TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016 DEER BREEDERS STILL DON'T GET IT $
Chronic Wasting Unease
The emergence of a deadly disease has wildlife officials and deer breeders
eyeing each other suspiciously.
January 2016By Brantley Hargrove - See more at: http://www.texasmonthly.com/articles/chronic-wasting-unease/#sthash.UnSGN5Cs.dpuf
Chronic Wasting Unease
The emergence of a deadly disease has wildlife officials and deer breeders
eyeing each other suspiciously.
January 2016 By Brantley Hargrove
snip...
Eddie Ray, like most of the animals on this ranch outside Chico, has never
met his father; he was conceived by way of frozen semen that arrived in the
mail. Terrie and Steve artificially inseminate many of their does with this
high-dollar substance and sell the resulting progeny to outfitters and other
breeders. They’ve even gotten into the supply business themselves; Eddie Ray’s
semen goes for $1,250 a straw, a fraction of a teaspoon. “Used to be that if you
had a deer this big, he’s five years old,” Steve says, pointing to a buck in a
nearby paddock. “I have a yearling with a two-hundred-inch rack. It’s all about
genetics.”
Thanks to these innovations, the Texas deer-breeding industry has thrived,
swelling from just over 100 breeders in the early nineties to some 1,300 today.
Breeders like to say they’ve democratized trophy hunting, providing even small
outfitters with monster bucks befitting the King Ranch. That’s been a boon not
only for the deer business but for a way of life that’s central to the state’s
identity; the industry has kept land in the hands of families who might
otherwise have sold out to developers.
But in recent years this progress has come with a price. Since 2002, the
industry has been bedeviled by a fatal pathogen that’s endemic in parts of
Colorado, Wisconsin, Wyoming, Nebraska, Utah, and New Mexico. Chronic wasting
disease (CWD), as it’s known, isn’t caused by a virus, bacteria, or parasite but
by an abnormal protein called a prion that can destroy a deer’s brain and spinal
cord. Deer contract it by interacting with infected animals or coming into
contact with their saliva, urine, or feces. They can even pick it up from
contaminated soil. It’s the cervid equivalent of mad cow disease, scrapie in
sheep, or Creutzfeldt-Jakob disease in humans. It transforms once majestic
animals into staggering husks that die well before their time. “You don’t want
this out in the Texas Hill Country, we’ll put it that way,” says Bryan Richards,
a CWD expert at the National Wildlife Health Center.
snip...
Chronic wasting disease might as well have been purpose-built to ignite old
animosities between TPWD and deer breeders. The industry has always loathed a
provision of Texas statute that classifies all whitetail deer as wildlife and
thus a public trust. Technically, a breeder doesn’t own deer, though in practice
they can sell them for a tidy sum.
TPWD’s supporters in this fight—conservationists, wildlife managers, and
traditional outfitters who disdain the intense focus on antler size—say the
breeders’ commodification of wildlife and fixation on the antler arms race has
warped Texas’s hunting culture. Breeders claim that the crackdown stems from the
rack envy of wild-game ranches. CWD, they allege, is the perfect pretext for
making their lives miserable. “Parks and Wildlife is picking winners and
losers,” says Texas Deer Association director Patrick Tarlton.
Breeders have long known that CWD would eventually find its way here. And
it didn’t take long for word to circulate that the disease had been detected at
Texas Mountain; almost immediately, TPWD’s deer-transfer permit system saw a
spike in activity as South Texas breeders raced to get ahead of the coming
regulatory freeze. In an unprecedented step to halt the movement of potentially
infected animals, TPWD deactivated the system for two months.
When business resumed in late summer, it was under a new regime of
emergency rules. Breeders like the Mosses, who can show negative tests for deer
purchased from Texas Mountain, have seen their hold orders lifted. If for
whatever reason breeders can’t demonstrate this—because, say, an animal died
earlier—they will fall to the bottom rung of a newly created caste system of
potential disease risk. To shake off the designation, they have to meet a number
of stringent requirements, such as proving that they have tested a certain
percentage of their animals. In most cases, that necessitates the sacrifice of
healthy deer, each worth hundreds if not thousands of dollars. Add to that the
cost of testing, which can run $150 per animal, and getting right with TPWD
becomes an expensive proposition.
Talk to any breeder and it becomes clear that they and the regulators exist
in separate factual galaxies. The breeders don’t even agree that CWD is a major
threat. “This is a political disease,” Steve says. Terrie notes that of the
legions of deer tested, only a handful have come up positive.
“We do not feel like it’s contained, because we don’t know where it came
from,” counters TPWD’s Wolf. All that investigators know about the infected deer
at Texas Mountain is that they were artificially inseminated on the same night
by the same vet. But they haven’t determined if that event was the source of the
disease. In September the state forced Texas Mountain to kill 173 more deer—the
remainder of its penned whitetail population. None of them tested positive. Now
the state has told the ranch’s owner, Robert E. Patterson, to kill the rest of
the deer in his pastures. Patterson says he has already suffered $3.2 million in
inventory losses.
At a TPWD meeting in Austin in November, breeders came from all over the
state to protest the proposed extension of the emergency rules into next summer.
