TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE Prion Testing
Thursday, September 24, 2015 TEXAS
Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE Prion
Testing
News Release Media Contact: Steve Lightfoot, 512-389-4701,
steve.lightfoot@tpwd.texas.gov
Sept. 23, 2015
Hunters Asked to Submit Samples for CWD Testing TPWD Steps Up Free-Ranging
Deer Disease Surveillance
AUSTIN — With the recent discovery of Chronic Wasting Disease (CWD) in two
captive deer breeding facilities in south-central Texas, the Texas Parks and
Wildlife Department will be stepping up efforts to strategically sample hunter
harvested deer at a greater level during the 2015-16 hunting season.
Hunters are encouraged to assist with this statewide monitoring effort by
voluntarily submitting samples this fall. TPWD biologists will collect and
submit samples to the Texas A&M Veterinary Diagnostic Lab at no cost to the
hunter. Tissue samples from the heads of harvested deer must be collected within
24 hours of harvest, up to 48 hours if kept chilled. It is very important that
the deer head not be frozen.
Since 2003, TPWD biologists have been monitoring the state’s free-ranging
deer population for CWD. Using statistical sampling tables commonly used by
animal disease experts, biologists set a sampling goal that would detect the
disease with 95 percent confidence if at least one out of every 100 deer was
infected. Thus far, biologists have collected nearly 30,000 samples from
hunter-harvested deer across Texas’ eight ecological regions, in most cases
surpassing 95 percent confidence standards. To date, CWD has not been found in
Texas free-ranging white-tailed deer.
The sampling strategy for the 2015-16 hunting season is being refined to
target disease risk levels within the state’s 33 unique Resource Management
Units (RMU); wildlife conservation areas that TPWD uses for all other deer
management decisions. Criteria for establishing risk levels include factors such
as deer density, susceptible species importation history, proximity to a
CWD-positive site, etc.
Sampling goals will rely upon hunter harvest submissions ranging from 60 to
433 (lowest to highest risk) deer for each RMU, and if biologists can achieve
these goals, will result in excess of 7,000 samples. TPWD will also specifically
target sampling efforts within a 5-mile radius around the CWD index facility in
Medina County to determine the prevalence and geographic extent of the disease
in that specific area.
“In the wake of our increased concern about CWD we are ramping up our
sampling effort state wide,” said Mitch Lockwood, TPWD Big Game Program
Director. “We will be collecting samples from deer and elk, and other cervid
species, in every county where deer hunting occurs.”
Hunters wishing to submit samples can go online to find their local TPWD
biologist, listed by county at http://tpwd.texas.gov/landwater/land/technical_guidance/biologists/
. The biologist will provide a sample receipt hunters can use to track test
results online. TPWD anticipates test results could take 3-4 weeks to process.
In some cases, biologists may request to retain the entire deer head for later
sample collection; a resource document will be given to the hunter as proof of
sex in those instances.
More information about CWD, including safe carcass handling tips and
precautions, can be found online at http://tpwd.texas.gov/huntwild/wild/diseases/cwd/.
SL 2015-09-23
*** I cannot stress enough to all of you, for the sake of your family and
mine, before putting anything in the freezer, have those deer tested for CWD.
see video and latest transmission studies and warnings below. ...terry
State seeks help from hunters in monitoring deer disease
By Shannon Tompkins
Updated 8:40 pm, Saturday, September 26, 2015
In the wake of the discovery this summer of chronic wasting disease (CWD)
in captive white-tailed deer in two fenced deer breeding/production operations
in Texas, state wildlife officials are expanding a long-running program aimed at
monitoring the state's free-ranging whitetail herd for the fatal, untreatable,
transmissible neurological disease.
In addition, the state's 700,000-plus deer hunters are being asked to aid
in that effort by volunteering tissue samples from whitetails they take during
the 2015-16 hunting season.
That season begins Saturday with the statewide opening of archery-only
hunting for whitetails and the opening of whitetail season on many tracts
enrolled in Texas' Managed Lands Deer Permit program. The general whitetail deer
hunting season opens statewide Nov. 7.
"We've had a very robust CWD sampling program of hunter-harvested deer for
years; we've collected and tested almost 30,000 samples," Mitch Lockwood,
director of big-game programs for Texas Parks and Wildlife Department, said,
noting none of the samples from free-ranging whitetails has been positive for
the degenerative disease that has proven transmissible among cervids such as
deer and elk but has not been shown to be a health risk to humans. "This year,
we're going to be doing more than we've done before. We'll be collecting samples
from every area, but concentrating on getting larger numbers of samples from
areas where assessments indicate risk levels are higher."
7,600 samples targeted
Those higher-risk areas include counties where the two captive deer
operations are located (Medina and Lavaca) and those around the 46 sites where
deer tied to the Medina County breeding operation were released, Lockwood said.
Under the expanded program, TPWD has set an overall target of collecting
tissue samples from 7,600 free-range whitetails. The state's previous sampling
regime for free-range whitetails produced a statistical confidence level of 95
percent based on a goal of determining if CWD was present in as few as 1 percent
of the deer population. The new sampling program will provide a confidence level
of 99 percent or higher, Lockwood said.
Those samples will come from hunters who voluntarily offer TPWD biologists
the opportunity to remove tissue from the brain of whitetails the hunters take.
The most reliable and, currently, only certified test for CWD, which evidence
indicates is caused by a prion (abnormal protein) that triggers
neurodegeneration resulting in progressive deterioration of the infected animal,
involves testing tissue from the brain.
