Elk Cull Coming To Wind Cave National Park South Dakota Due To CWD TSE PRION DISEASE
GFP News - september 14, 2016 82 77 0 4
Wind Cave National Park and GFP Seek Volunteers to Reduce Elk Population in
the Park WIND CAVE NATIONAL PARK, S.D. -- The National Park Service (NPS),
working with South Dakota Game, Fish and Parks (GFP), will use skilled
volunteers to reduce its elk herd at Wind Cave National Park (Wind Cave) to help
address the high rate of Chronic Wasting Disease (CWD) in the park. Beginning in
mid-November, trained volunteers selected through a lottery system managed by
GFP will work with NPS staff to reduce the number of elk inside the park.
Volunteers will be selected by lottery through GFP and will be trained by
park staff.
The elk management plan for Wind Cave has a targeted population objective
of 232 to 475 elk. Current population estimates indicate numbers of around 550
elk in the park. A recently released report by the United States Geological
Survey (USGS) estimates the CWD prevalence rate in the park’s elk herd is around
9.5 percent, which is higher than previously understood. Scientists seek to
determine if this increased prevalence is linked to the higher density of elk in
the park. It is believed that by reducing the elk population within the boundary
of the park, it will also reduce the prevalence of CWD. The effectiveness of
this management action will be evaluated over the next several years to coincide
with the lifespan of the disease in elk. This action is consistent with the
range of options presented in the Wind Cave Elk Management Plan/ Environmental
Impact Statement signed in 2009.
“Our scientists believe the density of the park’s elk population and CWD
are related,” Wind Cave Superintendent Vidal Dávila said. “We will be following
the herd’s health over the next several years to determine if the reduced
density of elk lowers the prevalence of CWD in the park,” Dávila said. Every
animal taken during this operation will be tested for CWD.
The NPS is partnering with GFP to distribute meat with a “non-detected”
finding for CWD to Feeding South Dakota, an organization dedicated to
eliminating hunger in the state, to be distributed. Also, volunteers who work an
entire week on this operation will be eligible to receive some of the elk meat.
Only meat with a ‘not-detected’ test result for CWD will be distributed.
Four different volunteers will be needed each week for this operation. Each
day two teams will be formed: consisting of an NPS team leader and 2 volunteers.
Anyone wishing to volunteer should submit an online application. A lottery,
similar to those conducted for elk permits, will be conducted.
Applications will be accepted from September 14, 2016 to September 28, 2016
at 8 am CDT.
Only online applications will be accepted.
No paper applications will be allowed.
Applicants need to be over 18 years of age, a South Dakota resident, not
have a felony record, and be willing to undergo a background check.
Participant Requirements
Submit an online application.
Contact Tom Farrell at 605.745.1130 for additional details on this
operation. On their first day, volunteers will be required to demonstrate
advanced firearms proficiency and physical fitness to participate. This will
include shooting a minimum of 3 out of 5 shots into an 8-inch circle at 200
yards using their own firearm and non-lead ammunition. During the week,
volunteers will be required to hike up to 10-miles over rough terrain and carry
packs up to 70lbs. The operation is expected to continue through February.
“As people fill out the application, they have to understand that this is
difficult work that includes several hard days in the field under strenuous
hiking and weather conditions,” said Dávila.
For more information visit https://www.nps.gov/wica/learn/nature/elk-cervus-elaphus.htm.
Administrative Report
Evaluate Elk Population Control and Support Adaptive
Management at Wind Cave National Park
GLEN A. SARGEANT, U.S. Geological Survey, Northern Prairie Wildlife
Research Center, 8711 37th St. SE, Jamestown, ND 58401; gsargeant@usgs.gov;
701-253-5528 DANIEL E. RODDY, National Park Service, Wind Cave National Park,
26611 U.S. Highway 385, Hot Springs, SD 57747-9430; dan roddy@nps.gov;
605-745-1157 DUANE C. WEBER, National Park Service, Wind Cave National Park,
26611 U.S. Highway 385, Hot Springs, SD 57747-9430; duane weber@nps.gov;
605-745-1188
Revised July 27, 2016
Abstract
Since 2010, when the National Park Service (NPS) replaced a 6.65-km section
of 1.2-m-tall woven-wire fencing along the southwestern boundary, Wind Cave Na-
tional Park (WICA) has been fully enclosed by a 2.4-m-tall woven-wire fence. To
enter or leave the park, elk (Cervus elaphus) must negotiate either the fence,
cat- tle guards on roadways, or 7.3-m-wide drop down gates. The NPS proposed to
open gates to allow egress and close gates during summer and fall to prevent elk
from returning, thereby increasing hunter harvest and causing a gradual decline
in population. We used pre-treatment and post-treatment estimates of
distribution and vital rates, obtained from elk marked with global positioning
system collars, to evaluate e ects of the fence renovation on voluntary
movements and mortal- ity of elk captured within WICA during winter. During
2005{14, female elk at WICA comprised distinct eastern and western subsets. Elk
residing in eastern WICA were essentially con ned to the park, whereas elk
distribution in western WICA was continuous with elk distribution on adjacent
public and private lands. However, the proportion of marked western elk with
summer centers of activity outside the park declined from 32% during 2005{09 to
14% during 2011{14. This decline was accompanied by a 32{78% reduction in
voluntary use of lands outside the park during January{August. Although the
renovated fence and gate system discouraged egress, it did not e ectively
prevent elk from returning to the park. Consequently, hunting mortality declined
from 0.052 (SE = 0.016) during 2005{09 to 0.024 (SE = 0.012) during 2011{14. E
ects of reduced mortality from hunting were masked by a coincidental increase in
mortality from chronic wasting disease, from 0:034 (SE = 0.012) to 0:094 (SE
= 0.022). Annual mortality thus in- creased from 0.132 (SE = 0.024) to 0.187 (SE
= 0.030) and projected population growth declined from ^ = 0:976 (SE = 0.018)
to ^ = 0:936 (SE = 0.028). Without knowledge of distribution and cause-speci c
mortality, changes in population would have created an illusion of success. Our
results emphasize inherent risk of interpreting population trend without
knowledge of population processes that are directly a ected by wildlife
management practices, land use, disease, and environmental variation.
snip...
Translocations of elk from WICA were sus- pended in 1997, when the rst
documented case of chronic wasting disease (CWD) in South Dakota was observed in
a captive elk herd on adjacent private land. Although state o cials ordered the
captive herd de- stroyed to prevent the disease from spread- ing, an infected
elk was discovered at WICA in 2002. The NPS subsequently terminated shipments of
potentially infected ungulates from parks (R. Jones, National Park Service 2002,
written communication). By 2004, ap- proximately 800 elk occupied WICA for a
density of 7.0 elk/km2, 12{15 times greater than in hunting units surrounding
the park and twice the park management objective. The NPS responded by
initiating develop- ment of an Environmental Impact Statement and Elk Management
Plan for Wind Cave National Park [EMP] (National Park Service 2009).
snip...
The rst cases of CWD in South Dakota were documented in 1997 in a captive
elk herd held on the Casey addition. The dis- ease was not known to occur in
free-ranging deer until 2001 or in elk until 2002 (Gigliotti (2004); S. Gri n,
South Dakota Game Fish and Parks [SDGFP], oral communication). In 2002, WICA
became the only national park outside the core endemic area described by
Williams et al. (2002) where CWD was then known to occur.
snip...
Because CWD was known to occur in elk at WICA, we took great care to
prevent transmission during capture or via GPS collars. When we recovered and
refurbished collars, we removed and destroyed belting before soaking the
receiver and associated metal container in an aqueous solution of 10% Environ
LpH (Steris Corporation, St. Louis, Missouri, USA) for 1 h. Members of the
capture crew wore disposable surgical gloves while handling elk and did not
reuse syringes, needles, or gloves. Each year, after completion of capture
operations, nets were either destroyed or 1) washed in hot soap and water to
remove gross contamination, 2) soaked in 10% solution of Environ LpH for 1 h,
and 3) triple rinsed and air-dried.
