MONTANA CHRONIC WASTING DISEASE CWD TSE PRION UPDATE STILL SHOWS ONLY 9 CAPTIVE CASES CONFIRMED FROM Philipsburg Kesler Game game since 1999
MONTANA CHRONIC WASTING DISEASE CWD TSE PRION UPDATE STILL SHOWS ONLY 9
CAPTIVE CASES CONFIRMED FROM Philipsburg Kesler Game game since 1999
In Montana CWD has only been found in one captive elk herd near Philipsburg
(Montana Dept. of Livestock 2004). Last year (2003) over 2,000 samples were
collected in Montana from free-ranging elk and deer, all of which tested
negative (N. Anderson, pers. comm.). Even so, it has been found in free-ranging
cervids in adjacent states, including South Dakota and Wyoming and the Canadian
Province of Saskatchewan (National Wildlife Health Center 2004) within 60 miles
of the Montana border.
Montana FWP has conducted CWD surveillance since 1998. Between 1998 and
2011, FWP collected and tested 17,269 samples from free-ranging elk, deer, and
moose from across the state, all of which were negative for CWD. Federal funding
for CWD surveillance was drastically reduced in 2012, and since that time, FWP
has restricted surveillance to high-risk areas and to elk, deer, or moose
exhibiting symptoms consistent with CWD. To date, no evidence of CWD has been
found in Montana’s free-ranging wildlife populations. In 2015, the US Geological
Survey and FWP published a study (Russell et al. 2015; see “Reports”) that
identified priority surveillance areas for CWD in mule deer populations across
Montana. Going forward, this information will be used to craft additional
targeted surveillance efforts for CWD within Regions 4, 6, and 7 in Montana.
Beginning in 2014/2015, FWP initiated a cooperative study with the US Fish
and Wildlife Service to better understand the movement patterns of deer within
the high-CWD risk areas on the northern border with Canada. This study has
entailed capturing and radio-collaring mule deer and collecting rectal biopsy
samples for CWD testing. To date, CWD has not been detected from any of these
samples.
More information on CWD is available at www.cwd-info.org/.
Chronic Wasting Disease Surveillance in Montana 1998-2011
A Summary of Surveillance Efforts
Montana CWD Survey Methods
1998-1999
The goal of surveillance in 1998 and 1999 was to conduct broad geographical
surveillance across the state in an effort to get baseline information on CWD
presence or absence. During the 1998 and 1999 hunting seasons, elk and deer
heads were collected from hunters on a voluntary basis at game check stations
and designated drop points across Montana. Kits containing information about
CWD, the location of game check stations and drop points, and collection
protocols were mailed to deer and elk permit holders. Technicians were employed
to work check stations and collect heads for testing. Symptomatic animals from
across the state were tested for CWD.
2000-2001
In 2000 surveillance efforts shifted from statewide collections to
collection of samples in areas considered to be “high risk” for movement of CWD
into the state. In January 2000, deer and elk from the area surrounding the
Kessler Game Farm near Philipsburg, MT were lethally removed by ground based
sharpshooters and through aerial gunning from a helicopter, following detection
of CWD in elk from the game farm in 1999. MFWP also participated in the removal
and testing of mule deer from the Sunlight Game Farm near Hardin, MT. The
Sunlight Game Farm was going out of business and wanted to remove its fences. It
also shared a fence line with the Elk Valley Game Farm, which had previously
received elk from Kessler’s Game Farm. The Elk Valley Game Farm was under
quarantine and ultimately depopulated in June of 2000. MFWP assisted in the
depopulation and testing of elk from Elk Valley as well. Surveillance during the
fall hunting season focused on the area surrounding the Kessler Game Farm near
Philipsburg and the southeastern border with Wyoming. These two areas were
selected because of concern over the potential transmission of CWD from infected
game farm elk and the potential movement of CWD infected deer into Montana from
northeastern Wyoming. Heads from hunter-harvested deer and elk were collected at
check stations and drop points within the Philipsburg and southeastern border
areas. Surveillance in 2001 again focused on the Philipsburg area, but efforts
in eastern Montana shifted to the northeastern border with Saskatchewan rather
than the southeastern border with Wyoming, a result of the detection of CWD in
wild deer near the Saskatchewan-Montana border. Statewide surveillance consisted
of testing symptomatic animals reported to MFWP.
2002 – 2005
USDA-APHIS agreed to cover laboratory testing costs in 2002 and 2003, and
federal funding of the national “Plan to Assist States, Federal Agencies and
Tribes in Managing Chronic Wasting Disease in Captive and Free Ranging Cervids”
in 2004 allowed for increased surveillance for CWD. As a result, surveillance
was conducted simultaneously in “high risk” areas near Montana’s northeastern
border, southeastern border, southern border with September 26, 2012
6
Yellowstone National Park, and the Philipsburg area. The Philipsburg area
was dropped from the “high risk” designation and collection of hunter-harvested
and road-killed animals was discontinued in 2004 Voluntary participation by
hunters remained the primary method of collecting elk and deer heads in the
remaining areas. Collections occurred at drop barrels, game check stations and
selected game processors. Cooperating game processors were paid $1 per head
collected. Efforts were taken to improve the accuracy of information regarding
harvest location, and databases were updated to conform to national standards.
Targeted surveillance continued for all symptomatic elk and deer reported to the
MFWP Wildlife Laboratory.
Sample size goals for the 2003 and 2004 surveys were 500 samples from FWP
administrative regions 3, 5, 6 and 7, and 450 samples in FWP administrative
region 2 (2003 only). These goals exceeded recommendations proposed by Samuel et
al (2003) and considered sufficient to detect one CWD positive animal from a
large populations assuming a 1% infection rate and a 99% confidence interval.
Collection points were located throughout the survey area in an effort to
achieve an even distribution of samples across the surveillance area in regions
2, 5, 6 and 7. In 2004 and 2005 sample size goals were reduced to 400 samples
and surveillance concentrated on the “high risk” areas of regions 3, 5, 6, and
7. Goals were reduce to be more consistent with Samuel et al. (2003), and were
believed to be more achievable, based on previous experience.
A research project assessing mule deer demographics and potential
transmission of CWD through deer movements between Wyoming and Montana was
initiated in the winter of 2004- 2005 (see Carnes 2009). In conjunction with the
study, surveillance goals were increased by 200 samples for the southern portion
of the survey area in region 7. A cooperative agreement was also reached with
the Charles M. Russell Wildlife Refuge (CMR) to collect an additional 200
samples from hunting districts containing refuge lands in the northeastern
portion of Montana in 2004.
Game processors within regions 5, 6 and 7 were contacted to solicit
cooperation starting in 2002. Samples in region 3 were collected primarily from
check stations within the Madison Valley west of YNP and a game check station
located north of Gardiner, Montana during the late elk hunt in the months of
January and February. A cooperative agreement was reached with the National Park
Service for payment of testing costs for samples from elk harvested during the
Gardiner late hunt (which consists primarily of elk migrating from Yellowstone
National Park) in 2004 and 2005. In an effort to improve location information
associated with each sample, game processors and drop barrels were not used
during the 2005 general hunting in region 7. Technicians obtained samples during
game check station operations by collecting road kills, through assistance of
taxidermists and contacts with hunters in the field.
2006-2008
Surveillance in 2006-2008 was conducted in a similar manner to the surveys
conducted since 2003, with a few exceptions. Collection of samples from
hunter-harvested animals was not conducted in region 3 due to decreases in
federal funding and in attempts to focus efforts in eastern Montana, which was
viewed as a higher priority area. Goals for regions 5, 6 and 7 remained at 400
samples from each region with the exception of region 6. Within this region the
September 26, 2012
7
goal was 400 samples in areas north and east of hunting districts
containing CMR lands. MFWP entered into a cooperative agreement with the CMR to
conduct surveillance in hunting districts containing CMR lands during 2006-2008.