Coordination is key
Under the plan, hunters who want to participate in the program will be
asked to coordinate tissue collection though TPWD wildlife division staff in the
area they hunt. Ahead of this deer season, TPWD biologists in some areas of the
state already have been working with landowners and deer hunters to arrange
tissue collection from successful deer hunters, Lockwood said. In other areas,
hunters wanting to participate will be asked to contact their local TPWD
wildlife biologist; the agency's website, tpwd.texas.gov, includes names and
contact information of TPWD wildlife biologists, by county.
Also, Lockwood said, the agency plans to include on its website an icon
hunters can click to see a schedule of when and were TPWD biologists will be
stationed at local deer processing businesses or other public locations where
hunters can bring their deer for tissue sample collection.
The agency plans to set up check stations in Hondo and Bandera, towns
nearest the site of the Medina County deer breeding/production operation, where
the first CWD-positive whitetail found in Texas was documented in June and three
more deer subsequently were confirmed infected with the transmissible spongiform
encephalopathy. Those two check stations will be staffed each day from
mid-October through January, Lockwood said.
No cost to hunters
The sampling program is strictly voluntary, Lockwood said, and no fee will
be charged hunters who offer their deer for sampling. Samples must be collected
within 24 hours of the deer being taken, 48 hours if the carcass is kept
refrigerated. In most cases, biologists will be able to relatively quickly
remove the tissue and the hunter can take the entire animal. But in some cases,
biologists will ask that the hunter allow them to retain the deer's entire head.
In those cases, the hunter will be given a document legally necessary as proof
of the deer's sex, required until the deer reached the hunter's home or a deer
processing business.
The hunter, who will be asked to provide contact information and location
where the deer was taken, also will be given a receipt that includes an ID
number for the sample. Samples will be sent to the Texas A&M Veterinary
Diagnostic Lab and results, which could take three to four weeks to process,
will be posted online where the hunter can access them.
Lockwood said he is optimistic the sampling will not find CWD-positive
individuals in the state's free-ranging whitetail herd - the nation's largest at
almost 4 million animals.
"I'm really hoping not to find it. I'm not expecting to find it in the
free-ranging whitetail herd," he said, adding the agency has developed response
plans should a CWD-positive free-range whitetail be found.
Texas has some experience dealing with CWD. In 2012, CWD was detected in a
free-ranging mule deer in the Hueco Mountains of far West Texas. That deer and
eight subsequent CWD-positive mule deer found in the same area are believed to
have contracted the disease from CWD-positive mule deer in southern New Mexico.
TPWD and Texas Animal Health Commission response was to adopt regulations
restricting movement of deer, elk, and other susceptible species within or from
a "containment" zone around the isolated area, and enhance surveillance efforts.
Texas is one of 23 states and two Canadian provinces where chronic wasting
disease has been found in either captive-held or free-range cervids such as
whitetail, mule deer and elk.
The disease can take months or years to manifest, is progressive and in its
later stages often results in significant loss of weight and body condition.
CWD has not proven transmissible to humans. But the World Health
Organization and the U.S. Centers for Disease Control and Prevention recommend
not consuming meat from infected animals.
*** I cannot stress enough to all of you, for the sake of your family and
mine, before putting anything in the freezer, have those deer tested for CWD.
see video and latest transmission studies and warnings below. ...terry
Wednesday, November 07, 2012
Chronic Wasting Disease CWD, Texas, Houston Chronicle Shannon Thomkins 1998
- 2012 what happened ???
From: Terry S. Singeltary Sr.
Sent: Sunday, August 26, 2012 11:19 AM
To: Shannon.Tompkins@chron.com
Cc: news@chron.com ; sports@chron.com ; viewpoints@chron.com ;
readerrep@chron.com ; lbagley@hearst.com ; jblumencranz@hearst.com ;
pmurphy@hearst.com ; jloughlin@hearst.com
Subject: Chronic Wasting Disease CWD, Texas, Houston Chronicle Shannon
Thomkins 1998 - 2012 what happened ???
Greetings,
I am amazed, and concerned, that the Houston Chronicle can put out a
complete paper magazine addition in the Sunday Paper about Deer Hunting in Texas
(and other hunting) Sunday 25, 2012, (32 pages), promoting it, ‘’come on down,
the water is fine” type mentality, but yet not mention a word of the fact that
after trying to hide CWD for a decade, by not testing properly, and only after
having New Mexico force Texas to finally test in the very place I told TAHC and
Shannon Thomkins and the Houston Chronicle some 10 years ago, and every year
there from, to date, they finally documented CWD, yet not a word, NOT A WORD
from the chronicle in this magazine about it. I find that very deceiving, and
very disturbing, that the Houston Chronicle and Shannon Thomkins, when in comes
to TEXAS and CWD, I find it very disturbing that you have decided to stick you
head in the sand, look the other way, and ignore this. that’s why we are in this
mess, TSE prion disease. Mr. Thomkins wrote a few good articles in the past,
when CWD was NOT documented in Texas, but where is your pen at now Mr. Thomkins,
when we finally are forced into documenting it ??? where is your pen now Sir ???
you are a prized and honored author of the wild, where is your ink now Sir, when
we need it the most? you may think ehd is more concerning than the TSE prion
disease CWD, but I can assure you, don’t let the incubation period, and the fact
of transmission between species, and the lateral transmission, environmental
factors, I can assure you, you will only fool yourself and your readers. they
are both deadly diseases.
A huge difference the type ink you have now Sir, when the shoe is on the
other foot, compared to years past, when Texas was one of the elites i.e. had
the gold card, i.e. CWD free. same as with BSE aka mad cow, everything was just
fine, as long as the other states, countries had it, but when the shoe was put
on the other foot there, my oh my, how things changed then.
it’s all about money, and that is what keeps spreading this damn disease
i.e. the TSE prion mad cow type disease.
