnesota.
Immediately, DNR officials will conduct a local deer survey to determine
the number of wild deer in the area. It is expected that not many deer will be
found because the area is highly agricultural, with little deer habitat
surrounding the farm. DNR will conduct opportunistic sampling of deer, like road
kills, in the immediate area now and will conduct intensive hunter-harvested
surveillance during the 2006 firearm deer season.
Although this positive animal is a captive deer, DNR has conducted
surveillance for CWD in wild deer in the area. The farm is located near the
northern boundary of deer permit area 447, where wild deer surveillance for CWD
last occurred in 2003.
Lou Cornicelli, DNR big game program coordinator, said, "In 2003, we
conducted wild deer CWD surveillance in adjoining permit areas 433, 446 and 447.
In total, we collected 392 samples from those permit areas during the regular
firearm deer season and CWD was not detected."
The sampling of wild deer was designed statistically to have a 95 percent
confidence of detecting a 1 percent infection rate, according to Mike DonCarlos,
DNR wildlife programs manager.
"This situation is very similar to the positive elk farm discovered in
Stearns County in 2003, which followed the first discovery of CWD in an Aitkin
County elk farm," DonCarlos said. “The DNR response will be similar to the
Stearns County action and will include an initial assessment of wild deer
populations in the area and development of a surveillance program for next
fall."
From 2002 to 2004, DNR staff collected nearly 28,000 CWD samples statewide
and no disease found in the wild herd.
"The intensive surveillance conducted in 2003 indicated CWD was not
present in wild deer," Cornicelli said. “In addition, all indications are that
this positive captive deer has not contacted any wild deer, but we will conduct
additional surveillance this fall to be sure."
CWD disease detected on Lac qui Parle County cervid farm southwestern
Minnesota (2006-03-15) Date: March 15, 2006 at 12:36 pm PST
Chronic wasting disease detected on Lac qui Parle County cervid farm
(2006-03-15) The Board of Animal Health announced today that chronic wasting
disease (CWD) has been detected in one domestic white-tailed deer on a cervid
farm in Lac qui Parle County, which is located in southwestern Minnesota.
Immediately, DNR officials will conduct a local deer survey to determine
the number of wild deer in the area. It is expected that not many deer will be
found because the area is highly agricultural, with little deer habitat
surrounding the farm. DNR will conduct opportunistic sampling of deer, like road
kills, in the immediate area now and will conduct intensive hunter-harvested
surveillance during the 2006 firearm deer season.
Although this positive animal is a captive deer, DNR has conducted
surveillance for CWD in wild deer in the area. The farm is located near the
northern boundary of deer permit area 447, where wild deer surveillance for CWD
last occurred in 2003.
Lou Cornicelli, DNR big game program coordinator, said, "In 2003, we
conducted wild deer CWD surveillance in adjoining permit areas 433, 446 and 447.
In total, we collected 392 samples from those permit areas during the regular
firearm deer season and CWD was not detected."
The sampling of wild deer was designed statistically to have a 95 percent
confidence of detecting a 1 percent infection rate, according to Mike DonCarlos,
DNR wildlife programs manager.
"This situation is very similar to the positive elk farm discovered in
Stearns County in 2003, which followed the first discovery of CWD in an Aitkin
County elk farm," DonCarlos said. “The DNR response will be similar to the
Stearns County action and will include an initial assessment of wild deer
populations in the area and development of a surveillance program for next
fall."
From 2002 to 2004, DNR staff collected nearly 28,000 CWD samples statewide
and no disease found in the wild herd.
"The intensive surveillance conducted in 2003 indicated CWD was not
present in wild deer," Cornicelli said. “In addition, all indications are that
this positive captive deer has not contacted any wild deer, but we will conduct
additional surveillance this fall to be sure."
IT is my opinion, that these states are going to have to significantly
increase their CWD TSE PRION testing, in order to truly know what the rate of
cwd tse prion is in that state. Minnesota seems to be another state that needs
to do this...imo...terry
Friday, July 29, 2016
IOWA CHRONIC WASTING DISEASE CWD TSE PRION TOTAL TO DATE 304 CASES WILD AND
CAPTIVE REPORT UPDATE JULY 2016
Sunday, May 08, 2016
WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE
ABYSS UPDATE http://chronic-wasting-disease.blogspot.com/2016/05/wisconsin-chronic-wasting-disease-cwd.html
Wednesday, July 27, 2016
Arkansas CWD 101 positive cases documented to date, Biologists to take
additional samples in in southern Pope County, Aug. 1-5
Sunday, January 17, 2016
Wisconsin Captive CWD Lotto Corporate Welfare Pays Out Again indemnity
payment of $298,770 for 228 white-tailed deer killed on farm
Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of $298,770
for 228 white-tailed deer killed on farm
Tuesday, February 11, 2014
Wisconsin tracks 81 deer from game farm with CWD buck to seven other states
Friday, April 04, 2014
Wisconsin State officials kept silent on CWD discovery at game farm
Saturday, March 29, 2014
Game Farm, CWD Concerns Rise at Boone and Crockett Club
Saturday, March 10, 2012
CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow protein
feed CUSTOM MADE for deer and elk
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
Friday, July 01, 2016
*** TEXAS Thirteen new cases of chronic wasting disease (CWD) were
confirmed at a Medina County captive white-tailed deer breeding facility on June
29, 2016***
*** How Did CWD Get Way Down In Medina County, Texas?
DISCUSSION Observations of natural outbreaks of scrapie indicated that the
disease spread from flock to flock by the movement of infected, but apparently
normal, sheep which were incubating the disease.