In this area, efforts were maximized to collect as many samples as possible
given the remote locations and difficulty in accessing hunters. Within region 7
the goal was 400 samples with a minimum of 200 coming from the southern portion
of the survey area along the border with Wyoming.
2009-2011
The discovery of a CWD positive moose near Jackson Hole, WY in 2008 raised
concern that CWD might find its way into the elk feedgrounds in Wyoming. As a
result, the southern portion of region 3 was again elevated to a high risk area.
Due to the large area in Montana considered to be at high risk for movement of
CWD into the state and limited available funding, the state was divided into two
surveillance areas. The eastern half of the state, primarily regions 4, 6 and 7,
comprised one area and the south central and southwestern portions of the state,
primarily regions 3 and 5 comprised the other area. Surveillance activities
alternated between the two areas, occurring in the central/southwest one year
and the eastern regions the following year. Surveillance efforts focused on
regions 3 and 5 in 2009.
Prior to 2009, elk, mule deer and white-tailed deer samples were pooled
when determining sample size goals, in effect considering the three species one
population. Starting in 2009, each species within a MFWP region was considered a
unique population. Sample size goals for each population were based on
recommendations within the USDA-APHIS cooperative agreement and based on
statistical tables referenced by Samuel et al. (2003). Those goals consisted of
collecting a large enough sample to be 95% confident that we would detect a
single CWD positive animal assuming a 1% infection rate. However, in areas and
for species where harvest was limited, the sampling goal was 25% of the prior
hunting season’s estimated harvest. Moose were tested on a state-wide level as
available. The cooperative agreement with the CMR to conduct surveillance in
hunting districts containing CMR lands was renewed in 2009 but discontinued in
2010 and 2011. The goal for the CMR sampling effort was to maximize sample sizes
for white-tailed deer, mule deer and elk. Local game processors were offered a
reimbursement of $5 for elk and deer heads collected within the surveillance
area in an effort to increase the numbers of samples and the quality of data
associated with the samples.
Montana CWD Survey Results
From 1998 through the 2011 survey season, 17,269 samples from free-ranging
elk, deer and moose were tested for the presence of PrPcwd as part of MFWP’s
annual CWD surveillance program. The number of samples tested varied by year and
region (Table 2, Figure 2), and was dependent on the goals of the surveillance
program as referenced above. Regions 5, 6 and 7 accounted for over 73% of the
samples collected from 1998-2011, and sampling effort in these areas increase
considerably after MFWP began focusing surveillance in SW, NE and SE Montana
beginning in 2004 (Table 2). Elk, moose, mule deer and white-tailed deer
comprised 20.4%, 0.7%, 55.4% and 23.5% of the samples tested, respectively
(Table 3). The primary species tested varied by survey season (Table 3) and
general area of the state (Figure 3). Hunterharvested animals consistently
comprised the majority of samples tested, accounting for 93.5% of all samples;
however, increased emphasis was placed on collecting road-kills starting in 2004
(Table 4). Targeted surveillance of symptomatic animals remained a focus of
state-wide surveillance, but overall numbers varied greatly by season (Table
4).
SNIP...
2003 Judith River Elk Captive Escapees from alternative livestock facility
12
2007 Beaverhead County Elk Captive Escapees from alternative livestock
facility 2
Research Article
Identifying Priority Chronic Wasting Disease Surveillance Areas for Mule
Deer in Montana
ROBIN E. RUSSELL,1 US Geological Survey, National Wildlife Health Center,
6006 Schroeder Road, Madison, WI 53711, USA JUSTIN A. GUDE, Montana Fish,
Wildlife and Parks, 1420 East 6th Avenue, Helena, MT 59620, USA NEIL J.
ANDERSON,2 Montana Fish, Wildlife, and Parks, 1400 South 19th Avenue, Bozeman,
MT 59717, USA JENNIFER M. RAMSEY, Montana Fish, Wildlife, and Parks, 1400 South
19th Avenue, Bozeman, MT 59717, USA
ABSTRACT Chronic wasting disease (CWD) is a fatal prion disease that
affects a variety of ungulate species including mule deer (Odocoileus hemionus).
As of 2014, no CWD cases had been reported in free-ranging ungulates in Montana.
However, nearby cases in Canada, Wyoming, and the Dakotas indicated that the
disease was encroaching on Montana’s borders. Mule deer are native and common
throughout Montana, and they represent a significant portion of the total
hunter-harvested cervids in the state. The arrival of CWD in Montana may have
significant ecosystem and socioeconomic impacts as well as potential
consequences for wildlife management. We used 18,879 mule deer locations from
892 individual deer collected during 1975– 2011 and modeled habitat selection
for 7 herds in 5 of the 7 wildlife management regions in Montana. We estimated
resource selection functions (RSF) in a Bayesian framework to predict summer and
winter habitat preferences for mule deer. We estimated deer abundance from
flyover counts for each region, and used the RSF predictions as weights to
distribute the deer across the region. We then calculated the distance to the
nearest known infected herds. We predicted areas of high risk of CWD infection
in mule deer as areas with densities above the median density estimate and
within the lowest quartile of distances to known infected herds. We identified
these areas, the southeast corner of Montana and the north-central border near
Alberta and Saskatchewan, as priority areas for CWD surveillance and management
efforts. Published 2015. This article is a U.S. Government work and is in the
public domain in the USA.
SNIP...
KEY WORDS chronic wasting disease, disease surveillance, Montana,
Odocoileus hemionus, resource selection, risk mapping. http://onlinelibrary.wiley.com/doi/10.1002/jwmg.914/abstract
Chronic Wasting Disease Surveillance in Montana 1998-2011 2 MB
Environmental Assessment for Detection and Management of Chronic Wasting
Disease in Montana 2013 507 KB
Decision Notice - CWD Plan for Free Ranging Wildlife in MT 2014 185 KB
USFWS-FWP_Chronic Wasting Disease Risk Assessment for Mule Deer in
Northeastern MT 2015 483 KB
Lewis et al 2013_MT public survey on CWD 735 KB
Russell et al 2015_Identifying Priority Chronic Wasting Disease
Surveillance Areas for Mule Deer in Montana 5889 KB
Environmental Assessment for Detection and Management of Chronic Wasting
Disease (CWD) in Montana
4.4.4 Effect on the Alternative Livestock Industry
MFWP currently licenses 39 alternative livestock ranches (game farms) in
Montana. Those licensed facilities reported an inventory of 1086 animals in
their December, 2012 inventory reports to the department. Elk are farmed for
breeding stock, velvet antler production, meat production, and sale to out of
state “game parks” for the harvest of trophy bulls.
