Politicians ignore alarming CWD spike in Wyoming valley Wisconsin
Patrick Durkin column: Politicians ignore alarming CWD spike in Wyoming
valley
About one out of every three bucks age 2.5 years and older carries CWD in
north-central Iowa County, as does one out of every six yearling bucks (1.5
years old). / Patrick Durkin/For Wisconsinoutdoorfun.com
Written by Patrick Durkin
Those who think Wisconsin should just “learn to live” with chronic wasting
disease are seeing their surrender take shape as “nature takes its course” on
our deer herd.
In fact, folks near Spring Green are living the realities of such clichés.
One farmer in the Wyoming valley of north-central Iowa County has shot 21
CWD-positive deer from his family’s 700 acres since 2008, with 11 falling since
April 2012.
Those are just a few of the sick deer in a 144-square-mile area where CWD
is rising at “unprecedented” rates. That one-word assessment came from Bryan
Richards, CWD project leader at the U.S. Geological Survey’s National Wildlife
Health Center in Madison after reviewing the latest CWD reports from Robert
Rolley, a Department of Natural Resources researcher in the wildlife science
bureau.
Rolley, Richards and about 50 other citizens, biologists and agency staff
were at the University of Wisconsin-Stevens Point on April 6 to help implement
62 recommendations from the “Deer Trustee Report,” Dr. James Kroll’s guide to
revamping Wisconsin deer management.
Rolley, too, used one word — “frightening” — to assess CWD’s increase in
the 12-by-12-mile area around the Wyoming valley. The eastern border of this
diseased block abuts CWD’s core area (northeastern Iowa and northwestern Dane
counties), where the disease was first discovered 11 years ago.
What constitutes “unprecedented” and “frightening”? First, realize the
infection rate in the core area is increasing about 10 percent annually. That
resembles annual infection rates of mule deer in southeastern Wyoming’s Converse
area, where 40 to 50 percent of the herd is infected.
Now consider north-central Iowa County:
■ CWD’s annual growth rate for all deer (both sexes combined) 2.5 years and
older is 27 percent.
■ Annual disease rates for adult bucks (18 months and older) are doubling
every two to three years.
■ Roughly every third buck 2.5 years and older is infected, as is one in
every six yearling bucks (18 months old). Infected deer live two years or less.
(Page 2 of 2)
■ Although the number of diseased females is lower, the infection rate for
does 2.5 years and older is growing 38 percent annually, faster than for
males.
“I’m not aware of data anywhere showing wild, free-range deer with similar
infection rates,” Richards said. “The only thing worse was the Stan Hall farm
(Buckhorn Flats, near Almond), whose penned herd of 76 deer went from one sick
deer to 60 in five years.”
That might sound like mere statistics to some, but not to Matt Limmex, 49,
an Iowa County dairy farmer who has spent his life on the family’s property. Of
the 11 sick deer killed on Limmex’s lands the past year, six fell during 2012
gun seasons.
The other five? Limmex shot them at the DNR’s request after noticing the
“droolers and shakers” near his farmyard. In three cases, they were so sick they
couldn’t flee when Limmex approached. The DNR retrieved the carcasses for
testing and disposal.
“I hate to see this,” Limmex said. “It’s disheartening. I just want to get
sick deer off the landscape.”
Limmex said his family deploys about 14 hunters each year during gun
season. They’ve also used agricultural shooting permits since 1991 to control
the herd. Even so, this is the first time he senses deer numbers
decreasing.
“It seems like the disease might be affecting the herd now,” he said.
So, what’s causing CWD rates in the Wyoming valley to exceed those in the
original disease zone? And will it shrink local herds, as experts have long
predicted? No one knows, and our state and federal governments aren’t inclined
to find out.
The only current DNR-funded deer research by the University of Wisconsin is
studying whether predators are affecting Northwoods whitetails. Meanwhile,
Professor Michael Samuel at UW-Madison is using federal funds to study if deer
leave CWD-causing prions in feces, breeding scrapes and mineral licks. But
that’s ending soon.
“We’re puzzled by what’s going on in the Wyoming valley,” Samuel said.
“It’s very disturbing, but CWD research is on the way out. We could generate
hypotheses and proposals to study what’s behind the increases, but I doubt we’d
get the funding. There’s little interest in CWD these days, Wisconsin and
nationwide.”
Imagine that. The world’s most “disturbing,” “frightening” and
“unprecedented” CWD case is growing next door to our capital and flagship
university, and our government won’t crack a window to sniff it.
Meanwhile, no group or coalition of hunters, doctors, veterinarians or
environmentalists is holding politicians accountable or funding the research
themselves.
There’ll be no shortage of shame as this stench spreads.
> There’ll be no shortage of shame as this stench spreads.
it’s all about money. no one cares about a long incubating disease, that
once clinical, is 100% fatal in all species, i.e. the TSE prion disease.
