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
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 IS THE TEXAS DEER CZAR DR. DOUGH DOING FOR WISCONSIN AFTER HIS
RECOMMENDATIONS FOR CWD $$$
Tuesday, July 14, 2015
*** TWO Escaped Captive Deer on the loose in Eau Claire County Wisconsin
CWD postive farm Yellow ear tag
Wednesday, March 04, 2015
Disease sampling results provide current snapshot of CWD in Wisconsin
finding 324 positive detections statewide in 2014
Tuesday, February 11, 2014
*** Wisconsin tracks 81 deer from game farm with CWD buck to seven other
states
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
Wednesday, March 04, 2015
*** Disease sampling results provide current snapshot of CWD in Wisconsin
finding 324 positive detections statewide in 2014
Friday, April 04, 2014
*** Wisconsin State officials kept silent on CWD discovery at game farm ***
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
Wisconsin : 436 Deer Have Escaped From Farms to Wild
Date: March 18, 2003 Source: Milwaukee Journal Sentinel
Hundreds of deer escape
The DNR found a total of 671 deer that escaped farms - 436 of which were
never found - because of storm-damaged fences, gates being left open or the
animals jumping over or through fences.
In one example in Kewaunee County, a deer farmer's fence was knocked down
in a summer storm. Ten deer escaped, and the farmer told the DNR he had no
intention of trying to reclaim them. The DNR found five of the deer, killed them
and cited the farmer for violation of a regulation related to fencing.
24 farmers were unlicensed. One had been operating illegally since 1999
after he was denied a license because his deer fence did not meet minimum
specifications.
Records maintained by operators ranged from "meticulous documentation to
relying on memory." At least 227 farms conducted various portions of their deer
farm business with cash. Over the last three years, 1,222 deer died on farms for
various reasons. Disease testing was not performed nor required on the majority
of deer. Farmers reported doing business with people in 22 other states and one
Canadian province. ..
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats)
FarmUpdate 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 80acres of land for
$465,000 for the Statewide Wildlife Habitat Program inPortage County and approve
the restrictions on public use of the site.
SUMMARY:
yep, while the Texas deer czar dr. dough was off to Wisconsin pushing the
privately owned shooting pen industry (livestock cervids industry), Texas fell
to CWD.
for your information...
According to Wisconsin’s White-Tailed Deer Trustee Dr. James Kroll, people
who call for more public hunting opportunities are “pining for socialism.” He
further states, “(Public) Game management is the last bastion of
communism.”
“Game Management,” says James Kroll, driving to his high-fenced,
two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.”
Kroll, also known as Dr. Deer, is the director of the Forestry Resources
Institute of Texas at Stephen F. Austin State University, and the “management”
he is referring to is the sort practiced by the State of Texas. The 55-year-old
Kroll is the leading light in the field of private deer management as a means to
add value to the land. His belief is so absolute that some detractors refer to
him as Dr. Dough, implying that his eye is on the bottom line more than on the
natural world.
Kroll, who has been the foremost proponent of deer ranching in Texas for
more than thirty years, doesn’t mind the controversy and certainly doesn’t fade
in the heat. People who call for more public lands are “cocktail
conservationists,” he says, who are really pining for socialism. He calls
national parks “wildlife ghettos” and flatly accuses the government of gross
mismanagement. He argues that his relatively tiny acreage, marked by eight-foot
fences and posted signs warning off would-be poachers, is a better model for
keeping what’s natural natural while making money off the land.
WHICH SIDE OF THE FENCE ARE YOU ON ?
According to Wisconsin’s White-Tailed Deer Trustee
Dr. James Kroll, people who call for more public hunting opportunities are
“pining for socialism.” He further states, “(Public) Game management is the last
bastion of communism.”
OPINION BLOG
These are just two insights into the man who has been asked to provide
analysis and recommended changes to Wisconsin’s deer management program. Kroll’s
insights are from an article entitled “Which Side of the Fence Are You On?” by
Joe Nick Patoski for a past edition of Texas Monthly.
If nothing more, the article gives an unabashed look into the mind-set that
will be providing the Wisconsin DNR with recommendations on how to change their
deer management practices. James Kroll (also known as “Deer Dr.”) was appointed
to the Wisconsin “deer czar” position last fall. He was hired by the Department
of Administration and instructed to complete a review of the state’s deer
management program.
Here’s a sample of the article:
“Game Management,” says James Kroll, driving to his high-fenced,
two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.”