Data collection
Collars estimated and recorded locations of marked elk at 5-h (2005) or 7-h
(2006{14) intervals throughout the year. Sampling at primary intervals provided
3{4 locations per elk per day and evenly distributed sampling throughout the day
and night. For exam- ple, if an elk was located one day at 0100, 0800, 1500, and
2200 hours, it was located the next day at 0500, 1200, and 1900 hours and a day
later at 0200, 0900, 1600, and 2300 hours. This rotating schedule assured repre-
sentative sampling and eliminated bias that might otherwise result from temporal
activ- ity patterns. In addition, we monitored each marked elk at 15-minute
intervals for 24 h on dates selected to maximize coverage of biologically signi
cant periods, within con- straints imposed by battery life.
GPS collars included very high frequency (VHF) transmitters, which operated
for 4 days per week. The VHF transmitters included mortality sensors, which were
checked weekly so that causes of death could be determined and collars could be
recovered if elk died during the course of our study. Whenever possible, we
collected a sample of brain tissue for immunohisto- logical CWD testing by the
Colorado State University Veterinary Diagnostic Laboratory and assigned elk to 1
of 3 condition classes (Table 1). Proximate causes of death were inferred from
physical condition, infection with CWD, harvest reports (hunting),
characteristic injuries or caching of carcasses (cougar predation; Shaw et al.
2007), fatal bullet wounds (poaching), entanglement of carcasses in fences
(fence), vehicle accident reports and massive blunt trauma (vehicle), and
restricted post-marking movements of otherwise healthy elk (excluded from
analysis). We used cessation of move- ment, determined from GPS locations and
activity-sensor records stored by collars, to determine dates of death. We
terminated survival records for elk at death, when col- lars failed (indicated
by low-battery signals or malfunctioning VHF radio transmitters), or at
scheduled dates of collar retrieval.
Thirty-four collared elk were herded out of the park by the NPS during 2013
(28) and 2014 (6). Return times and fates are shown in Figure 10. At least 50%
(17) successfully negotiated the boundary fence and returned within
approximately 4 months (124 days).
Collared elk that were herded out of the park during 2013 were pushed
northward, into Custer State Park, on 1 or 8 March. Thirteen of those elk
returned to the park by 3 July 2013 and 1 returned on 20 May of 2014 (Figure
10). Of the 14 that did not re- turn while they were still under observation, 4
died outside the park from con rmed (3) or presumptive (1) CWD. In addition, one
elk that returned to the park died subsequently from CWD.
All marked elk that were herded northward remained in the vicinity of WICA:
60% of lo- cations were within 1 km, 90% were within 2 km, 98% were within 3 km
of the park. Movement may have been impaired by fences on the east, northeast,
and west, as evinced by corresponding locations of fences and dis- continuities
in the distribution of activity. However, fences apparently did not prevent elk
from dispersing to the north if they were so inclined (Appendix II).
Collared elk that were herded out of the park during 2014 were pushed
westward, into the Black Hills National Forest, on March 12. Three of these elk
were apparently together when they were last located outside the park on March
21, in the vicinity of Custer County Road 391, which traverses the park bound-
ary at 620970 E, 4830851 N, Universal Trans- verse Mercator (UTM) zone 13. The
fourth returned via a similar route on March 23 or 24. One elk remained outside
the park un- til it was killed by a hunter on October 20, 2014, and was also
infected with CWD. One elk survived outside the park until collar re- covery on
December 18, 2014.
Unlike elk that were herded northward, the two elk that remained west of
the park prob- ably were not displaced from their own tradi- tional ranges. Both
occupied ranges within the park that were previously bounded by 1.2-m woven-wire
fence, and both occupied ranges outside the park that were contigu- ous with
their ranges in the park (Appendix III). Moreover, both probably were adults,
based on dentition, when the park fence was renovated in 2010.
Mortality We obtained survival records for 84 subadult male and 215 female
elk. Records encom- passed 132,183 elk-days of observation and 61 deaths.
Mortality rates and numbers of deaths attributed to various causes are shown in
Table 2.
In 25 cases, collared elk simply \laid down and died" without evidence of
injury. Such elk, when tested for CWD, were invariably infected [Table 2, rst
row and Sargeant et al. (2011)]. Given the strength of this associa- tion, CWD
was likely the cause of death for similar, untested cases (Table 2, second row).
Annual mortality rates for con rmed and presumptive CWD, combined, were 0.034
(SE = 0.012) during 2005{09 and 0.094 (SE = 0.022) during 2011{14. In addition,
ap- proximately one-third of deaths (32%, SE = 10.2%, n = 22 tests) attributed
to other prox- imate causes were associated with CWD in- fection. If CWD was
regarded as the under- lying cause for known cases, the mortality rate from CWD
reached 0.042 (SE = 0.013) during 2005{09 and 0.125 (SE =0.025) dur- ing
2011{14.
Prior to renovation of the park boundary fence in 2010, hunting outside the
park was the leading proximate cause of adult mortal- ity, at 5.2% (SE = 0.016)
annually, followed by CWD (Table 2). With renovation of the fence and
restriction of movements across the park boundary, hunting mortality declined to
2.4% (SE = 0.012) annually. However, this decline was o set by increased mortal-
ity from CWD. Accordingly, our point esti- mate of total mortality increased
from 13.2% (SE = 0.024) during 2005{09 to 18.7% (SE = 0.030) during 2011{14.
Rates of mortal- ity from other causes were relatively stable during
2005{14.
snip...
Although attempted management of volun- tary movements failed to increase
use of adjacent lands or increase mortality from hunting, renovation of the park
boundary fence coincided with a presumably unre- lated increase in mortality
from CWD and a concomitant decline in population growth. If we relied on
knowledge of elk numbers rather than elk distribution and vital rates, we would
have concluded|incorrectly|that renovation of the park fence accomplished
management objectives. Whereas popula- tion growth embodies collective e ects of
all in uences on vital rates and distribution, fo- cusing on processes targeted
by management actions reduces the likelihood of confounding and spurious
inference when replication and experimental control are not possible. Fur- ther,
knowledge of vital rates and distribu- tion can|as in this case|elucidate
reasons for outcomes and inform adaptation of man- agement plans.
Elk numbers within WICA were reduced e ectively by herding elk northward
into Custer State Park and westward into the Black Hills National Forest.
However, elk that were herded away from traditional range into Custer State Park
remained concen- trated along the WICA boundary fence, which was clearly more e
ective in deterring egress than entry. We suspect philopatry and social
relationships had opposite e ects on voluntary egress of elk from the park and
return of displaced elk to traditional range within the park. Because displaced
elk are highly motivated to return, prompt detection and repair of damaged
fencing are likely to be essential components of any plan to exclude resident
elk from WICA.
Estimation of mortality is predicated on rep- resentative sampling,
noninformative censor- ing, and independence of events. Longitudi- nal studies
of CWD in wild elk are unlikely to satisfy these conditions, and ours did not,
so management implications warrant careful consideration. At WICA, we selected
out- wardly healthy elk and did not pursue ani- mals that showed signs of
distress; hence we did not capture elk with advanced CWD. In- fection with CWD
may elevate risk of pre- dation, accidents, or even capture and han- dling
(Krumm et al. 2005, Williams 2005). Removal of animals from those at risk of
death from CWD because they are infected with CWD exempli es informative
censoring, and we found evidence of such an e ect in the relatively high rate of
infection among elk that died of other causes. Our estimates of mortality from
CWD were therefore con- servative (i.e., subject to foreseeable nega- tive
bias). However, CWD is an infectious disease, elk are gregarious animals, and we
observed broad overlap of individual ranges. Temporal variation in prevalence
and mor- tality may thus be considerably more vari- able than would be expected
for independent events.
In context with typically high survival rates and typically low prevalence
of CWD in elk, annual mortality of elk at WICA dur- ing 2011{14 and mortality
associated with con rmed or presumptive CWD were ex- ceptional and present
substantial long-term challenges for elk management. In combina- tion with low
pregnancy rates and high peri- natal losses, adult mortality rates were not
sustainable. Vital rates were indicative of a population decline that may not be
alleviated by compensatory responses to falling elk den- sity. In particular,
studies in adjacent Custer State Park have implicated cougar predation as the
cause of similar neonatal losses (Chad P. Lehmann, SDGFP, oral communication).
Mortality from cougar predation probably is not proportional to population size,
hence is likely to increase, rather then decrease, as elk numbers decline.