Dozens of men in boots and hats embossed with the names of their ranches milled
about the halls of TPWD’s bunker-like concrete building, grousing about anemic
sales. “I’ve moved six deer,” Niederwald breeder Bobby Schmidt said of his
business since the emergency rules went into effect. “That’s normally one
hundred and fifty deer.”
So many had shown up for the meeting, in fact, that TPWD set aside a second
room just to accommodate the overflow. But when the hearing began, everyone
crowded into the small, wood-paneled council chambers, some clutching pieces of
paper scrawled with the grievances they planned to air. After waiting through
some early agenda items, the breeders began filing to the lectern. Parks and
Wildlife, they lamented, had effectively slapped a scarlet letter of disease
onto many ranchers who had done nothing wrong. “I feel like I’m being
discriminated against,” said Van Bruns, a breeder and outfitter from Live Oak
County.
David Yeates, the CEO of the San Antonio–based conservation group Texas
Wildlife Association, saw it very differently. “We haven’t found the source,” he
said. “This is an opportunity to nip this in the bud and react in a responsible
manner.” After about an hour of testimony, no one was particularly shocked when
the commission ratified the rules.
For now, at least, breeders have no choice but to settle in under the new
normal while TPWD investigators hunt for a Patient Zero they may never find.
“Everything has changed. When it changes, you conform to it and go on,” Terrie
says. “What choice do we have? We’ve invested everything in this.”
Tags: Ranching, Science, The Culture, chico, chronic wasting disease, deer,
ranching - See more at: http://www.texasmonthly.com/articles/chronic-wasting-unease/#sthash.KA9YDYT3.dpuf
sporadic CJD has now been linked to scrapie and mad cow disease, and
concerns are growing about a possible link to humans from CWD TSE Prion in
cervid.
you can continue to ignore this as the media usually does, or report it.
sadly, it’s not being reported to the public.
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary:
The transmissible spongiform encephalopathies (also called prion diseases)
are fatal neurodegenerative diseases that affect animals and humans. The agent
of prion diseases is a misfolded form of the prion protein that is resistant to
breakdown by the host cells. Since all mammals express prion protein on the
surface of various cells such as neurons, all mammals are, in theory, capable of
replicating prion diseases. One example of a prion disease, bovine spongiform
encephalopathy (BSE; also called mad cow disease), has been shown to infect
cattle, sheep, exotic undulates, cats, non-human primates, and humans when the
new host is exposed to feeds or foods contaminated with the disease agent. The
purpose of this study was to test whether non-human primates (cynomologous
macaque) are susceptible to the agent of sheep scrapie. After an incubation
period of approximately 10 years a macaque developed progressive clinical signs
suggestive of neurologic disease. Upon postmortem examination and microscopic
examination of tissues, there was a widespread distribution of lesions
consistent with a transmissible spongiform encephalopathy. This information will
have a scientific impact since it is the first study that demonstrates the
transmission of scrapie to a non-human primate with a close genetic relationship
to humans. This information is especially useful to regulatory officials and
those involved with risk assessment of the potential transmission of animal
prion diseases to humans.
Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion
disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the
past decades, c-BSE's zoonotic potential has been the driving force in
establishing extensive protective measures for animal and human health. In
complement to the recent demonstration that humanized mice are susceptible to
scrapie, we report here the first observation of direct transmission of a
natural classical scrapie isolate to a macaque after a 10-year incubation
period. Neuropathologic examination revealed all of the features of a prion
disease: spongiform change, neuronal loss, and accumulation of PrPres throughout
the CNS.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
==========================================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==========================================
PRION 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.***
================
From: Terry S. Singeltary Sr.
Sent: Saturday, November 15, 2014 9:29 PM
To: Terry S. Singeltary Sr.
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
R. G. WILL
1984
*** 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). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT
THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
snip...
85%+ of all human tse prion disease is sporadic CJD.
see what the NIH prion Gods say themselves ;
‘’In the Archives of Neurology you quoted (the abstract of which was
attached to your email), we did not say CWD in humans will present like variant
CJD. That assumption would be wrong.’’
‘’Also, we do not claim that "no-one has ever been infected with prion
disease from eating venison." Our conclusion stating that we found no strong
evidence of CWD transmission to humans in the article you quoted or in any other
forum is limited to the patients we investigated.’’
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
*** 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 tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat. you can take the ash and
mix it with saline and inject that ash into a mouse, and the mouse will go down
with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the
environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of
protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple
autoclave will not kill this TSE prion agent.
cwd to humans, consumption, exposure, sub-clinical, iatrogenic, what if ?