There was no evidence that the disease spread to adjacent flocks in the
absent of such movements or that vectors or other host species were involved in
the spread of scrapie to sheep or goats; however, these possibilities should be
kept open...
Monday, July 18, 2016
Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers
Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster
Tuesday, August 02, 2016
TEXAS TPWD Sets Public Hearings on Deer Movement Rule Proposals in Areas
with CWD Rule Terry S. Singeltary Sr. comment submission
Tuesday, April 12, 2016
The first detection of Chronic Wasting Disease (CWD) in Europe free-ranging
reindeer from the Nordfjella population in South-Norway.
Tuesday, June 14, 2016
*** Chronic Wasting Disease (CWD) in a moose from Selbu in Sør-Trøndelag
Norway ***
Thursday, July 07, 2016
Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd
Norwegian moose
14/06/2016 - Norway reports a third case
Saturday, July 16, 2016
Chronic wasting Disease in Deer (CWD or Spongiform Encephalopathy) The
British Deer Society 07/04/2016
Sunday, July 17, 2016
*** CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
***
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild ***
Thursday, August 4, 2016
Secretary's Advisory Committee on Animal Health [Docket No.
APHIS-2016-0046] TSE PRION DISEASE ?
Thursday, August 04, 2016
*** MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
***
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
with CWD TSE Prions, I am not sure there is any absolute yet, other than
what we know with transmission studies, and we know tse prion kill, and tse
prion are bad. science shows to date, that indeed soil, dirt, some better than
others, can act as a carrier. same with objects, farm furniture. take it with
how ever many grains of salt you wish, or not. if load factor plays a role in
the end formula, then everything should be on the table, in my opinion. see
;
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil
Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable
neurological diseases likely caused by a misfolded form of the prion protein.
TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’
disease) in cattle, chronic wasting disease in deer and elk, and
Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are
unique among TSEs because they can be transmitted between animals, and the
disease agents appear to persist in environments previously inhabited by
infected animals. Soil has been hypothesized to act as a reservoir of
infectivity and to bind the infectious agent. In the current study, we orally
dosed experimental animals with a common clay mineral, montmorillonite, or whole
soils laden with infectious prions, and compared the transmissibility to unbound
agent. We found that prions bound to montmorillonite and whole soils remained
orally infectious, and, in most cases, increased the oral transmission of
disease compared to the unbound agent. The results presented in this study
suggest that soil may contribute to environmental spread of TSEs by increasing
the transmissibility of small amounts of infectious agent in the
environment.
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
>>>Particle-associated PrPTSE molecules may migrate from locations
of deposition via transport processes affecting soil particles, including
entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several
years. Significant interest remains in developing methods that could be applied
to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests
that serine proteases and the microbial consortia in stimulated soils and
compost may partially degrade PrPTSE. Transition metal oxides in soil (viz.
manganese oxide) may also mediate prion inactivation. Overall, the effect of
prion attachment to soil particles on its persistence in the environment is not
well understood, and additional study is needed to determine its implications on
the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding,
inferring a durable environmental reservoir, and an efficient mechanism for
indirect horizontal CWD transmission.
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY
Friday, August 14, 2015
*** Susceptibility of cattle to the agent of chronic wasting disease from
elk after intracranial inoculation ***
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Summary
The previous assessment concentrated on the incursion of disease from North
America through the imports of animal feed or the movement of contaminated
clothing, footwear and equipment. The results suggested that import of pet feed
was a non-negligible risk, but given the unlikely contact of resident deer in GB
with such non-ruminant feed, this was considered overall a negligible to very
low risk. The movement of contaminated clothing, footwear or equipment
(particularly hunting equipment) could pose a very low risk, although the volume
of contaminated soil which would need to be ingested to give rise to an
infection is likely to be higher than would be present. There is a variable
level uncertainty in all these assessments.
The new assessment focuses on an additional potential route of entry: the
importation of natural deer urine lures. The main conclusions from this
assessment are:
In areas of North America where CWD has been reported, given that CWD is
excreted in faeces, saliva, urine and blood, and survives in the environment for
several years there is a medium probability that the deer urine in North America
contains CWD (high uncertainty; depends on the source of deer used for
production).
The risk of a deer in GB being infected per 30 ml bottle of urine
imported from the USA is very low, albeit with high uncertainty. Overall it is
concluded that the risk of at least one infection of deer in the UK with CWD per
year from deer urine lures imported from the USA is medium. This assumes a high
number of 30 ml bottles imported per year from all areas of the USA.
None of the species affected by CWD in North America are present in GB.