Kroll, also known as Dr. Deer, is the director of the Forestry Resources
Institute of Texas at Stephen F. Austin State University, and the “management”
he is referring to is the sort practiced by the State of Texas. The 55-year-old
Kroll is the leading light in the field of private deer management as a means to
add value to the land. His belief is so absolute that some detractors refer to
him as Dr. Dough, implying that his eye is on the bottom line more than on the
natural world.
Kroll, who has been the foremost proponent of deer ranching in Texas for
more than thirty years, doesn’t mind the controversy and certainly doesn’t fade
in the heat. People who call for more public lands are “cocktail
conservationists,” he says, who are really pining for socialism. He calls
national parks “wildlife ghettos” and flatly accuses the government of gross
mismanagement. He argues that his relatively tiny acreage, marked by eight-foot
fences and posted signs warning off would-be poachers, is a better model for
keeping what’s natural natural while making money off the land.
A trip to South Africa six years ago convinced Kroll that he was on the
right track. There he encountered areas of primitive, lush wildlife-rich
habitats called game ranches. They were privately owned, privately managed, and
enclosed by high fences. He noticed how most of the land outside those fences
had been grazed to the nub, used up. “Game ranches there derive their income
from these animals — viewing them, hunting them, selling their meat,” he says.
“There are no losers.” At his own ranch Kroll has set up a smaller version of
the same thing. His land is indeed lush, verdant, with pine groves, an abundance
of undergrowth, wild orchids, New Jersey tea, jack-in-the-pulpits, and other
native plants. He has also set up a full-scale breeding research center and is
one of twenty Texas deer breeders using artificial insemination to improve his
herd. “We balance sex and age ratio,” he says. “We manage habitat. We control
the population and manage for hunting. I want to leave the deer herd better than
it was before we came.”
It is interesting to note that, in 2001, the State of Texas shifted its
deer management strategies toward the same leanings that Kroll has suggested for
Wisconsin. In Texas, the change was brought about via heavy lobbying from the
high-fence deer ranching industry. This pressure helped convince the Texas Parks
and Wildlife to change their regulations and allow private landowners to select
the own deer biologists.
“That has given landowners more freedom,” Kroll told Texas Monthly.
“(However,) You still have to let the state on your land to get a
wildlife-management permit.”
The key difference here is that 98 percent of Texas is comprised of private
land.
Wisconsin, on the other hand, consists of approximately 34.8 million acres
of land, and 25.5 percent of the state’s 638,000 gun-hunters reported hunting on
public land at some point during the season (2010, Duey, Rees).
According to the Wisconsin Realtors Association, more than 5.7 million
acres of this land, or 16.5 percent, is publicly owned and used for parks,
forests, trails, and natural resource protection. [Note: these statistics do not
include the public land used for roads, government buildings, military bases,
and college/school campuses.] This 5.7 million acres of public land is owned as
follows:
Federal government owns approximately 1.5 million acres (4.4 percent of the
state’s land area). Almost all of the federal forestland in Wisconsin is located
in Chequamegon-Nicolet National Forest.
State government owns approximately 1.6 million acres (4.6 percent of the
state’s land area). The land is managed by two agencies, the Board of
Commissioners of Public Land (who manages lands granted by federal government)
and the DNR (managing land owned by the state).
County government owns approximately 2.6 million acres (7.5 percent of the
state’s land area).
Public land is located in 71 of Wisconsin’s 72 counties, with the most
public land located in Bayfield County (464,673 acres). [Note: Menominee County
does not have any public land, but 98 percent of the land is held in trust by
the Menominee Tribe.] Twenty counties have more than 100,000 acres of public
land, while only 12 counties have fewer than 10,000 acres.
What does this all mean? My initial reaction, which is one that I predicted
when Kroll was named to the state’s deer trustee position, is that his team’s
final recommendations — if implemented — will be heavily skewed toward the
state’s larger landowners (500+ acres) and folks who own small parcels in areas
comprised mostly of private land.
It is also my prediction that the final recommendations (again, if
implemented) will do little, if anything, to improve deer herds and deer hunting
on Wisconsin’s 5.7 million acres of public land.
Where does this leave the public-land hunter? “It will suck to be you,”
said one deer manager who asked to remain anonymous out of fear for his job.
“The resources and efforts will go toward improving the private land sector.
This is all about turning deer hunting away from the Public Land Doctrine and
more toward a European-style of management — like they have in Texas.”
