Wisconsin doing what it does best, procrastinating about CWD yet again thanks to Governor Walker
Wisconsin doing what it does best, procrastinating about CWD yet again.
Texas is doing the same thing, and will look like Wisconsin, before this pig is
done dancing...tss
Deer still alive on farm hit by CWD
posted 12:27 a.m. | updated 12:45 a.m. (CDT)
by / Joe Knight
Nearly two months after chronic wasting disease was found at a Fairchild
game farm, those animals remain alive.
Those 280 deer won’t be put down until federal agricultural officials come
up with the money to compensate the game farm owner, state officials said.
“We would all like to get the deer off the landscape as soon as possible,
and we’re working through the proper channels to get that done,” said state
veterinarian Paul McGraw.
In June, a 7-year-old doe at the farm tested positive for CWD, and the
protocol for any deer farm where the disease is found is to kill the entire
captive herd and test every deer at the farm. Owners of farms where the disease
is detected are compensated for each animal based on a U.S. Department of
Agriculture formula. Compensation payments are as high as $3,000 per
animal.
There is no process for testing live deer for the disease.
Previous reports had the number of deer at the farm at about 160 animals,
but when fawns are included, the number of captive deer needing to be put down
will be around 280, McGraw said. Killing and testing the herd will be conducted
by the Wisconsin Department of Agriculture, Trade and Consumer Protection and
the U.S. Department of Agriculture, McGraw said.
USDA officials were not available for comment.
Deer at large
Two bucks that escaped from the farm remain at large, and the state
Department of Natural Resources is asking anyone seeing a deer with a yellow or
blue ear tag to report it to the DNR. A number of deer escaped from the farm in
May, when a tree fell on a fence. All but two of the escaped animals have been
accounted for, officials said.
The DNR wants the two deer not captured to be eliminated, said Bill
Hogseth, DNR wildlife manager for Eau Claire County.
“We're trying to keep that issue on people’s radar,” he said. “We're really
hoping people let us know if they see one.”
The DNR can give authorization over the phone for someone to shoot an
ear-tagged deer, which they did a few weeks ago with a logger who reported an
ear-tagged deer in the area where he was cutting.
The DNR asked if he could shoot it, which he did the following day,
bringing the at-large number down to two.
As of Aug. 1, baiting and feeding deer in Eau Claire, Clark and Jackson
counties is prohibited.
All of those counties were within a 10-mile radius of the farm where CWD
was detected, which triggered the ban under state law.
Hogseth said hunters seem to be aware of the ban.
Contact: 715 830-5835, joe.knight@
ecpc.com
Wisconsin doing what it does best, procrastinating about CWD yet again.
what happens when CWD is left alone, while the good Governor of Wisconsin
sides with the Texas deer czar and recommendations to let CWD and cervid fend
for themselves, to save the industry. what happens then ?
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)
*** 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.
Wednesday, March 04, 2015
*** Disease sampling results provide current snapshot of CWD in Wisconsin
finding 324 positive detections statewide in 2014
Tuesday, October 07, 2014
*** Wisconsin white-tailed deer tested positive for CWD on a Richland
County breeding farm, and a case of CWD has been discovered on a Marathon County
hunting preserve
Thursday, June 25, 2015
Wisconsin CWD-positive white-tailed deer found on Eau Claire County farm
Tuesday, July 14, 2015
TWO Escaped Captive Deer on the loose in Eau Claire County Wisconsin CWD
postive farm Yellow ear tag
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Saturday, July 18, 2015
CHARLES "SAM" JAMES, Columbia, Missouri, was charged in a one-count federal
indictment for violations of the Lacey Act involved the sale of white-tailed
deer transported in violation of Missouri and Florida law
Tuesday, November 27, 2012
Pennsylvania ‘Pink 23’ Adams County exposed CWD Escaped Deer shot, but
where are the other escapees ?
Saturday, June 29, 2013
PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN
INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA
Tuesday, June 11, 2013
CWD GONE WILD, More cervid escapees from more shooting pens on the loose in
Pennsylvania
Earl Ray Tomblin, Governor Frank Jezioro, Director
News Release: November 4, 2011
Facebook: WV Commerce - State Parks
Hoy Murphy, Public Information Officer (304) 957-9365 hoy.r.murphy@wv.gov
Contact: Curtis Taylor, Wildlife Resources Section Chief 304-558-2771
DNR.Wildlife@wv.gov
Elk escape from captive cervid facility in Pennsylvania near West Virginia
border
SOUTH CHARLESTON, W.Va. – The West Virginia Division of Natural Resources
(WVDNR) has confirmed with officials from the Pennsylvania Department of
Agriculture (PDA) that at least two elk, including one adult bull and one cow,
have escaped from a captive cervid facility (deer and elk farms) in Greene
County, Pa. Greene County shares a common border with Marshall, Wetzel and
Monongalia counties in West Virginia. The elk escaped from a captive cervid
facility located approximately three miles from the West Virginia-Pennsylvania
border.
The PDA regulates captive cervid facilities in Pennsylvania. A
representative of the agency was unaware if the recent escaped elk were tagged.
The WVDNR regulates captive cervid facilities in West Virginia. In West
Virginia, all captive cervids in breeding facilities must be ear-tagged, and
there are currently no reported elk escapes from any facility in West Virginia.
A bull elk has been seen recently in Wetzel County, W.Va., according to
WVDNR officials. There have been no reports of cow elk sightings in either
Wetzel County, W.Va., or Greene County, Pa. No free-ranging wild elk live within
150 miles of Wetzel County. The elk sighted in Wetzel County is likely the
escaped animal from the captive facility in Pennsylvania.
Friday, September 28, 2012
Stray elk renews concerns about deer farm security Minnesota
Monday, June 11, 2012
*** OHIO Captive deer escapees and non-reporting ***
Thursday, October 23, 2014
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
Thursday, April 02, 2015
OHIO CONFIRMS SECOND POSTIVE CHRONIC WASTING DISEASE CWD on Yoder's
properties near Millersburg
Wednesday, February 11, 2015
World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with
two counts of tampering with evidence
GRASSHOPPER TO MASTER Obi-Wan Kenobi CWD TEXAS CAPTIVE
‘’I see no evidence whatsoever here for a genetic link. The numbers are
statistically insignificant and co-housing in contaminated facilities would
strongly predispose to this outcome.’’