For a British species to become infected with CWD following exposure, the dose
and inherent susceptibility of the species will be important. Based on current
scientific evidence Red deer (Cervus elaphus elaphus) are susceptible to CWD,
Fallow deer (Dama dama) are likely to be less susceptible and Roe deer
(Capreolus capreolus) have a gene conferring susceptibility. Therefore, it is
likely that given exposure to an infectious dose of CWD, deer in GB could become
infected with CWD.
Overall, the probability of importing CWD into GB from North America and
causing infection in British deer is uncertain but likely to be negligible to
very low via movement of deer hunters, other tourists and British servicemen and
very low via imported (non-
2
ruminant) animal feed and medium for the use of lures. However, if it was
imported and (a) deer did become infected with CWD, the consequences would be
severe as eradication of the disease is impossible, it is clinically
indistinguishable from BSE infection in deer (Dalgleish et al., 2008) and
populations of wild and farmed deer would be under threat.
The USA has implemented a Herd Certification Programme for farmed and
captive cervids. So far, 29 States are approved for HCP status (APHIS, 2015).
The list includes States such as Colorado, where CWD is present, therefore it is
recommended that any sourcing of such natural urine lures should be not only
from States with an HCP programme, but also from a herd which is registered as
being regularly tested free of CWD.
Animal urine is not considered a commodity which is subject to animal
by-products legislation for imports. Internet sales are common and although a
license would be required, there are no conditions for the safe sourcing of such
products. Deer urine lures are also available in Europe and may be produced from
carcases of hunted deer. The use of deer urine produced from a species not
present in Europe (such as white tailed deer) is questioned for its value with
native GB deer according to the British Deer Society survey.
Background
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and
behavioural changes that can span weeks or months (Williams, 2005). In addition,
signs might include excessive salivation, behavioural alterations including a
fixed stare and changes in interaction with other animals in the herd, and an
altered stance (Williams, 2005). These signs are indistinguishable from cervids
experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB,
for example, infected deer populations would need to be tested to differentiate
if they were infected with CWD or BSE to minimise the risk of BSE entering the
human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
What is the risk of chronic wasting disease being introduced into Great
Britain? A Qualitative Risk Assessment October 2012
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids, as well as non-ruminants such as cats and dogs as
well, as soon as possible for the following reasons...
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Terry Singeltary Sr. comment ;
THIS IS most important as well, and you may not be aware of this, if not,
you and your colleagues should please take note ‘After a natural route of
exposure, 100% of white-tailed deer were susceptible to scrapie’, and below this
as well, I am now beginning to question the Red Deer Ataxia back in the 70s and
80s, as I did the infamous ‘hound ataxia’.
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie. ***
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie. ***
Primary transmission of CWD versus scrapie prions from small ruminants to
ovine and cervid PrP transgenic mice
Authors: Sally A. Madsen-Bouterse1, David A. Schneider2, Dongyue Zhuang3,
Rohana P. Dassanayake4, Aru Balachandran5, Gordon B. Mitchell6, Katherine I.
O'Rourke7 VIEW AFFILIATIONS
Published Ahead of Print: 08 July, 2016 Journal of General Virology doi:
10.1099/jgv.0.000539 Published Online: 08/07/2016
Development of mice expressing either ovine (Tg338) or cervid (TgElk) prion
protein (PrP) have aided in characterization of scrapie and chronic wasting
disease (CWD), respectively. Experimental inoculation of sheep with CWD prions
has demonstrated the potential for interspecies transmission but, infection with
CWD versus classical scrapie prions may be difficult to differentiate using
validated diagnostic platforms. In this study, mouse bioassay in Tg338 and TgElk
was utilized to evaluate transmission of CWD versus scrapie prions from small
ruminants. Mice (>5/homogenate) were inoculated with brain homogenates from
clinically affected sheep or goats with naturally-acquired classical scrapie,
white-tailed deer with naturally-acquired CWD (WTD-CWD), or sheep with
experimentally-acquired CWD derived from elk (sheep-passaged-CWD). Survival time
(time to clinical disease) and attack rates (brain accumulation of protease
resistant PrP, PrPres) were determined. Inoculation with classical scrapie
prions resulted in clinical disease and 100% attack rates in Tg338, but no
clinical disease at endpoint (>300 days post inoculation, dpi) and low attack
rates (6.8%) in TgElk. Inoculation with WTD-CWD prions yielded no clinical
disease or brain PrPres accumulation in Tg338 at endpoint (>500dpi) but rapid
onset of clinical disease (~121dpi) and 100% attack rate in TgElk.
Sheep-passaged-CWD resulted in transmission to both mouse lines with 100% attack
rates at endpoint in Tg338 and an attack rate of ~73% in TgElk with some culled
due to clinical disease. These primary transmission observations demonstrate the
potential of bioassay in Tg338 and TgElk to help differentiate possible
infection with CWD versus classical scrapie prions in sheep and goats.
P.97: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum
Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and
Robert Kunkle1
1National Animal Disease Center; Ames, IA USA;
2Iowa State University; Ames, IA USA
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 D 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 2
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, 2
distinct molecular profiles of PrPSc are present in the tissues of affected
deer, and inoculum of either profile readily passes to deer.
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.
Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)
Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National
Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie
and CWD in inoculated deer. Interspecies transmission studies afford the
opportunity to better understand the potential host range and origins of prion
diseases. We inoculated white-tailed deer intracranially (IC) and by a natural
route of exposure (concurrent oral and intranasal inoculation) with a US scrapie
isolate. All deer inoculated by the intracranial route had evidence of PrPSc
accumulation and those necropsied after 20 months post-inoculation (PI) (3/5)
had clinical signs, spongiform encephalopathy, and widespread distribution of
PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6
months PI did not have clinical signs, but had widespread distribution of PrPSc.
This highlights the facts that 1) prior to the onset of clinical signs PrPSc is
widely distributed in the CNS and lymphoid tissues and 2) currently used
diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical
signs. The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in white-tailed deer 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 consistent with 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 white-tailed deer 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 scrapie by
IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil,
retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and
spleen. While two WB patterns have been detected in brain regions of deer
inoculated by the natural route, unlike the IC inoculated deer, the pattern
similar to the scrapie inoculum predominates.
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 ;
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
The possibility of any reservoir of infection in wild cervids originating
from scrapie in domestic sheep flocks seems remote. Scrapie has been recorded in
only three flocks in Wyoming since 1947 and Beth Williams could recall only one
previous occurrence in 1966. This had involved a Suffolk flock close to the
border with Nebraska. However, there has been one new confirmed and a suspected
affected flock this year in Wyoming. In the latter a ewe bought-in from an
Illinois flock is incriminated.
Spraker suggested an interesting explanation for the occurrence of CWD. The
deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob
Davis. At or about that time, allegedly, some scrapie work was conducted at this
site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep. Whether they were scrapie infected sheep or
not is unclear. There were domestic sheep and goats present in the facility also
in the 1960's but there is not evidence that these animals developed scrapie.
During the 60's hybridization studies between the Bighorn and domestic sheep
were carried
PAGE 30
out, again, without evidence of scrapie. Domestic goats were also kept at
Sybille in the 1960's.
Spraker considers that the nasal route is responsible for transmission of
CWD through nose to nose contact, which may well occur also between captive and
free-living individuals.
In domestic cattle of which about 15-20 adults were necropsied per year at
the Diagnostic Laboratory, CSU., Spraker had not encountered any lesions
suggesting BSE. Polioencephalomalacia (PEM) and Encephalic Listeriosis were the
most common morphologic neuropathological diagnoses. No bovine rabies was seen.
PAGE 31
Appendix I
VISIT TO USA - DR A E WRATHALL - INFO ON BSE AND SCRAPIE
1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has
successfully transmitted ovine and caprine scrapie to cattle. The experimental
results have not been published but there are plans to do this. This work was
initiated in 1978. A summary of it is:-
Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a
2nd Suffolk scrapie passage:-
i/c 1ml i/m, 5ml; s/c 5ml; oral 30ml.
1/6 went down after 48 months with a scrapie/BSE-like disease.
Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus
2/6 went down similarly after 36 months.
Expt C Mice inoculated from brains of calves/cattle in expts A & B were
resistant, only 1/20 going down with scrapie and this was the reason given for
not publishing.
Diagnosis in A, B, C was by histopath. No reports on SAF were given.
Dr Warren Foote indicated success so far in eliminating scrapie in
offspring from experimentally- (and naturally) infected sheep by ET. He had
found difficulty in obtaining emhryos from naturally infected sheep (cf SPA).
3. Prof. A Robertson gave a brief account of BSE. The US approach was to
PAGE 32
accord it a very low profile indeed. Dr A Thiermann showed the picture in
the "Independent" with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. BSE was not reported in USA.
4. Scrapie incidents (ie affected flocks) have shown a dramatic increase
since 1978. In 1953 when the National Control Scheme was started there were
10-14 incidents, in 1978 - 1 and in 1988 so far 60.
5. Scrapie agent was reported to have been isolated from a solitary
fetus.
6. A western blotting diagnostic technique (? on PrP} shows some promise.
7. Results of a questionnaire sent to 33 states on the subject of the
national sheep scrapie programme survey indicated;
17/33 wished to drop it 6/33 wished to develop it 8/33 had few sheep and
were neutral
Information obtained from Dr Wrathall's notes of a meeting of the U.S.
Animal Health Association at Little Rock, Arkansas Nov. 1988.
kind regards,
Terry S. Singeltary Sr., Bacliff, Texas USA -July 29, 2000-
please see ;
Their concern deepened as they experimented with ways to sanitize the
holding pens in Fort Collins and Sybille. All the deer and elk in the
contaminated pens at Sybille were killed, and the pens were left empty for six
months to a year. When deer and elk were reintroduced to the pens, they were
animals that weren't known to have had direct contact with infected deer and
elk. In spite of these efforts, elk in the pens came down with chronic wasting
disease within five years after the attempt at sterilizing the facility.
In Fort Collins, the effort was even more intense. All the deer and elk in
the facility were killed and buried. Then personnel plowed up the soil in the
pens in an effort to bury possible disease organisms and sprayed structures and
pastures repeatedly with a strong disinfectant. A year later, they took twelve
elk calves from the wild and released them in the sanitized holding areas. In
the next five years, two of these elk died from chronic wasting disease.