Likewise, reduced density may not alleviate adult mortality from acci- dents or
hunting. Persistent environmental contamination, the gregarious nature of elk,
and the long course of disease from infection to mortality are all likely to
diminish e ects of density on CWD infection; hence, reduc- ing elk densities may
not reverse the increase in prevalence that occurred during ca. 2000 to 2015. If
survival and fecundity do not in- crease, the population will continue declining
at similar or greater rates after population objectives have been reached.
Regardless of population trend, elk densi- ties at WICA exceed management
objec- tives established by the NPS to protect na- tive vegetation and other
wildlife (National Park Service 2009). Moreover, high elk den- sities combined
with year-round occupation of elk range at WICA, which are likely to promote
animal-to-animal transmission and environmental contamination, are a plausi- ble
explanation for rapidly increasing preva- lence and observed high rates of
mortality from CWD (Almberg et al. 2011), which were much greater for marked elk
than for elk in the greater Black Hills region, where preva- lence is reportedly
< 1% (Sargeant et al. 2011).
In the context of this report, our model is primarily a device for
understanding the collective implications of various in uences on population and
for estimating perina- tal mortality and population trend. Our estimates of
should not be used directly for long-term population projection and management
planning because discrepancies between model projections and actual pop- ulation
performance compound over time. Further, discrepancies generally arise be- cause
models are simpli ed representations of actual dynamics, parameter estimates are
subject to sampling error, and environ- mental in uences (including risks, e.g.,
of disease or predation) are subject to change. With these limitations
acknowledged, our model and parameter estimates nevertheless provide an
objective basis for exploring potential management strategies or hypo- thetical
population responses to changing density.
Elk Cull Coming To Wind Cave National Park
By NPT Staff on September 16th, 2016
An elk culling operation at Wind Cave National Park in South Dakota will
run this coming winter/NPS
A slightly larger than preferred population of elk in Wind Cave National
Park, one carrying Chronic Wasting Disease, has led to a decision to cull the
herd this November.
A release from the park says the National Park Service, working with South
Dakota Game, Fish and Parks, plans to use skilled volunteers to reduce the Wind
Cave elk herd from about 550 animals to between 232 and 475. Volunteers will be
selected by lottery through the South Dakota Game, Fish and Parks Department,
and will be trained by park staff.
A recently released report by the United States Geological Survey estimates
the Chronic Wasting Disease prevalence rate in the park’s elk herd is around 9.5
percent, which is higher than previously understood. Scientists seek to
determine if this increased prevalence is linked to the higher density of elk in
the park. It is believed that by reducing the elk population within the boundary
of the park, it will also reduce the prevalence of CWD. The effectiveness of
this management action will be evaluated over the next several years to coincide
with the lifespan of the disease in elk. This action is consistent with the
range of options presented in the Wind Cave Elk Management Plan/ Environmental
Impact Statement signed in 2009.
“Our scientists believe the density of the park’s elk population and CWD
are related,” Wind Cave Superintendent Vidal Dávila said. “We will be following
the herd’s health over the next several years to determine if the reduced
density of elk lowers the prevalence of CWD in the park. Every animal taken
during this operation will be tested for CWD.”
The NPS is partnering with GFP to donate meat with a “non-detected” finding
for CWD to Feeding South Dakota, an organization dedicated to eliminating hunger
in the state, to be distributed. Also, volunteers who work an entire week on
this operation will be eligible to receive some of the elk meat. Only meat with
a ‘not-detected’ test result for CWD will be distributed.
Four different volunteers will be needed each week for this operation. Each
day two teams will be formed: consisting of an NPS team leader and two
volunteers. Anyone wishing to volunteer should submit an online application
through GFP website. A lottery, similar to those conducted for elk permits, will
be conducted. Applications are being accepted until September 28 at 8 a.m. CDT.
Only online applications will be accepted. Applicants need to be over 18 years
of age, a South Dakota resident, not have a felony record, and be willing to
undergo a background check.
On their first day, volunteers will be required to demonstrate advanced
firearms proficiency and physical fitness to participate. This will include
shooting a minimum of three out of five shots into an 8-inch circle at 200 yards
using their own firearm and non-lead ammunition. During the week, volunteers
will be required to hike up to 10 miles over rough terrain and carry packs up to
70 pounds. The operation is expected to continue through February.
“As people fill out the application, they have to understand that this is
difficult work that includes several hard days in the field under strenuous
hiking and weather conditions,” said Superintendent Dávila.
Wind Cave National Park
CWD in South Dakota
Eliminating CWD is difficult, given the limited understanding of its cause
and transmission and the lack of any vaccine or treatment.
The Animal Industry Board established specific requirements after CWD was
first diagnosed in private, captive elk herds to prevent further introductions
or recurrences in private, captive elk and deer herds. All captive herds that
were infected or exposed have been depopulated, and a voluntary cervidae (deer
and elk) CWD surveillance and control program for captive cervids is now being
implemented.
Joint management strategies for CWD have been, aimed at intensified
surveillance to determine to what degree CWD occurs in free-roaming animals.
GFP, in cooperation with South Dakota State University and Wind Cave National
Park, tested hunter-harvested animals, vehicle killed animals, sick animals, and
research animals starting in 1997. Emphasis has been placed on testing elk and
deer from areas near previously quarantined CWD private elk herd sites, areas
where CWD has been found in wild animals, and sick animals from anywhere in
South Dakota.
Animals tested from 1997-2014 by GFP and Wind Cave National Park consisted
of 6,060 elk, 6,032 mule deer and 13,205 white-tailed deer and 2 moose. Two
hundred and eighty-two animals (178 deer, 104 elk) tested positive for CWD
during this time period.
Animals tested from July 1, 2014 to June 30, 2015 by GFP and Wind Cave
National Park consisted of 129 elk, 19 mule deer, and 30 white-tailed deer.
Twenty-two animals tested positive for CWD during this CWD surveillance period.
Ten deer and 5 elk were found by South Dakota Game, Fish, and Parks that tested
positive for CWD. Wind Cave National Park found 7 elk that tested positive for
CWD.
As of June 30, 2015, a total of 25,299 wild deer and elk have been tested
for CWD in South Dakota and 104 elk and 178 deer have been found to have the
disease. All CWD detected to-date in free-roaming wildlife has been in
southwestern South Dakota and includes Lawrence County, Pennington County, Fall
River County, and Custer County, Wind Cave National Park, and Custer State Park.
Sick deer from several areas of the state are being tested as part of our CWD
Surveillance Program, and no CWD has been found in other areas in South Dakota.
South Dakota agencies, in cooperation with citizens of the state, will
continue to keep a close watch for the disease and determine its distribution
and prevalence. This program will incorporate testing of hunter-harvested deer
and elk, as well as sick deer and elk that are found and reported to GFP. The
AIB will continue its CWD control and monitoring program involving private,
captive elk and deer herds.Â
FOR MORE INFORMATION: South Dakota Game, Fish and Parks 4130 Adventure
Trail Rapid City, SD 57702 605.394.2391 or 605.394.6786 South Dakota Game, Fish
and Parks Information Office 20641 SD Highway 1806 Fort Pierre, SD 57532
605.223.7684 e-mail: wildinfo@state.sd.us South Dakota Animal Industry Board 411
South Fort Street Pierre, SD 57501 605.773.3321
see a bit of cwd positive history here ;
Tuesday, February 26, 2013
Planned elk drive from Wind Cave National Park raises question about spread
of disease
snip...
just when you think it can’t get worse, dumb and dumber step up to the
plate. this is about as dumb, if not dumber, than the blunder at Colorado
Division of Wildlife Foothills Wildlife Research Facility in Fort Collins, where
cwd was first documented.