DECISION NOTICE: CHRONIC WASTING DISEASE MANAGEMENT PLAN FOR FREE RANGING
WILDLIFE IN MONTANA
*** A more advanced test shows 9 of the 81 elk killed at a Philipsburg game
farm last year had chronic wasting disease (CWD), Published Date: 2000-07-18
23:50:00
Subject: PRO/AH> Chronic wasting disease, elk - USA (Montana) (02)
Archive Number: 20000718.1186
CHRONIC WASTING DISEASE, ELK - USA (MONTANA) (02)
*************************************************
A ProMED-mail post
See Also Chronic wasting dis., elk - Canada (Saskatchewan) 2000.0662
Chronic wasting disease, elk - USA (Montana) 2000.0086 1999
----
Chronic wasting disease, elk - USA (Oklahoma, Montana) 990629124708
Chronic wasting disease, deer & elk - USA (western) 991015094435
1998
----
Chronic wasting dis., deer & elk - USA (Colorado)(04)
980201013730
Chronic wasting dis., deer & elk - Canada (02) 980213223510
Chronic wasting dis., deer & elk - Canada: surveillance 980210202901
1997
----
Chronic wasting dis., deer & elk - USA (Colorado)(03) 971122110009
Chronic wasting disease, deer & elk - USA (Colorado) (02) 971113131710
Chronic wasting disease, deer & elk - USA (Colorado) 970601002126 1996
----
Chronic wasting disease - Canada 960501
Chronic wasting disease - Canada & USA 960613
Chronic wasting disease - USA 960503
Date: Sun, 16 Jul 2000 01:24:21 –0400
From: "Marjorie P. Pollack"
Source: Billings Gazette, 15 July 2000 [edited
Test shows 5 Philipsburg elk had CWD
A more advanced test shows 9 of the 81 elk killed at a Philipsburg game
farm last year had chronic wasting disease (CWD), 5 more than the number
identified in previous testing, state veterinarian Arnold Gertonson said Friday.
He also said the disease has not spread from the Philipsburg facility to any
other Montana game farm. Gertonson said the second-generation test is more
sensitive than the previous testing method available to diagnose the disease,
which is deadly to deer and elk and causes a slow wasting away of the animal.
The newer test was used in the testing of elk recently euthanized by the
state Department of Fish, Wildlife and Parks at the Elk Valley Game Ranch near
Hardin, a herd having been under quarantine since June of 1998. No cases of CWD
were found in the Elk Valley herd, even though 4 of the 29 adult elk at the site
originated from the Kesler game farm at Philipsburg. The Elk Valley herd was
euthanized because the license had not been renewed and the facility was
closing.
Montana regulations require that whenever any game-farm animal 16 months or
older dies, it must immediately be tested for chronic wasting disease. Since
April 1999, 560 samples have been submitted from 41 game farms. "No elk other
than the 9 from the one facility in Philipsburg have been diagnosed with CWD,"
Gertonson said. "The Kesler facility in Philipsburg did not provide elk to any
other Montana alternative livestock facility except the Elk Valley Game Ranch,
where all elk recently tested negative for the disease. Therefore it appears the
Kesler facility did not spread the disease to any other facility in
Montana."
In February, the state veterinarian ordered a 5-year surveillance under
which no deer or elk can be imported into Montana without first having been
under continuous surveillance for CWD for 5 years.
The animal also must have lived within a captive herd where no case of the
disease has been found for 5 years. Montana regulations are the strongest in the
nation, and other states are considering adopting them, Gertonson indicated. The
Montana Legislature this year enacted a moratorium on the licensing of any new
game farms until a live-animal test for CWD can be developed.
--
ProMED-mail
[There are a number of Transmissible Spongiform Encephalopathies (TSE) such
as CWD, scrapie, Bovine Spongiform Encephalopathies (BSE). This herd has been a
reason for concern for several years. - Mod.TG
...........................................tg/es
Published Date: 1999-06-29 23:50:00
Subject: PRO/AH/EDR> Chronic wasting disease, elk - USA (Oklahoma,
Montana?)
Archive Number: 19990629.1098
CHRONIC WASTING DISEASE, ELK - USA (OKLAHOMA, MONTANA?)
******************************************
A ProMED-mail post
See Also
Chronic wasting dis., deer & elk - Canada (05) 980723220304
Chronic wasting dis., deer & elk - Canada: surveil...
980210202901
Chronic wasting dis., deer & elk - USA (Colorado)(06)
980314214051
Date: Tue, 29 Jun 1999
From: *Chan Yow Cheong* ProMED-mail
Regional Moderator for Asia
Source: Missoulian Online, 28 Jun 1999 [edited
A second elk from a Philipsburg game farm recently diagnosed with chronic
wasting disease (CWD) in Oklahoma raises concerns about public health as well as
risks to Montana's wild deer and elk, according to the Montana Wildlife
Federation.
Two elk traced to the Kesler Game Farm [in Montana have been diagnosed with
CWD at an Oklahoma game farm. The most recent case of the deadly brain disease
was diagnosed in May. The disease is similar to "mad cow disease'' (Bovine
Spongiform Encephalopathy, BSE) that has affected cattle in Great Britain. It
has been found in wild deer and elk in Wyoming and Colorado. It is always fatal.
It has been linked by some scientists to the fatal human brain ailment,
Creutzfeldt-Jakob disease (CJD).
Montana Department of Livestock officials have said no CWD has been found
in the state, either in the wild, or in game farm animals. But transfer
documents make it appear very unlikely the infected Oklahoma elk contracted the
disease after being shipped from the Kesler Game Farm, a Wildlife Federation
spokesman said this week.
"We did some digging and found some interesting things we think need to be
brought to the public's attention,'' said John Kober, a western Montana field
representative of the Wildlife Federation. Kober examined records of Kesler Game
Farm elk from Montana Fish, Wildlife and Parks and Montana Department of
Livestock. The 2 agencies share regulatory responsibility for game farms.
The records show that the most recent elk diagnosed with CWD in Oklahoma
was born and raised on the Kesler Game Farm. It was shipped directly to a game
farm in Oklahoma City owned by Don Kaspereit in April 1997. CWD can only be
diagnosed through a necropsy. The elk, which died after it was gored by another
elk, had no clinical signs of the disease.David Kesler, who owns Kesler Game
Farm, said in an earlier interview he has no idea where the elk he sold to the
Oklahoma farm may have contracted CWD. He added no animals at his game farm have
ever shown signs of the disease.
But according to Oklahoma state veterinarian Gene Eskew, Kesler supplied
all of Kaspereit's elk. Kaspereit's game farm has been quarantined with the only
cases of CWD yet found in the state. No additional animals have been added to
the herd.
Of the 84 elk that were sold to Kaspereit by Kesler, the Wildlife
Federation's research showed, only one animal, a bull elk from Utah, did not
originate from Kesler's Montana herd. Fifty of those animals were shipped to
Oklahoma directly from Montana; while 33 of the elk were shipped from Montana to
Idaho, where they spent about 2 months before being shipped to Oklahoma. All of
those animals, except the bull from Utah, came from the Kesler Game Farm. The
Utah bull is still alive.
"To act responsibly, and protect wildlife,'' said Kober, the Livestock
Department "should absolutely admit that this animal did come directly from
Montana, and that the possibility exists this infection occurred in Montana is
actually likely, more likely than anywhere else.''
Tom Linfield, a veterinarian for the Montana Department of Livestock, said
"it's certainly a possibility'' the CWD was present in Kesler's Montana elk
herd.
"The difficulty for us,'' Linfield said, "is to determine where the source
of the problem is. If it's here, where did it come from? Kesler's game farm was
under quarantine for 5 years for TB. There's been no introduction of elk
there.'' The Montana Wildlife Federation believes more thorough testing for CWD
should be done by the Livestock Department on Montana game farms, Kober
said.
Linfield said CWD has not been found on the Kesler Game Farm, which has
been under quarantine since June 1998, after the first elk from there was
diagnosed with the disease in Oklahoma. He said the quarantine means no elk can
be shipped from the game farm except for slaughter. Any elk from the Kesler Game
Farm that dies or is killed for slaughter will be tested for the disease,
Linfield said. Any animal that shows neurological signs of the disease also will
be tested, he said.