‘’if the father did have a bad amino acid variant allele, it would be
diluted to heterozygozity with a normal gene in the half the four descendants
since the father never would have survived to breeding age with two bad copies.
sort of like met/val at position 129 in humans with greatly lengthened
incubation times if prnp is propagating at all. Mutations such as repeat
expansion leading to positive dominant infection have not been documented in
cervids.’’
On 09 08 15, at 9:09 AM, Terry S. Singeltary Sr.
wrote: ‘’
cwd Texas and then there were 4?
genetic link ?
He said 42 deer have been killed and tested since July 28, and three
additional positives were the result.
***He added that all four deer confirmed to have the disease were males
from the same father, which leads him to believe the problem is genetic.
snip...
HAVE YOU BEEN THUNDERSTRUCK ?
on my mothers grave, when I wrote up the ‘have you been thunderstruck’
about super ovulation, and what if? I had no clue about all this. hell, I had it
in draft for a month. then a week or so later, bam.
it’s been like this all along Obi-Wan Kenobi.
every shooting pen owner in Texas are praying this familial cwd is the
going thing now.
no link to sperm.
no link to super ovulation.
they sell those sperm straws like the meth heads and crack heads sell meth
and crack.
genetic link with four deer in the same herd, same father ?
familial ?
sperm ?
super ovulation ?
what say ye master ?
grasshopper
Friday, August 07, 2015
Texas CWD Captive, and then there were 4 ?
Thursday, August 06, 2015
WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
Article Citation: (2015)
AGE AND REPEATED BIOPSY INFLUENCE ANTEMORTEM PRPCWD TESTING IN MULE DEER
(ODOCOILEUS HEMIONUS) IN COLORADO, USA.
Journal of Wildlife Diseases In-Press. doi: http://dx.doi.org/10.7589/2014-12-284
Ahead of Print
AGE AND REPEATED BIOPSY INFLUENCE ANTEMORTEM PRPCWD TESTING IN MULE DEER
(ODOCOILEUS HEMIONUS) IN COLORADO, USA
Chris Geremia1,6,7 Jennifer A. Hoeting2, Lisa L. Wolfe3, Nathan L.
Galloway4, Michael F. Antolin4, Terry R. Spraker5, Michael W. Miller3, and N.
Thompson Hobbs1
1 Natural Resource Ecology Laboratory, Graduate Degree Program in Ecology,
Colorado State University, Fort Collins, Colorado, 80523-1499, USA
2 Department of Statistics, Colorado State University, Fort Collins,
Colorado 80523, USA
3 Colorado Division of Parks and Wildlife, Wildlife Health Program, 4330
Laporte Avenue, Fort Collins, Colorado 80521, USA
4 Department of Biology, Colorado State University, Fort Collins, Colorado
80523-1878, USA
5 Colorado State University Diagnostics Laboratory, Colorado State
University, Fort Collins, Colorado 80523, USA
Key words: Bayesian, capture–mark–recapture, chronic wasting disease, mule
deer, prion, test sensitivity
Abstract
Biopsy of rectal-mucosa associated lymphoid tissue provides a useful, but
imperfect, live-animal test for chronic wasting disease (CWD) in mule deer
(Odocoileus hemionus). It is difficult and expensive to complete these tests on
free-ranging animals, and wildlife health managers will benefit from methods
that can accommodate test results of varying quality. To this end, we developed
a hierarchical Bayesian model to estimate the probability that an individual is
infected based on test results. Our model was estimated with the use of data on
210 adult female mule deer repeatedly tested during 2010−2014. The ability to
identify infected individuals correctly declined with age and may have been
influenced by repeated biopsy. Fewer isolated lymphoid follicles (where PrPCWD
accumulates) were obtained in biopsies of older deer and the proportion of
follicles showing PrPCWD was reduced. A deer’s genotype in the prion gene (PRNP)
also influenced detection. At least five follicles were needed in a biopsy to
assure a 95% accurate test in PRNP genotype 225SS deer.
Received: December 15, 2014; Accepted: April 23, 2015
6 Current address: Yellowstone Center for Resources, P.O. Box 168,
Yellowstone National Park, Mammoth Hot Springs, Wyoming 82190, USA
7 Corresponding author (email: chris_geremia@nps.gov)
the cwd 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.
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
NOW, here is the most frightening aspect of all this, is the proven
secondhand transmission, i.e. pass if forward mode, via iatrogenic (medical,
surgical, dental, blood, tissue). you may never eat meat, but go to a hospital
near you, it’s a proven risk factor, our hospitals have been exposed. I have
countless articles on hospitals DEAR JOHN mad cow letters i.e. you have been
exposed via surgery).
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD
20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
SOURCE REFERENCES
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.
============================================================================
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Tuesday, August 4, 2015
*** FDA U.S. Measures to Protect Against BSE aka MAD COW DISEASE ***
20097 Section Contents Menu Recalls, Market Withdrawals, & Safety
Alerts8
Archive for Recalls, Market Withdrawals & Safety Alerts9 200910 Recall
-- Firm Press Release
FDA posts press releases and other notices of recalls and market
withdrawals from the firms involved as a service to consumers, the media, and
other interested parties. FDA does not endorse either the product or the
company.
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin
Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic
Wasting Disease
Contact: Exotic Meats USA 1-800-680-4375
FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San
Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may
contain meat derived from an elk confirmed to have Chronic Wasting Disease
(CWD). The meat with production dates of December 29, 30 and 31, 2008 was
purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk
Farm LLC in Pine Island, MN and was among animals slaughtered and processed at
USDA facility Noah’s Ark Processors LLC.
Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease
found in elk and deer. The disease is caused by an abnormally shaped protein
called a prion, which can damage the brain and nerves of animals in the deer
family. Currently, it is believed that the prion responsible for causing CWD in
deer and elk is not capable of infecting humans who eat deer or elk contaminated
with the prion, but the observation of animal-to-human transmission of other
prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has
raised a theoretical concern regarding the transmission of CWD from deer or elk
to humans. At the present time, FDA believes the risk of becoming ill from
eating CWD-positive elk or deer meat is remote. However, FDA strongly advises
consumers to return the product to the place of purchase, rather than disposing
of it themselves, due to environmental concerns.
Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The
Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was
packaged in individual vacuum packs weighing approximately 3 pounds each. A
total of six packs of the Elk Tenderloins were sold to the public at the Exotic
Meats USA retail store. Consumers who still have the Elk Tenderloins should
return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX
78209. Customers with concerns or questions about the Voluntary Elk Recall can
call 1-800-680-4375. The safety of our customer has always been and always will
be our number one priority.
Exotic Meats USA requests that for those customers who have products with
the production dates in question, do not consume or sell them and return them to
the point of purchase. Customers should return the product to the vendor. The
vendor should return it to the distributor and the distributor should work with
the state to decide upon how best to dispose. If the consumer is disposing of
the product he/she should consult with the local state EPA office.
#
RSS Feed for FDA Recalls Information11 [what's this?12]
http://www.fda.gov/Safety/Recalls/ArchiveRecalls/2009/ucm128543.htm
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease
Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic
Association Volume 111, Issue 6 , Pages 858-863, June 2011.
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 ;
==============================
*** 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.
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
Chronic wasting disease (CWD) is a widespread and expanding prion disease
in free-ranging and captive cervid species in North America. The zoonotic
potential of CWD prions is a serious public health concern. Current literature
generated with in vitro methods and in vivo animal models (transgenic mice,
macaques and squirrel monkeys) reports conflicting results. The susceptibility
of human CNS and peripheral organs to CWD prions remains largely unresolved. In
our earlier bioassay experiments using several humanized transgenic mouse lines,
we detected protease-resistant PrPSc in the spleen of two out of 140 mice that
were intracerebrally inoculated with natural CWD isolates, but PrPSc was not
detected in the brain of the same mice. Secondary passages with such
PrPSc-positive CWD-inoculated humanized mouse spleen tissues led to efficient
prion transmission with clear clinical and pathological signs in both humanized
and cervidized transgenic mice. Furthermore, a recent bioassay with natural CWD
isolates in a new humanized transgenic mouse line led to clinical prion
infection in 2 out of 20 mice. 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
The propensity for trans-species prion transmission is related to the
structural characteristics of the enciphering and heterologous PrP, but the
exact mechanism remains mostly mysterious. Studies of the effects of primary or
tertiary prion protein structures on trans-species prion transmission have
relied primarily upon animal bioassays, making the influence of prion protein
structure vs. host co-factors (e.g. cellular constituents, trafficking, and
innate immune interactions) difficult to dissect. As an alternative strategy, we
used real-time quakinginduced conversion (RT-QuIC) to investigate trans-species
prion conversion.
To assess trans-species conversion in the RT-QuIC system, we compared
chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions,
as well as feline CWD (fCWD) and feline spongiform encephalopathy (FSE). Each
prion was seeded into each host recombinant PrP (full-length rPrP of
white-tailed deer, bovine or feline). We demonstrated that fCWD is a more
efficient seed for feline rPrP than for white-tailed deer rPrP, which suggests
adaptation to the new host.
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.***
================
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.19: Characterization of chronic wasting disease isolates from freeranging
deer (Odocoileus sp) in Alberta and Saskatchewan, Canada
Camilo Duque Velasquez1, Chiye Kim1, Nathalie Daude1, Jacques van der
Merwe1, Allen Herbst1, Trent Bollinger2, Judd Aiken1, and Debbie McKenzie1
1Centre for Prions and Protein Folding Diseases; University of Alberta;
Edmonton, Canada; 2Western College of Veterinary Medicine; University of
Saskatchewan; Saskatoon, Canada
Chronic wasting disease (CWD) is an emerging prion disease of free ranging
and captive species of Cervidae. In North America, CWD is enzootic in some wild
cervid populations and can circulate among different deer species. The
contagious nature of CWD prions and the variation of cervid PRNP alleles, which
influence host susceptibility, can result in the emergence and adaptation of
different CWD strains. These strains may impact transmission host range, disease
diagnosis, spread dynamics and efficacy of potential vaccines. We are
characterizing different CWD agents by biochemical analysis of the PrPCWD
conformers, propagation in vitro cell assays1 and by comparing transmission
properties and neuropathology in Tg33 (Q95G96) and Tg60 (Q95S96) mice.2 Although
Tg60 mice expressing S96- PrPC have been shown resistant to CWD infectivity from
various cervid species,2,3
***these transgenic mice are susceptible to H95 C CWD, a CWD strain derived
from experimental infection of deer expressing H95G96-PrPC. The diversity of
strains present in free-ranging mule deer (Odocoileus hemionus) and white-tailed
deer (Odocoileus virginianus) from Alberta and Saskatchewan is being determined
and will allow us to delineate the properties of CWD agents circulating in CWD
enzootic cervid populations of Canada.
References
1. van der Merwe J, Aiken J, Westaway D, McKenzie D. The standard scrapie
cell assay: Development, utility and prospects. Viruses 2015; 7(1):180–198;
PMID:25602372; http://dx.doi.org/10.3390/v7010180
2. Meade-White K, Race B, Trifilo M, Bossers A, Favara C, Lacasse R, Miller
M, Williams E, Oldstone M, Race R, Chesebro B. Resistance to chronic wasting
disease in transgenic mice expressing a naturally occurring allelic variant of
deer prion protein. J Virol 2007; 81(9):4533–4539; PMID: 17314157; http://dx. doi.org/10.1128/JVI.02762-06
3. Race B, Meade-White K, Miller MW, Fox KA, Chesebro B. In vivo comparison
of chronic wasting disease infectivity from deer with variation at prion protein
residue 96. J Virol 2011; 85(17):9235–9238; PMID: 21697479; http://dx.doi.org/10.1128/JVI.00790-11
=========
***these transgenic mice are susceptible to H95 C CWD, a CWD strain derived
from experimental infection of deer expressing H95G96-PrPC.