Sunday, July 10, 2016
Primary transmission of CWD versus scrapie prions from small ruminants to
ovine and cervid PrP transgenic mice
2016 PRION CONFERENCE TOKYO
‘’These results demonstrate that scrapie prions have a zoonotic potential
and raise new questions about the possible link between animal and human
prions.’’
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
snip...
Do our transmission results in tgHu imply that sheep scrapie is the cause
of sCJD cases in humans? This question challenges well-established dogma that
sCJD is a spontaneous disorder unrelated to animal prion disease. In our
opinion, our data on their own do not unequivocally establish a causative link
between natural exposure to sheep scrapie and the subsequent appearance of sCJD
in humans. However, our studies clearly point out the need to re-consider this
possibility. Clarification on this topic will be aided by informed and modern
epidemiological studies to up-date previous analysis that was performed at the
end of the last century3, 4. The value of such an approach is highlighted by the
implementation in the year 2000 of large-scale active animal TSE surveillance
programs around the world that provided an informed epidemiological-based view
of the occurrence and geographical spread of prion disease in small ruminant
populations51. The fact that both Australia and New-Zealand, two countries that
had been considered for more than 50 years as TSE-free territories, were finally
identified positive for atypical scrapie in their sheep flocks provides an
example of how prion dogma can be reversed52. However, the incubation period for
prion disease in humans after exposure to prions via the peripheral route, such
as in iatrogenic CJD transmission and Kuru, can exceed several decades53, 54. In
this context, it will be a challenge to combine epidemiological data collected
contemporarily in animal populations and humans to investigate the existence of
a causative link between prion disease occurrence in these different hosts.
Furthermore, it is crucial to bear in mind that sporadic sCJD in humans is a
rare disease (1–2 individuals per million of the population per year) and that
scrapie has been circulating in small ruminants populations used for food
purposes for centuries. Consequently, it is our opinion that even if a causative
link was established between sheep scrapie exposure and the occurrence of
certain sCJD cases, it would be wrong to consider small ruminant TSE agents as a
new major threat for public health. Despite this, it remains clear that our data
provide a new impetus to establish the true zoonotic potential of sheep scrapie
prions.
Subject terms: Biological sciences• Medical research At a glance
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.
2015
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
PRION 2016 CONFERENCE TOKYO
IL-13 Transmission of prions to non human-primates: Implications for human
populations
Jean-Philippe Deslys, Emmanuel E. Comoy
CEW, Institute of Emerging Diseases and Innovative Therapies (iMETI),
Division of Prions and Related Diseases (SEPIA), Fontenay-aux-Roses, France
Prion diseases 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 prion
disease might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, prion diseases, like the other
proteinopathies, are reputed to occur spontaneously (atypical animal prion
strains, sporadic CJD summing 80 % of human prion cases).
Non-human primate models provided the first evidences supporting the
transmissibility of human prion strains and the zoonotic potential of BSE. Among
them, cynomolgus macaques brought major information for BSE risk assessment for
human health1, according to their phylogenetic proximity to humans and extended
lifetime. We used this model to assess the risk of primary (oral) and secondary
(transfusional) risk of BSE, and also the zoonotic potential of other animal
prion diseases 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' . longer incubation than BSE2. Scrapie, as recently evoked in
humanized mice3, is the third potentially zoonotic prion disease (with BSE and
L-type BSE4), thus questioning the origin of human sporadic cases. We also
observed hidden prions transmitted by blood transfusion in primate which escape
to the classical diagnostic methods and extend the field of healthy carriers. We
will present an updated panorama of our different long-term transmission studies
and discuss the implications on risk assessment of animal prion diseases for
human health and of the status of healthy carrier5.
1. Chen, C. C. & Wang, Y. H. Estimation of the Exposure of the UK
Population to the Bovine Spongiform Encephalopathy Agent through Dietary Intake
During the Period 1980 to 1996. PLoS One 9, e94020 (2014).
2. Comoy, E. E. et al. Transmission of scrapie prions to primate after an
extended silent incubation period. Sci Rep 5, 11573 (2015).
3. Cassard, H. et al. Evidence for zoonotic potential of ovine scrapie
prions. Nat Commun 5, 5821-5830 (2014).
4. Comoy, E. E. et al. Atypical BSE (BASE) transmitted from asymptomatic
aging cattle to a primate. PLoS One 3, e3017 (2008).
5. Gill O. N. et al. Prevalent abnormal prion protein in human appendixes
after bovine spongiform encephalopathy epizootic: large scale survey. BMJ. 347,
f5675 (2013).
Curriculum Vitae
Dr. Deslys co-authored more than one hundred publications in international
scientific journals on main aspects of applied prion research (diagnostic,
decontamination techniques, risk assessment, and therapeutic approaches in
different experimental models) and on underlying pathological mechanisms. He
studied the genetic of the first cases of iatrogenic CJD in France. His work has
led to several patents including the BSE (Bovine Spongiform Encephalopathy)
diagnostic test most widely used worldwide. He also wrote a book on mad cow
disease which can be downloaded here for free (http://www.neuroprion.org/pdf_docs/documentation/madcow_deslys.pdf).