Politicians have been ignoring all TSE prions, and risks there from. somebody
better start caring, soon. ...tss
Tuesday, April 16, 2013
Cervid Industry Unites To Set Direction for CWD Reform and seem to ignore
their ignorance and denial in their role in spreading Chronic Wasting Disease
Monday, April 01, 2013
Dr. Deer/Dough from Texas on Wisconsin’s CWD implementation survey, is now
available
Tuesday, December 18, 2012
*** A Growing Threat How deer breeding could put public trust wildlife at
risk
yep, while the Texas deer czar dr. dough was off to Wisconsin pushing the
privately owned shooting pen industry (livestock cervids industry), Texas fell
to CWD, and just reported 4 more CWD postives. ...
for your information...
According to Wisconsin’s White-Tailed Deer Trustee Dr. James Kroll, people
who call for more public hunting opportunities are “pining for socialism.” He
further states, “(Public) Game management is the last bastion of communism.”
“Game Management,” says James Kroll, driving to his high-fenced,
two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.”
Kroll, also known as Dr. Deer, is the director of the Forestry Resources
Institute of Texas at Stephen F. Austin State University, and the “management”
he is referring to is the sort practiced by the State of Texas. The 55-year-old
Kroll is the leading light in the field of private deer management as a means to
add value to the land. His belief is so absolute that some detractors refer to
him as Dr. Dough, implying that his eye is on the bottom line more than on the
natural world.
Kroll, who has been the foremost proponent of deer ranching in Texas for
more than thirty years, doesn’t mind the controversy and certainly doesn’t fade
in the heat. People who call for more public lands are “cocktail
conservationists,” he says, who are really pining for socialism. He calls
national parks “wildlife ghettos” and flatly accuses the government of gross
mismanagement. He argues that his relatively tiny acreage, marked by eight-foot
fences and posted signs warning off would-be poachers, is a better model for
keeping what’s natural natural while making money off the land.
Tuesday, July 10, 2012
Dr. James C. Kroll Texas deer czar final report on Wisconsin
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Thursday, March 29, 2012
TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT
CALLING KETTLE BLACK
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Monday, April 15, 2013
Deer farmers in the state of Louisiana are under a quarantine due to
Chronic Wasting Disease CWD
Monday, January 16, 2012
9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD
pens, PENS, PENS ???
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
now, decades later ;
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. The purpose
of these experiments was to determine susceptibility of white-tailed deer (WTD)
to scrapie and to compare the resultant clinical signs, lesions, and molecular
profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD
intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral
and intranasal (IN); n = 5) with a US scrapie isolate. All deer were inoculated
with a 10% (wt/vol) brain homogenate from sheep with scrapie (1ml IC, 1 ml IN,
30 ml oral). All deer inoculated by the intracranial route had evidence of PrPSc
accumulation. PrPSc was detected in lymphoid tissues as early as 7
months-post-inoculation (PI) and a single deer that was necropsied at 15.6
months had widespread distribution of PrPSc highlighting that PrPSc is widely
distributed in the CNS and lymphoid tissues prior to the onset of clinical
signs. IC inoculated deer necropsied after 20 months PI (3/5) had clinical
signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural
and lymphoid tissues. The results of this study suggest that there are many
similarities in the manifestation of CWD and scrapie in WTD after IC inoculation
including early and widespread presence of PrPSc in lymphoid tissues, clinical
signs of depression and weight loss progressing to wasting, and an incubation
time of 21-23 months. Moreover, western blots (WB) done on brain material from
the obex region have a molecular profile similar to CWD and distinct from
tissues of the cerebrum or the scrapie inoculum. However, results of microscopic
and IHC examination indicate that there are differences between the lesions
expected in CWD and those that occur in deer with scrapie: amyloid plaques were
not noted in any sections of brain examined from these deer and the pattern of
immunoreactivity by IHC was diffuse rather than plaque-like. After a natural
route of exposure, 100% of WTD were susceptible to scrapie. Deer developed
clinical signs of wasting and mental depression and were necropsied from 28 to
33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB.
Similar to IC inoculated deer, samples from these deer exhibited two different
molecular profiles: samples from obex resembled CWD whereas those from cerebrum
were similar to the original scrapie inoculum. On further examination by WB
using a panel of antibodies, the tissues from deer with scrapie exhibit
properties differing from tissues either from sheep with scrapie or WTD with
CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive
when probed with mAb P4, however, samples from WTD with scrapie are only weakly
immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from
sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from
WTD with scrapie are strongly positive. This work demonstrates that WTD are
highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is
differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)
Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National
Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie
and CWD in inoculated deer. Interspecies transmission studies afford the
opportunity to better understand the potential host range and origins of prion
diseases. We inoculated white-tailed deer intracranially (IC) and by a natural
route of exposure (concurrent oral and intranasal inoculation) with a US scrapie
isolate. All deer inoculated by the intracranial route had evidence of PrPSc
accumulation and those necropsied after 20 months post-inoculation (PI) (3/5)
had clinical signs, spongiform encephalopathy, and widespread distribution of
PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6
months PI did not have clinical signs, but had widespread distribution of PrPSc.