==========
P.136: Mother to offspring transmission of CWD—Detection in fawn tissues
using the QuIC assay
Amy Nalls, Erin McNulty, Clare Hoover, Jeanette Hayes-Klug, Kelly Anderson,
Edward Hoover, and Candace Mathiason Colorado State University; Fort Collins, CO
USA
To investigate the role mother to offspring transmission plays in chronic
wasting disease (CWD), we have employed a small, polyestrous breeding, indoor
maintainable cervid model, the Reeves’ muntjac deer. Muntjac doe were inoculated
with CWD and tested positive by lymphoid biopsy at 4 months post inoculation.
From these CWD-infected doe, we obtained 3 viable fawns. These fawns tested
IHC-positive for CWD by lymphoid biopsy as early as 40 d post birth, and all
have been euthanized due to clinical disease at 31, 34 and 59 months post birth.
The QuIC assay demonstrates sensitivity and specificity in the detection of
conversion competent prions in peripheral IHC-positive tissues including tonsil,
mandibular, partotid, retropharyngeal, and prescapular lymph nodes, adrenal
gland, spleen and liver. In summary, using the muntjac deer model, we have
demonstrated CWD clinical disease in offspring born to CWD-infected doe and
found that the QuIC assay is an effective tool in the detection of prions in
peripheral tissues. ***Our findings demonstrate that transmission of prions from
mother to offspring can occur, and may be underestimated for all prion
diseases.
===============
***Our findings demonstrate that transmission of prions from mother to
offspring can occur, and may be underestimated for all prion diseases.
===============
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? ***
Singeltary et al
31 Jan 2015 at 20:14 GMT
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely
unchanged when attention was restricted to pairs with data obtained from
relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Friday, May 22, 2015
*** Chronic Wasting Disease and Program Updates - 2014 NEUSAHA Annual
Meeting 12-14 May 2014 ***
Saturday, May 30, 2015
PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS
***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.
Longitudinal Detection of Prion Shedding in Saliva and Urine by
CWD-Infected Deer by RT-QuIC
Davin M. Henderson1, Nathaniel D. Denkers1, Clare E. Hoover1, Nina
Garbino1, Candace K. Mathiason1 and Edward A. Hoover1# + Author
Affiliations
1Prion Research Center, Department of Microbiology, Immunology, and
Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado
State University, Fort Collins, CO 80523 ABSTRACT Chronic Wasting Disease (CWD)
is an emergent, rapidly spreading prion disease of cervids. Shedding of
infectious prions in saliva and urine is thought to be an important factor in
CWD transmission. To help elucidate this issue, we applied an in vitro
amplification assay to determine the onset, duration, and magnitude of prion
shedding in longitudinally collected saliva and urine samples from CWD-exposed
white-tailed deer. We detected prion shedding as early as 3 months after CWD
exposure and sustained shedding throughout the disease course. We estimated that
a 50% lethal dose (LD50) for cervidized transgenic mice would be contained in 1
ml of infected deer saliva or 10 ml or urine. Given the average course of
infection and daily production of these body fluids, an infected deer would shed
thousands of prion infectious dosesover the course of CWD infection. The direct
and indirect environmental impact of this magnitude of prion shedding for cervid
and non-cervid species is surely significant.
Importance: Chronic wasting disease (CWD) is an emerging and uniformly
fatal prion disease affecting free ranging deer and elk and now recognized in 22
United States and 2 C anadian Provinces. It is unique among prion diseases in
that it is transmitted naturally though wild populations. A major hypothesis for
CWD's florid spread is that prions are shed in excreta and transmitted via
direct or indirect environmental contact. Here we use a rapid in vitro assay to
show that infectious doses of CWD prions are in fact shed throughout the
multi-year disease course in deer. This finding is an important advance in
assessing the risks posed by shed CWD prions to animals as well as humans.
FOOTNOTES
↵#To whom correspondence should be addressed: Edward A. Hoover, Prion
Research Center, Department of Microbiology, Immunology and Pathology, Colorado
State University, Fort Collins, Colorado, US Email: edward.hoover@colostate.edu
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.
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...
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
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? ***
Singeltary et al
31 Jan 2015 at 20:14 GMT
Tuesday, July 21, 2015
Texas CWD Medina County Herd Investigation Update July 16, 2015
• 66 Texas sites, 2 Mexico sites
Wednesday, July 22, 2015
Texas Certified Chronic Wasting Disease CWD Sample Collector, like the Wolf
Guarding the Henhouse
Thursday, July 23, 2015
*** Chronic Wasting Disease (CWD) 101 Drs. Walter Cook & Donald S.
Davis
Sunday, July 26, 2015
*** TEXAS IN MELT DOWN MODE OVER CAPTIVE CWD AND THEY ARE PUTTING LIPSTICK
ON THAT PIG AND TAKING HER TO THE DANCE LIKE MAD COW DISEASE ***
how many have been consumed?
how many are exposed?
how many more will die?
iatrogenic, what if?
spontaneous atypical BSE ???
don’t let anyone fool you. spontaneous TSE prion disease is a hoax in
natural cases, never proven.
all one has to do is look at France. France is having one hell of an
epidemic of atypical BSE, probably why they stopped testing for BSE, problem
solved $$$ same as the USA, that’s why they stopped testing for BSE mad cow
disease in numbers they could find any with, after those atypical BSE cases
started showing up. shut down the testing to numbers set up by OIE that are so
low, you could only by accident find a case of BSE aka mad cow disease. and this
brilliant idea by the WHO et al, to change the name of mad cow disease, thinking
that might change things is preposterous. it’s all about money now folks, when
the OIE, USDA and everyone else went along and made the TSE prion disease aka
mad cow type disease a legal trading commodity by the BSE MRR policy, I would
say everyone bit off more then they can chew, and they will just have to digest
those TSE Prions coming from North America, and like it, and just prey you don’t
get a mad cow type disease i.e. Transmissible Spongiform Encephalopathy TSE
prion disease in the decades to come, and or pass it to some other poor soul via
the iatrogenic medical surgical tissue friendly fire mode of transmission i.e.
second hand transmission. it’s real folks, just not documented much, due to lack
of trace back efforts. all iatrogenic cjd is, is sporadic cjd, until the
iatrogenic event is tracked down and documented, and put into the academic and
public domain, which very seldom happens. ...
As of December 2011, around 60 atypical BSE cases have currently been
reported in 13 countries, *** with over one third in France.