Linfield said at least 3 elk have been tested for CWD at the Kesler Game
Farm. None tested positive.But records show that since 1995, 29 elk have died of
causes other than for slaughter or market on the Kesler Game Farm, including 7
since 1998, Kober said.
"That's an inordinate number of game farm animals dead,'' Kober said.
"Something is going on.''
Recent studies indicate that there is a real possibility that CWD, or its
related brain diseases, can be transmitted between species, according to the
Federation.
---
ProMED-mail .........................tg/jw
The Atlantic Online - June 2000
Money Game
Impatient hunters seeking guaranteed trophy antlers -- and impatient Asians
seeking aphrodisiacs -- have made elk farms a thriving business. We’re just
starting to assess the damage
by Hal Herring
ON a hot September afternoon the small town of Hamilton, Montana, is a busy
place. Expensive Jeep Cherokees are towing rafts and drift boats. Sport utility
vehicles cruise by full of camping and fishing and rock-climbing gear. Old
pickups loaded with firewood and a .22 rifle or a shotgun in the gun rack wait
at stoplights. Conspicuous in the traffic is a brand-new flatbed
four-wheel-drive with tinted windows and a special rack in the back, from which
hangs a truly monumental bull elk, the smooth mahogany-colored surface of its
antlers protected by a wrap of rubber inner tube. The metal of the flatbed shows
a long wash of blood, and trickles of blood streak the license plate.
Even in Hamilton, where a dead deer or elk in the back of a pickup is a
common sight, this rig slows traffic, as tourists stare and visiting hunters
look on in envy. The locals are less impressed. They know that the spectacular
animal hanging there is just another “shooter bull,” on its way to a nearby
meat-packing plant. Behind those tinted windows is a wealthy man who has paid
thousands of dollars for the privilege of killing an elk that has been raised
and confined within the fences of the Big Velvet Ranch, twenty miles to the
south -- one of a growing number of game farms in the United States.
The rise of the elk game-farming industry is a relatively recent
development, but the notion has been around since the 1920s, when an eccentric
Montana character named Courtland DuRand set up a dude ranch where elk pulled
wagons and rowboats, and customers applauded as trained bison dropped from a
forty-foot-high platform into an artificial lake.
The modern industry is a more serious business. North American farmed elk
produce 100 tons a year of blood-rich immature “velvet” antler, cut from bulls’
heads annually in June and sold mostly by the Asian medicine trade, which
markets it as a general tonic and an aphrodisiac -- by some estimates a $3
billion industry worldwide. Farmed elk also provide shoots for trophy seekers
who have neither the time nor the inclination to take their chances in the Rocky
Mountain wilderness. The number of people taking part in these staged hunts is
growing. Last year the Big Velvet broke its own record, providing trophy heads
for more than 140 clients. The price for a bull varies according to how large
the antlers are. Hunts at the Big Velvet start at $5,500 and may cost $20,000 or
more.
Colorado is the current leader in elk ranching, with more than 140 game
farms holding more than 10,000 elk captive. In 1994 the game-farming industry in
Colorado successfully lobbied the state to transfer the regulation of elk game
farms from the Division of Wildlife -- which worried about habitat loss and the
spread of disease from captive elk to native wildlife populations -- to the
Department of Agriculture, which is less concerned with such matters. Wyoming is
the only Rocky Mountain state that has outlawed game farming and captive
shooting -- after a campaign that took several years and a great deal of public
money. In Montana, despite the efforts of industry lobbyists, state wildlife
officials still share jurisdiction with the Department of Livestock. And even
here the property-rights movement, whose interests dominate the state
legislature, has successfully deflected attempts by wildlife advocates to ban or
further regulate the industry. Across the state, as new game farms are
established, their fenced-in herds displace native deer, elk, antelope -- and
just about every other wild creature except birds, which have probably benefited
from the creation of large areas newly freed of natural predators.
Because wildlife is considered a public resource, the land to be fenced for
a game farm must first be cleared of all wild game. The “game-proof” fences that
went up for the Big Velvet, in 1993, enclosed some particularly valuable deer
habitat and elk winter range. Len Wallace, the Big Velvet’s owner, hired local
teenagers to run through the gullies and coulees of the property, driving mule
deer to the proposed fenceline. Helicopters buzzed the scattered herds of deer
to keep them moving. The area was then opened to hunters who held unused deer
tags from the past season. Finally game wardens moved in and shot forty-nine
mule deer that refused to leave the area. The wild elk were still in the high
country, so they escaped slaughter. When snow brought them down to their winter
range, they encountered an eight-foot-high fence and came face to face with
their captive brethren.
Prospective clients of the Big Velvet are sent photographs of available
shooter bulls and a promotional video narrated by Wallace, who shows the bulls
wandering around the property and reports exactly what each animal will score on
the Boone and Crockett scale -- a standard measure of the horns and antlers of
North American big game. In the video’s finale happy trophy seekers -- including
a bow hunter in full camouflage garb and facepaint -- pose with their elk.
“Finally I got one exactly the way I wanted it,” one client says.
In game-magazine advertisements the Big Velvet boasts of “The Worlds Most
Successful Trophy Elk Hunt! 100% Success, No Kill, No Pay” and promises a “video
of your hunt” along with transportation and lodging. Other ads show giant bull
elk killed by clients of the fenced Yellowstone Game Ranch, near Sidney,
Montana, far out on the plains. Fenced trophy shoots are in themselves nothing
new. In Texas, which has very little public land and almost no opportunities for
public hunting, they have been around for decades. A client in Texas can choose
from an array of exotic game on dozens of fenced ranches and make guaranteed
kills of everything from greater kudu to gemsbok to addax to giant white-tailed
deer fed on supplements and selectively bred for fantastic antler production.
What is new is the growth of captive shooting in the Rocky Mountain states,
where wild herds still roam public lands and the tradition of “fair chase”
hunting has attained an almost religious status.
THE modern version of farming elk for breeding stock and velvet came to
Montana in the mid-1970s, when a Corwin Springs outfitter and restaurant owner
named Welch Brogan started the Cinnabar Game Farm, in Paradise Valley, north of
Yellowstone National Park. Brogan, with help from a Korean entrepreneur, was the
first to exploit the Asian market for velvet antler. Beginning in 1974, he also
air-freighted over 300 head of elk to buyers in Korea. In the late 1980s state
game officials began to suspect that Brogan and others were supplementing their
herds with elk captured from the wild.
Brogan was found guilty in 1991 of capturing eighty wild elk, and lost his
license to operate. One outspoken critic of the growing game-farming industry is
Jim Posewitz. Posewitz spent thirty-two years as a fish-and-wildlife biologist
in Montana before retiring to start Orion The Hunter’s Institute, a kind of
think tank dedicated to conservation and the preservation of ethical hunting
traditions. He is the author of Beyond Fair Chase (1994), an eloquent discourse
on the ethics of hunting which is often used as a text in state-sponsored
hunting-education programs, and Inherit the Hunt, A Journey Into the Heart of
American Hunting (1999). Posewitz is appalled by the growth of captive shooting.
“It is killing,” he says, “and nothing more. The worst crime is that it
prostitutes and trivializes both hunting and wild game animals.”
Game farmers have little concern for such pieties. Mark Taylor, a lawyer in
Helena and a representative of the Montana Alternative Livestock Producers,
views captive shooting pragmatically. “You have a product,”Taylor says, “and as
a business owner you have a responsibility to explore the markets that will
yield the best profits. If a harvest situation is your best market, then you go
with that.” Len Wallace said in a 1997 interview that state wildlife officials
had persecuted the Big Velvet because they were in direct competition with him
to provide big game for hunters. “People who hunt on my property don’t have to
buy a hunting license,” he said. “Besides, I produce a better product, and [the
wardens] know that.”