I do, of course, hope these assumptions are wrong. As with all things in
life, we should maintain an open mind to change. Life is all about change.
However, change for the sake of change is usually a recipe for disaster.
Especially when that change is driven by something more than a sincere desire to
manage public resources for the greater good.
As noted yesterday (Dr. James Kroll Report: Is That All You Get For Your
Money), I will provide more of my opinions and interpretation on this important
issue in forthcoming installments of this blog. Read his full preliminary report
here.
Thursday, March 29, 2012
TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT
CALLING KETTLE BLACK
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Tuesday, July 10, 2012
Dr. James C. Kroll Texas deer czar final report on Wisconsin
$$$ now, what happened in TEXAS since the deer czar from Texas Dr. Dough
went to Wisconsin to solve their cwd problems $$$
Thursday, July 09, 2015
*** TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed
Herd with Testing of Exposed Animals ***
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
Wednesday, July 01, 2015
*** TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Wednesday, March 18, 2015
*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18,
2015
Wednesday, March 25, 2015
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
Thursday, May 02, 2013
*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY
TEXTING
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
2001 - 2002
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
========================
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.
snip...
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...
snip...end
***for anyone interested, here is some history of CWD along the Texas, New
Mexico border, and my attempt to keep up with it...terry
snip...
see history CWD Texas, New Mexico Border ;
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER
Sunday, October 04, 2009
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009 2009 Summary of Chronic
Wasting Disease in New Mexico New Mexico Department of Game and Fish
Friday, January 30, 2015
*** Scrapie: a particularly persistent pathogen ***
Tuesday, December 16, 2014
*** Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. ***The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. ***These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
see more here ;
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 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
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
============================================================================
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
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE AND 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.***
================
cwd environmental load factor in the land and surrounding plants and
objects.
transportation of cervids and HUMANS from cwd zone should be regarded as a
great risk factor, and environmental contamination.
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentallyrelevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
and take note here ;
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
I7 Early Trafficking and Dissemination of CWD Prions in Deer
Edward A. Hoover1*, Clare E. Hoover1, Davin M. Henderson1, Nathaniel D.
Denkers1, Kristin A. Davenport1, Shannon Bartelt-Hunt2, Alan M. Elder1, Anthony
E. Kincaid3, 4, Jason C. Bartz3, Mark D. Zabel1, Candace K. Mathiason1
1Prion Research Center, Department of Microbiology, Immunology, and
Pathology, Colorado State University, Fort Collins, Colorado, USA 2Department of
Civil Engineering, University of Nebraska-Lincoln, Prion2015 Program Guide
10 invited speakers PRION 2015 Omaha, Nebraska, USA, 3Department of Medical
Microbiology and immunology Creighton University, Omaha, Nebraska, USA
4Department of Pharmacy Science, Creighton University, Omaha, Nebraska,
USA
* P r e s e n t i n g a u t h o r ’ s e - m a i l :
edward.hoover@colostate.edu
Efficient horizontal infection is a hallmark of chronic wasting disease
(CWD) in freeranging cervids. The mechanisms and pathways that enable this
remarkable process, however, remain incompletely understood--in particular the
facile transmucosal entry, exit, and environmental persistence of CWD prions. We
have focused on trans-mucosal CWD infection in white-tailed deer, specifically
on early prion tissue tropism and later stage prion shedding and association
with environmental constituents using modifications of real-time quaking-induced
conversion combined with amplified immunohistochemistry. We have documented very
early trans-mucosal prion passage (within hours), followed by uptake and
amplification in upper digestive tract lymphoid t i s s u e s ( 4 w e e k s ) ,
and dissemination to more distant lymphoid and non-lymphoid tissue sites (8-12
weeks). We have used quantitative approaches to realtime conversion to estimate
the relatively low (i.e. vs. tissues) prion concentrations in body fluids and
excreta; i.e. >100 (cervidized mouse) LD50 are shed daily in the urine of one
CWD infected deer. Using similar methods, we have also demonstrated and
quantified the impressive
===========================
P183
Novel Detection of PrPCWD on Plants Collected from Rocky Mountain National
Park
Aimee Ortega1, Jeffrey Seligman1, Jan Leach2, Mark Zabel1 1Colorado State
University, Prion Research Center, Department of Microbiology, Immunology and
Pathology, Fort Collins, CO, USA, 2Colorado State University, Department of
Bioagricultural Sciences and Pest Management, Fort Collins, CO, USA
Chronic wasting disease (CWD) affects animals such as elk, deer, and moose
and has become endemic over the last decade. The disease is one of many
transmissible spongiform encephalopathies which occur due to the accumulation of
an abnormally folded, proteinase K resistant, form of the normal cellular prion
protein PrPC. This abnormally folded form, PrPCWD, seeds conversion of PrPC into
PrPCWD and eventually forms amyloid fibrils. The exact mechanisms behind
transmission and spread of CWD are unknown but research has shown that it can be
spread through h o r i z o n t a l , v e r t i c a l , and i n d i r e c t /
environmental routes. PrPCWD has been found in both soil and water.