This highlights the facts that 1) prior to the onset of clinical signs PrPSc is
widely distributed in the CNS and lymphoid tissues and 2) currently used
diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical
signs. The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in white-tailed deer after IC inoculation
including early and widespread presence of PrPSc in lymphoid tissues, clinical
signs of depression and weight loss progressing to wasting, and an incubation
time of 21-23 months. Moreover, western blots (WB) done on brain material from
the obex region have a molecular profile consistent with CWD and distinct from
tissues of the cerebrum or the scrapie inoculum. However, results of microscopic
and IHC examination indicate that there are differences between the lesions
expected in CWD and those that occur in deer with scrapie: amyloid plaques were
not noted in any sections of brain examined from these deer and the pattern of
immunoreactivity by IHC was diffuse rather than plaque-like. After a natural
route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 months PI. Tissues from these deer were positive for scrapie by
IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil,
retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and
spleen. While two WB patterns have been detected in brain regions of deer
inoculated by the natural route, unlike the IC inoculated deer, the pattern
similar to the scrapie inoculum predominates.
Committee Business:
The Committee discussed and approved three resolutions regarding CWD. They
can be found in the report of the Reswolutions Committee. Essentially the
resolutions urged USDA-APHIS-VS to:
Continue to provide funding for CWD testing of captive cervids
Finalize and publish the national CWD rule for Herd Certification and
Interstate Movement
Evaluate live animal test, including rectal mucosal biopsy, for CWD in
cervids
2011 Annual Report
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
2011 Annual Report
In Objective 1, Assess cross-species transmissibility of transmissible
spongiform encephalopathies (TSEs) in livestock and wildlife, numerous
experiments assessing the susceptibility of various TSEs in different host
species were conducted. Most notable is deer inoculated with scrapie, which
exhibits similarities to chronic wasting disease (CWD) in deer suggestive of
sheep scrapie as an origin of CWD.
snip...
4.Accomplishments 1. Deer inoculated with domestic isolates of sheep
scrapie. Scrapie-affected deer exhibit 2 different patterns of disease
associated prion protein. In some regions of the brain the pattern is much like
that observed for scrapie, while in others it is more like chronic wasting
disease (CWD), the transmissible spongiform encephalopathy typically associated
with deer. This work conducted by ARS scientists at the National Animal Disease
Center, Ames, IA suggests that an interspecies transmission of sheep scrapie to
deer may have been the origin of CWD. This is important for husbandry practices
with both captive deer, elk and sheep for farmers and ranchers attempting to
keep their herds and flocks free of CWD and scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
how many states have $465,000., and can quarantine and purchase there from,
each cwd said infected farm, but how many states can afford this for all the cwd
infected cervid game ranch type farms ???
? game farms in a state X $465,000., do all these game farms have insurance
to pay for this risk of infected the wild cervid herds, in each state ???
how many game farms, are too many game farms ?
when you have states handing out shooting pen permits like candy on
halloween, just to advance their coffers, then other states wanting to do the
same thing, with most all of them ignoring the science on shooting pens and cwd,
what do you expect is going to happen.
when is enough, enough ?
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
Form 1100-001
(R 2/11)
NATURAL RESOURCES BOARD AGENDA ITEM
SUBJECT: Information Item: Almond Deer Farm Update
FOR: DECEMBER 2011 BOARD MEETING
TUESDAY
TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief
SUMMARY:
SEE MORE USAHA REPORTS HERE, 2012 NOT PUBLISHED YET...TSS
the captive cervid industry has been helping spreading cwd for decades into
the wild, to other farms, and to other countries (Korea), and it's high time to
stop it. if you are fortunate enough to have a bunch of land and a bunch of
money, that should not give you the right to pen up a bunch of cervids, modify
these cervids to look like an alien with it's man made spreads, then put a cow
bell on the back of a truck at feeding time, pay an absurd fee to shoot these
straw bred bucks, call it livestock, and then go out and shoot it and call it
hunting i.e. a sport, and then spread cwd to hail and back. to me, it would be
like going out on a big hunt, in the pasture down the street and killing a cow
every time i want to eat a steak, mounting the head, hanging it on the wall, and
calling it a sport. i just don't see it, but if some folks have to do it, for
whatever reason, and it's legal, i think you must have an insurance policy from
Loyd's of London or whom ever, that would cover what ever cost to that state you
are in, if a case of cwd is detected on your farm, to cover the cost to that
state, for ever farm that is confirmed with cwd. that should put a fast track on
validated a cwd live test, which they have, to test cervids, and rapidly
expedite the validating of the many other cwd/tse/prion test that are in the
pipeline. but if you don't test, if you don't test correctly, if you don't test
all ages, if you don't test in large enough numbers to find, if you don't test
where you know it might be, you probably will not find it. ...