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
so 20 cases of atypical BSE in France, compared to the remaining 40 cases
in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+
cases per country, besides Frances 20 cases. you cannot explain this away with
any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
*** We describe the transmission of spongiform encephalopathy in a
non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie.
Because of this extended incubation period in a facility in which other prion
diseases are under study, we are obliged to consider two alternative
possibilities that might explain its occurrence. We first considered the
possibility of a sporadic origin (like CJD in humans). Such an event is
extremely improbable because the inoculated animal was 14 years old when the
clinical signs appeared, i.e. about 40% through the expected natural lifetime of
this species, compared to a peak age incidence of 60–65 years in human sporadic
CJD, or about 80% through their expected lifetimes. ***Moreover, sporadic
disease has never been observed in breeding colonies or primate research
laboratories, most notably among hundreds of animals over several decades of
study at the National Institutes of Health25, and in nearly twenty older animals
continuously housed in our own facility.***
>>> Moreover, sporadic disease has never been observed in breeding
colonies or primate research laboratories, most notably among hundreds of
animals over several decades of study at the National Institutes of Health25,
and in nearly twenty older animals continuously housed in our own facility.
<<<
Saturday, July 18, 2015
SPONTANEOUS TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD COW
TYPE DISEASE, DOES IT EXIST NATURALLY IN THE FIELD?
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
Enforcement Report for March 18, 2009 The FDA Enforcement Report is
published weekly by the Food and Drug Administration, Department of Health and
Human Services. It contains information on actions taken in connection with
agency Regulatory activities.
RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
___________________________________
PRODUCT a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging.
Each package is approximately 2 lbs., and each case is approximately 16 lbs.;
Item number 755125, Recall # F-129-9;
b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;
c) Elk Meat, French Rack, Chilled. Item number 755132, Recall #
F-131-9;
d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;
e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall #
F-133-9;
f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9; CODE
Elk Meats with production dates of December 29, 30, and 31 RECALLING
FIRM/MANUFACTURER Recalling Firm: Sierra Meats, Reno, NV, by telephone on
January 29, 2009 and press release on February 9, 2009. Manufacturer: Noah’s Ark
Holding, LLC, Dawson, MN. Firm initiated recall is ongoing. REASON Elk products
contain meat derived from an elk confirmed to have Chronic Wasting Disease
(CWD). VOLUME OF PRODUCT IN COMMERCE Unknown DISTRIBUTION NV, CA, TX, CO, NY,
UT, FL, OK
___________________________________
Singeltary trying to warn where cwd is at in Trans Pecos region 2001-2002
- 2012
TEXAS OLD STATISTICS BELOW FOR PAST CWD TESTING;
Subject: CWD testing in Texas
Date: Sun, 25 Aug 2002 19:45:14 –0500
From: Kenneth Waldrup
To: flounder@wt.net
CC: mcoats@tahc.state.tx.us
Dear Dr. Singletary,
In Fiscal Year 2001, seven deer from Texas were tested by the National
Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed
deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer).
During these two years, an additional six elk and one white-tailed deer were
tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal
Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least
eight other white-tailed deer have been tested at TVMDL. One elk has been tested
at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke
of the Texas Parks and Wildlife Department also has records of 601 clinically
ill white-tailed deer which were necropsied at Texas A&M during the late
1960's and early 1970's, and no spongiform encepalopathies were noted. Thank you
for your consideration.
Ken Waldrup, DVM, PhD Texas Animal Health Commission
========================
From: Ken Waldrup, DVM, PhD (host25-207.tahc.state.tx.us)
Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border)
Date: December 15, 2003 at 3:43 pm PST
In Reply to: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border) posted by TSS on December 12, 2003 at 2:15 pm:
Dear sirs:
With regard to your comment about Texas NOT looking for CWD along the New
Mexico border, it is painfully obvious that you do not know or understand the
natural distribution of mule deer out there or the rights of the land owners in
this state. As of 15 December 2003, a total of 42 deer had been sampled from
what we call "Trans-Pecos", beyond the Pecos River. Mule deer are very widely
dispersed through this area, sometimes at densities of one animal per 6 square
miles. The Texas Parks and Wildlife Department does not have the legal authority
to trepass on private property to collect deer. Some landowners are cooperative.
Some are not. Franklin State Park is at the very tip of Texas, and deer from the
park have been tested (all negative). One of the single largest land owners
along the border is the National Park Service. Deer and elk from the Guadalupe
Peak National Park cannot be collected with federal permission. The sampling
throughout the state is based on the deer populations by eco-region and is
dictated by the availability of funds. I am concerned about your insinuation
that CWD is a human health risk. We are at a stand-off - you have no proof that
it is and I have no definitive proof that it isn't. However I would say that the
inferred evidence from Colorado, Wyoming and Wisconsin suggests that CWD is not
a human health concern (i.e. no evidence of an increased incidence of human
brain disorders within the CWD "endemic" areas of these states). From my
professional interactions with the Texas Parks and Wildlife Department, I can
definitely say that they want to do a thorough and sound survey throughout the
state, not willy-nilly "look here, look there". There are limitations of
manpower, finances and, in some places, deer populations. I would congratulate
TPWD for doing the best job with the limitations at hand rather than trying to
browbeat them when you obviously do not understand the ecology of West Texas.
Thank you for your consideration.
======================
From: TSS (216-119-139-126.ipset19.wt.net)
Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border)
Date: December 16, 2003 at 11:03 am PST
In Reply to: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border) posted by Ken Waldrup, DVM, PhD on December 15, 2003 at 3:43 pm:
HEllo Dr. Waldrup,
thank you for your comments and time to come to this board.
Ken Waldrup, DVM, PhD states;
> it is painfully obvious that you do not know or understand the natural
distribution of mule deer out there or the rights of the land owners in this
state...
TSS states;
I am concerned about all deer/elk not just mule deer, and the rights of
land owners (in the case with human/animal TSEs) well i am not sure of the
correct terminology, but when the States deer/elk/cattle/sheep/humans are at
risk, there should be no rights for land owners in this case. the state should
have the right to test those animals. there are too many folks out there that
are just plain ignorant about this agent. with an agent such as this, you cannot
let landowners (and i am one) dictate human/animal health, especially when you
cannot regulate the movement of such animals...