Many hunters prefer not to discuss the origins of the trophy head that
hangs on the living-room wall or above the office desk. One Big Velvet client
willing to talk is Mike Ferrari, an international hunter and the owner of a
successful southern- California greenhouse business. The experience changed the
way Ferrari thinks about hunting. “I wouldn’t want my name out there as a
pro-game-ranch hunter,” he says. “At the same time, I don’t want to take
anything away from the Big Velvet. Len Wallace is a hell of a nice guy, and so
are his guides. But I’m sitting here right now looking at that animal on my
wall, and it just doesn’t mean very much to me. And if somebody asks, I have to
tell them how I really got it.” Ferrari says that he has also hunted at game
ranches in Texas, and that the trophy animals there are even easier to kill than
elk at the Big Velvet. “In Texas they have what they call a Texas Grand Slam,”
he says, “where you shoot all the species of sheep, and some of these animals,
you have to honk the horn on the truck to make them get out of the way.” Ferrari
has given up shooting game-farm trophies.
FROM the beginning, many biologists warned that if game farms were
permitted in areas that had served as traditional range for wild game, there was
a severe risk that captive animals would pass on troublesome and exotic diseases
to their free-ranging brethren. Since captive herds are usually made up of
animals from many different farms in various parts of the country, there is
always the possibility that diseases to which native wildlife have little or no
natural resistance will be transmitted. Game farmers dismissed the fear as
baseless, but it wasn’t. In 1988 shipments of elk from the United States were
thought to be responsible for introducing bovine tuberculosis to game farms
across Alberta, including the Elgersma Game Farm, one of the country’s first and
largest.
The Canadian industry was then producing more than $1.5 million worth of
velvet antler a year, and operations were being established or expanded across
the country, resulting in the trade and transport of large numbers of animals.
In an effort to control the rapid spread of the disease, livestock officials
“depopulated” fifty game farms, slaughtering 2,500 infected and exposed elk.
Forty-one people received preventive treatment for tuberculosis.
In a very controversial decision Alberta game farmers were paid $13 million
in compensation for the eradicated herds, even though they had been permitted to
establish a portion of their breeding stock free, through the capture of wild
elk. Six game farms in Montana were placed under quarantine, and one, the Elk
Valley Farm, on the prairie near Hardin, was found to have infected some of the
wild game that lived just outside its fences. So far at least seventy-five
game-farm elk across the state are known to have escaped, and no one can say
what effect they are having on wild herds, or what diseases or parasites they
may have introduced.
Valerius Geist, a professor emeritus of environmental science at the
University of Calgary, had been warning the Canadian government for years that
disease would sooner or later sweep the game-farming industry. One of the
infections that Geist had predicted would show up in captive elk and deer was
chronic wasting disease (CWD) -- a member of the mysterious family of
degenerative brain diseases that includes mad-cow disease, which devastated the
British beef industry in the early 1990s, and Creutzfeldt-Jakob disease, which
produces dementia and rapid death in human beings.
The diseases, known as transmissible spongiform encephalopathies (TSEs),
cause destructive changes in the protein structures of the brain but trigger no
response from the immune system, so there is no test that can determine
infection. “We knew that CWD existed in the wild, in a small area of Colorado
and Wyoming,” Geist says, “and we knew that theft of wild elk was occurring, so
it was just a matter of time.” By the end of last year elk farms in South
Dakota, Montana, Oklahoma, Nebraska, and Colorado were under quarantine for CWD.
The brisk trade in shooter bulls and breeding stock had given speed to a disease
that had been extremely slow to spread on its own.
The Kesler Game Farm, near Philipsburg, Montana, was one of the six Montana
game farms placed under TB quarantine during the early 1990s in response to the
epidemic in Alberta. After the quarantine ended, the owner, Dave Kesler, made a
series of shipments totaling eighty-four elk to a rancher in Oklahoma in 1996
and 1997. In May of 1998 one cow elk fell sick. The animal lost weight rapidly,
slobbered uncontrollably, and demonstrated the staggering that is symptomatic of
TSE infection. The elk died, and a lab test of fresh brain tissue revealed the
presence of CWD. A year later an apparently healthy bull elk was killed in a
brawl with other bulls on the ranch, and it, too, was found to be infected. The
Oklahoma ranch was placed under quarantine, and a new quarantine was imposed on
the Kesler farm. A trace of intrastate elk shipments from Kesler led to the Elk
Valley Farm, placing that farm under a separate quarantine.
For three days early last December the Kesler ranch was sealed off from the
outside world. Game wardens and livestock officials provided security and kept
the press at bay. Strategically placed farm equipment and haystacks blocked
photographers. Eighty-one elk were killed, and dozens of tissue samples were
collected by a team of researchers and biologists from state and federal
agencies. The elk carcasses were packed into plastic-lined dumpsters to await
disposal, the nature of which sparked an angry debate. One of the mysteries of
TSE is the resilience of the infectious agent: CWD is suspected of persisting in
soil for years and resists most routine disinfectants. Finally, livestock
officials imported a special incinerator from Mandan, North Dakota, and burned
the elk carcasses and ranch equipment suspected of CWD contamination. Wildlife
officials have begun trying to determine if the disease has escaped into the
wild mule deer and elk that use the land around the Kesler ranch; shooting from
the ground and from a helicopter, they have killed nine mule deer and one elk
for testing.
ONE result of the emergence of chronic wasting disease is that the
game-farming industry may never again enjoy the kind of free-for-all expansion
that characterized it in the late 1980s and early 1990s. In 1996 Wallace applied
for a new permit to enclose another 1,100 acres of his Big Velvet property. The
enclosure would have displaced both a herd of wild elk and more than 750 mule
deer. “There is absolutely no benefit for me in feeding the public’s wildlife,”
Wallace said at the time, “and I have no intention of doing so.” Wildlife
officials, citing negative impact on public hunting opportunities due to loss of
winter range and overwhelming negative public opinion, denied the permit request
and successfully fought subsequent legal appeals. This was the only gamefarm
permit ever denied by the Department of Fish, Wildlife, and Parks.
Prices for breeder cow elk are down, and the marketing of elk meat has so
far been slow to get off the ground. In South Dakota the brains of farm-raised
elk must be certified CWDfree by a lab before the carcasses can be sold for
meat. Game farmers complain that CWD-infected wild game is threatening their
industry, and that they must be protected from the wild elk and deer that
surround their enclosures. Experts disagree. “CWD is just not a widespread
problem in freeranging wild game,” says Michael Miller, a veterinarian for the
Colorado Division of Wildlife. “And the only tool we have to deal with the
disease in the small area of the wild where it does occur is to do a density
reduction, which basically means clobbering the wild game animals. I don’t think
the public really wants us to do that.”
Nevertheless, there remains a financial base for game farming. The Asian
financial crises temporarily stymied the market for velvet antler, but prices
have recently rebounded. Paula Southman, a spokesperson for the North American
Elk Breeders Association, says the alternative-medicine market in the United
States is in any case picking up the slack created by the fall in Asian demand.
The market for shooter bulls is thriving.
Game farming will be an issue in the upcoming Montana governor’s race.