I think (my opinion), you have done a great harm to your readers, by making
lite of the cwd recently discovered in Texas, and this recent magazine shows it.
It would have been a great opportunity to educate your readers, and even a word,
let alone a sentence, or maybe even a whole paragraph, wow, would that have been
nice, I know a complete page would have been too much$
big difference here in Texas when the TSE prion shoe is on the other foot.
...
Brain-eating disease found in Texas deer
By Shannon Tompkins Updated 5:47 a.m., Wednesday, July 11, 2012
Two mule deer taken recently from west Texas tested positive for Chronic
Wasting Disease, the first time the invariably fatal illness affecting deer and
other cervids has been documented in Texas, adding urgency to proposals by
wildlife and animal health officials to prohibit or severely restrict movement
of susceptible animals from that corner of the state.
"This is definitely not a crisis," Clayton Wolf, wildlife division director
for Texas Parks and Wildlife Department, said of the confirmation Monday from
the National Veterinary Services Laboratories that two of 31 mule deer shot
along the Texas/New Mexico border were infected with the incurable disease which
can be spread to other cervids. The wildlife agency shot the animals as part of
a plan monitoring the disease.
The agency and the Texas Animal Health Commission want to impose
regulations aimed at minimizing risks of the disease spreading to other parts of
Texas. The commission in June proposed regulations establishing a "containment
zone" covering El Paso County and portions of Hudspeth and Culberson counties
and a "high-risk zone" covering portions of Culberson and Reeves counties from
which movement of privately-owned cervids susceptible to the disease would be
prohibited or restricted. The deer that tested positive were taken from the
Hueco Mountains in El Paso and Hudspeth counties.
The wildlife agency plans later this month to officially propose similar
rules which would cover movement of wild deer or captive deer held under agency
permits.
http://www.chron.com/news/houston-texas/article/Brain-eating-disease-found-in-Texas-deer-3697731.php
what a difference a decade makes. seems to be different kind of ink. I know
the science has not found anything to change the CWD TSE prion agent, and risk
factors there from, only that it’s in Texas now. ...
Tompkins: There are a lot of reasons to be concerned about CWD
SHANNON TOMPKINS, Copyright 2002 Houston Chronicle Published 5:30 a.m.,
Thursday, March 14, 2002
Today, most Texas deer hunters probably yawn at the mention of Chronic
Wasting Disease. After all, the number of wild deer documented as killed,
nationwide, by the unusual malady probably is less than annually are crushed by
tractor-trailer rigs scorching Interstate 10 between Kerrville and Fort
Stockton.
And, so far, no cases of the fatal, incurable, communicable,
brain-destroying cervid disease have been documented in Texas.
What's so bad about a little-understood disease responsible for the death
of scattered pockets of deer in a handful of Rocky Mountain states?
If Texas' deer herd survived screwworms and can thrive despite endemic
bluetongue and anthrax and even the constant gnawing away of habitat, then why
worry about a little Chronic Wasting Disease?
There is abundant reason to be concerned.
CWD carries potential for incredible impacts on Texas' 4 million deer, its
half-million deer hunters, the hunting-based economy of rural areas and private
landowners and even the future of the state agency responsible for overseeing
those deer and all other natural resources.
Just how seriously many Texas wildlife managers and those with economic or
other interest in deer take the CWD threat was manifestly evident over the past
week.
In the wake of news that Wisconsin officials had discovered CWD in three of
26 wild deer taken by hunters in a small area of that state, Katharine Armstrong
Idsal, presiding officer of the Texas Parks and Wildlife Commission, called an
emergency meeting of the TPW Commission to address the issue of deer importation
into Texas.
A proposal to suspend all imports of deer into Texas was, and is, on the
TPW Commission's agenda for its scheduled April 4 meeting, with the
recommendation having been triggered by discovery over the past few months of
CWD in wild deer in Nebraska and South Dakota.
The emergency TPW Commission meeting was arranged Friday, the day the Texas
Wildlife Association, a politically active, landowner-based organization, sent
to the governor, members of the Legislature and the TPW Commission a resolution
calling for sealing the state's borders to deer imports because of the chance
some might be carrying CWD.
At the TPW Commission's hastily called Monday meeting, the group approved
and adopted an emergency rule prohibiting importation of white-tailed and mule
deer into Texas.
That emergency rule, which is effective for 45 days, took effect Tuesday.
It is the first time the TPW Commission has used its emergency rule-making
authority.
Justifications for the emergency action were laid out in the preamble to
the regulation change. CWD, the document states, "constitutes a direct threat to
wild deer populations in Texas and therefore to the multi-billion dollar hunting
industry, as well as a potential threat to human health, safety and welfare."
To understand the threat to deer and, perhaps, public health and the
subsequent potentially devastating impact on Texas' deer-based economy, it's
necessary to understand CWD.
CWD is one of a group of transmissible spongiform encephalopathies (TSE)
diseases that destroy brain cells. Triggering the destruction is a prion, an
abnormal form of protein. The prion mutates normal cellular protein into the
abnormal form.
This "eats away" at the brain and damages an infected animal's ability to
maintain normal functions such as converting food and body fat to energy.
Animals suffering from CWD begin wasting away as their body tries to
convert protein to energy, a very inefficient process.
Eventually, the animal loses motor control and even goes blind, giving rise
to the pitiful "blind staggers" seen in livestock suffering from CWD's close
relative, Bovine Spongiform Encephalopathy, better known as "Mad Cow Disease."
Death is inevitable and horrible.
Scientists know relatively little about CWD.
"We don't really know what triggers it. Does the prion create the disease
or does the disease create the prion?" said Jerry Cooke, game mammal branch
chief of the Texas Parks and Wildlife Department's wildlife division. "What we
do know is that it is transmissible to other cervids."