Ken Waldrup, DVM, PhD states;
> Deer and elk from the Guadalupe Peak National Park cannot be collected
with federal permission.
TSS states;
I do not understand this? so there is no recourse of action even if every
deer/elk was contaminated with CWD in this area (hypothetical)?
Ken Waldrup, DVM, PhD states;
> I am concerned about your insinuation that CWD is a human health risk.
We are at a stand-off - you have no proof that it is and I have no definitive
proof that it isn't. However I would say that the inferred evidence from
Colorado, Wyoming and Wisconsin suggests that CWD is not a human health concern
(i.e. no evidence of an increased incidence of human brain disorders within the
CWD "endemic" areas of these states)...
TSS states;
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging
Cervids and see where the CWD cluster in NM WSMR borders TEXAS;
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
Ecoregions of TEXAS
IF you look at the area around the NM WSMR where the CWD cluster was and
where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my
Geography and my Ciphering is correct ;-) that region only tested 55% of it's
goal. THE most important area on the MAP and they only test some 96 samples,
this in an area that has found some 7 positive animals? NOW if we look at the
only other border where these deer from NM could cross the border into TEXAS,
this area is called the High Plains ecoregion, and again, we find that the
sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD
sampling was met, only 16 samples were tested from some 175 that were suppose to
be sampled.
AS i said before;
> SADLY, they have not tested enough from the total population to
> know if CWD is in Texas or not.
BUT now, I will go one step further and state categorically that they are
not trying to find it. just the opposite it seems, they are waiting for CWD to
find them, as with BSE/TSE in cattle, and it will eventually...
snip...end...TSS
===============================
2005
SEE MAP OF CWD ON THE BORDER OF NEW MEXICO VERY CLOSE TO TEXAS ;
NO update on CWD testing in Texas, New Mexico that i could find. I have
inquired about it though, no reply yet...
-------- Original Message --------
Subject: CWD testing to date TEXAS ?
Date: Mon, 09 May 2005 12:26:20 –0500
From: "Terry S. Singeltary Sr."
To: kristen.everett@tpwd.state.tx.us
Hello Mrs. Everett,
I am most curious about the current status on CWD testing in Texas. could
you please tell me what the current and past testing figures are to date and
what geographical locations these tests have been in. good bust on the illegal
deer trapping case. keep up the good work there.........
thank you, with kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
-------- Original Message --------
Subject: CWD testing in New Mexico
Date: Mon, 09 May 2005 14:39:18 –0500
From: "Terry S. Singeltary Sr."
To: ispa@state.nm.us
Greetings,
I am most curious of the current and past CWD testing in New Mexico, and
there geographical locations...
thank you,
Terry S. Singeltary SR. CJD Watch
#################### https://lists.aegee.org/bse-l.html
####################
2006
----- Original Message -----
From: "Terry S. Singeltary Sr." flounder9@VERIZON.NET
To: BSE-L@aegee.org
Sent: Saturday, December 23, 2006 1:47 PM
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing
sampling figures -- what gives TAHC ???
Date: December 23, 2006 at 11:25 am PST
Greetings BSE-L members,
i never know if i am going crazy or just more of the same BSe. several
years ago i brought up the fact to the TAHC that CWD was literally at the Texas
borders and that the sample size for cwd testing was no where near enough in the
location of that zone bordering NM. well, i just wrote them another letter
questioning this again on Dec. 14, 2006 (see below) and showed them two
different pdf maps, one referencing this url, which both worked just fine then.
since then, i have NOT received a letter from them answering my question, and
the url for the map i used as reference is no longer working? i had reference
this map several times from the hunter-kill cwd sampling as of 31 August 2005
pdf which NO longer works now??? but here are those figures for that zone
bordering NM, for those that were questioning the url. the testing samples
elsewhere across Texas where much much more than that figure in the zone
bordering NM where CWD has been documented bordering TEXAS, near the White Sands
Missile Range. SO, why was the Texas hunter-kill cwd sampling as of 31 August
2005 document removed from the internet??? you know, this reminds me of the
infamous TEXAS MAD COW that i documented some 7 or 8 months before USDA et al
documented it, when the TAHC accidentally started ramping up for the
announcement on there web site, then removed it (see history at bottom). i am
not screaming conspiracy here, but confusious is confused again on the ciphering
there using for geographical distribution of cwd tissue sample size survey, IF
they are serious about finding CWD in TEXAS. common sense would tell you if cwd
is 35 miles from the border, you would not run across state and have your larger
samples there, and least samples 35 miles from where is what
found..........daaa..........TSS
THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of
Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare
to the other sample locations ;
TPWD has been conducting surveys of hunter-kill animals since 2002 and has
collected more than 7300 samples (as of 31 August 2005). In total, there have
been over 9400 samples, both hunter-kill and private samples, tested in Texas to
date, and no positives have been found.
SO, out of a total of 9,400 samples taken for CWD surveillance in TEXAS
since 2002 of both hunter-kill and private kill, ONLY 191 samples have been
taken in the most likely place one would find CWD i.e. the border where CWD has
been documented at TEXAS and New Mexico
latest map NM cwd old data
CWD in New Mexico ;
What is the Department doing to prevent the spread of CWD?
Chronic wasting disease (CWD) was recently detected in a mule deer from
Unit 34. Until 2005, CWD had only been found in Unit 19. With this discovery,
the Department will increase its surveillance of deer and elk harvested in Units
29, 30 and 34.
Lymph nodes and/or brain stems from every harvested deer and brain stems
from all elk taken in Unit 34 will be sampled.
snip...
CWD SURVEILLANCE TEXAS
SNIP...SEE FULL TEXT ;
2011 – 2012
Friday, October 28, 2011
CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS
Greetings TAHC et al,
A kind greetings from Bacliff, Texas.
In reply to ;
Texas Animal Health Commission (TAHC) Announcement October 27, 2011
I kindly submit the following ;
TEXAS CWD STATUS
Captive Cervids
There have been no reported CWD infections of captive elk or deer in Texas.
There is currently no mandatory surveillance program for susceptible cervids
kept on game farms, although, there has been voluntary surveillance since 1999,
which requires owners of participating herds to maintain an annual herd
inventory and submit samples for all mortalities of animals over 16 months of
age.