Additionally, PrPCWD is very resistant to degradation which makes it stable in
the environment for long periods of time. A study has shown that the
Prion2015 Program Guide 29
abnormal prion protein can remain viable in the environment for as long as
16 years. We wanted to further explore the latter and determine whether prions
could be detected in grasses and other plants in Rocky Mountain National Park
(RMNP) by use of the protein misfolding cyclic amplification (PMCA) assay.
This past summer we surveyed three sites within RMNP and collected a total
of 32 plants. Plants were collected from both outside and inside enclosures that
serve to keep wildlife out and allow for restoration and regrowth of the flora.
Plant samples were assayed by PMCA and we are now reporting for the first time
the novel detection of PrPCWD from the surface on a number of plants
assayed.
P195 Chronic wasting disease prions detected during early stages of
infection by mbPMCA in tissues from white-tailed deer o r a l l y inoculated
with f r e e and microparticle-bound prions
Alexandra Chesney1, Chad Johnson1, Tracy Nichols2, Hannah Kornely1, Dania
Shoukfeh1, Joel Pedersen1
1University of Wisconsin, Madison, WI, USA, 2United States Department of
Agriculture (USDA), Animal and Plant Health Inspection Service (APHIS), Wildlife
Services (WS), National Wildlife Research Center (NWRC), Fort Collins, CO,
USA
Enhanced oral transmission of rodenta d a p t e d p r i o n d i s e a s e
has been demonstrated with the disease agent bound to several types of mineral
microparticles; however, the generalizability of this finding to ruminants has
not been established. Contaminated soil is believed to represent a reservoir for
environmental prions and may contribute to horizontal transmission of chronic
wasting disease (CWD) in captive and wild cervid populations. Here, we examined
the impact of CWD agent association with microparticles o f montmorillonite, an
aluminosilicate clay
Prion2015 Program Guide 35
mineral that showed the largest disease transmission enhancement in rodent
bioassays, on early disease in orally inoculated white-tailed deer.
Amplification of prions by PMCA has been achieved from various contaminated
organs and excretions at late stages in disease. Using microplatebased PMCA
(mbPMCA), we detected different accumulation patterns in white-tailed deer
tissues 42 days after oral inoculation with CWD prions bound to montmorillonite.
We expected mbPMCA to be more sensitive than immunohistochemistry (IHC) to
determine prion accumulations in tissues. Through evaluation of mb-PMCA positive
tissues, we found that mbPMCA is more sensitive than IHC by at least a factor of
106.3, and detected CWD prions in multiple tissue types that were negative by
IHC. These findings suggest that microparticles can enhance the transmission of
CWD in white-tailed deer and also demonstrates the consistency and
high-throughput utility of the mbPMCA assay. Furthermore, our results indicate
that enhanced transmission of microparticle-bound CWD agent warrants
consideration in evaluating the relative importance o f d i r e c t and i n d i
r e c t (environmental) transmission of CWD in natural populations and in
disease management.
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods. *** We recently observed
the direct transmission of a natural classical scrapie isolate to macaque after
a 10-year silent incubation period, ***with features similar to some reported
for human cases of sporadic CJD, albeit requiring fourfold longe incubation than
BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), ***is the
third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the
origin of human sporadic cases. We will present an updated panorama of our
different transmission studies and discuss the implications of such extended
incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases...TSS
===============
From: Terry S. Singeltary Sr.
Sent: Saturday, November 15, 2014 9:29 PM
To: Terry S. Singeltary Sr.
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL
1984
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
R. G. WILL
1984
*** The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) ***
snip...
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. ...
human cwd will NOT look like nvCJD. in fact, see ;
*** 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).***
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.