State Auditor Mark O’Keefe, who has announced his candidacy, is the first
politician to fight the game-farming lobby, which involves the risk of also
angering the loud and forceful property-rights movement. “We have to decide
whether to bring this whole thing to a halt before we do irreparable harm to our
wildlife,”O’Keefe says. “No new permits, no more transport of game animals into
the state.” Under such a moratorium, many newcomers would fold. Game-farm
representatives are already talking about “takings legislation” and what
compensation farmers would accept if new regulations made conducting their
business impossible.
Len Wallace should not be concerned. With so many breeding elk within his
fences, he will probably be able to weather any coming regulatory storm. If the
worst occurs and the state shuts down the Big Velvet, Wallace can be expected to
demand ample payment for the loss of his products -- which is, after all, the
point of game farming.
Hal Herring writes for Field and Stream, High Country News, and Bugle, the
magazine of the Rocky Mountain Elk Foundation. Copyright © 2000 by The Atlantic
Monthly Company. All rights reserved.
The Atlantic Monthly; June 2000; Money Game - 00.06; Volume 285, No. 6;
page 20-25.
Montana burns game farm elk
Hal Herring | Jan. 31, 2000 | From the print edition | Print
Share
On a cold and windy morning last Dec. 7, livestock officials began killing
the elk on the Kesler Game Farm near Philipsburg, Mont.
The herd had been under quarantine for chronic wasting disease for over a
year when an elk that had just died on the ranch was found to be infected. Local
game wardens and officials from the Montana Department of Livestock provided
security for what they call "the depopulation," blocking the press and any
gawkers.
The ranch was a beehive of activity. Elk were sorted and separated by
veterinarians armed with syringes containing a lethal mixture of drugs. Teams of
pathologists and technicians followed, taking blood samples and packing brains
and spinal cords and tissues for laboratory study.
Three days later, the killing was complete. Eighty-nine elk carcasses were
packed into plastic lined dumpsters. Then the looming question: what to do with
them?
Given the few known facts and the many mysteries of chronic wasting disease
(CWD), it was a hot question (HCN, 9/27/99). No one knows how it is transmitted;
only testing a dead animal reveals its certain presence. Before the expansion of
the game farm industry, it was found only in elk in a small area of Wyoming and
Colorado.
The disease belongs to a group of deadly maladies known as TSEs, or
transmissible spongiform encephalopathies, a group which includes the so-called
"mad cow" disease which devastated the British beef industry in the early '90s.
Also among the TSEs is scrapie, which has been recognized as a killer of
domestic sheep for centuries, and Creutzfeldt-Jakob disease, which affects
humans.
A new variant of Creutzfeldt-Jakob disease appeared in Britain during the
"mad cow" epidemic and was linked to consumption of TSE-infected beef products.
Since 1995, the new variant has killed over 50 people in that country.
Scientists don't know the precise origin and makeup of TSEs. What is
certain is that the infectious agent is resilient. At a wildlife research
facility in Fort Collins, Colo., where CWD was first recognized in 1967,
researchers tried to eradicate the disease by killing all the deer and elk held
there, plowing the ground to a depth of over a foot, and spraying the entire
area with a powerful chlorine solution.
A year later, 12 wild elk calves were brought into the pens, said Wyoming
biologist Beth Williams, one of the early researchers into chronic wasting
disease. Within five years, two were dead of CWD.
At the Kesler Game Farm, livestock officials proposed shipping the 89
carcasses to a landfill in Great Falls, Mont., 250 miles away. That idea swiftly
ran afoul of public opinion.
Arnold Gertonson, the state veterinarian, told the Missoulian, "People are
saying, "We don't want them here, we don't want them there." But nobody is
telling me where they want them, or how to handle them, or at what cost."
Gertonson proposed burning the carcasses, and figured it would take about
104 cords of firewood to get the job done. But no one could say for certain if
the CWD agent would survive an open-air fire, or if it could be spread in
blowing ashes or smoke.
Livestock officials finally imported a special waste incinerator from
Mandan, N.D. Known as an air curtain incinerator, the device is set up over a
deep pit and forces air down into the fire, operating on the same principle as a
blacksmith's forge. Temperatures are supposed to reach from 1,700 to 2,200
degrees.
Burning - a month later
This Jan. 6, the burning began. Feed troughs and other equipment went into
the fire with the elk. One hundred forty-five cords of firewood later, it was
finished. Even the ashes were buried on site.
"When it warms up, we'll try to disinfect the grounds and the fences with a
chlorine bath and continue to operate our surveillance," said veterinarian
Gertonson, "and we'll take responsibility for maintaining the fences until July
2001. After that, it's up to Dave Kesler. We've accomplished what we set out to
do."
The whole operation cost Montana about $60,000, Gertonson said.
If the Department of Livestock is satisfied with its handling of the Kesler
problem, it is pretty much alone.
"The DOL is claiming some kind of victory when actually they have done
everything possible to ignore this issue," said John Kober, of the Montana
Wildlife Federation.
"We petitioned, yelled, and screamed for something to be done about the
Kesler herd a long time ago. They did everything in their power to ignore the
scientific evidence and advocate for the game farm industry at the expense of
the Montana public."
Kober says his group also asked the state to test the Kesler farm's
domestic sheep and cattle, since they were close to the elk herd: "They said
that because there's no proof that CWD crosses species, they have no
responsibility to test for it."
The state of Montana paid Kesler $56,000 as compensation for the death of
his herd. While well below the market values of domestic elk, the payment
outraged conservationists like Kober. The money came from funds held by the
Montana Fish, Wildlife and Parks Department, the Department of Livestock and the
Montana Alternative Livestock Producers.
"Once again, sportsmen are forced to pay for an industry that threatens
both hunting and wildlife," said Kober, who was also not happy to learn that the
state paid Kesler an additional $9,700 for providing firewood used to burn the
dead elk.
Before the quarantine, elk from the Kesler Game Farm were shipped to a
rancher in Oklahoma, and to a game farm near Hardin, Mont. Two of the Oklahoma
elk were found to be infected with CWD, and officials suspect that the Hardin
elk are also infected. Both game farms are currently under quarantine for the
disease.
Game farm operations in other states are experiencing similar
problems:
* In South Dakota, one elk herd has been voluntarily "depopulated" and
incinerated by its owner after CWD was found. Another 200 elk are under
quarantine elsewhere in the state.
* In September 1999, a small Colorado herd was killed.
* Two herds are under quarantine in Nebraska.
Canada, which has a large game farm industry of its own, has banned the
importation of elk or deer from the U.S.
Montana state wildlife officials must now step in to try to determine if
CWD has spread into the wild elk and mule deer that live around the Kesler
ranch. There are wintering herds less than two miles away, according to Warden
John Firebaugh, who will direct the shooting of 15 to 20 wild mule deer and elk
in the area. State vets will be on hand to extract the brains of the animals and
transport them to a lab in Bozeman. Firebaugh said that if the brains show no
indication of infection, the meat will be donated to charity.
Hal Herring has reported extensively the spread of chronic wasting disease.
He lives in Corvallis, Montana.
You can contact ...
* Montanans Against the Commercialization of Wildlife, Gary Holmquist,
13320 Sapphire Drive, Lolo, MT 59847 (406/273-7862);
* State Veterinarians, Animal Health Office at the Montana Department of
Livestock, 406/444-2043.
New York State Conservation Council, Inc.
A non-profit organization preserving and protecting the world we live
in
Testimony of Wally John on behalf of the New York State Conservation
Council, Inc Made at the Emerging Food Related Diseases Public Hearing
March 29th, 2001
Good morning, Assemblyman Felix Ortiz and other members of the New York
State Assembly Task Force on Food Farm and Nutrition Policy. Thank you for the
opportunity to testify on the issue of wild game and its relationship to human
nutrition and safety. Of particular concern to the New York State Conservation
Council are the assumptions and implications of Question Number 8 on your list
of selected issues to be addressed by this hearing: "Should the State warn
hunters about the safety of handling and eating deer meat? Should the donation
of deer meat to emergency food programs be allowed to continue?"