to the breeders and industry that care more about their bottom dollar,
ignore science, and the ones crying about their poor deer being
slaughtered...crying me a river$$$
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations 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.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Wednesday, March 18, 2015
*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015
(8 cases CWD in wild to date Texas)
Wednesday, March 25, 2015
*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
Saturday, December 12, 2015
CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
Tuesday, December 15, 2015
*** Chronic Wasting Disease will cause a Wyoming deer herd to go virtually
extinct in 41 years, a five-year study predicts
*** Study: Chronic Wasting Disease kills 19% of deer herd annually
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
***Title: Transmission of chronic wasting disease to sentinel reindeer
(Rangifer tarandus tarandus)
Authors
item Moore, S - item Kunkle, Robert item Nicholson, Eric item Richt,
Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A
Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring,
fatal neurodegenerative disease of North American cervids. Reindeer (Rangifer
tarandus tarandus) are susceptible to CWD following oral challenge, but CWD has
not been reported in free-ranging caribou (Rangifer tarandus caribou) or farmed
reindeer. Potential contact between CWD-affected cervids and Rangifer species
that are free-ranging or co-housed on farms presents a potential risk of CWD
transmission. The aims of this study were to 1) investigate the transmission of
CWD from white-tailed deer (Odocoileus virginianus; CWD-wtd), mule deer
(Odocoileus hemionus; CWD-md), or elk (Cervus elaphus nelsoni; CWD-elk) to
reindeer via the intracranial route, and 2) to assess for direct and indirect
horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer
fawns were challenged intracranially with CWD-wtd, CWD-md, or CWD-elk. Two years
after challenge of inoculated reindeer, non-inoculated control reindeer were
introduced into the same pen as the CWD-wtd inoculated reindeer (n=4) or into a
pen adjacent to the CWD-md inoculated reindeer (n=2). Reindeer were allowed to
develop clinical disease. At death/euthanasia a complete necropsy examination
was performed, including immunohistochemical testing of tissues for
disease-associated CWD prion protein (PrP-CWD). Intracranially challenged
reindeer developed clinical disease from 21 months post-inoculation (MPI).
PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed
clinical disease during the study period (<57 div="" mpi="">
***We have shown that reindeer are susceptible to CWD from various cervid
sources and can transmit CWD to naive reindeer both directly and indirectly.
Last Modified: 12/3/2015
***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6
developed clinical disease during the study period (<57 div="" mpi="">
***We have shown that reindeer are susceptible to CWD from various cervid
sources and can transmit CWD to naive reindeer both directly and indirectly.
Tuesday, September 29, 2015
*** Transmission of chronic wasting disease to sentinel reindeer (Rangifer
tarandus tarandus) can transmit CWD to naive reindeer both directly and
indirectly
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
*** 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.
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
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.
SUMMARY:
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or
Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after gaining approval
from surrounding landowners, and confirmed that the fenced had been cut or
removed in at least four separate locations; that the fence had degraded and was
failing to maintain the enclosure around the Quarantined Premises in at least
one area; that at least three gates had been opened;and that deer tracks were
visible in and around one of the open areas in the sand on both sides of the
fence, evidencing movement of deer into the Quarantined Premises.
The overall incidence of clinical CWD in white-tailed deer was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)
”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.
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
CWD, spreading it around...
for the game farm industry, and their constituents, to continue to believe
that they are _NOT_, and or insinuate that they have _NEVER_ been part of the
problem, will only continue to help spread cwd. the game farming industry, from
the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet
mills, shooting pens, to large ranches, are not the only problem, but it is
painfully obvious that they have been part of the problem for decades and
decades, just spreading it around, as with transportation and or exportation and
or importation of cervids from game farming industry, and have been proven to
spread cwd. no one need to look any further than South Korea blunder ;
===========================================
spreading cwd around...
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of
farmed elk in Saskatchewan in a single epidemic. All of these herds were
depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease
eradication program. Animals, primarily over 12 mo of age, were tested for the
presence CWD prions following euthanasia. Twenty-one of the herds were linked
through movements of live animals with latent CWD from a single infected source
herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily
infected herds.
***The source herd is believed to have become infected via importation of
animals from a game farm in South Dakota where CWD was subsequently diagnosed
(7,4). A wide range in herd prevalence of CWD at the time of herd depopulation
of these herds was observed. Within-herd transmission was observed on some
farms, while the disease remained confined to the introduced animals on other
farms.
spreading cwd around...
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim,
Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research
Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion
disease in native North America deer and Rocky mountain elks. The disease is a
unique member of the transmissible spongiform encephalopathies (TSEs), which
naturally affects only a few species. CWD had been limited to USA and Canada
until 2000.
On 28 December 2000, information from the Canadian government showed that a
total of 95 elk had been exported from farms with CWD to Korea. These consisted
of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72
elk in 1997, which had been held in pre export quarantine at the “source
farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD
surveillance program was initiated by the Ministry of Agriculture and Forestry
(MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994
were impossible to identify. CWD control measures included stamping out of all
animals in the affected farm, and thorough cleaning and disinfection of the
premises. In addition, nationwide clinical surveillance of Korean native
cervids, and improved measures to ensure reporting of CWD suspect cases were
implemented.
Total of 9 elks were found to be affected. CWD was designated as a
notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and
2005.
Since February of 2005, when slaughtered elks were found to be positive,
all slaughtered cervid for human consumption at abattoirs were designated as
target of the CWD surveillance program. Currently, CWD laboratory testing is
only conducted by National Reference Laboratory on CWD, which is the Foreign
Animal Disease Division (FADD) of National Veterinary Research and Quarantine
Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the
human consumption was confirmed as positive. Consequently, all cervid – 54 elks,
41 Sika deer and 5 Albino deer – were culled and one elk was found to be
positive. Epidemiological investigations were conducted by Veterinary
Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary
services.
Epidemiologically related farms were found as 3 farms and all cervid at
these farms were culled and subjected to CWD diagnosis. Three elks and 5
crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and
confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were
linked to the importation of elks from Canada in 1994 based on circumstantial
evidences.