Free-Ranging (Wild) Cervids
There have been no reported CWD infections of free-ranging susceptible
cervids in Texas. Currently targeted surveillance of free-ranging cervids having
clinical symptoms is ongoing in Texas with no positives identified.
Additionally, sampling of hunter-killed animals was initiated statewide during
the 2002-2003 deer hunting season and sampling will be continued for the next
three to five years.
Historic Status
snip...
NO update on CWD testing in Texas, New Mexico that i could find. I have
inquired about it though, no reply yet...
-------- Original Message --------
Subject: CWD testing to date TEXAS ?
Date: Mon, 09 May 2005 12:26:20 –0500
From: "Terry S. Singeltary Sr."
To: kristen.everett@tpwd.state.tx.us
Hello Mrs. Everett,
I am most curious about the current status on CWD testing in Texas. could
you please tell me what the current and past testing figures are to date and
what geographical locations these tests have been in. good bust on the illegal
deer trapping case. keep up the good work there.........
thank you, with kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
CJD WATCH
-------- Original Message --------
Subject: CWD testing in New Mexico
Date: Mon, 09 May 2005 14:39:18 –0500
From: "Terry S. Singeltary Sr."
To: ispa@state.nm.us
Greetings,
I am most curious of the current and past CWD testing in New Mexico, and
there geographical locations...
thank you,
Terry S. Singeltary SR. CJD Watch
#################### https://lists.aegee.org/bse-l.html
####################
-------- Original Message --------
Subject: CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS ?
Date: Mon, 16 Aug 2004 15:09:58 –0500
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy
Greetings List members,
as i stated in my previous email;
> >> CWD has not been detected in Texas, SADLY, they have not
tested enough from the total population to know if CWD is in Texas or not. time
will tell though. IF they get serious about finding and documenting CWD in
sufficient numbers here in TEXAS, sadly, i am afraid they will find it. ITs
already at NM, Texas border, TSEs knows no borders. HOWEVER, with the recent
finding of a CNS cow with high potential for BSE/TSE in TEXAS, with one high
official over ruling another official that wanted it tested, with the high
official winning out and the damn thing going to render without being tested,
head spinal cord and all. THIS weighs heavy on the credibility of any
surveillance for any TSE in TEXAS, and speaks a great deal for the over all
surveillance of TSE in the USA...TSS
SO, i thought i would just see where these Ecoregions were, and just how
the CWD testing was distributed. YOU would think that with the cluster of CWD
bordering TEXAS at the WPMR in NM, you would have thought this would be where
the major CWD testing samples were to have been taken? wrong! let's have a look
at the sample testing. here is map of CWD in NM WPMR bordering TEXAS;
NEW MEXICO 7 POSITIVE CWD WHITE SANDS MISSILE RANGE MAP
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging
Cervids and see where the CWD cluster in NM WSMR borders TEXAS;
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
Ecoregions of TEXAS
IF you look at the area around the NM WSMR where the CWD cluster was and
where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my
Geography and my Ciphering is correct ;-) that region only tested 55% of it's
goal. THE most important area on the MAP and they only test some 96 samples,
this in an area that has found some 7 positive animals? NOW if we look at the
only other border where these deer from NM could cross the border into TEXAS,
this area is called the High Plains ecoregion, and again, we find that the
sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD
sampling was met, only 16 samples were tested from some 175 that were suppose to
be sampled.
AS i said before;
> SADLY, they have not tested enough from the total population to >
know if CWD is in Texas or not.
BUT now, I will go one step further and state categorically that they are
not trying to find it. just the opposite it seems, they are waiting for CWD to
find them, as with BSE/TSE in cattle, and it will eventually...
TSS
CWD TEXAS TAHC OLD FILE HISTORY
updated from some of my old files. ...
Subject: CWD SURVEILLANCE STATISTICS TEXAS (total testing figures less than
50 in two years)
Date: Sun, 25 Aug 2002 21:06:49 –0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
Singeltary trying to warn TAHC that they were covering up mad cow disease
and correspondence with OIG
BUT FIRST, THE FIRST STUMBLING AND STAGGERING MAD COW THAT GOT AWAY FROM
SINGELTARY, 2004, highly suspect stumbling and staggering mad cow reported,
however, NO TESTING DONE, ON ORDERS FROM AUSTIN $
May 4, 2004
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30th, the Food and Drug Administration learned that a cow
with central nervous system symptoms had been killed and shipped to a processor
for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began
an investigation. On Friday and throughout the weekend, FDA investigators
inspected the slaughterhouse, the rendering facility, the farm where the animal
came from, and the processor that initially received the cow from the
slaughterhouse.
FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over the
weekend FDA was able to track down all the implicated material. That material is
being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known as "mad
cow disease," can exhibit such symptoms. In this case, there is no way now to
test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit
the feeding of its rendered protein to other ruminant animals (e.g., cows,
goats, sheep, bison)...
USDA regulations, any cow that exhibits signs of central nervous system
(CNS)
According to a 1997 Animal and Plant Health Inspection Service (NHIS)
Memorandum, brain samples all of such animals should be sent for BSE testing.2
The memorandum notes that "it is essential that brain specimens be collected
from adult cattle condemned for CNS signs as part of our national surveillance
of BSE."
The cow slaughtered at the Lone Star Beef slaughterhouse last week
staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a
request from APHIS personnel at the plant to conduct BSE testing, however, an
APHIS supervisor in Austin reportedly refused the test and instructed the plant
to send the carcass for rendering.5
May 13,2004
Page 2
snip...
The cow slaughtered at the Lone Star Beef slaughterhouse last week
staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a
request from APHIS personnel at the plant to conduct BSE testing, however, an
APHIS supervisor in Austin reportedly refused the test and instructed the plant
to send the carcass for rendering.5
This sequence of events is troubling, and it raises the question of
whether this is an isolated incident. In 1997, USDA noted a major gap between
the number of cattle condemned for CNS symptoms and the number of these cows
actually tested for mad cow disease. The Department found:
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at
OIG, ...............
snip...
There will be several more emails of my research to follow. I respectfully
request a full inquiry into the cover-up of TSEs in the United States of America
over the past 30 years. I would be happy to testify...