*** sometimes, you just can’t fix stupid.
*** this should never happen!
*** yes, it did take place, I called to confirm.
*** insanity at it’s finest...tss
Tuesday, March 05, 2013
Chronic Wasting Disease Management Plan/Environmental Impact Statement,
Shenandoah National Park Virginia
Chronic Wasting Disease closes in on Yellowstone
By Ralph Maughan On May 17, 2013
Saturday, May 25, 2013
Wyoming Game and Fish Commission Alkali Creek Feedground #39126 Singeltary
comment submission
Friday, November 16, 2012
Yellowstone elk herds feeding grounds, or future killing grounds from CWD
Thursday, July 08, 2010
CWD Controversy still stalking elk feedgrounds in Wyoming 2010
Greetings,
This is very serious, please notice that one of the CWD clusters is only 45
miles from ELK feeding grounds in Wyoming, the second elk feeding ground is 98
miles from CWD cluster, and the third elk feeding ground is 130 miles from the
CWD cluster. Common sense tells us we need to stop those feeding grounds, if you
want your Elk to survive. There is no politics or plot against the hunters or
elk about it. read the science please. ...TSS
chronic wasting disease proximity to elk feedgrounds in wyoming 2009-2010
Wednesday, October 29, 2014
Chronic wasting disease now rings Greater Yellowstone in Wyoming
Tuesday, December 01, 2015
DRAFT for Public Review and Comment – November 30, 2015 WYOMING GAME AND
FISH DEPARTMENT CHRONIC WASTING DISEASE MANAGEMENT PLAN Singeltary
Submission
Wednesday, November 12, 2014
Shenandoah National Park, Chronic Wasting Disease Management
Plan/Environmental Assessment
Friday, February 22, 2013
SOUTH DAKOTA CHRONIC WASTING DISEASE CWD UPDATE FEBRUARY 22, 2013
http://chronic-wasting-disease.blogspot.com/2013/02/south-dakota-chronic-wasting-disease.html
Published Date: 2011-03-01 14:00:06
Published Date: 2011-03-01 14:00:06
Subject: PRO/AH/EDR> Chronic wasting disease, cervid - USA (06): (SD),
summary
Archive Number: 20110301.0671
CHRONIC WASTING DISEASE, CERVID - USA (06): (SOUTH DAKOTA), SUMMARY
*******************************************************************
A ProMED-mail post <http://www.promedmail.org> ProMED-mail
is a program of the International Society for Infectious Diseases <http://www.isid.org>
Date: Mon 28 Feb 2011 [accessed]
Source: South Dakota Game Fish and Prks
Latest chronic wasting disease [CWD] testing results
----------------------------------------------------
In the South Dakota CWD Surveillance period of 1 Jul 2010-31 Jan 2011, a
total of 1650 samples have been collected for CWD surveillance. In addition, 71
samples were collected from North Dakota hunters in cooperation with the North
Dakota Game and Fish Department.
Breakdown of the SD sampling is as follows:
- 243 elk sampled: 236 results returned as NOT positive; 4 results pending;
3 positive
- 332 mule deer sampled: 324 results returned as NOT positive; 8 positive
- 1075 white-tailed deer: 1061 results returned as NOT positive; 14
positive
To date, South Dakota has found 165 cases of CWD (118 deer and 47 elk) in
free ranging deer and elk since testing began in 1997. Wind Cave National Park
accounts for 34 of these animals (25 elk, 9 deer). 4 elk and 1 deer have been
found in Custer State Park. A total of 23 143 wild deer and elk have been tested
for CWD since 1997.
--
Communicated by: Terry S Singeltary Sr
[The South Dakota Game Fish and Parks did not post a date on this release,
so I am uncertain how long it has been on their website. There is more
information as to breakdown by counties on which deer are positive. For more
information please visit their website at the source URL above. - Mod.TG]
[South Dakota can be seen on the HealthMap/ProMED-mail interactive map at
<http://healthmap.org/r/0x4C>. -
Sr.Tech.Ed.MJ]
Monday, February 28, 2011
South Dakota finds 25 more cases of Chronic Wasting Disease
Latest Chronic Wasting Disease Testing Results
Thursday, May 20, 2010
South Dakota CWD cases mounting
Thursday, December 10, 2009
SOUTH DAKOTA'S CHRONIC WASTING DISEASE (CWD) TESTING UPDATE –2009
Published Date: 2008-02-18 23:50:00
Subject: PRO/AH/EDR> Chronic wasting disease, cervids - USA: (02)(SD),
2007
Archive Number: 20080218.0653
CHRONIC WASTING DISEASE, CERVIDS - USA: (02)(SOUTH DAKOTA), 2007
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A ProMED-mail post <http://www.promedmail.org> ProMED-mail
is a program of the International Society for Infectious Diseases <http://www.isid.org>
Date: Wed 30 Jan 2008
Source: South Dakota Division of Wildlife (accessed 17 Feb 2008) [edited]
South Dakota's chronic wasting disease (CWD) testing update – 2007
-------------------------------------------------------------------
A total of 2532 total samples were collected since 1 Jul 2007. Most samples
are from the Black Hills and from prairie hunting units in Fall River, Custer,
and eastern Pennington counties of western South Dakota. Some samples were
collected in Grant and Deuel Counties in East River. Most samples were taken
from hunter-harvested animals.
Results
-------
As of 30 Jan 2008 we have received results from the SDSU (South Dakota
State University) Diagnostic Lab or Wind Cave National Park on 2531 samples
listed below; one result is pending. [These comprised] 474 elk, 600 mule deer,
and 1457 white-tailed deer
Of the 2531 samples tested to date, we have found one CWD positive elk and
15 CWD positive deer. Below is a summary of these animals:
1. White-tailed female from Unit BD3 in Pennington County. (Hunter Harvest)
2. Elk female from Unit H3B in Custer County. (Hunter harvest)
3. White-tailed female from Unit BD3 in Pennington County. (Vehicle Kill)
4. White-tailed male from Rapid City in Pennington County. (Vehicle Kill)
5. White-tailed female from Unit 21A in Pennington County. (Hunter Harvest)
6. White-tailed male from Unit 27B in Fall River County. (Hunter Harvest)
7. Mule deer male from Unit 27A in Fall River County. (Hunter Harvest)
8. Mule deer female from Unit 27B in Fall River County. (Hunter Harvest)
9. White-tailed female from Unit CU1 in CSP [Custer State Park] in Custer
County. (Hunter Harvest)
10. White-tailed male from Unit 27A in Fall River County. (Hunter Harvest)
11. White-tailed female from Unit 27B in Fall River County. (Hunter
Harvest)
12. Mule deer male from Unit 27B in Fall River County. (Hunter Harvest)
13. Mule deer male from Unit 27A in Fall River County. (Hunter Harvest)
14. Mule deer female from Unit BD4 in Fall River County.
(Sick/Surveillance)
15. Mule deer female from Unit 27B in Fall River County. (Hunter Harvest)
16. White-tailed female from Unit 27B in Fall River County. (Hunter
Harvest)
In summary:
South Dakota Department of Game Fish and Parks has found 16 cases of CWD
(one elk, 15 deer) in free ranging cervids in the testing period 1 Jul 2007 to
present.
To date, South Dakota has found 74 cases of CWD (54 deer and 20 elk) in
free ranging deer and elk since testing began in 1997. Wind Cave National Park
accounts for 17 of these animals (9 elk, 8 deer). A total of 17 378 wild deer
and elk have been tested for CWD since 1997.
Hunters may get their animal tested for chronic wasting disease by making
their own arrangements directly through the SDSU Diagnostic Lab at (605)
688-5171
[Related news accounts: <" target=_blank>http://www.keloland.com/News/NewsDetail6371.cfm?Id=0,66495
--
Communicated by: Terry S. Singeltary Sr.
[Fall River County is in the southeastern corner of SD (see map at <http://en.wikipedia.org/wiki/Fall_River_County,_South_Dakota>;
Custer adjoins it immediately to the north; and Pennington is on Custer's
eastern border and north of the Pine Ridge Reservation. Or all these affected
deer came from one tight corner of the state. Even without denominators of deer
submitted from other counties there appears to be a region of high risk for
cervid CWD in south eastern SD. This raises a question as to how many deer were
submitted from the Pine Ridge Reservation as from these data it would not be at
all unlikely for this disease to be there, or at least needs investigation if
this disease is ever to be cost-effectively controlled.
If you go to the Nebraska Game & Parks Commission "Chronic Wasting
Disease" you can click on their CWD map & tabular data sub-page: <http://www.ngpc.state.ne.us/wildlife/guides/cwd/maps.asp>.