In December 2010, one elk was confirmed as positive at Farm 5.
Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer –
were culled and one Manchurian Sika deer and seven Sika deer were found to be
positive. This is the first report of CWD in these sub-species of deer.
Epidemiological investigations found that the owner of the Farm 2 in CWD
outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced
from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed
(species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as
negative.
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600°C. It has been assumed, without proof, that incineration totally inactivates
the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Histochemical analysis of hamster brains inoculated with the solid residue
showed typical spongiform degeneration and vacuolation. Re-inoculation of these
brains into a new cohort of hamsters led to onset of clinical scrapie symptoms
within 75 days, suggesting that the specific infectivity of the prion protein
was not changed during the biodiesel process. The biodiesel reaction cannot be
considered a viable prion decontamination method for MBM, although we observed
increased survival time of hamsters and reduced infectivity greater than 6 log
orders in the solid MBM residue. Furthermore, results from our study compare for
the first time prion detection by Western Blot versus an infectivity bioassay
for analysis of biodiesel reaction products. We could show that biochemical
analysis alone is insufficient for detection of prion infectivity after a
biodiesel process.
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative
assessment is described that estimates the amount of TSE infectivity that is
present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for
cattle and classical/atypical scrapie for sheep and lambs) and the amounts that
subsequently fall to the floor during processing at facilities that handle
specified risk material (SRM). BSE in cattle was found to contain the most oral
doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to
a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep
infected with classical and atypical scrapie, respectively. Lambs contained the
least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie
and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity
falling to the floor and entering the drains from slaughtering a whole carcass
at SRM facilities were found to be from cattle infected with BSE at rendering
and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate
plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and
collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains
are from lambs infected with classical and atypical scrapie at intermediate
plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO
ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key
inputs for the model in the companion paper published here.
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
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.
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...
98 | Veterinary Record | January 24, 2015
EDITORIAL
Scrapie: a particularly persistent pathogen
Cristina Acín
Resistant prions in the environment have been the sword of Damocles for
scrapie control and eradication. Attempts to establish which physical and
chemical agents could be applied to inactivate or moderate scrapie infectivity
were initiated in the 1960s and 1970s,with the first study of this type focusing
on the effect of heat treatment in reducing prion infectivity (Hunter and
Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate
the prion protein are based on the method developed by Kimberlin and
collaborators (1983). This procedure consists of treatment with 20,000 parts per
million free chlorine solution, for a minimum of one hour, of all surfaces that
need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so
on). Despite this, veterinarians and farmers may still ask a range of questions,
such as ‘Is there an official procedure published somewhere?’ and ‘Is there an
international organisation which recommends and defines the exact method of
scrapie decontamination that must be applied?’
From a European perspective, it is difficult to find a treatment that could
be applied, especially in relation to the disinfection of surfaces in lambing
pens of affected flocks. A 999/2001 EU regulation on controlling spongiform
encephalopathies (European Parliament and Council 2001) did not specify a
particular decontamination measure to be used when an outbreak of scrapie is
diagnosed. There is only a brief recommendation in Annex VII concerning the
control and eradication of transmissible spongiform encephalopathies (TSE
s).
Chapter B of the regulation explains the measures that must be applied if
new caprine animals are to be introduced to a holding where a scrapie outbreak
has previously been diagnosed. In that case, the statement indicates that
caprine animals can be introduced ‘provided that a cleaning and disinfection of
all animal housing on the premises has been carried out following
destocking’.
Issues around cleaning and disinfection are common in prion prevention
recommendations, but relevant authorities, veterinarians and farmers may have
difficulties in finding the specific protocol which applies. The European Food
and Safety Authority (EFSA ) published a detailed report about the efficacy of
certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and
even a formulation of copper or iron metal ions in combination with hydrogen
peroxide, against prions (EFSA 2009). The report was based on scientific
evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006,
Solassol and others 2006) but unfortunately the decontamination measures were
not assessed under outbreak conditions.
The EFSA Panel on Biological Hazards recently published its conclusions on
the scrapie situation in the EU after 10 years of monitoring and control of the
disease in sheep and goats (EFSA 2014), and one of the most interesting findings
was the Icelandic experience regarding the effect of disinfection in scrapie
control. The Icelandic plan consisted of: culling scrapie-affected sheep or the
whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of
stables, sheds, barns and equipment with high pressure washing followed by
cleaning with 500 parts per million of hypochlorite; drying and treatment with
300 ppm of iodophor; and restocking was not permitted for at least two years.
Even when all of these measures were implemented, scrapie recurred on several
farms, indicating that the infectious agent survived for years in the
environment, even as many as 16 years after restocking (Georgsson and others
2006).
In the rest of the countries considered in the EFSA (2014) report,
recommendations for disinfection measures were not specifically defined at the
government level. In the report, the only recommendation that is made for sheep
is repopulation with sheep with scrapie-resistant genotypes. This reduces the
risk of scrapie recurrence but it is difficult to know its effect on the
infection.