This issue is of critical importance to the 900,000 big game hunters who
purchase and use a hunting license each fall in all areas of New York State,
excluding New York City and Nassau County (where hunting is prohibited), because
the question implies strongly that such a public health threat exists, when it
does not! At present and in the past, there has not been any documented concern
by any public health or environmental agency in this state or the nation that
New York's whitetail deer are a food hazard, either to hunters or to the
recipients of donated meat.
There are potential threats to the State's food supply from Bovine
Spongiform Encephalopathy (BSE), commonly called "Mad Cow Disease" from farmed
animal meats which must be guarded against and deserve investigation. Facts and
scientific research should guide our actions in relation to how we treat the
prion-related disease, because we really do know very little about the formation
of prions, how they react with healthy cells, how they are transmitted, and how
they may be controlled.
It is possible to look at the existing reports of BSE and other forms of
Chronic Wasting Disease (CWD) in animals and draw some conclusions about what
actions should be considered.
1. BSE and CWD have been and continue to be confirmed in farm animals in
Europe, Canada, and some other states.
2. Other highly contagious diseases also continue to be confirmed in farm
animals, including "Hoof and Mouth Disease" in Europe, T.B., Brucellosis, Blue
Tongue, Johnnes Disease, and Anthrax.
3. Farmed deer and elk can contract T.B., and there have been cases in New
York State in the past.
4. The New York State Department of Agriculture and Markets has the
authority, under existing law, to confine and destroy any farmed animal,
including but not limited to sheep, cows, pigs, poultry, and farmed deer and
elk, that present a public health threat or a threat to other animals.
5. The food supply that is consumed in New York State is worldwide in
origin, and the State alone cannot completely control disease threats due to
interstate and international marketing of food.
6. Other forms of food-borne disease, such as Sammenella, E. Coli., and
Lysteria, are a greater threat to human health and life, simply due to the ease
of spread and frequency of occurrence.
That said, we should examine some of the actual cases as reported and
investigated and as they relate to CWD or BSE. Canadian health inspectors
confirmed one case of CWD which killed a farmed elk in a Saskatchewan game farm
in 2000 and that same farm had another elk die in 1998 of CWD. All high-risk
animals were destroyed in 1998. The farm animals in 2000 were under quarantine,
and no other elk have shown any symptoms. Further research indicates only one
case in 1996 of CWD in farmed elk in Sedley, Canada, and in that case, the
entire herd was destroyed by the Canadian Government. Those elk had been
imported from a game farm in the United State and had been in Canada for seven
years before they died.
In June of 2000, Montana wildlife and livestock officials destroyed more
than thirty elk at the Elk Valley Game Farm, near Harden, due to the discovery
of CWD at an elk farm in nearby Philipburg, Montana. This site, the Kessler Game
Farm, had an elk die of CWD in October 1999. Montana officials destroyed more
than eighty elk at that farm. The thirty-plus farm elk destroyed at Elk Valley
are currently being tested for CWD.
Montana wildlife officials killed wild elk and deer found outside the
fence of the Kessler and Elk Valley Game Farms and tested them for CWD. None of
the wild animals tested positive for CWD.The Montana Legislature, in 2000,
enacted a moratorium on new game farm applications, until a live animal test for
CWD can be developed. This fact is important to note, because a significant
number of game farms exist in New York State, and they generally import stock
from out-of-state game farms. Also, no test exists for BSE or CWD that allows
the animal to live. The head and brain must be removed from the suspect animal
for examination to confirm CWD or BSE.
The State of Wyoming also tracks cases of CWD and other wildlife diseases,
like Blue Tongue and Brucellosis. Their Department of Game and Fish actively use
the pathology units' Sybille Field Station to evaluate wildlife samples. This
unit is considered to be one of the best worldwide and is presently monitoring
CWD in a small area of southeastern Wyoming. That state's system of deer and elk
licensing by management unit allows them to control hunting efforts in the
suspect area, and a mandatory check area permits them to inspect every animal
taken in that area.
The area of suspected CWD in wild deer and elk is primarily located in
Colorado, just south of Wyoming's area. This area, north of Fort Collins, has
had a CWD problem for several years. In November 2000, the Colorado Wildlife
Commission approved an experimental late season either-sex deer hunt in that
area as part of a Department of Wildlife study on CWD. The hunt had a two-fold
purpose. One was to reduce the deer herd by fifty percent, and the second was to
provide samples for CWD testing. The hunt was conducted by Colorado hunters, who
received written CWD information with their license. This information included
hygiene handling instructions and notice of the requirement that the deer's head
had to be submitted within five days to the Department of Wildlife. Hunters were
then notified of the positive tests.
Colorado hunters and wildlife officials are working together to provide
the scientific sample necessary to better understand the transmission of CWD in
wild deer. This data will help determine if the fifteen- percent suspected
disease rate is accurate and to also help define the boundary of the diseased
herd.
Hunters are concerned with CWD, because laboratory experiments have shown
prion transfer between diseased animal flesh and human proteins in a test tube.
This fact does not indicate a theoretical risk to humans, but it is still not
known how one animal can pass the prion to another.
Approximately fifteen million Americans Hunt and consume game, and this
number is increasing in many states. If wildlife disease is a threat to human
health, it will impact some of this hunting population; hunters have a right to
the best information available. New York State has provided excellent
information in this regard to people who fish, listing types of fish and water
bodies that should be avoided due to chemical and industrial pollution. The
Department of Environmental Conservation and the Department of Health have the
ability to communicate factually about actual and suspected health threats, as
has been seen in the case of Lyme disease and rabies. Hunters have their own
information network through newsletters, organizational notes, national
magazines, and meetings. The word of the problem is communicated quickly
throughout the State by this network.
In conclusion, the answer to Question 8 is that the State should continue
to fund the Division of Fish and Wildlife at the highest possible levels, so
that biologists and wildlife experts will be available to evaluate the health of
our wildlife resources and deal with the potential of disease transmission from
farmed animals to wild animals. The proposed license fee increase should be
enacted this year, because hunters and other sportsmen want to pay their part in
protecting the health and the viability of the State's wildlife. Additional
funds should be made available to the State Veterinarian in the Department of
Agriculture and Markets to monitor imported farm animals for CWD and BSE.
The deer donation program should be allowed to continue as long as poverty
and hunger are present within New York State. Hunters stand ready and willing to
assist the State, when and if a real food safety restriction is needed. Only if
CWD becomes a major human health problem, should restrictions on deer meat
donation be implemented. It is far more apt to become a problem from farmed
animals than from wild animals, and no restrictions have been considered by this
Task Force for farmed elk or deer.
This statement may be reproduced if copied in whole and credit given to
NYSCC.
1992 – 2000 MONTANA escapes from Montana game farm operations
Since 1992, the state has recorded 39 animal escapes from Montana game farm
operations. During the same period there were 22 cases in which native wildlife
got into a game farm. Here's a look at the number of animals escaping from game
farms vs. the number of wildlife getting into the farms from the outside.
1992: Six escapes of game farm animals compared with seven animals entering
the pen.
1993: Six escapes compared with one animal getting in from the outside.
1994: Nine escapes compared with one animal getting in from the outside.
1995: Six escapes compared with two animals getting in.
1996: Four escapes compared with two animals getting in.
1997: Two escapes compared with two getting in.