From this you will see that nearly all the cases seen in NE deer are in the
"Panhandle" or far western segment of the state, with a tight little cluster in
Sioux County, NE, abutting Fall River County, SD. Historically there is a larger
series in the SE corner of that panhandle indicating problems in northern
Colorado.
For maps & data on CWD in Colorado go to: <http://wildlife.state.co.us/Hunting/BigGame/CWD/>
Wyoming Game & Fish Department -- <http://gf.state.wy.us/index.asp>
-- has yet to release their CWD data for 2007.
Our thanks to Terry for this report. - Mod MHJ]
From: TSS
Subject: SOUTH DAKOTA Seven deer, four elk found to have CWD
Date: October 10, 2007 at 7:33 am PST
Chronic wasting persists in Hills Seven deer, four elk found to have
chronic wasting disease. By The Associated Press
PIERRE -- Seven deer and four elk were found to have chronic wasting
disease from 2,539 samples in the most recent testing done for the state
Department of Game, Fish & Parks.
All of the infected animals were from Custer, Fall River and Pennington
counties in southwest South Dakota -- the location of all previous CWD cases in
the wild.
Chronic wasting disease attacks the brain in deer and elk and is always
fatal. It's been found in the wild in more than a half-dozen states.
Researchers test for the disease from samples submitted by hunters and from
sick animals observed in the wild.
The positive cases in the July 1, 2006 to June 30, 2007 period included two
elk from Custer State Park and an elk from Wind Cave National Park.
Samples also were taken in the past year from deer killed by hunters in
Grant and Deuel counties in eastern South Dakota. Those counties were added to
the surveillance plan because a CWD-infected deer was discovered at a farm in
Minnesota.
The GF&P said testing will again be done on elk and deer taken by
hunters this fall in the Black Hills and Fall River, Custer, Pennington, Deuel
and Grant counties.
Thirty-nine cases of CWD have been found in deer and 19 in elk from the
18,846 samples tested in South Dakota since 1997, the GF&P said. Seventeen
of the infected animals came from Wind Cave National Park.
South Dakota: [1]
-- First CWD diagnosis in game farm elk on 8 Dec 97; now 5 infected
herds,11 exposed herds
-- all 5 infected herds placed on 5 year quarantine; animals in 1 herd
given to research project.
-- 38/86 animals from infected herds tested positive for CWD.
-- 2 wild white-tailed deer or ingress offspring within premises of an
infected facility tested posivitve.[4]
--30 deer on elk farm premises killed, 1 tested positive for CWD.
-- one suspected case reported in antelope on infected premises [4]
-- index herd tested at USDA: 10 of 17 positive by IHC, only 3 by
histopathology, only 2 animals clinical
-- Wisconsin has additional trace-forward game farms from affected South
Dakota game farms [7]
"Dr. Sam Holland, State Veterinarian for South Dakota, gave a brief summary
of his state's experience with CWD in captive elk. After an initial diagnosis of
CWD on December 8, 1997, his investigation revealed three infected and five
exposed captive elk farms. All infected herds have been placed on quarantine for
5 years, and animals in one herd have become part of a research project.
Eighty-six animals have been tested from positive herds, and 38 have been
infected with CWD. Of the exposed herds, 2 of 35 animals tested were infected.
The Department of Agriculture has developed a memorandum of understanding with
the state wildlife agency to evaluate the wild cervids in the state. To date,
two white-tailed deer within the enclosures of an infected premise were
positive. One deer was a wild animal and the other was privately owned."
snip... "Experiences with captive and free-ranging cervids in Colorado and
Wyoming suggest deer (Odocoileus spp.) may be more susceptible then elk;
however, recent epidemics in farmed South Dakota elk show a different pattern
that could be explained by herd management and/or PrPCWD strain differences.
Both sexes and all age classes of animals can be affected, underscoring the
likely importance of animal-to-animal (lateral) transmission in sustaining
epidemics. Both intra- and inter-specific transmission (e.g., mule
deerwhite-tailed deer, elkwhite-tailed deer) can occur. Precise transmission
mechanisms are unknown, but shedding in saliva, feces, urine, and/or other
excretions have been hypothesized; although transmission via tissue-contaminated
feed could occur, this route appears unimportant in sustaining epidemics. "
"Persistence of the agent in the environment may exacerbate epidemics and
present an obstacle to eradicating CWD from infected premises. The potential
role of invertebrate and/or vertebrate reservoirs in CWD epidemiology warrants
further study, as does the influence of climate on disease persistence,
especially in free-ranging populations. Epidemiological uncertainties, combined
with lack of reliable live-animal tests, present significant obstacles to the
prospects for effectively controlling or eradicating CWD. "
"Sam Holland, DVM, State Veterinarian from South Dakota, presented "CWD,
the State Regulatory Experience." In December 1997, South Dakota confirmed the
diagnosis of CWD in a captive elk herd. This occurrence was treated as an animal
health emergency. Dr. Holland reviewed a program to prevent, prepare, respond
and recover. Great pains were taken to include all stakeholders in the process.
The response included quarantine, immediate epidemiologic traceback, and the
notification of all stakeholders, which included fact sheets and letter writing.
A meeting of all stakeholders was organized to glean support from the industry,
support from regulators, to determine a scientific based process, to devise a
risk based program, and attempt an indemnity program (the latter being
unsuccessful.)"
"The group consensus was that a mandatory control program needed to be
enacted. Legislation was passed to enforce the control program. The control
program includes detailed definitions, outlines official tests, and delineates
movement criteria. "
"Dr. Holland reviewed the present status of CWD in South Dakota. There have
been a total of three affected herds, those with confirmed CWD. A total of five
herds were exposed to the affected herds and have been quarantined from one to
five years. The source elk herd had 30 free-ranging white-tailed deer that were
on the property but did not share a pasture. It was uncertain whether there had
been contact. These 30 white-tailed deer were harvested, and one was found
positive for CWD. A surveillance program of free-ranging wildlife was developed
via cooperation between the various state agencies involved. About 0.5 percent
of annual hunter harvest in designated areas are being examined for CWD. "
"Glen Zebarth, DVM, gave the North American Elk Breeders Association
(NAEBA) perspective on CWD. He updated the committee on the activities of the
Elk Research Council and presented a study plan for the ante-mortem diagnosis,
pathogenesis and epidemiology of CWD in elk. The objectives of the study plan
are to evaluate the potential utility of early diagnosis using third eyelid and
tonsilar lymphoid tissue; characterize the biochemical properties of CWD using
capillary electrophoresis; and determine the pathogenesis as well as the
epidemiology of CWD. The elk breeders have identified two sets of study animals.
The first is the index herd from the South Dakota outbreak. The second herd has
a negative history for the disease. They plan to utilize these animals in
extensive and comprehensive ante-mortem and post-mortem testing. The NAEBA put
forth two resolutions and one recommendation for this Committee's consideration.
"
snip...see more history here on cwd and South Dakota
*** 2016 2015 2014 PRION CONFERENCE UPDATES ON CWD, BSE, SCRAPIE, AND
ZOONOSIS POTENTIAL, PRICE OF PRIONPOKER GOES UP ***
Monday, September 05, 2016
*** Pathological features of chronic wasting disease in reindeer and
demonstration of horizontal transmission Major Findings for Norway ***
see more here ;
Monday, September 05, 2016
*** Pathological features of chronic wasting disease in reindeer and
demonstration of horizontal transmission Major Findings for Norway ***
Wednesday, August 31, 2016
*** NORWAY CONFIRMS 4TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN
SECOND CARIBOU
Wednesday, September 7, 2016
*** An assessment of the long-term persistence of prion infectivity in
aquatic environments
Friday, September 02, 2016
*** Chronic Wasting Disease Drives Population Decline of White-Tailed
Deer
Wednesday, September 21, 2016
ILLINOIS -- Deer disease CWD meetings set Oct. 18 at the Nash Recreation
Center in Oregon, Illinois, and Oct. 19 at the Big Rock Park District Community
Building in Big Rock
Wednesday, September 21, 2016
Pennsylvania Game commission to present forum on deer chronic wasting
disease cwd tse prion
Monday, September 19, 2016
TPWD Agency Partners Set CWD Informational Meetings in Texas Panhandle
Monday, August 29, 2016
*** NWHC USGS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Thursday, August 18, 2016
*** PROCEEDINGS ONE HUNDRED AND Nineteenth ANNUAL MEETING of the USAHA BSE,
CWD, SCRAPIE, PORCINE TSE PRION October 22 28, 2015 ***
Sunday, August 28, 2016
*** CONFIDENTIAL ***
*** Felines and Canines and TSE prions ***
Transmissible Spongiform Encephalopathy TSE Prion and how Politics and
Greed by the Industry spread madcow type diseases from species to species and
around the globe
*** TSE PRIONS AKA MAD COW TYPE DISEASE, LIONS AND TIGERS AND BEARS, OH MY!
***
Saturday, December 12, 2015
NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE
Prion REPORT December 14, 2015
Friday, August 14, 2015
Carcass Management During a Mass Animal Health Emergency Draft Programmatic
Environmental Impact Statement—August 2015
***at present, no cervid PrP allele conferring absolute resistance to prion
infection has been identified.