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER
AND ELK ;
NOR IS THE FDA recalling this CWD positive elk meat for the well being of
the dead elk ;
Wednesday, March 18, 2009 Noah's Ark Holding, LLC, Dawson, MN RECALL Elk
products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO,
NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
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.
Wednesday, July 15, 2015
*** Additional BSE TSE prion testing detects pathologic lesion in unusual
brain location and PrPsc by PMCA only, how many cases have we missed? ***
not sure if you all are aware, but there has now been a captive deer
confirmed with cwd in Texas, and they will have a difficult time tracing back
all the deer from that facility. all cwd is mad cow disease in cervid. this is a
nightmare for Texas, that the TPWD, the TDAH, and the captive deer industry have
managed to put liptstick on and take her to the dance. see the map, but that’s
just what Texas did with mad cow disease. they let one slip away, and then let
the other mad cow sit on a shelf for 7 months with the BSE MRR policy was
ratified. that was long ago, this cwd in captive is now ...Prion2015 conference
out of Ft. Collins and other recent science shows what the real risk factors are
long term. the captive game farming is a huge industry in Texas, and they will
do what ever they can to protect it. recent science shows indeed that cwd is a
risk factor to humans. check out the map of the trace out to other facilities in
Texas.
Just got off the phone with TAHC, and I wanted to confirm this. but it
seems true, that in the state of Texas, even if you are a Captive game farmer,
breeder, part of the captive industry at all, if you want to sample your own
cervid for cwd, instead of the TAHC, TPWD, or Doctor, all you have to do is pass
the Certified CWD Sample Collector course, and bingo, you sample your own herd.
reminds me of the obex only criteria for testing of TSE prion. wonder how many
that policy missed?
The new Subchapter C, which is entitled “Chronic Wasting Disease” includes
standards and requirements for persons authorized by the commission to perform
work as a Certified CWD Sample Collector. The provisions also establish
application, training and recordkeeping requirements. A Certified CWD Sample
Collector is an individual who has completed commission provided or approved
training on the collection and preservation of samples for CWD testing and on
proper recordkeeping, and who has been authorized to perform these activities by
the commission.
For more information about the CWD herd program, call your TAHC region
office or 800-550-8242 x777.
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
how to hide a mad cow for 7 months in Texas ;
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ??? Date: Mon, 22 Nov 2004
21:07:51 –0600 From: "Terry S. Singeltary Sr." To: Carla Everett References:
snip
ok, thank you Carla. i hate rumors and 'inconclusive' announcements.
kind regards, terry
Carla Everett wrote: > 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. I still want my Texas mad cows
confirmed BY WB! TSS
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ??? Date: Mon, 22 Nov 2004
21:07:51 –0600 From: "Terry S. Singeltary Sr." To: Carla Everett References:
ok, thank you Carla. i hate rumors and 'inconclusive' announcements.
kind regards, terry
Carla Everett wrote:
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.
I still want my Texas mad cows confirmed BY WB!
TSS
Terry S. Singeltary Sr. wrote:
##################### Bovine Spongiform Encephalopathy
#####################
Greetings list members,
I find this very very disturbing. IN fact i will say that if the USDA/APHIS
do not get a second opinion from the experts overseas, I would say that there is
a cover-up. WE now know that they are willing to do anything to cover-up BSE in
the USA by what they did with the other stumbling and staggering cow they
refused to TSE test and sent to the render in TEXAS. IN fact I am hearing from
International experts on TSE that they do NOT buy the latest USDAs test result.
why should they? Seems they did not even do a western blot from what i was told.
They run two rapid test that turn up positive, but the USDA finds that to be
inconclusive. They also said they would not be telling us of any 'inconclusive',
but they did. SO, why was it announced? I will tell you why, because the
likelihood of it being positive was very high. Even the CEO of BioRAD and
Prionics said this. IN fact, USDA has never said they would run 2 IHC, so again,
why did they this time? I will tell you why, they wanted a negative so bad, they
would test the samples until they found a portion of the brain/tissue sample
that would not show a positive. THIS REEKs of industry/political manipulation. I
cannot believe that our foreign alies/exporting countries (if there is any
left), continue to risk there people through the lies from this administration.
why won't USDA et al send samples for independent examinations if they are still
having such a hard time with this? what do they have to hide? IF both the TSE
laboratory in Waybride, England and the University of Bern, Switzerland (OIE
Reference Laboratory) dont get a sample of this tissue from this cow to give
second opinions, then in my opinion that cow was positive. Hell, we get official
slides of Japan's infected samples to survey. but in the USA, it's all closed
doors now and they will test the damn animal as many times as it takes to get a
negative. total bull sh!t encephalopathy this is, what i call BSeee, politics at
it's finest hour. when will it all end$
IF we look at the original U.S. Emergency Bovine Spongiform Encephalopathy
Response Plan Summary i posted in 1999, it states very clearly;
If additional tests do suggest a presumptive diagnosis of BSE, an NVSL
pathologist will hand carry the sample to the United Kingdom for confirmation.