First documented in the 1960s in penned herds in Colorado, CWD "jumped"
into the wild cervid population there, being confirmed in wild deer and elk in
the 1980s.
A common suspicion is that CWD is a mutated form of "scrapie," a TSE long
confined to sheep.
There is some evidence that the cervids in the Colorado pen where CWD was
first documented were fed protein feeds containing sheep parts and that those
parts could have contained brain material infected with scrapie.
One of the scrapie-triggering prions might have mutated just enough to
break the molecular barrier of a deer's brain cell, and the disease was off and
running.
Scientists are convinced CWD is spread by close contact between uninfected
and infected animals. That can happen between animals in a pen or behind a
fence, or by nose-to-nose contact between deer or elk inside the fence and those
outside the enclosure.
From Colorado, CWD spread throughout the northwest corner of the state into
wild herds in Wyoming and Nebraska.
Its spread was accelerated over the past decade by a burgeoning market in
deer and elk triggered by elk farming and deer ranching.
Thousands of deer and elk are bought and transported each year, most to
penned facilities where they are either raised for food or, in the case of
white-tailed deer, used in an effort to produce bucks with large antlers to feed
a market in trophy hunting.
To test for CWD, brain tissue is needed. And such tissue samples can be
obtained only if the animal is dead.
Plus, getting rid of the disease has proved difficult, if not impossible,
even in penned facilities.
In at least one case, a penned facility holding CWD-infected deer was
"depopulated" (the animals slaughtered and destroyed) and the site left with no
animals for three years.
When uninfected deer were placed in the pens, they contracted CWD.
As deer and elk from areas with CWD have been traded and transported across
the nation, they have brought the disease with them
Currently, CWD-infected, free-ranging deer have been confirmed in Colorado,
Nebraska, Wyoming, South Dakota and Wisconsin, plus the Canadian province of
Saskatchewan.
CWD has been found in captive herds in Saskatchewan, Colorado, South
Dakota, Nebraska, Kansas, Oklahoma and Montana.
Texas has been a big player in the deer trade over the past decade, as
hundreds of deer-breeding facilities have sprung up in the state to feed the
interest in building bucks with bigger antlers.
Today, more than 450 individuals in Texas hold a TPWD-issued "scientific
breeder permit" allowing them to manipulate deer. Some of these breeders and
other landowners over the past four years have imported 2,107 deer from outside
Texas.
Because deer can be traded so often -- a deer may be sold as a fawn in
Nebraska to a broker in Missouri who sells it to a breeder in Pennsylvania who
sells it to a landowner in Texas -- it often is nearly impossible to determine
the provenance of individual animals.
Whether any of the thousands of deer imported into Texas over the past
decade carried CWD remains an unsettling question.
Texas has no CWD-testing program for wild deer and only a voluntary program
for elk and other animals under the jurisdiction of the Texas Animal Health
Commission.
"Ten years ago, elk and deer (imported into Texas) were not regulated at
all," said Dr. Ken Waldrup, an epidemiologist with the Texas Animal Health
Commission and one of the agency's point men on CWD. "If Texas doesn't already
have CWD, then I say that proves that God is a Texan.
"For everyone's sake, I sure hope He is."
CWD has not been proved to be transmissible to any animal other than deer
and elk.
But that was the original thought with BSE, which did "jump" into humans
who ate BSE-infected meat in Europe and contracted Creutzfeldt-Jakob Disease
(CJD), the human form of TSE. CJD, like CWD and BSE, is fatal, incurable and
untreatable. It is blamed for at least 80 deaths in Europe.
While there is no proof CWD can jump to humans, there is no absolute proof
it can't if given enough opportunities.
And that issue scares wildlife managers.
If CWD shows up in a deer herd and the deer-hunting public gets spooked
about the possibility -- no matter how tiny -- that by cleaning or eating a deer
they will contract CJD and face a certain and horrible death, they could, en
masse, abandon deer hunting.
This could destroy the $2 billion-plus deer hunting economy in Texas.
Also, if deer hunters abandon their recreation, natural resource agencies
such as TPWD, which depend almost entirely on hunting license fees to fund their
diverse wildlife programs, would be maimed, perhaps mortally.
"It's not the immediate impact on the deer herds that (is) the most
frightening thing about CWD," Waldrup said. "It's the secondary impacts that are
really scary.
"People better just pray it doesn't show up here. If it does, things could
get very ugly."
Shannon Tompkins covers the outdoors for the Chronicle. His column appears
Thursdays, Fridays and Sundays.
now, don’t get me wrong Mr. Thompkins, you have written some great articles
on the wild and on the fisheries.
snip...tss
but Mr. Thomkin Sir, you have written some great articles. a few here ;
Sunday, November 30, 2008
Commentary: Crimes hurt essence of hunting
Commentary on Houston Chronicle article [below] by Dr. Thomas Pringle
From: tom@cyber-dyne.com
Date: Fri, 10 May 2002 11:03:29 –0800
To: shannon.tompkins@chron.com
Subject: nice cwd reporting Shannon,
My compliments on these superb CWD Houston Chronical articles: not mincing
words, they display an excellent -- and most rare -- journalistic understanding
of the origin and continuing spread of CWD. (A couple of technical points were
not quite on target, see bottom.)
It is really refreshing to see in print the probable origin as sheep
scrapie-to-penned cervids in 1967 at Foothills Research Station, after decades
of relentless PR out of Colorado DOW seeking to distance itself from
responsibility (and liability). Facility workers at Colorado Dept of Wildlife
commented on the similarity to scrapie already in 1967 but never autopsied any
of their many dead research animals until 1979, discovering immediately an
obvious spongiform encephalopathy.