Until the EFSA was established (in May 2003), scientific opinions about TSE
s were provided by the Scientific Steering Committee (SSC) of the EC, whose
advice regarding inactivation procedures focused on treating animal waste at
high temperatures (150°C for three hours) and high pressure alkaline hydrolysis
(SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory
Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe
working and the prevention of TSE infection. Annex C of the ACDP report
established that sodium hypochlorite was considered to be effective, but only if
20,000 ppm of available chlorine was present for at least one hour, which has
practical limitations such as the release of chlorine gas, corrosion,
incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its
active chemicals and the stability of dilutions (ACDP 2009).
In an international context, the World Organisation for Animal Health (OIE)
does not recommend a specific disinfection protocol for prion agents in its
Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General
recommendations on disinfection and disinsection (OIE 2014), focuses on
foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on
prion disinfection. Nevertheless, the last update published by the OIE on bovine
spongiform encephalopathy (OIE 2012) indicates that few effective
decontamination techniques are available to inactivate the agent on surfaces,
and recommends the removal of all organic material and the use of sodium
hydroxide, or a sodium hypochlorite solution containing 2 per cent available
chlorine, for more than one hour at 20ºC.
The World Health Organization outlines guidelines for the control of TSE s,
and also emphasises the importance of mechanically cleaning surfaces before
disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO
1999).
Finally, the relevant agencies in both Canada and the USA suggest that the
best treatments for surfaces potentially contaminated with prions are sodium
hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution,
while most commercial household bleaches contain 5.25 per cent sodium
hypochlorite. It is therefore recommended to dilute one part 5.25 per cent
bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency
2013).
So what should we do about disinfection against prions? First, it is
suggested that a single protocol be created by international authorities to
homogenise inactivation procedures and enable their application in all
scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available
chlorine seems to be the procedure used in most countries, as noted in a paper
summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015).
But are we totally sure of its effectiveness as a preventive measure in a
scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease
be needed?
What we can conclude is that, if we want to fight prion diseases, and
specifically classical scrapie, we must focus on the accuracy of diagnosis,
monitoring and surveillance; appropriate animal identification and control of
movements; and, in the end, have homogeneous and suitable protocols to
decontaminate and disinfect lambing barns, sheds and equipment available to
veterinarians and farmers. Finally, further investigations into the resistance
of prion proteins in the diversity of environmental surfaces are required.
References
snip...
98 | Veterinary Record | January 24, 2015
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc
MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C.
Maddison, BSc, PhD3 + Author Affiliations
1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey
KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of
Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS
UK, School of Veterinary Medicine and Science, The University of Nottingham,
Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for
correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and
chronic wasting disease of deer/elk are contagious prion diseases where
environmental reservoirs are directly implicated in the transmission of disease.
In this study, the effectiveness of recommended scrapie farm decontamination
regimens was evaluated by a sheep bioassay using buildings naturally
contaminated with scrapie. Pens within a farm building were treated with either
20,000 parts per million free chorine solution for one hour or were treated with
the same but were followed by painting and full re-galvanisation or replacement
of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype
VRQ/VRQ were reared within these pens and their scrapie status was monitored by
recto-anal mucosa-associated lymphoid tissue. All animals became infected over
an 18-month period, even in the pen that had been subject to the most stringent
decontamination process. These data suggest that recommended current guidelines
for the decontamination of farm buildings following outbreaks of scrapie do
little to reduce the titre of infectious scrapie material and that environmental
recontamination could also be an issue associated with these premises.
SNIP...
Discussion
Thorough pressure washing of a pen had no effect on the amount of
bioavailable scrapie infectivity (pen B). The routine removal of prions from
surfaces within a laboratory setting is treatment for a minimum of one hour with
20,000 ppm free chlorine, a method originally based on the use of brain
macerates from infected rodents to evaluate the effectiveness of decontamination
(Kimberlin and others 1983). Further studies have also investigated the
effectiveness of hypochlorite disinfection of metal surfaces to simulate the
decontamination of surgical devices within a hospital setting. Such treatments
with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower
than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous
treatment of the pen surfaces did not effectively remove the levels of scrapie
infectivity over that of the control pens, indicating that this method of
decontamination is not effective within a farm setting. This may be due to the
high level of biological matrix that is present upon surfaces within the farm
environment, which may reduce the amount of free chlorine available to
inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had
also became scrapie positive within nine months, with all animals in this pen
being RAMALT positive by 18 months of age. Pen D was no further away from the
control pen (pen A) than any of the other pens within this barn. Localised hot
spots of infectivity may be present within scrapie-contaminated environments,
but it is unlikely that pen D area had an amount of scrapie contamination that
was significantly different than the other areas within this building.
Similarly, there were no differences in how the biosecurity of pen D was
maintained, or how this pen was ventilated compared with the other pens. This
observation, perhaps, indicates the slower kinetics of disease uptake within
this pen and is consistent with a more thorough prion removal and
recontamination. These observations may also account for the presence of
inadvertent scrapie cases within other studies, where despite stringent
biosecurity, control animals have become scrapie positive during challenge
studies using barns that also housed scrapie-affected animals (Ryder and others
2009). The bioassay data indicate that the exposure of the sheep to a farm
environment after decontamination efforts thought to be effective in removing
scrapie is sufficient for the animals to become infected with scrapie. The main
exposure routes within this scenario are likely to be via the oral route, during
feeding and drinking, and respiratory and conjunctival routes. It has been
demonstrated that scrapie infectivity can be efficiently transmitted via the
nasal route in sheep (Hamir and others 2008), as is the case for CWD in both
murine models and in white-tailed deer (Denkers and others 2010, 2013).