WILD DEER AND ELK
NUMBER OF CWD TESTING WILD DEER AND ELK 2002 - 2012 = 910,136.
VOLUNTARY captive shooting pen farmed deer and elk program
number of CWD testing samples 2002-2012 = 188,624.
this is minus the SSS policy of the dead captive cervids found $ (old
mountain lion must have eaten it???), or (that old sickly looking deer that
might have CWD, just happened to escape???) ;
i have included in this report, SOME HISTORY ON CAPTIVE SHOOTING PENS IN
NORTH AMERICA, AND CWD THERE FROM...
see full text ;
Saturday, April 13, 2013
Tennessee Launches CWD Herd Certification Program in the wake of
legislation for game farms
P35
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.
PPo3-7:
Prion Transmission from Cervids to Humans is Strain-dependent
Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi
Gambetti and Liuting Qing Department of Pathology; Case western Reserve
University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial
Sloan-Kettering Cancer Center; New York, NY USA
Key words: CWD, strain, human transmission
Chronic wasting disease (CWD) is a widespread prion disease in cervids
(deer and elk) in North America where significant human exposure to CWD is
likely and zoonotic transmission of CWD is a concern. Current evidence indicates
a strong barrier for transmission of the classical CWD strain to humans with the
PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD
strains. What remain unknown is whether individuals with the PrP-129VV/MV
genotypes are also resistant to the classical CWD strain and whether humans are
resistant to all natural or adapted cervid prion strains. 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. Preliminary results on CWD transmission in transgenic mice
expressing human PrP-129V will also be discussed.
Acknowledgement Supported by NINDS NS052319 and NIA AG14359.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A.
Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and
related Brain disorders; Dept of Neurology; University of Texas Houston Medical
School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular
Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky
Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve
University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago;
Chicago, IL USA
Prion diseases are infectious neurodegenerative disorders affecting humans
and animals that result from the conversion of normal prion protein (PrPC) into
the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of
cervids is a prion disorder of increasing prevalence within the United States
that affects a large population of wild and captive deer and elk. CWD is highly
contagious and its origin, mechanism of transmission and exact prevalence are
currently unclear. The risk of transmission of CWD to humans is unknown.
Defining that risk is of utmost importance, considering that people have been
infected by animal prions, resulting in new fatal diseases. To study the
possibility that human PrPC can be converted into the infectious form by CWD
PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification
(PMCA) technique, which mimic in vitro the process of prion replication. Our
results show that cervid PrPSc can induce the pathological conversion of human
PrPC, but only after the CWD prion strain has been stabilized by successive
passages in vitro or in vivo. Interestingly, this newly generated human PrPSc
exhibits a distinct biochemical pattern that differs from any of the currently
known forms of human PrPSc, indicating that it corresponds to a novel human
prion strain. 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
Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin,
Germany
Key words: CWD, strains, FT-IR, AFM
Chronic wasting disease (CWD) is one of three naturally occurring forms of
prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie
in sheep. CWD is contagious and affects captive as well as free ranging cervids.
As long as there is no definite answer of whether CWD can breach the species
barrier to humans precautionary measures especially for the protection of
consumers need to be considered. In principle, different strains of CWD may be
associated with different risks of transmission to humans. Sophisticated strain
differentiation as accomplished for other prion diseases has not yet been
established for CWD. However, several different findings indicate that there
exists more than one strain of CWD agent in cervids. We have analysed a set of
CWD isolates from white-tailed deer and could detect at least two biochemically
different forms of disease-associated prion protein PrPTSE. Limited proteolysis
with different concentrations of proteinase K and/or after exposure of PrPTSE to
different pH-values or concentrations of Guanidinium hydrochloride resulted in
distinct isolate-specific digestion patterns. Our CWD isolates were also
examined in protein misfolding cyclic amplification studies. This showed
different conversion activities for those isolates that had displayed
significantly different sensitivities to limited proteolysis by PK in the
biochemical experiments described above. We further applied Fourier transform
infrared spectroscopy in combination with atomic force microscopy. This
confirmed structural differences in the PrPTSE of at least two disinct CWD
isolates. The data presented here substantiate and expand previous reports on
the existence of different CWD strains.
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
November 2012
Friday, December 14, 2012
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005
– December 14, 2012
Monday, November 14, 2011
WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Wednesday, November 16, 2011
Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Sunday, November 13, 2011
COLORADO CWD CJD TSE PRION REPORTING 2011
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.
TSS
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