It is at this critical point, when NVSL suggests a diagnosis of BSE and is
preparing to send the sample to the United Kingdom, that this BSE Response Plan
is initiated. The Plan begins the preliminary notification from NVSL to
APHIS...
snip...end
OIG AND THE HONORABLE FONG CONFIRMS TEXAS MAD AFTER AN ACT OF CONGRESS 7
MONTHS LATER
TEXAS MAD COW
THEY DID FINALLY TEST AFTER SITTING 7+ MONTHS ON A SHELF WHILE GW BORE THE
BSE MRR POLICY, i.e. legal trading of all strains of TSE. now understand, i
confirmed this case 7 months earlier to the TAHC, and then, only after i
contacted the Honorable Phyllis Fong and after an act of Congress, this animal
was finally confirmed ;
During the course of the investigation, USDA removed and tested a total of
67 animals of interest from the farm where the index animal's herd originated.
All of these animals tested negative for BSE. 200 adult animals of interest were
determined to have left the index farm. Of these 200, APHIS officials determined
that 143 had gone to slaughter, two were found alive (one was determined not to
be of interest because of its age and the other tested negative), 34 are
presumed dead, one is known dead and 20 have been classified as untraceable. In
addition to the adult animals, APHIS was looking for two calves born to the
index animal. Due to record keeping and identification issues, APHIS had to
trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter
channels, four are presumed to have entered feeding and slaughter channels and
one calf was untraceable.
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.
THE TEXAS MAD COW THAT GOT AWAY 2004
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:
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)...
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
***
Posted by flounder on 03 Jul 2015 at 16:53 GMT
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain
location and PrPsc by PMCA only, how many cases have we missed?
HOUND STUDY
*** AS implied in the Inset 25 we must not _ASSUME_ that transmission of
BSE to other species will invariably present pathology typical of a scrapie-like
disease. ***
snip...
full text ;
Saturday, July 18, 2015
SPONTANEOUS TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD COW
TYPE DISEASE, DOES IT EXIST NATURALLY IN THE FIELD?
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Australia
COMMONWEALTH OF AUSTRALIA Official Committee Hansard SENATE RURAL AND
REGIONAL AFFAIRS AND TRANSPORT REFERENCES COMMITTEE Reference: Import
restrictions on beef FRIDAY, 5 FEBRUARY 2010 CANBERRA BY AUTHORITY OF THE
SENATE
RRA&T 2 Senate Friday, 5 February 2010 RURAL AND REGIONAL AFFAIRS AND
TRANSPORT
[9.03 am]
BELLINGER, Mr Brad, Chairman, Australian Beef Association
CARTER, Mr John Edward, Director, Australian Beef Association
CHAIR—Welcome. Would you like to make an opening statement?
Mr Bellinger—Thank you. The ABA stands by its submission, which we made on
14
December last year, that the decision made by the government to allow the
importation of beef from BSE affected countries is politically based, not
science based. During this hearing we will bring forward compelling new evidence
to back up this statement. When I returned to my property after the December
hearing I received a note from an American citizen. I will read a small excerpt
from the mail he sent me in order to reinforce the dangers of allowing the
importation of beef from BSE affected countries. I have done a number of press
releases on this topic, and this fellow has obviously picked my details up from
the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He
states, and rightfully so:
snip...end
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
We have shown that cattle-adapted TME is the third cattle prion strain
(joining classical and L-type BSE) to be transmissible both to non-human
primates and transgenic mice overexpressing human PrP. However, the successful
transmission of raccoon TME to primate, inducing a disease with similar features
as cattle TME, extends this notion to TME-related strains independent of host
origin. Pathological, biochemical and bioassay investigations converged to
demonstrate the similarity between cattle-adapted TME and L-BSE.