Recently, it has also been demonstrated that CWD prions presented as dust when
bound to the soil mineral montmorillonite can be infectious via the nasal route
(Nichols and others 2013). When considering pens C and D, the actual source of
the infectious agent in the pens is not known, it is possible that biologically
relevant levels of prion survive on surfaces during the decontamination regimen
(pen C). With the use of galvanising and painting (pen D) covering and sealing
the surface of the pen, it is possible that scrapie material recontaminated the
pens by the movement of infectious prions contained within dusts originating
from other parts of the barn that were not decontaminated or from other areas of
the farm.
Given that scrapie prions are widespread on the surfaces of affected farms
(Maddison and others 2010a), irrespective of the source of the infectious prions
in the pens, this study clearly highlights the difficulties that are faced with
the effective removal of environmentally associated scrapie infectivity. This is
likely to be paralleled in CWD which shows strong similarities to scrapie in
terms of both the dissemination of prions into the environment and the facile
mode of disease transmission. These data further contribute to the understanding
that prion diseases can be highly transmissible between susceptible individuals
not just by direct contact but through highly stable environmental reservoirs
that are refractory to decontamination.
The presence of these environmentally associated prions in farm buildings
make the control of these diseases a considerable challenge, especially in
animal species such as goats where there is lack of genetic resistance to
scrapie and, therefore, no scope to re-stock farms with animals that are
resistant to scrapie.
Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE)
Accepted October 12, 2014. Published Online First 31 October 2014
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
PPo3-22:
Detection of Environmentally Associated PrPSc on a Farm with Endemic
Scrapie
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh
Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of
Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories
Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University
of Nottingham; Sutton Bonington, Loughborough UK
Key words: scrapie, evironmental persistence, sPMCA
Ovine scrapie shows considerable horizontal transmission, yet the routes of
transmission and specifically the role of fomites in transmission remain poorly
defined. Here we present biochemical data demonstrating that on a
scrapie-affected sheep farm, scrapie prion contamination is widespread. It was
anticipated at the outset that if prions contaminate the environment that they
would be there at extremely low levels, as such the most sensitive method
available for the detection of PrPSc, serial Protein Misfolding Cyclic
Amplification (sPMCA), was used in this study. We investigated the distribution
of environmental scrapie prions by applying ovine sPMCA to samples taken from a
range of surfaces that were accessible to animals and could be collected by use
of a wetted foam swab. Prion was amplified by sPMCA from a number of these
environmental swab samples including those taken from metal, plastic and wooden
surfaces, both in the indoor and outdoor environment. At the time of sampling
there had been no sheep contact with these areas for at least 20 days prior to
sampling indicating that prions persist for at least this duration in the
environment. These data implicate inanimate objects as environmental reservoirs
of prion infectivity which are likely to contribute to disease transmission.
Willingham, Erin McNulty, Kelly Anderson, Jeanette Hayes-Klug, Amy Nalls,
and Candace Mathiason Colorado State University; Fort Collins, CO USA
Chronic wasting disease (CWD) is the transmissible spongiform
encephalopathy (TSE), of free-ranging and captive cervids (deer, elk and moose).
The presence of infectious prions in the tissues, bodily fluids and
environments of clinical and preclinical CWD-infected animals is thought to
account for its high transmission efficiency. Recently it has been recognized
that mother to offspring transmission may contribute to the facile transmission
of some TSEs. Although the mechanism behind maternal transmission is not yet
known, the extended asymptomatic TSE carrier phase (lasting years to decades)
suggests that it may have implications in the spread of prions.
Placental trafficking and/or secretion in milk are 2 means by which
maternal prion transmission may occur. In these studies we explore these avenues
during early and late infection using a transgenic mouse model expressing cervid
prion protein. Na€ıve and CWD-infected dams were bred at both timepoints, and
were allowed to bear and raise their offspring. Milk was collected from the dams
for prion analysis, and the offspring were observed for TSE disease progression.
Terminal tissues harvested from both dams and offspring were analyzed for
prions.
We have demonstrated that
(1) CWDinfected TgCerPRP females successfully breed and bear offspring, and
(2) the presence of PrPCWD in reproductive and mammary tissue from
CWD-infected dams.
We are currently analyzing terminal tissue harvested from offspring born to
CWD-infected dams for the detection of PrPCWD and amplification competent
prions. These studies will provide insight into the potential mechanisms and
biological significance associated with mother to offspring transmission of
TSEs.