P-145 Estimating chronic wasting disease resistance in cervids using real
time quaking- induced conversion
Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David
Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2
1 Department of Microbiology and Immunology, Midwestern University, United
States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State
University; 3Prion Research Center; Colorado State University; 4U.S. Geological
Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural
Research Service, United States Department of Agriculture; 6Canadian Food
Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWO
In mammalian species, the susceptibility to prion diseases is affected, in
part, by the sequence of the host's prion protein (PrP). In sheep, a gradation
from scrapie susceptible to resistant has been established both in vivo and in
vitro based on the amino acids present at PrP positions 136, 154, and 171, which
has led to global breeding programs to reduce the prevalence of scrapie in
domestic sheep. In cervids, resistance is commonly characterized as a delayed
progression of chronic wasting disease (CWD); at present, no cervid PrP allele
conferring absolute resistance to prion infection has been identified. To model
the susceptibility of various naturally-occurring and hypothetical cervid PrP
alleles in vitro, we compared the amplification rates and efficiency of various
CWD isolates in recombinant PrPC using real time quaking-induced conversion. We
hypothesized that amplification metrics of these isolates in cervid PrP
substrates would correlate to in vivo susceptibility - allowing susceptibility
prediction for alleles found at 10 frequency in nature, and that there would be
an additive effect of multiple resistant codons in hypothetical alleles. Our
studies demonstrate that in vitro amplification metrics predict in vivo
susceptibility, and that alleles with multiple codons, each influencing
resistance independently, do not necessarily contribute additively to
resistance. Importantly, we found that the white-tailed deer 226K substrate
exhibited the slowest amplification rate among those evaluated, suggesting that
further investigation of this allele and its resistance in vivo are warranted to
determine if absolute resistance to CWD is possible.
***at present, no cervid PrP allele conferring absolute resistance to prion
infection has been identified.
PRION 2016 CONFERENCE TOKYO
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base
Scrapie Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
Confucius ponders...
Could the Scrapie experiments back around 1964 at Moore Air Force near
Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides
the CWD cases that have waltzed across the Texas, New Mexico border near WSMR
Trans Pecos region since around 2001)?
Epidemiology of Scrapie in the United States 1977
snip...
Scrapie Field Trial Experiments Mission, Texas
A Scrapie Field Trial was developed at Mission, Texas, to provide
additional information for the eradication program on the epidemiology of
natural scrapie. The Mission Field Trial Station is located on 450 acres of
pastureland, part of the former Moore Air Force Base, near Mission, Texas. It
was designed to bring previously exposed, and later also unexposed, sheep or
goats to the Station and maintain and breed them under close observation for
extended periods to determine which animals would develop scrapie and define
more closely the natural spread and other epidemiological aspects of the
disease.
The 547 previously exposed sheep brought to the Mission Station beginning
in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were
purchased as field outbreaks occurred, and represented 21 bloodlines in which
scrapie had been diagnosed. Upon arrival at the Station, the sheep were
maintained on pasture, with supplemental feeding as necessary. The station was
divided into 2 areas: (1) a series of pastures and-pens occupied by male animals
only, and (2) a series of pastures and pens occupied by females and young
progeny of both sexes. ...
snip...see full text ;
Thursday, June 09, 2016
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base
Scrapie TSE Prion Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was
detected in a Mule Deer
Monday, July 18, 2016
Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers
Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster
Wednesday, February 10, 2016
*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD
***
Sunday, January 17, 2016
*** Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of
$298,770 for 228 white-tailed deer killed on farm ***
Sunday, May 08, 2016
WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE
ABYSS UPDATE
Friday, April 22, 2016
COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM IS MINIMAL AND LIMITED
*** SEE CWD HIGH INFECTION RATE MAPS FOR COLORADO ! ***
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier
Andréoletti1, Affiliations Contributions Corresponding author Journal name:
Nature Communications Volume: 5, Article number: 5821 DOI:
doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014
Published 16 December 2014 Article tools Citation Reprints Rights &
permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated.
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains.
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
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.***
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.***
CWD TSE PRION HUMAN ZOONOSIS POTENTIAL, has it already happened, and being
masked as sporadic CJD? and what about iatrogenic, or the pass if forward,
friendly fire mode of transmission of cwd to humans, same thing, sporadic cjd ?
*** WDA 2016 NEW YORK ***
We found that CWD adapts to a new host more readily than BSE and that human
PrP was unexpectedly prone to misfolding by CWD prions. In addition, we
investigated the role of specific regions of the bovine, deer and human PrP
protein in resistance to conversion by prions from another species. We have
concluded that the human protein has a region that confers unusual
susceptibility to conversion by CWD prions.
Student Presentations Session 2
The species barriers and public health threat of CWD and BSE prions
Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr.
Edward Hoover1 1Colorado State University
Chronic wasting disease (CWD) is spreading rapidly through cervid
populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease)
arose in the 1980s because cattle were fed recycled animal protein. These and
other prion diseases are caused by abnormal folding of the normal prion protein
(PrP) into a disease causing form (PrPd), which is pathogenic to nervous system
cells and can cause subsequent PrP to misfold. CWD spreads among cervids very
efficiently, but it has not yet infected humans. On the other hand, BSE was
spread only when cattle consumed infected bovine or ovine tissue, but did infect
humans and other species. The objective of this research is to understand the
role of PrP structure in cross-species infection by CWD and BSE. To study the
propensity of each species’ PrP to be induced to misfold by the presence of PrPd
from verious species, we have used an in vitro system that permits detection of
PrPd in real-time. We measured the conversion efficiency of various combinations
of PrPd seeds and PrP substrate combinations. We observed the cross-species
behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found
that CWD adapts to a new host more readily than BSE and that human PrP was
unexpectedly prone to misfolding by CWD prions. In addition, we investigated the
role of specific regions of the bovine, deer and human PrP protein in resistance
to conversion by prions from another species. We have concluded that the human
protein has a region that confers unusual susceptibility to conversion by CWD
prions. CWD is unique among prion diseases in its rapid spread in natural
populations. BSE prions are essentially unaltered upon passage to a new species,
while CWD adapts to the new species. This adaptation has consequences for
surveillance of humans exposed to CWD.
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust
Administration Exploring perceptions about chronic wasting disease risks among
wildlife and agriculture professionals and stakeholders
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
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.
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.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
Yet, it has to be noted that our assessments of PrPTSE levels in skeletal
muscles were based on findings in presumably pre- or subclinically infected
animals. Therefore, the concentration of PrPTSE in skeletal muscles of WTD with
clinically manifest CWD may possibly exceed our estimate which refers to
clinically inconspicuous animals that are more likely to enter the human food
chain. Our tissue blot findings in skeletal muscles from CWD-infected WTD would
be consistent with an anterograde spread of CWD prions via motor nerve fibres to
muscle tissue (figure 4A). Similar neural spreading pathways of muscle infection
were previously found in hamsters orally challenged with scrapie [28] and
suggested by the detection of PrPTSE in muscle fibres and muscle-associated
nerve fascicles of clinically-ill non-human primates challenged with BSE prions
[29]. Whether the absence of detectable PrPTSE in myofibers observed in our
study is a specific feature of CWD in WTD, or was due to a pre- or subclinical
stage of infection in the examined animals, remains to be established. In any
case, our observations support previous findings suggesting the precautionary
prevention of muscle tissue from CWD-infected WTD in the human diet, and
highlight the need to comprehensively elucidate of whether CWD may be
transmissible to humans. While the understanding of TSEs in cervids has made
substantial progress during the past few years, the assessment and management of
risks possibly emanating from prions in skeletal muscles of CWD-infected cervids
requires further research.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C.
Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡,
Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ + Author
Affiliations
1 Department of Microbiology, Immunology and Molecular Genetics, University
of Kentucky, Lexington, KY 40536, USA. 2 Sanders Brown Center on Aging,
University of Kentucky, Lexington, KY 40536, USA. 3 Department of Neurology,
University of Kentucky, Lexington, KY 40536, USA. 4 Department of Microbiology,
Immunology and Pathology, Colorado State University, Fort Collins, CO 80523,
USA. 5 Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO
80526, USA. ↵§ To whom correspondence should be addressed. E-mail:
gtell2@uky.edu ↵* These authors contributed equally to this work.
↵† Present address: Department of Infectology, Scripps Research Institute,
5353 Parkside Drive, RF-2, Jupiter, FL 33458, USA.
↵‡ Present address: Institute of Neuropathology, University of Zurich,
Schmelzbergstrasse 12, 8091 Zurich, Switzerland.
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure.
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin
Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic
Wasting Disease
Contact: Exotic Meats USA 1-800-680-4375
FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San
Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may
contain meat derived from an elk confirmed to have Chronic Wasting Disease
(CWD). The meat with production dates of December 29, 30 and 31, 2008 was
purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk
Farm LLC in Pine Island, MN and was among animals slaughtered and processed at
USDA facility Noah’s Ark Processors LLC.
Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease
found in elk and deer. The disease is caused by an abnormally shaped protein
called a prion, which can damage the brain and nerves of animals in the deer
family. Currently, it is believed that the prion responsible for causing CWD in
deer and elk is not capable of infecting humans who eat deer or elk contaminated
with the prion, but the observation of animal-to-human transmission of other
prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has
raised a theoretical concern regarding the transmission of CWD from deer or elk
to humans. At the present time, FDA believes the risk of becoming ill from
eating CWD-positive elk or deer meat is remote. However, FDA strongly advises
consumers to return the product to the place of purchase, rather than disposing
of it themselves, due to environmental concerns.
Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The
Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was
packaged in individual vacuum packs weighing approximately 3 pounds each. A
total of six packs of the Elk Tenderloins were sold to the public at the Exotic
Meats USA retail store. Consumers who still have the Elk Tenderloins should
return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX
78209. Customers with concerns or questions about the Voluntary Elk Recall can
call 1-800-680-4375. The safety of our customer has always been and always will
be our number one priority.
Exotic Meats USA requests that for those customers who have products with
the production dates in question, do not consume or sell them and return them to
the point of purchase. Customers should return the product to the vendor. The
vendor should return it to the distributor and the distributor should work with
the state to decide upon how best to dispose. If the consumer is disposing of
the product he/she should consult with the local state EPA office.
#
COLORADO: Farmer's market meat recalled after testing positive for CWD
24.dec.08 9News.com Jeffrey Wolf
Elk meat that was sold at a farmer's market is being recalled because tests
show it was infected with chronic wasting disease. The Boulder County Health
Department and Colorado Department of Public Health and Environment issued the
recall Wednesday after the meat was sold at the Boulder County Fairgrounds on
Dec. 13. Although there isn't any human health risk connected with CWD, the
recalled was issued as a precaution. About 15 elk were bought from a commercial
ranch in Colorado in early December and processed at a licensed plant. All 15
were tested for CWD and one came up positive. The labeling on the product would
have the following information: *Seller: High Wire Ranch *The type of cut:
"chuck roast," "arm roast," "flat iron," "ribeye steak," "New York steak,"
"tenderloin," "sirloin tip roast," "medallions" or "ground meat." *Processor:
Cedaredge Processing *The USDA triangle containing the number "34645" People
with questions about this meat can contact John Pape, epidemiologist at the
Colorado Department of Public Health and Environment at 303-692-2628.
COULD NOT FIND any warning or recalls on these two sites confirming their
recall of CWD infected meat. ...TSS
Wednesday, April 06, 2011
Presence and Seeding Activity of Pathological Prion Protein (PrPTSE) in
Skeletal Muscles of White-Tailed Deer Infected with Chronic Wasting Disease
Prion Infectivity in Fat of Deer with Chronic Wasting Disease
Brent Race,# Kimberly Meade-White,# Richard Race, and Bruce Chesebro* Rocky
Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840
Received 2 June 2009/ Accepted 24 June 2009
ABSTRACT Top ABSTRACT TEXT REFERENCES
Chronic wasting disease (CWD) is a neurodegenerative prion disease of
cervids. Some animal prion diseases, such as bovine spongiform encephalopathy,
can infect humans; however, human susceptibility to CWD is unknown. In
ruminants, prion infectivity is found in central nervous system and lymphoid
tissues, with smaller amounts in intestine and muscle. In mice, prion
infectivity was recently detected in fat. Since ruminant fat is consumed by
humans and fed to animals, we determined infectivity titers in fat from two
CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD
infectivity and might be a risk factor for prion infection of other species.
snip...
The highest risk of human contact with CWD might be through exposure to
high-titer CNS tissue through accidental skin cuts or corneal contact at the
time of harvest and butchering. However, the likelihood of a human consuming fat
infected with a low titer of the CWD agent is much higher. It is impossible to
remove all the fat present within muscle tissue, and fat consumption is
inevitable when eating meat. Of additional concern is the fact that meat from an
individual deer harvested by a hunter is typically consumed over multiple meals
by the same group of people. These individuals would thus have multiple
exposures to the CWD agent over time, which might increase the chance for
transfer of infection.
In the Rocky Mountain region of North America, wild deer are subject to
predation by wolves, coyotes, bears, and mountain lions. Although canines such
as wolves and coyotes are not known to be susceptible to prion diseases, felines
definitely are susceptible to BSE (9) and might also be infected by the CWD
agent. Deer infected with the CWD agent are more likely to be killed by
predators such as mountain lions (11). Peripheral tissues, including lymph
nodes, muscle, and fat, which harbor prion infectivity are more accessible for
consumption than CNS tissue, which has the highest level of infectivity late in
disease. Therefore, infectivity in these peripheral tissues may be important in
potential cross-species CWD transmissions in the wild.
The present finding of CWD infectivity in deer fat tissue raises the
possibility that prion infectivity might also be found in fat tissue of other
infected ruminants, such as sheep and cattle, whose fat and muscle tissues are
more widely distributed in both the human and domestic-animal food chains.
Although the infectivity in fat tissues is low compared to that in the CNS,
there may be significant differences among species and between prion strains.
Two fat samples from BSE agent-infected cattle were reported to be negative by
bioassay in nontransgenic RIII mice (3, 6). However, RIII mice are
10,000-fold-less sensitive to BSE agent infection than transgenic mice
expressing bovine PrP (4). It would be prudent to carry out additional
infectivity assays on fat from BSE agent-infected cattle and scrapie
agent-infected sheep using appropriate transgenic mice or homologous species to
determine the risk from these sources.
0C7.04
North American Cervids Harbor Two Distinct CWD Strains
Authors
Angers, R. Seward, T, Napier, D., Browning, S., Miller, M., Balachandran
A., McKenzie, D., Hoover, E., Telling, G. 'University of Kentucky; Colorado
Division of Wildlife, Canadian Food Inspection Agency; University Of Wisconsin;
Colorado State University.