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff,
Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST In
Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford,
Regarding further analysis of BSE Inconclusive Test Results posted by TSS on
June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days
later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary
for Marketing and Regulatory Programs resigns. Three days later same mad cow
found in November turns out to be positive. Both resignation are unexpected.
just pondering... TSS
MAD COW IN TEXAS NOVEMBER 2004 SINGELTARY’S MAD COW THAT DID NOT GET AWAY,
JUST DELAYED FOR POLITICAL PURPOSES...TRADE $$$
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to
unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up
forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION
YET...can you confirm???
terry
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 –0600
From: Carla Everett
To: "Terry S. Singeltary Sr." References: <[log in to unmask]>
The USDA has made a statement, and we are referring all callers to the
USDA web site. We have no information about the animal being in Texas. Carla At
09:44 AM 11/19/2004, you wrote:>Greetings Carla,>>i am getting
unsubstantiated claims of this BSE 'inconclusive' cow is from>TEXAS. can you
comment on this either way please?>>thank you,>Terry S. Singeltary
Sr.>>
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600 From: Carla Everett
To: "Terry S. Singeltary Sr."
References: ...sniptss
our computer department was working on a place holder we could post USDA's
announcement of any results. There are no results to be announced tonight by
NVSL, so we are back in a waiting mode and will post the USDA announcement when
we hear something. At 06:05 PM 11/22/2004,
you wrote:
>why was the announcement on your TAHC site removed?
>>Bovine Spongiform Encephalopathy:
>November 22: Press Release title here
>>star image More BSE information
>>>>terry
>>Carla Everett wrote:
>>>no confirmation on the U.S.' inconclusive test...
>>no confirmation on location of animal.>>>>>>
==========================
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to
unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up
forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION
YET...can you confirm???
terry
=====7 MONTHS LATER, SINGELTARY’S MAD COW WAS CONFIRMED=====
*** HOW TEXAS DOES TRACE OUTS...
Executive Summary In June 2005, an inconclusive bovine spongiform
encephalopathy (BSE) sample from November 2004, that had originally been
classified as negative on the immunohistochemistry test, was confirmed positive
on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA)
identified the herd of origin for the index cow in Texas; that identification
was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal
Health Commission (TAHC), established an incident command post (ICP) and began
response activities according to USDA’s BSE Response Plan of September 2004.
Response personnel removed at-risk cattle and cattle of interest (COI) from the
index herd, euthanized them, and tested them for BSE; all were negative. USDA
and the State extensively traced all at-risk cattle and COI that left the index
herd. ***The majority of these animals entered rendering and/or slaughter
channels well before the investigation began. USDA’s response to the Texas
finding was thorough and effective.
snip...
Trace Herd 3 The owner of Trace Herd 3 was identified as possibly having
received an animal of interest. The herd was placed under hold order on 7/27/05.
The herd inventory was conducted on 7/28/05. The animal of interest was not
present within the herd, and the hold order was released on 7/28/05. The person
who thought he sold the animal to the owner of Trace Herd 3 had no records and
could not remember who else he might have sold the cow to. Additionally, a
search of GDB for all cattle sold through the markets by that individual did not
result in a match to the animal of interest. The animal of interest traced to
this herd was classified as ***untraceable because all leads were exhausted.
Trace Herd 4 The owner of Trace Herd 4 was identified as having received
one of the COI through an order buyer. Trace Herd 4 was placed under hold order
on 7/29/05. A complete herd inventory was conducted on 8/22/05 and 8/23/05.
There were 233 head of cattle that were examined individually by both State and
Federal personnel for all man-made identification and brands. ***The animal of
interest was not present within the herd. Several animals were reported to have
died in the herd sometime after they arrived on the premises in April 2005. ***A
final search of GDB records yielded no further results on the eartag of interest
at either subsequent market sale or slaughter. ***With all leads having been
exhausted, this animal of interest has been classified as untraceable. The hold
order on Trace Herd 4 was released on 8/23/05.
Trace Herd 5 The owner of Trace Herd 5 was identified as having received
two COI and was placed under hold order on 8/1/05. Trace Herd 5 is made up of 67
head of cattle in multiple pastures. During the course of the herd inventory,
the owner located records that indicated that one of the COI, a known birth
cohort, had been sold to Trace Herd 8 where she was subsequently found alive.
***Upon completion of the herd inventory, the other animal of interest was not
found within the herd. ***A GDB search of all recorded herd tests conducted on
Trace Herd 5 and all market sales by the owner failed to locate the
identification tag of the animal of interest and she was subsequently classified
as ***untraceable due to all leads having been exhausted. The hold order on
Trace Herd 5 was released on 8/8/05.
Trace Herd 6 The owner of Trace Herd 6 was identified as possibly having
received an animal of interest and was placed under hold order on 8/1/05. This
herd is made up of 58 head of cattle on two pastures. A herd inventory was
conducted and the animal of interest was not present within the herd. ***The
owner of Trace Herd 6 had very limited records and was unable to provide further
information on where the cow might have gone after he purchased her from the
livestock market. A search of GDB for all cattle sold through the markets by
that individual did not result in a match to the animal of interest.
Additionally, many of the animals presented for sale by the owner of the herd
had been re-tagged at the market effectually losing the traceability of the
history of that animal prior to re-tagging. ***The animal of interest traced to
this herd was classified as ***untraceable due to all leads having been
exhausted. The hold order on Trace Herd 6 was released on 8/3/05.
Trace Herd 7 The owner of Trace Herd 7 was identified as having received
an animal of interest and was placed under hold order on 8/1/05. Trace Herd 7
contains 487 head of cattle on multiple pastures in multiple parts of the State,
including a unit kept on an island. The island location is a particularly rough
place to keep cattle and the owner claimed to have lost 22 head on the island in
2004 due to liver flukes. Upon completion of the herd inventory, the animal of
interest was not found present within Trace Herd 7. ***A GDB search of all
recorded herd tests conducted on Trace Herd 7 and all market sales by the owner
failed to locate the identification tag of the animal of interest. ***The cow
was subsequently classified as untraceable. It is quite possible though that she
may have died within the herd, especially if she belonged to the island unit.
The hold order on Trace Herd 7 was released on 8/8/05.
TSS
posted by Terry S. Singeltary Sr. at
11:33 AM
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