By that time of course, release to the wild and transfer of surplus animals
to zoos, game farms, and sister facilities had seeded widespread dissemination
of the disease. This was subsequently aggravated by the explosive growth in game
farms and intra- and inter-state cervid shipping, which at industry insistence
was in essence unregulated (eg regulated by state ag dept boosters). It is not
just the shoot-deer-in-a-barrel industry --elk velvet nutriceutical was never
tested by anyone for abnormal prions despite its troublesome composition (the
market collapsed from live CWD exported to Korea).
DOW itself did nothing to change its practises or control the disease until
very recently. Only last year, in the face of published evidence [below] that
the disease is expected to transfer to humans at the same low efficency as BSE
(129 human deaths to date), did they back off from encouraging human consumption
of venison from the endemic area. Nebraska fish and game even offered a
deer-neck stew recipe on its web site, even though spinal cord was long known to
have high infectious titres.
State fish and game depts are basically unfenced game farms. They have a
commercial concession that allows them earn a salary from sale of antler tags.
This motivates them to set up winter feeding stations, watering holes, salt
blocks, control predators, fight CWD testing, anything and everything that
increases numbers and leads to more or continued sales. Unfortunately, practises
leading to high cervid concentrations and testing avoidance are highly conducive
to the spread of CWD.
States such as Montana require testing of every game farm cervid dead for
any reason and an accounting of each animal's provenance and disposition; other
states adopt a "don't look, don't find" policy of testing avoidance with no
monitoring whatsoever of facilities. Absence of evidence is not evidence of
absence when it comes to TSEs. This disease just does not go away on its own, be
it kuru in New Guinea or scrapie in the US.
Given the numbers of Texas game farms, massive importation statistics, and
the high likelihood of trace-backs to affected facilities, it would be most
surprising if CWD were not already entrenched in Texas along the lines of
Wisconsin. It really questionable if stonewalling really is in the industry's
best interest -- who is going to hunt in a state that fears to test? The longer
infectious foci are allowed to operate, the greater the probability of multiple
introductions into wild deer. To ban imports (only after everyone has finished
importing all they want) just locks the barn door after the horse is long gone.
Half-measures on prion diseases are worse than no measures because they put
off the day of reckoning while exacerbating it immensely. Wisconsin's hasty
policy of culling 15,000 wild deer, yet business as usual (no testing, no
trace-backs, no inspection, no recordkeeping, no culls) at its sacrosanct 535
game farms. will result in CWD in perpetuity. The focus is on temporary
abatement for purposes of hunter reassurance. Dr. Charles Southwick
southwic@stripe.colorado.edu is a good source of scientific information on cwd
control strategies.
A few technical notes. First, the word mutation is reserved for genetic
change affecting DNA. It is not applicable to mere protein conformational
changes and fibril formation seen in amyloid diseases such as Alzheimer and CWD.
Mutation has been ruled out in CWD amplification. The prion gene of hundreds of
CWD and non-CWD animals have been sequenced by Dr. O'Rourke at Pullman. There is
no counterpart to the mutations that cause 15% of human CJD, much to the
disappointment of DOW.
No TSE has ever been seen in natural populations of any wild animal
anywhere in the world, making Colorado's story of a natural pocket (by
coincidence located adjacent to Foothills and Sybille research stations) a bit
far-fetched. Now by golly another natural pocket has flared up next to a game
farm in Wisconsin. How about the supposed natural pocket adjacent to the
massively infected game farm in the Black Hills -- despite its import history,
the industry PR firm in Ketchum turned this around 180 degrees -- now it's the
wild animals infecting innocent game farms!?! There has invariably been a nexus
to intensive livestock operations, be that cows fed rendered cows, mink farms
fed downer cows or deer quartered in a scrapie research facility.
Second, the "best available scientific evidence" upon which public policy
is normally based (more studies are needed, they always are, but something must
be used for the interim) is that published by Byron Caughey's group at Rocky Mtn
labs (after two years of delay by co-author Mike Miller of DOW who controlled
sample access). A proxy test was used since human volunteers cannot be
considered. Transmission efficiencies to human were similar to BSE -- low, but
hardly reassuring given England's experience.
Third, CWD has already been experimentally transferred to 6-7 species
including rodents, primates, and bovids, as published in peer-reviewed
scientific journals. The first round of transmission can be inefficient in TSEs;
after that, no species barrier. It is really the human-to-human second round
(plasma donation, childhood vaccines, cornea transplants) that has cause the
greatest consternation in England. A Ft. Collins hunter/blood donor with
preclinical cwd-induced CJD would have no idea he is ill.
It is currently impossible to test humans for cwd-induced CJD because there
is no known signature. Rises in baseline CJD cannot be monitored, contrary to
CDC, because of very large numbers of missed diagnoses, swings in ascertainment
effort, and diagnostic changes.
Best wishes and keep up the good work! Tom
Dr. Thomas Pringle Sperling Biomedical Foundation 3295 Kincaid St. Eugene,
OR 97405
CWD archives
Wisconsin latest to be hit by deer brain disease
May 10, 2002
The Houston Chronicle by Shannon Tompkins
Wisconsin drew the black bean in the continent's expanding war with chronic
wasting disease, and that simple twist of fate promises to be expensive and
painful for the state's deer and human populations. It also serves as a sobering
study for Texas in what can happen when the poorly understood but invariably
fatal brain disease shows up in a state's wild deer herd.
Just three months after CWD was documented in a handful of white-tailed
deer taken by hunters in southwestern Wisconsin, the state is preparing to kill
thousands of deer; Gov. Scott McCallum is calling for a special session of the
state Legislature to address the issue; politicians are asking for millions of
dollars to fight CWD spread; and the hunting-based economies of the region are
preparing to take a stunning blow.