His research group is Associate Laboratory to National Reference Laboratory for
CJD in France and has high security level microbiological installations
(NeuroPrion research platform) with different experimental models (mouse,
hamster, macaque). The primate model of BSE developed by his group with
cynomolgus macaques turned out to mimick remarkably well the human situation and
allows to assess the primary (oral) and secondary (transfusional) risks linked
to animal and human prions even after very long silent incubation periods. For
several years, his interest has extended to the connections between PrP and
Alzheimer and the prion mechanisms underlying neurodegenerative diseases. He is
coordinating the NeuroPrion international association (initially european
network of excellence now open to all prion researchers).
- 59-
P-088 Transmission of experimental CH1641-like scrapie to bovine PrP
overexpression mice
Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1,
Takashi Yokoyama2
1Influenza and Prion Disease Research Center, National Institute of Animal
Health, NARO, Japan; 2Department of Planning and General Administration,
National Institute of Animal Health, NARO
Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke
scrapie is characterized by a lower molecular mass of the unglycosylated form of
abnormal prion protein (PrpSc) compared to that of classical scrapie. It is
worthy of attention because of the biochemical similarities of the Prpsc from
CH1641-like and BSE affected sheep. We have reported that experimental
CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice
(Yokoyama et al. 2010). We report here the further details of this transmission
study and compare the biological and biochemical properties to those of
classical scrapie affected TgBoPrP mice.
Methods: The details of sheep brain homogenates used in this study are
described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were
intracerebrally inoculated with a 10% brain homogenate of each scrapie strain.
The brains of mice were subjected to histopathological and biochemical analyses.
Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice
was similar to that of classical scrapie affected mice. Mean survival period of
CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it
was significantly shorter than that of classical scrapie affected mice (439
days). Lesion profiles and Prpsc distributions in the brains also differed
between CH1641-like and classical scrapie affected mice.
Conclusion: We succeeded in stable transmission of CH1641-like scrapie to
TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is
likely to be more virulent than classical scrapie in cattle.
WS-02
Scrapie in swine: A diagnostic challenge
Justin J Greenlee1, Robert A Kunkle1, Jodi D Smith1, Heather W. Greenlee2
1National Animal Disease Center, US Dept. of Agriculture, Agricultural
Research Service, United States; 2Iowa State University College of Veterinary
Medicine
A naturally occurring prion disease has not been recognized in swine, but
the agent of bovine spongiform encephalopathy does transmit to swine by
experimental routes. Swine are thought to have a robust species barrier when
exposed to the naturally occurring prion diseases of other species, but the
susceptibility of swine to the agent of sheep scrapie has not been thoroughly
tested.
Since swine can be fed rations containing ruminant derived components in
the United States and many other countries, we conducted this experiment to test
the susceptibility of swine to U.S. scrapie isolates by intracranial and oral
inoculation. Scrapie inoculum was a pooled 10% (w/v) homogenate derived from the
brains of clinically ill sheep from the 4th passage of a serial passage study of
the U.S scrapie agent (No. 13-7) through susceptible sheep that were homozygous
ARQ at prion protein residues 136, 154, and 171, respectively. Pigs were
inoculated intracranially (n=19) with a single 0.75 ml dose or orally (n=24)
with 15 ml repeated on 4 consecutive days. Necropsies were done on a subset of
animals at approximately six months post inoculation (PI), at the time the pigs
were expected to reach market weight. Remaining pigs were maintained and
monitored for clinical signs of TSE until study termination at 80 months PI or
when removed due to intercurrent disease (primarily lameness). Brain samples
were examined by immunohistochemistry (IHC), western blot (WB), and
enzyme-linked immunosorbent assay (ELISA). Brain tissue from a subset of pigs in
each inoculation group was used for bioassay in mice expressing porcine PRNP.
At six-months PI, no evidence of scrapie infection was noted by any
diagnostic method. However, at 51 months of incubation or greater, 5 animals
were positive by one or more methods: IHC (n=4), WB (n=3), or ELISA (n=5).
Interestingly, positive bioassay results were obtained from all inoculated
groups (oral and intracranial; market weight and end of study).
Swine inoculated with the agent of scrapie by the intracranial and oral
routes do not accumulate abnormal prion protein (PrPSc) to a level detectable by
IHC or WB by the time they reach typical market age and weight. However, strong
support for the fact that swine are potential hosts for the agent of scrapie
comes from positive bioassay from both intracranially and orally inoculated pigs
and multiple diagnostic methods demonstrating abnormal prion protein in
intracranially inoculated pigs with long incubation times.
Curriculum Vitae
Dr. Greenlee is Research Veterinary Medical Officer in the Virus and Prion
Research Unit at the National Animal Disease Center, US Department of
Agriculture, Agricultural Research Service. He applies his specialty in
veterinary anatomic pathology to focused research on the intra- and interspecies
transmission of prion diseases in livestock and the development of antemortem
diagnostic assays for prion diseases. In addition, knockout and transgenic mouse
models are used to complement ongoing experiments in livestock species. Dr.