1998: Four escapes compared with six getting in.
1999: Two escapes compared with two getting in from the outside.<
ABOUT that deer antler spray and CWD TSE PRION...
I have been screaming this since my neighbors mom died from cjd, and she
had been taking a supplement that contained bovine brain, bovine eyeball, and
other SRMs specified risk materials, the most high risk for mad cow disease.
just saying...
Volume 15, Number 5—May 2009
Research
Chronic Wasting Disease Prions in Elk Antler Velvet
I made a submission to the BSE Inquiry long ago during the BSE Inquiry
days, and they seemed pretty interested. see on down ;
Sender: "Patricia Cantos"
To: "Terry S Singeltary Sr. (E-mail)"
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100
3 July 1998
Mr Terry S Singeltary Sr.
E-Mail: Flounder at wt.net
Ref: E2979
Dear Mr Singeltary,
Thank you for your E-mail message of the 30th of June 1998 providing the
Inquiry with your further comments.
Thank you for offering to provide the Inquiry with any test results on the
nutritional supplements your mother was taking before she died.
As requested I am sending you our general Information Pack and a copy of
the Chairman's letter. Please contact me if your system cannot read the
attachments.
Regarding your question, the Inquiry is looking into many aspects of the
scientific evidence on BSE and nvCJD. I would refer you to the transcripts of
evidence we have already heard which are found on our internet site at ;
Could you please provide the Inquiry with a copy of the press article you
refer to in your e-mail? If not an approximate date for the article so that we
can locate it?
In the meantime, thank you for you comments. Please do not hesitate to
contact me on...
snip...end...tss
everyone I tell this too gets it screwed up...MY MOTHER WAS NOT TAKING
THOSE SUPPLEMENTS IPLEX (that I ever knew of). this was my neighbors mother that
died exactly one year _previously_ and to the day of sporadic CJD that was
diagnosed as Alzheimer’s at first. my mother died exactly a year later from the
Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, and exceedingly rare
strains of the ever growing sporadic CJD’s. _both_ cases confirmed. ...kind
regards, terry
TSEs i.e. mad cow disease's BSE/BASE and NUTRITIONAL SUPPLEMENTS
IPLEX, mad by standard process;
vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver
powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine
stomach.
also;
what about potential mad cow candy bars ?
see their potential mad cow candy bar list too...
THESE are just a few of MANY of just this ONE COMPANY...TSS
DEPARTMENT OF HEALTH AND HUMAN SERVICES
FOOD AND DRUG ADMINISTRATION CENTER FOR BIOLOGICS EVALUATION AND RESEARCH
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE
Friday, January 19, 2001 snip...
17 But I think that we could exhibit some quite
18 reasonable concern about blood donors who are taking dietary
19 supplements that contain a certain amount of unspecified-
20 origin brain, brain-related, brain and pituitary material.
21 If they have done this for more than a sniff or something
22 like that, then, perhaps, they should be deferred as blood
23 donors.
24 That is probably worse than spending six months in
25 the U.K.
1/19/01
3681t2.rtf(845) page 501
see full text ;
Sunday, November 10, 2013
LARGE CJD TSE PRION POTENTIAL CASE STUDY AMONG HUMANS WHO TAKE DEER ANTLER
VELVET WILL BE ONGOING FOR YEARS IF NOT DECADES, but who's cares $
CHRONIC WASTING DISEASE TSE PRION UPDATE ON RECENT SCIENCE AND THE
POTENTIAL FOR ZOONOTIC TRANSMISSION GROWS
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 CONFERENCE TOKYO
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.
*** now, let’s see what the authors said about this casual link, personal
communications years ago, and then the latest on the zoonotic potential from CWD
to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS
casual evidence ???? “Our conclusion stating that we found no strong evidence of
CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** NIH awards $11 million to UTHealth researchers to study deadly CWD
prion diseases Claudio Soto, Ph.D. ***
Public Release: 29-Jun-2016
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Tuesday, July 12, 2016
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE,
TSE, Prion Zoonosis Science History
see history of NIH may destroy human brain collection
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.
SCRAPIE AND CWD ZOONOSIS
PRION 2016 CONFERENCE TOKYO
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Transmission of scrapie prions to primate after an extended silent
incubation period
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
Wednesday, June 29, 2016
CWD, SCRAPIE, ZOONOSIS, it’s for real folks, the risk factors have
increased greatly, and science has spoken, cwd and scrapie to humans as sporadic
cjd may have already happened.
Transmission of scrapie prions to primate after an extended silent
incubation period
Emmanuel E. Comoy , Jacqueline Mikol , Sophie Luccantoni-Freire , Evelyne
Correia , Nathalie Lescoutra-Etchegaray , Valérie Durand , Capucine Dehen ,
Olivier Andreoletti , Cristina Casalone , Juergen A. Richt , Justin J. Greenlee
, Thierry Baron , Sylvie L. Benestad , Paul Brown & Jean-Philippe Deslys
Abstract
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion
disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD)
in humans and having guided protective measures for animal and human health
against animal prion diseases. Recently, partial transmissions to humanized mice
showed that the zoonotic potential of scrapie might be similar to c-BSE. We here
report the direct transmission of a natural classical scrapie isolate to
cynomolgus macaque, a highly relevant model for human prion diseases, after a
10-year silent incubation period, with features similar to those reported for
human cases of sporadic CJD. Scrapie is thus actually transmissible to primates
with incubation periods compatible with their life expectancy, although fourfold
longer than BSE. Long-term experimental transmission studies are necessary to
better assess the zoonotic potential of other prion diseases with high
prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98
scrapie.
snip...
In addition to previous studies on scrapie transmission to primate1,8,9 and
the recently published study on transgenic humanized mice13, our results
constitute new evidence for recommending that the potential risk of scrapie for
human health should not be dismissed. Indeed, human PrP transgenic mice and
primates are the most relevant models for investigating the human transmission
barrier. To what extent such models are informative for measuring the zoonotic
potential of an animal TSE under field exposure conditions is unknown. During
the past decades, many protective measures have been successfully implemented to
protect cattle from the spread of c-BSE, and some of these measures have been
extended to sheep and goats to protect from scrapie according to the principle
of precaution. Since cases of c-BSE have greatly reduced in number, those
protective measures are currently being challenged and relaxed in the absence of
other known zoonotic animal prion disease. We recommend that risk managers
should be aware of the long term potential risk to human health of at least
certain scrapie isolates, notably for lymphotropic strains like the classical
scrapie strain used in the current study. Relatively high amounts of infectivity
in peripheral lymphoid organs in animals infected with these strains could lead
to contamination of food products produced for human consumption. Efforts should
also be maintained to further assess the zoonotic potential of other animal
prion strains in long-term studies, notably lymphotropic strains with high
prevalence like CWD, which is spreading across North America, and atypical/Nor98
scrapie (Nor98)50 that was first detected in the past two decades and now
represents approximately half of all reported cases of prion diseases in small
ruminants worldwide, including territories previously considered as scrapie
free. Even if the prevailing view is that sporadic CJD is due to the spontaneous
formation of CJD prions, it remains possible that its apparent sporadic nature
may, at least in part, result from our limited capacity to identify an
environmental origin.
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
2015
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
***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.***
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
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
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
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.
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
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.
HIDING THE BODY BAGS...
Tuesday, July 12, 2016
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE,
TSE, Prion Zoonosis Science History
*** see history of NIH may destroy human brain collection ***
Sunday, July 17, 2016
CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
Terry S. Singeltary Sr. Bacliff, Texas USA flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
2:32 PM
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