Add to that the uncertainty many of Wisconsin's 700,000 deer hunters are
expressing about the safety of eating venison, and you have the future of that
state's deer and deer hunting hanging in the balance. CWD is a recently
discovered transmissible spongiform encephalopathy that affects deer and elk. It
is similar to the TSE that causes "mad cow disease" in livestock, and which in
Europe "jumped" from infected livestock to humans as a variation of the TSE
Creutzfeldt-Jakob disease in humans.
The disease manifests itself via prions, or mutant proteins, which cause
deterioration of brain cells. The effects include loss of weight and muscle
control, blindness and dementia. There is no treatment and the disease is fatal.
CWD has been proved transmissible between deer and elk, but it has not been
shown to be transmittable to humans. But neither has it been proved
non-transmittable. The possibility, however minuscule, exists that a human could
contract the fatal disease.
Since it was discovered in 1967 in wild deer in the northeast corner of
Colorado, CWD has been a mystery. How it came to exist remains a question, but
the most accepted theory is that it is a mutation of a TSE called "scrapie"
found in sheep. A Colorado research facility that housed sheep, deer and elk in
close contact is assumed to have been the genesis of CWD.
The disease for most of the past three decades seems to have remained
localized in a small area of Colorado.
Interstate trade in "farmed" live elk and deer, some of which were infected
with CWD, is assumed to have begun the diseases' spread to other states.
CWD has been identified in a half-dozen states and a couple of Canadian
provinces, almost always associated with penned elk or deer.
The discovery of CWD in three wild deer in Wisconsin during a routine
sampling of hunter-taken animals stunned most wildlife scientists and managers.
The disease never had been documented east of the Mississippi River, and
never in an area where deer densities are as high as they are in Wisconsin.
The closest CWD cases were more than 900 miles from Wisconsin.
The discovery triggered a rush of states closing their borders to
importation of deer and elk.
Texas, which has for years been one of the major players in live deer and
elk traffic, shut its borders to all importation of deer and elk within a couple
of weeks of the Wisconsin discovery.
Wisconsin officials began addressing the issue by killing and testing 516
deer in the area that produced CWD-infected animals. (There is no certified
live-animal test for CWD; animals must be killed and brain or brain stem tissue
analyzed to document infection.)
When 11 of those 516 deer proved infected with CWD, the state's Department
of Natural Resources and politicians knew they had a severe problem.
In an effort to prevent the spread of CWD, Wisconsin wildlife officials are
proposing to kill every deer in a 287-square-mile (about 184,000 acres) area
where the infected deer have been found.
That will involve killing 14,000-15,000 deer, officials estimate.
Just how that will be accomplished remains a question. But the slaughter
almost certainly will begin next month.
CWD has become a white-hot political issue in the state, where fingers are
being pointed at agriculture officials who disregarded warnings about the
possibility of CWD-infected deer being brought into the state.
McCallum said this week he will call a special session of the state's
Legislature to address CWD-related issues such as regulation of feeding wild
deer, a practice that crowds deer together and is suspected of making it easier
for CWD to spread.
The Wisconsin Legislature has approved spending $ 4.4 million this year to
fight CWD. Officials say they need at least $ 22.5 million over the next three
years to contain CWD.
McCallum is asking the federal government for $ 18.5 million.
At least Wisconsin knows it has a CWD problem, and is addressing it. Other
states, including Texas, probably have CWD-infected deer within their borders.
But because they do no testing for the disease, they have no evidence of
its presence.
Other states are beginning to fashion CWD testing programs, though.
Iowa, which abuts the southwest corner of Wisconsin where the CWD-infected
deer have been found, this week announced it will begin collecting brain tissue
samples from road-killed deer and submitting them for CWD testing.
Iowa officials said they hope to collect 100-200 road-killed deer for
sampling each month.
Texas has no CWD testing program.
But the Texas Deer Association, a trade group representing many of the
state's 400-plus state-permitted deer and elk ranches, this past month promised
to put together a voluntary CWD monitoring program in cooperation with the Texas
Parks and Wildlife Department and Texas Animal Health Commission.
If the voluntary program is not accepted by TPWD and TAHC, the agencies
could issue regulations for mandatory CWD testing.
The issue will be discussed at May 29-30 TPW Commission meetings in Austin.
============end============
Mr. Thomkins, and Houston Chronicle, I think your disregard for concern
NOW, at least the same concern now, than you had back when the CWD TSE prion
disease was not on the other foot, I think your silence is deafening now, and
very disturbing, and is doing an injustice to your readers.
I wasted 12 years trying to get them to test, where New Mexico forced them
to test, i.e. White Sands Missle range side of Texas, and there about. course, I
did the same with mad cow disease too. to no avail. $$$
2001 – 2002
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...TSS
===============================
2005
SEE MAP OF CWD ON THE BORDER OF NEW MEXICO VERY CLOSE TO TEXAS ;
NO update on CWD testing in Texas, New Mexico that i could find. I have
inquired about it though, no reply yet...
-------- Original Message --------
Subject: CWD testing to date TEXAS ?
Date: Mon, 09 May 2005 12:26:20 –0500
From: "Terry S. Singeltary Sr."
Hello Mrs. Everett,
I am most curious about the current status on CWD testing in Texas. could
you please tell me what the current and past testing figures are to date and
what geographical locations these tests have been in. good bust on the illegal
deer trapping case. keep up the good work there.........
thank you, with kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
-------- Original Message --------
Subject: CWD testing in New Mexico
Date: Mon, 09 May 2005 14:39:18 –0500
From: "Terry S. Singeltary Sr."