==============
P.157: Uptake of prions into plants
Christopher Johnson1, Christina Carlson1, Matthew Keating1,2, Nicole
Gibbs1, Haeyoon Chang1, Jamie Wiepz1, and Joel Pedersen1 1USGS National Wildlife
Health Center; Madison, WI USA; 2University of Wisconsin - Madison; Madison, WI
USA
Soil may preserve chronic wasting disease (CWD) and scrapie infectivity in
the environment, making consumption or inhalation of soil particles a plausible
mechanism whereby na€ıve animals can be exposed to prions. Plants are known to
absorb a variety of substances from soil, including whole proteins, yet the
potential for plants to take up abnormal prion protein (PrPTSE) and preserve
prion infectivity is not known. In this study, we assessed PrPTSE uptake into
roots using laser scanning confocal microscopy with fluorescently tagged PrPTSE
and we used serial protein misfolding cyclic amplification (sPMCA) and detect
and quantify PrPTSE levels in plant aerial tissues. Fluorescence was identified
in the root hairs of the model plant Arabidopsis thaliana, as well as the crop
plants alfalfa (Medicago sativa), barley (Hordeum vulgare) and tomato (Solanum
lycopersicum) upon exposure to tagged PrPTSE but not a tagged control
preparation. Using sPMCA, we found evidence of PrPTSE in aerial tissues of A.
thaliana, alfalfa and maize (Zea mays) grown in hydroponic cultures in which
only roots were exposed to PrPTSE. Levels of PrPTSE in plant aerial tissues
ranged from approximately 4 £ 10 ¡10 to 1 £ 10 ¡9 g PrPTSE g ¡1 plant dry weight
or 2 £ 105 to 7 £ 106 intracerebral ID50 units g ¡1 plant dry weight. Both stems
and leaves of A. thaliana grown in culture media containing prions are
infectious when intracerebrally-injected into mice. ***Our results suggest that
prions can be taken up by plants and that contaminated plants may represent a
previously unrecognized risk of human, domestic species and wildlife exposure to
prions.
===========
***Our results suggest that prions can be taken up by plants and that
contaminated plants may represent a previously unrecognized risk of human,
domestic species and wildlife exposure to prions.***
SEE ;
Friday, May 15, 2015
Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions
Report
P.97: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum
Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and
Robert Kunkle1 1National Animal Disease Center; Ames, IA USA; 2Iowa State
University; Ames, IA USA
The purpose of this work was to determine susceptibility of white-tailed
deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to
that of the original inoculum and chronic wasting disease (CWD). We inoculated
WTD by a natural route of exposure (concurrent oral and intranasal (IN); n D 5)
with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc
accumulation. PrPSc was detected in lymphoid tissues at preclinical time points,
and deer necropsied after 28 months post-inoculation had clinical signs,
spongiform encephalopathy, and widespread distribution of PrPSc in neural and
lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular
profiles. WB on cerebral cortex had a profile similar to the original scrapie
inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc
with a higher profile resembling CWD. Homogenates with the 2 distinct profiles
from WTD with clinical scrapie were further passaged to mice expressing cervid
prion protein and intranasally to sheep and WTD. In cervidized mice, the 2
inocula have distinct incubation times. Sheep inoculated intranasally with WTD
derived scrapie developed disease, but only after inoculation with the inoculum
that had a scrapie-like profile. The WTD study is ongoing, but deer in both
inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary,
this work demonstrates that WTD are susceptible to the agent of scrapie, 2
distinct molecular profiles of PrPSc are present in the tissues of affected
deer, and inoculum of either profile readily passes to deer.
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
CENSORED, RAW, AND UNCUT...
Sunday, August 23, 2015
*** TEXAS CHRONIC WASTING DISEASE CWD DEER BREEDERS STILL DON'T GET IT,
BLINDED BY MONEY
Subject: Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a
pig and take her to the dance in Texas
I was listening to a radio show the other day here in the Galveston bay
area, and outdoor show, they had a breeder or someone from the industry on, and
I was amazed at the false information he was spewing. the part about the poor
little girl with her pet deer crying in the breeder pen, ......cry me a friggen
river, they are raising the damn deer to put in a pen to slaughter, or to breed
for that purpose, AND you ought to see a human die from this shit. my mother did
everything Linda Blair did in that movie the exorcist except spin her head 360
degrees. she DID levitate in bed because she would jerk so bad, where it took
three grown strong adults to hold her down to keep her from hurting herself, all
the while screaming God why can’t I stop this. so cry me a friking river on a
damn deer they are raising to have slaughtered, but whine because the TPWD et al
are going to kill it to try and prevent the spread of disease cwd. if the TPWD
et al had a better way of confirming or not whether those cervid had CWD, they
would do it. the live tests they have to date do not work 100%, so there for
they have not been validated. oh that’s fine with the pen owners, but it’s not
fine for Texas. you don’t want a cwd test that just works part of the time. it’s
total ignorance out there now, and they will put lipstick on this pig and take
her to the dance, just like TAHC did with mad cow disease, and that’s well
documented. they will change what ever law to meet their needs$$$ I will agree
with this much of what the industry said this morning, that cwd has been in
Texas for a long time, and in the pens to, and that the TAHC has not tested
enough, that much he got correct. I have been saying this year, after year,
after year, since back to 2001, to the TAHC, and told them exactly where they
should be testing back in 2001, and then year after year after year, up and
until 2012, where they finally did test there in enough numbers to find it a
decade later, exactly where I been saying it was. the cwd deer have been
waltzing across Texas from there for over a decade. it does not matter if I am
pro-pen or not. that will not and does not change the science. why in the hell
did they speak about the 4 confirmed deer from that index herd, yes, I said 4
now. why is not the TAHC TPWD telling that to the public now. why did not that
guy today speak of 4? all the newspapers are reporting it, and I ask about the
4th case weeks and weeks ago? where is that information at on TAHC site? I am a
meat eater, I am pro-hunt, and extremely pro-gun, I am however anti-stupid and
anti-prion, prions can kill you, I don’t want to eat prions, you should not
either. but here is the kicker, you eat meat infected with CWD TSE prion, your
exposed, however you never go clinical in your life........BBBUT, your exposed
and if you go on to have surgical, dental, tissue, blood donations, etc. you
risk exposing my family and others...I will simply post this one short abstract
of an old study the late great Dr. Gibbs...SNIP...see full text ;
CENSORED, RAW, AND UNCUT...