Content
Despite the increasing geographic distribution and host range of CWD,
little is known about the prion strain(s) responsible for distinct outbreaks of
the disease. To address this we inoculated CWD-susceptible Tg(CerPrP)1536+/·
mice with 29 individual prion samples from various geographic locations in North
America. Upon serial passage, intrastudy incubation periods consistently
diverged and clustered into two main groups with means around 210 and 290 days,
with corresponding differences in neuropathology. Prion strain designations were
utilized to distinguish between the two groups: Type I CWD mice succumbed to
disease in the 200 day range and displayed a symmetrical pattern of vacuolation
and PrPSc deposition, whereas Type II CWD mice succumbed to disease near 300
days and displayed a strikingly different pattern characterized by large local
accumulations of florid plaques distributed asymmetrically. Type II CWD bears a
striking resemblance to unstable parental scrapie strains such as 87A which give
rise to stable, short incubation period strains such as ME7 under certain
passage conditions. In agreement, the only groups of CWD-inoculated mice with
unwavering incubation periods were those with Type I CWD. Additionally,
following endpoint titration of a CWD sample, Type I CWD could be recovered only
at the lowest dilution tested (10-1), whereas Type II CWD was detected in mice
inoculated with all dilutions resulting in disease. Although strain properties
are believed to be encoded in the tertiary structure of the infectious prion
protein, we found no biochemical differences between Type I and Type II CWD. Our
data confirm the co·existence of two distinct prion strains in CWD-infected
cervids and suggest that Type II CWD is the parent strain of Type I CWD.
see page 29, and see other CWD studies ;
Sunday, November 23, 2008
PRION October 8th - 10th 2008 Book of Abstracts
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A
WISCONSIN STRAIN OF CWD
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of
Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2
Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary
Research Institute, 4.Center for Prions and Protein Folding Diseases, 5
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
T6G 2P5
The identification and characterization of prion strains is increasingly
important for the diagnosis and biological definition of these infectious
pathogens. Although well-established in scrapie and, more recently, in BSE,
comparatively little is known about the possibility of prion strains in chronic
wasting disease (CWD), a disease affecting free ranging and captive cervids,
primarily in North America. We have identified prion protein variants in the
white-tailed deer population and demonstrated that Prnp genotype affects the
susceptibility/disease progression of white-tailed deer to CWD agent. The
existence of cervid prion protein variants raises the likelihood of distinct CWD
strains. Small rodent models are a useful means of identifying prion strains. We
intracerebrally inoculated hamsters with brain homogenates and phosphotungstate
concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD
endemic area) and experimentally infected deer of known Prnp genotypes. These
transmission studies resulted in clinical presentation in primary passage of
concentrated CWD prions. Subclinical infection was established with the other
primary passages based on the detection of PrPCWD in the brains of hamsters and
the successful disease transmission upon second passage. Second and third
passage data, when compared to transmission studies using different CWD inocula
(Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin
white-tailed deer population is different than the strain(s) present in elk,
mule-deer and white-tailed deer from the western United States endemic region.
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
with CWD TSE Prions, I am not sure there is any absolute yet, other than
what we know with transmission studies, and we know tse prion kill, and tse
prion are bad. science shows to date, that indeed soil, dirt, some better than
others, can act as a carrier. same with objects, farm furniture. take it with
how ever many grains of salt you wish, or not. if load factor plays a role in
the end formula, then everything should be on the table, in my opinion. see
;
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil
Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable
neurological diseases likely caused by a misfolded form of the prion protein.
TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’
disease) in cattle, chronic wasting disease in deer and elk, and
Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are
unique among TSEs because they can be transmitted between animals, and the
disease agents appear to persist in environments previously inhabited by
infected animals. Soil has been hypothesized to act as a reservoir of
infectivity and to bind the infectious agent. In the current study, we orally
dosed experimental animals with a common clay mineral, montmorillonite, or whole
soils laden with infectious prions, and compared the transmissibility to unbound
agent. We found that prions bound to montmorillonite and whole soils remained
orally infectious, and, in most cases, increased the oral transmission of
disease compared to the unbound agent. The results presented in this study
suggest that soil may contribute to environmental spread of TSEs by increasing
the transmissibility of small amounts of infectious agent in the
environment.
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
>>>Particle-associated PrPTSE molecules may migrate from locations
of deposition via transport processes affecting soil particles, including
entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several
years. Significant interest remains in developing methods that could be applied
to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests
that serine proteases and the microbial consortia in stimulated soils and
compost may partially degrade PrPTSE. Transition metal oxides in soil (viz.
manganese oxide) may also mediate prion inactivation. Overall, the effect of
prion attachment to soil particles on its persistence in the environment is not
well understood, and additional study is needed to determine its implications on
the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding,
inferring a durable environmental reservoir, and an efficient mechanism for
indirect horizontal CWD transmission.
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
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
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Summary
The previous assessment concentrated on the incursion of disease from North
America through the imports of animal feed or the movement of contaminated
clothing, footwear and equipment. The results suggested that import of pet feed
was a non-negligible risk, but given the unlikely contact of resident deer in GB
with such non-ruminant feed, this was considered overall a negligible to very
low risk. The movement of contaminated clothing, footwear or equipment
(particularly hunting equipment) could pose a very low risk, although the volume
of contaminated soil which would need to be ingested to give rise to an
infection is likely to be higher than would be present. There is a variable
level uncertainty in all these assessments.
The new assessment focuses on an additional potential route of entry: the
importation of natural deer urine lures. The main conclusions from this
assessment are:
In areas of North America where CWD has been reported, given that CWD is
excreted in faeces, saliva, urine and blood, and survives in the environment for
several years there is a medium probability that the deer urine in North America
contains CWD (high uncertainty; depends on the source of deer used for
production).
The risk of a deer in GB being infected per 30 ml bottle of urine
imported from the USA is very low, albeit with high uncertainty. Overall it is
concluded that the risk of at least one infection of deer in the UK with CWD per
year from deer urine lures imported from the USA is medium. This assumes a high
number of 30 ml bottles imported per year from all areas of the USA.
None of the species affected by CWD in North America are present in GB.
For a British species to become infected with CWD following exposure, the dose
and inherent susceptibility of the species will be important. Based on current
scientific evidence Red deer (Cervus elaphus elaphus) are susceptible to CWD,
Fallow deer (Dama dama) are likely to be less susceptible and Roe deer
(Capreolus capreolus) have a gene conferring susceptibility. Therefore, it is
likely that given exposure to an infectious dose of CWD, deer in GB could become
infected with CWD.
Overall, the probability of importing CWD into GB from North America and
causing infection in British deer is uncertain but likely to be negligible to
very low via movement of deer hunters, other tourists and British servicemen and
very low via imported (non-
2
ruminant) animal feed and medium for the use of lures. However, if it was
imported and (a) deer did become infected with CWD, the consequences would be
severe as eradication of the disease is impossible, it is clinically
indistinguishable from BSE infection in deer (Dalgleish et al., 2008) and
populations of wild and farmed deer would be under threat.
The USA has implemented a Herd Certification Programme for farmed and
captive cervids. So far, 29 States are approved for HCP status (APHIS, 2015).
The list includes States such as Colorado, where CWD is present, therefore it is
recommended that any sourcing of such natural urine lures should be not only
from States with an HCP programme, but also from a herd which is registered as
being regularly tested free of CWD.
Animal urine is not considered a commodity which is subject to animal
by-products legislation for imports. Internet sales are common and although a
license would be required, there are no conditions for the safe sourcing of such
products. Deer urine lures are also available in Europe and may be produced from
carcases of hunted deer. The use of deer urine produced from a species not
present in Europe (such as white tailed deer) is questioned for its value with
native GB deer according to the British Deer Society survey.
Background
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and
behavioural changes that can span weeks or months (Williams, 2005). In addition,
signs might include excessive salivation, behavioural alterations including a
fixed stare and changes in interaction with other animals in the herd, and an
altered stance (Williams, 2005). These signs are indistinguishable from cervids
experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB,
for example, infected deer populations would need to be tested to differentiate
if they were infected with CWD or BSE to minimise the risk of BSE entering the
human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
What is the risk of chronic wasting disease being introduced into Great
Britain? A Qualitative Risk Assessment October 2012
*** 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.
Thursday, August 04, 2016
MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
snip...
1979
SILENCE ON CJD AND SCRAPIE
1980
SILENCE ON CJD AND SCRAPIE
*** 1981 NOVEMBER
snip...see full text ;
Thursday, August 04, 2016
MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
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
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
Monday, August 22, 2016
CREUTZFELDT JAKOB DISEASE USA 2015 SPORADIC CJD TOTAL FIGURES REACHES
HIGHEST ANNUAL COUNT TO DATE AT 239 CONFIRMED CASES
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
4:45 PM
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