Greenlee has publications in a number of topic areas including prion agent
decontamination, effects of PRNP genotype on susceptibility to the agent of
sheep scrapie, characterization of US scrapie strains, transmission of chronic
wasting disease to cervids and cattle, features of H-BSE associated with the
E211 K polymorphism, and the development of retinal assessment for antemortem
screening for prion diseases in sheep and cattle. Dr. Greenlee obtained his DVM
degree and completed the PhD/residency program in Veterinary Pathology at Iowa
State University. He is a Diplomate of the American College of Veterinary
Pathologists.
PRION 2016 CONFERENCE TOKYO
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane
Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan
Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Prion 2016
Purchase options Price * Issue Purchase USD 198.00
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting
disease (CWD) is the prion disease affecting deer, elk and moose, and it is a
widespread and expanding epidemic affecting 22 US States and 2 Canadian
provinces so far. CWD poses the most serious zoonotic prion transmission risks
in North America because of huge venison consumption (>6 million deer/elk
hunted and consumed annually in the USA alone), significant prion infectivity in
muscles and other tissues/fluids from CWD-affected cervids, and usually high
levels of individual exposure to CWD resulting from consumption of the affected
animal among often just family and friends. However, we still do not know
whether CWD prions can infect humans in the brain or peripheral tissues or
whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no
essays to reliably detect CWD infection in humans. We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) CWD transmission to humans has already occurred. We will test these
hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in
vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain
or peripheral lymphoid tissues at low levels by conducting systemic bioassays in
a set of "humanized" Tg mouse lines expressing common human PrP variants using a
number of CWD isolates at varying doses and routes. Experimental "human CWD"
samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission
barrier is dependent on prion strain and influenced by the host (human) PrP
sequence by examining and comparing the transmission efficiency and phenotypes
of several atypical/unusual CWD isolates/strains as well as a few prion strains
from other species that have adapted to cervid PrP sequence, utilizing the same
panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD
infection in humans by examining in details the clinical, pathological,
biochemical and in vitro seeding properties of existing and future experimental
"human CWD" samples generated from Aims 1-2 and compare them with those of
common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by
examining a significant number of brain samples from prion-affected human
subjects in the USA and Canada who have consumed venison from CWD-endemic areas
utilizing the criteria and essays established in Aim 3. The findings from this
proposal will greatly advance our understandings on the potential and
characteristics of cervid prion transmission in humans, establish reliable
essays for CWD zoonosis and potentially discover the first case(s) of CWD
infection in humans.
Public Health Relevance There are significant and increasing human
exposure to cervid prions because chronic wasting disease (CWD, a widespread and
highly infectious prion disease among deer and elk in North America) continues
spreading and consumption of venison remains popular, but our understanding on
cervid-to-human prion transmission is still very limited, raising public health
concerns. This proposal aims to define the zoonotic risks of cervid prions and
set up and apply essays to detect CWD zoonosis using mouse models and in vitro
methods. The findings will greatly expand our knowledge on the potentials and
characteristics of cervid prion transmission in humans, establish reliable
essays for such infections and may discover the first case(s) of CWD infection
in humans.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 1R01NS088604-01A1
Application # 9037884
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2015-09-30
Budget End 2016-07-31
Support Year 1
Fiscal Year 2015
Total Cost $337,507
Indirect Cost $118,756
Institution
Name Case Western Reserve University
Department Pathology
Type Schools of Medicine
DUNS # 077758407
City Cleveland
State OH
Country United States
Zip Code 44106
===========================================================
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) *** CWD transmission to humans has already occurred. *** We will test
these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary
in vitro approaches.
============================================================
Key Molecular Mechanisms of TSEs
Zabel, Mark D.
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs),
are fatal neurodegenerative diseases affecting humans, cervids, bovids, and
ovids. The absolute requirement of PrPC expression to generate prion diseases
and the lack of instructional nucleic acid define prions as unique infectious
agents. Prions exhibit species-specific tropism, inferring that unique prion
strains exist that preferentially infct certain host species and confront
transmission barriers to heterologous host species. However, transmission
barriers are not absolute. Scientific consensus agrees that the sheep TSE
scrapie probably breached the transmission barrier to cattle causing bovine
spongiform encephalopathy that subsequently breached the human transmission
barrier and likely caused several hundred deaths by a new-variant form of the
human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human
health, emotion and economies can still be felt in areas like farming, blood and
organ donations and the threat of a latent TSE epidemic. This precedent raises
the real possibility of other TSEs, like chronic wasting disease of cervids,
overcoming similar human transmission barriers. A groundbreaking discovery made
last year revealed that mice infected with heterologous prion strains facing
significant transmission barriers replicated prions far more readily in spleens
than brains6. Furthermore, these splenic prions exhibited weakened transmission
barriers and expanded host ranges compared to neurogenic prions. These data
question conventional wisdom of avoiding neural tissue to avoid prion
xenotransmission, when more promiscuous prions may lurk in extraneural tissues.
Data derived from work previously funded by NIH demonstrate that Complement
receptors CD21/35 bind prions and high density PrPC and differentially impact
prion disease depending on the prion isolate or strain used. Recent advances in
live animal and whole organ imaging have led us to generate preliminary data to
support novel, innovative approaches to assessing prion capture and transport.