THE SECRET MAD COW POSITIVE TEST, THAT WAS COVERED UP
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform
Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February
2007 to charges of theft of Government funds, mail fraud, and wire fraud. The
owner and his company defrauded the BSE Surveillance Program when they falsified
BSE Surveillance Data Collection Forms and then submitted payment requests to
USDA for the services. In addition to the targeted sample population (those
cattle that were more than 30 months old or had other risk factors for BSE), the
owner submitted to USDA, or caused to be submitted, BSE obex (brain stem)
samples from healthy USDA-inspected cattle. As a result, the owner fraudulently
received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy detailed
critiques and recommendations to both the USDA and the Canadian Food Agency."
end...tss
Saturday, May 26, 2012
Are USDA assurances on mad cow case 'gross oversimplification'?
SNIP...
What irks many scientists is the USDA’s April 25 statement that the rare
disease is “not generally associated with an animal consuming infected feed.”
The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown,
one of the world’s experts on this type of disease who retired recently from the
National Institutes of Health. "(The agency) has no foundation on which to base
that statement.”
“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an
official with the USDA during the Clinton Administration now at Mississippi
State.
In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the
origins of atypical cases of BSE,” she said
The argument about feed is critical because if feed is the cause, not a
spontaneous mutation, the California cow could be part of a larger outbreak.
SNIP...
Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods. *** We recently observed
the direct transmission of a natural classical scrapie isolate to macaque after
a 10-year silent incubation period, ***with features similar to some reported
for human cases of sporadic CJD, albeit requiring fourfold longe incubation than
BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), ***is the
third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the
origin of human sporadic cases. We will present an updated panorama of our
different transmission studies and discuss the implications of such extended
incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases...TSS
===============
who’s kidding whom $$$ i.e. USDA INC AND THE OIE
2014
***Moreover, L-BSE has been transmitted more easily to transgenic mice
overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
***It has been suggested that some sporadic CJD subtypes in humans may
result from an exposure to the L-BSE agent.
*** Lending support to this hypothesis, pathological and biochemical
similarities have been observed between L-BSE and an sCJD subtype (MV genotype
at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and
another sCJD subtype (MM genotype) [15].
snip...
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC)
recently delivered a scientific opinion on any possible epidemiological or
molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far
*** but the possibility that a small proportion of human cases so far
classified as "sporadic" CJD are of zoonotic origin could not be excluded.
*** Moreover, transmission experiments to non-human primates suggest that
some TSE agents in addition to Classical BSE prions in cattle (namely L-type
Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME)
and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
*** Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
*** These atypical BSE cases constitute an unforeseen first threat that
could sharply modify the European approach to prion diseases.
Second threat
snip...
Thursday, January 15, 2015
41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE
Prion: Case Report
Subject: *** Becky Lockhart 46, Utah’s first female House speaker, dies
diagnosed with the extremely rare Creutzfeldt-Jakob disease aka mad cow type
disease
what is CJD ? just ask USDA inc., and the OIE, they are still feeding the
public and the media industry fed junk science that is 30 years old.
why doesn’t some of you try reading the facts, instead of rubber stamping
everything the USDA inc says.
sporadic CJD has now been linked to BSE aka mad cow disease, Scrapie, and
there is much concern now for CWD and risk factor for humans.
My sincere condolences to the family and friends of the House Speaker Becky
Lockhart. I am deeply saddened hear this.
with that said, with great respect, I must ask each and every one of you
Politicians that are so deeply saddened to hear of this needless death of the
Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am
seriously going to ask you all this...I have been diplomatic for about 17 years
and it has got no where. people are still dying. so, are you all stupid or
what??? how many more need to die ??? how much is global trade of beef and other
meat products that are not tested for the TSE prion disease, how much and how
many bodies is this market worth?
Saturday, January 17, 2015
*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed
with the extremely rare Creutzfeldt-Jakob disease
Sunday, December 14, 2014
*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD
strains, TSE prion aka Mad Cow Disease United States of America Update December
14, 2014 Report ***
*** HUMAN MAD COW DISEASE nvCJD TEXAS CASE NOT LINKED TO EUROPEAN TRAVEL
CDC ***
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
in June 2014 confirmed as USA case NOT European ***
the patient had resided in Kuwait, Russia and Lebanon. The completed
investigation did not support the patient's having had extended travel to
European countries, including the United Kingdom, or travel to Saudi Arabia. The
specific overseas country where this patient’s infection occurred is less clear
largely because the investigation did not definitely link him to a country where
other known vCJD cases likely had been infected.
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
12:50 PM
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