Sunday, August 23, 2015
*** TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a
pig and take her to the dance in Texas
from the other side of the fence... today’s Singeltary Sunday School class
‘thinking outside of the box, God’s Wrath’ at the bottom. ...tss
I asked someone recently, what sort of hunting legacy do you want to leave
your children, did you want to have where all you have are blind, slobbering,
drooling, stumbling, or maybe even healthy looking subclinical cwd infected
cervid, to go on and expose who knows what (cause cwd is spreading, it has
mutated, and nobody can stop it so far), but is this what we want to leave our
children? the only answer I ever seem to get from anyone in the industry, is
just let cwd take care of itself. well hell, how is that working for us so
far?
this cwd tse prion must be stopped. the vertical and lateral transmission
of this cwd tse prion agent amongst cervids, if cwd jumps species (if it has not
already), and transmits the same ways vertical and lateral in other species, and
the other species are as susceptible from so many different routes and sources,
simply put, we’re screwed. just saying. I am not trying to scare anyone, I am
simply presenting the facts, you must make your own decision or not. we have
ignored these tse prion disease way too long. ...tss
Thursday, December 17, 2015
Annual report of the Scientific Network on BSE-TSE 2015 EFSA-Q-2015-00738
10 December 2015
Saturday, December 12, 2015
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
Saturday, December 12, 2015
NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE
Prion REPORT December 14, 2015
Thursday, December 24, 2015
Infectious disease spread is fueled by international trade
Saturday, December 12, 2015
*** CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
***
Thursday, December 24, 2015
Revisiting the Heidenhain Variant of Creutzfeldt-Jakob Disease: Evidence
for Prion Type Variability Influencing Clinical Course and Laboratory Findings
Article type: Research Article
Congress is all set to give NIH it's largest increase in 12 years.
Included in the bill: $350 million increase for Alzheimer’s research and an
$85 million increase for the BRAIN Initiative, the project to map the human
brain.
Full story at: http://ow.ly/VYKBv
great news, with not a minute to spare...
Evidence for human transmission of amyloid-β pathology and cerebral amyloid
angiopathy
07 02:27 AM
Terry S. Singeltary Sr. said:
re-Evidence for human transmission of amyloid-? pathology and cerebral
amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26
April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated
online 11 September 2015 Erratum (October, 2015)
I would kindly like to comment on the Nature Paper, the Lancet reply, and
the newspaper articles.
snip...see full text ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO
PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have
recognised the public sensitivity of these findings and intend to report them in
their proper context. 'This hopefully will avoid misunderstanding and possible
distortion by the media to portray the results as having more greater
significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection)
the researchers have demonstrated the transmission of a pathological process
from two cases one of severe Alzheimer's disease the other of
Gerstmann-Straussler disease to marmosets. However they have not demonstrated
the transmission of either clinical condition as the "animals were behaving
normally when killed". As the report emphasises the unanswered question is
whether the disease condition would have revealed itself if the marmosets had
lived longer. They are planning further research to see if the conditions, as
opposed to the partial pathological process, is transmissible.
what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of
things highly unusual. However it could be argued that the results reveal a
potential risk, in that brain tissue from these two patients has been shown to
transmit a pathological process. Should therefore brain tissue from such cases
be regarded as potentially infective? Pathologists, morticians, neuro surgeons
and those assisting at neuro surgical procedures and others coming into contact
with "raw" human brain tissue could in theory be at risk. However, on a priori
grounds given the highly specific route of transmission in these experiments
that risk must be negligible if the usual precautions for handling brain tissue
are observed.
1
92/11.4/1.1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent
the GSS case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral injection. If other prion diseases can be transmitted in this way
it is little surprise that some pathological findings observed in GSS were also
transmissible to a marmoset. But the transmission of features of Alzheimer's
pathology is a different matter, given the much greater frequency of this
disease and raises the unanswered question whether some cases are the result of
a transmissible prion. The only tenable public line will be that "more research
is required’’ before that hypothesis could be evaluated. The possibility on a
transmissible prion remains open. In the meantime MRC needs carefully to
consider the range and sequence of studies needed to follow through from the
preliminary observations in these two cases. Not a particularly comfortable
message, but until we know more about the causation of Alzheimer's disease the
total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH
832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is
required’’ <<<
>>> possibility on a transmissible prion remains
open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is
"more research is required’’ enough time for evaluation ?
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Wednesday, September 2, 2015
Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses
in an Alzheimer’s Disease Database
these blogs are for educational use. I do not advertise or make money from
them.
MOM DOD 12/14/97 confirmed hvCJD, just made a promise to mom, never forget,
and never let them forget...
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
9:37 PM
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