We plan to test our unifying hypothesis for this proposal that CD21/35 control
the processes of peripheral prion capture, transport, strain selection and
xenotransmission in the following specific aims. 1. Assess the role of CD21/35
in splenic prion strain selection and host range expansion. 2. Determine whether
CD21/35 and C1q differentially bind distinct prion strains 3. Monitor the
effects of CD21/35 on prion trafficking in real time and space 4. Assess the
role of CD21/35 in incunabular prion trafficking
Public Health Relevance Transmissible spongiform encephalopathies, or
prion diseases, are devastating illnesses that greatly impact public health,
agriculture and wildlife in North America and around the world. The impact to
human health, emotion and economies can still be felt in areas like farming,
blood and organ donations and the threat of a latent TSE epidemic. This
precedent raises the real possibility of other TSEs, like chronic wasting
disease (CWD) of cervids, overcoming similar human transmission barriers. Early
this year Canada reported its first case of BSE in over a decade audits first
case of CWD in farmed elk in three years, underscoring the need for continued
vigilance and research. Identifying mechanisms of transmission and zoonoses
remains an extremely important and intense area of research that will benefit
human and other animal populations.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Allergy and Infectious Diseases (NIAID)
Type High Priority, Short Term Project Award (R56)
Project # 1R56AI122273-01A1
Application # 9211114
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Beisel, Christopher E
Project Start 2016-02-16
Project End 2017-01-31
Budget Start 2016-02-16
Budget End 2017-01-31
Support Year 1
Fiscal Year 2016
Total Cost
Indirect Cost Institution Name Colorado State University-Fort Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
PMCA Detection of CWD Infection in Cervid and Non-Cervid Species
Hoover, Edward Arthur
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Chronic wasting disease (CWD) of deer and elk is an emerging highly
transmissible prion disease now recognized in 18 States, 2 Canadian provinces,
and Korea. We have shown that Infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces, and in the tissues
generating those body fluids and excreta, thereby leading to facile transmission
by direct contact and environmental contamination. We have also shown that CWD
can infect some non-cervid species, thus the potential risk CWD represents to
domestic animal species and to humans remains unknown. Whether prions borne in
blood, saliva, nasal fluids, milk, or excreta are generated or modified in the
proximate peripheral tissue sites, may differ in subtle ways from those
generated in brain, or may be adapted for mucosal infection remain open
questions. The increasing parallels in the pathogenesis between prion diseases
and human neurodegenerative conditions, such as Alzheimer's and Parkinson's
diseases, add relevance to CWD as a transmissible protein misfolding disease.
The overall goal of this work is to elucidate the process of CWD prion
transmission from mucosal secretory and excretory tissue sites by addressing
these questions: (a) What are the kinetics and magnitude of CWD prion shedding
post-exposure? (b) Are excreted prions biochemically distinct, or not, from
those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the
source of excreted prions? and (d) Are excreted prions adapted for horizontal
transmission via natural/trans-mucosal routes? The specific aims of this
proposal are: (1) To determine the onset and consistency of CWD prion shedding
in deer and cervidized mice; (2); To compare the biochemical and biophysical
properties of excretory vs. CNS prions; (3) To determine the capacity of
peripheral tissues to support replication of CWD prions; (4) To determine the
protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To
compare the mucosal infectivity of excretory vs. CNS prions. Understanding the
mechanisms that enable efficient prion dissemination and shedding will help
elucidate how horizontally transmissible prions evolve and succeed, and is the
basis of this proposal. Understanding how infectious misfolded proteins (prions)
are generated, trafficked, shed, and transmitted will aid in preventing,
treating, and managing the risks associated with these agents and the diseases
they cause.
Public Health Relevance Chronic wasting disease (CWD) of deer and elk is
an emergent highly transmissible prion disease now recognized throughout the USA
as well as in Canada and Korea. We have shown that infected deer harbor and shed
high levels of infectious prions in saliva, blood, urine, and feces thereby
leading to transmission by direct contact and environmental contamination. In
that our studies have also shown that CWD can infect some non-cervid species,
the potential risk CWD may represents to domestic animal species and humans
remains unknown. The increasing parallels in the development of major human
neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and
prion diseases add relevance to CWD as a model of a transmissible protein
misfolding disease. Understanding how infectious misfolded proteins (prions) are
generated and transmitted will aid in interrupting, treating, and managing the
risks associated with these agents and the diseases they cause.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 4R01NS061902-07
Application # 9010980
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May Project Start 2009-09-30
Project End 2018-02-28
Budget Start 2016-03-01
Budget End 2017-02-28
Support Year 7
Fiscal Year 2016
Total Cost $409,868
Indirect Cost $134,234 Institution Name Colorado State University-Fort
Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane
Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western
Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples,
Italy, 3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion
of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING
FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid
prion protein (PrP) sequence through passage in cervidized transgenic mice
efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion
strain-dependent and humans can be vulnerable to novel cervid prion strains.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on
the existence of different CWD strains.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion
of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
======================================================
Wednesday, June 29, 2016
*** NIH awards $11 million to UTHealth researchers to study deadly CWD
prion diseases Claudio Soto, Ph.D. ***
Public Release: 29-Jun-2016
Terry S. Singeltary Sr. flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
12:32 PM
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