To: ispa@state.nm.us
Greetings,
I am most curious of the current and past CWD testing in New Mexico, and
there geographical locations...
thank you,
Terry S. Singeltary SR. CJD Watch
#################### https://lists.aegee.org/bse-l.html
####################
2006
----- Original Message -----
From: "Terry S. Singeltary Sr." flounder9@VERIZON.NET
To: BSE-L@aegee.org
Sent: Saturday, December 23, 2006 1:47 PM
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing
sampling figures -- what gives TAHC ???
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing
sampling figures -- what gives TAHC ???
Date: December 23, 2006 at 11:25 am PST
Greetings BSE-L members,
i never know if i am going crazy or just more of the same BSe. several
years ago i brought up the fact to the TAHC that CWD was literally at the Texas
borders and that the sample size for cwd testing was no where near enough in the
location of that zone bordering NM. well, i just wrote them another letter
questioning this again on Dec. 14, 2006 (see below) and showed them two
different pdf maps, one referencing this url, which both worked just fine then.
since then, i have NOT received a letter from them answering my question, and
the url for the map i used as reference is no longer working? i had reference
this map several times from the hunter-kill cwd sampling as of 31 August 2005
pdf which NO longer works now??? but here are those figures for that zone
bordering NM, for those that were questioning the url. the testing samples
elsewhere across Texas where much much more than that figure in the zone
bordering NM where CWD has been documented bordering TEXAS, near the White Sands
Missile Range. SO, why was the Texas hunter-kill cwd sampling as of 31 August
2005 document removed from the internet??? you know, this reminds me of the
infamous TEXAS MAD COW that i documented some 7 or 8 months before USDA et al
documented it, when the TAHC accidentally started ramping up for the
announcement on there web site, then removed it (see history at bottom). i am
not screaming conspiracy here, but confusious is confused again on the ciphering
there using for geographical distribution of cwd tissue sample size survey, IF
they are serious about finding CWD in TEXAS. common sense would tell you if cwd
is 35 miles from the border, you would not run across state and have your larger
samples there, and least samples 35 miles from where is what
found..........daaa..........TSS
THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of
Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare
to the other sample locations ;
snip...see full text ;
here are a few of my pleas to the TAHC about CWD waltzing into Texas for
over a decade.
see history of my failed attempts to get the TAHC to start testing for CWD
in far west Texas started back in 2001 – 2002 ;
Saturday, July 07, 2012
TEXAS Animal Health Commission Accepting Comments on Chronic Wasting
Disease Rule Proposal
Considering the seemingly high CWD prevalence rate in the Sacramento and
Hueco Mountains of New Mexico, CWD may be well established in the population and
in the environment in Texas at this time.
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
snip...see full text ;
P.97: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum
Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and
Robert Kunkle1 1National Animal Disease Center; Ames, IA USA; 2Iowa State
University; Ames, IA USA
The purpose of this work was to determine susceptibility of white-tailed
deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to
that of the original inoculum and chronic wasting disease (CWD). We inoculated
WTD by a natural route of exposure (concurrent oral and intranasal (IN); n D 5)
with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc
accumulation. PrPSc was detected in lymphoid tissues at preclinical time points,
and deer necropsied after 28 months post-inoculation had clinical signs,
spongiform encephalopathy, and widespread distribution of PrPSc in neural and
lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular
profiles. WB on cerebral cortex had a profile similar to the original scrapie
inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc
with a higher profile resembling CWD. Homogenates with the 2 distinct profiles
from WTD with clinical scrapie were further passaged to mice expressing cervid
prion protein and intranasally to sheep and WTD. In cervidized mice, the 2
inocula have distinct incubation times. Sheep inoculated intranasally with WTD
derived scrapie developed disease, but only after inoculation with the inoculum
that had a scrapie-like profile. The WTD study is ongoing, but deer in both
inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary,
this work demonstrates that WTD are susceptible to the agent of scrapie, 2
distinct molecular profiles of PrPSc are present in the tissues of affected
deer, and inoculum of either profile readily passes to deer.
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
Liuting Qing and Qingzhong Kong
Case Western Reserve University; Cleveland, OH USA
Chronic wasting disease (CWD) is a widespread prion disease in free-ranging
and captive cervid species in North America, and there is evidence suggesting
the existence of multiple CWD strains. The susceptibility of human CNS and
peripheral organs to the various CWD prion strains remains largely unclear.
Current literature suggests that the classical CWD strain is unlikely to infect
human brain, but the potential for peripheral infection by CWD in humans is
unknown. We detected protease-resistant PrpSc in the spleens of a few humanized
transgenic mice that were intracerebrally inoculated with natural CWD isolates,
but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our
ongoing bioassays in humanized Tg mice indicate that intracerebral challenge
with such PrpSc-positive humanized mouse spleen already led to prion disease in
most animals. ***These results indicate that the CWD prion may have the
potential to infect human peripheral lymphoid tissues.
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of
the ability of sheep, cattle and deer prion disease isolates to convert normal
human prion protein to its pathological isoform in a cell-free system
Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki
Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and
Mark W. Head1
1National CJD Research and Surveillance Unit; Centre for Clinical Brain
Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh,
UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food
Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious
Pathogen Research Section; Central Research Laboratory; Japan Blood Products
Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku
University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division;
The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush;
Midlothian; Edinburgh, UK
Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic
prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans.
In contrast, classical scrapie in sheep is thought to offer little or no danger
to human health. However, a widening range of prion diseases have been
recognized in cattle, sheep and deer. The risks posed by individual animal prion
diseases to human health cannot be determined a priori and are difficult to
assess empirically. The fundamemal event in prion disease pathogenesis is
thought to be the seeded conversion of normal prion protein (PrPC) to its
pathological isoform (PrPSc). Here we report the use of a rapid molecular
conversion assay to test whether brain specimens from different animal prion
diseases are capable of seeding the conversion of human PrPC ro PrPSc.
Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE,
classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain
homogenates were tested for their ability to seed conversion of human PrPC to
PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed
human PrPSc was detected by protease digestion and western blotting using the
antibody 3F4.
Results. C-type BSE and vCJD were found to efficiently convert PrPC to
PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion
diseases tested only chronic wasting disease appeared to have the capability ro
convert human PrPC to PrPSc. The results were consistent whether the human PrPC
came from human brain, humanised transgenic mouse brain or from cultured human
cells and the effect was more pronounced for PrPC with methionine at codon 129
compared with that with valine.
Conclusion. Our results show that none of the tested animal prion disease
isolates are as efficient as C-type BSE and vCJD in converting human prion
protein in this in vitro assay. ***However, they also show that there is no
absolute barrier ro conversion of human prion protein in the case of chronic
wasting disease.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood,
and mother to offspring transmission
From: Terry S. Singeltary Sr.
Sent: Saturday, November 15, 2014 9:29 PM
To: Terry S. Singeltary Sr.
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
R. G. WILL
1984
*** The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT
THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
snip...
*** 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. ***
*** IF CWD is not a risk factor for humans, then I guess the FDA et al
recalled all this CWD tainted elk tenderloin (2009 Exotic Meats USA of San
Antonio, TX) for the welfare and safety of the dead elk. ...tss
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin
Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic
Wasting Disease
Contact: Exotic Meats USA 1-800-680-4375
FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San
Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may
contain meat derived from an elk confirmed to have Chronic Wasting Disease
(CWD). The meat with production dates of December 29, 30 and 31, 2008 was
purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk
Farm LLC in Pine Island, MN and was among animals slaughtered and processed at
USDA facility Noah’s Ark Processors LLC.
Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease
found in elk and deer. The disease is caused by an abnormally shaped protein
called a prion, which can damage the brain and nerves of animals in the deer
family. Currently, it is believed that the prion responsible for causing CWD in
deer and elk is not capable of infecting humans who eat deer or elk contaminated
with the prion, but the observation of animal-to-human transmission of other
prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has
raised a theoretical concern regarding the transmission of CWD from deer or elk
to humans. At the present time, FDA believes the risk of becoming ill from
eating CWD-positive elk or deer meat is remote. However, FDA strongly advises
consumers to return the product to the place of purchase, rather than disposing
of it themselves, due to environmental concerns.
Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The
Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was
packaged in individual vacuum packs weighing approximately 3 pounds each. A
total of six packs of the Elk Tenderloins were sold to the public at the Exotic
Meats USA retail store. Consumers who still have the Elk Tenderloins should
return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX
78209. Customers with concerns or questions about the Voluntary Elk Recall can
call 1-800-680-4375. The safety of our customer has always been and always will
be our number one priority.
Exotic Meats USA requests that for those customers who have products with
the production dates in question, do not consume or sell them and return them to
the point of purchase. Customers should return the product to the vendor. The
vendor should return it to the distributor and the distributor should work with
the state to decide upon how best to dispose. If the consumer is disposing of
the product he/she should consult with the local state EPA office.
#
RSS Feed for FDA Recalls Information11 [what's this?12]
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease
Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic
Association Volume 111, Issue 6 , Pages 858-863, June 2011.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
* I urge everyone to watch this video.
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
July's Milwaukee Journal Sentinel article did prod state officials to ask
CDC to investigate the cases of the three men who shared wild game feasts. The
two men the CDC is still investigating were 55 and 66 years old. But there's
also Kevin Boss, a Minnesota hunter who ate Barron County venison and died of
CJD at 41. And there's Jeff Schwan, whose Michigan Tech fraternity brothers used
to bring venison sausage back to the frat house. His mother, Terry, says that in
May 2001, Jeff, 26, began complaining about his vision. A friend noticed
misspellings in his e-mail, which was totally unlike him. Jeff began losing
weight. He became irritable and withdrawn. By the end of June, he couldn't
remember the four-digit code to open the garage door or when and how to feed his
parents' cats. At a family gathering in July, he stuck to his parents and
girlfriend, barely talking. "On the night we took him to the hospital, he was
speaking like he was drunk or high and I noticed his pupils were so dilated I
couldn't see the irises," his mother says. By then, Jeff was no longer able to
do even simple things on his computer at work, and "in the hospital, he couldn't
drink enough water." When he died on September 27, 2001, an autopsy confirmed he
had sporadic CJD.
In 2000, Belay looked into three CJD cases reported by The Denver Post, two
hunters who ate meat from animals killed in Wyoming and the daughter of a hunter
who ate venison from a plant that processed Colorado elk. All three died of CJD
before they were 30 years old. The CDC asked the USDA to kill 1,000 deer and elk
in the area where the men hunted. Belay and others reported their findings in
the Archives of Neurology, writing that although "circumstances suggested a link
between the three cases and chronic wasting disease, they could find no 'causal'
link." Which means, says Belay, "not a single one of those 1,000 deer tested
positive for CWD. For all we know, these cases may be CWD. What we have now
doesn't indicate a connection. That's reassuring, but it would be wrong to say
it will never happen."
So far, says NIH researcher Race, the two Wisconsin cases pinpointed by the
newspaper look like spontaneous CJD. "But we don't know how CWD would look in
human brains. It probably would look like some garden-variety sporadic CJD."
What the CDC will do with these cases and four others (three from Colorado and
Schwan from Upper Michigan), Race says, is "sequence the prion protein from
these people, inject it into mice and wait to see what the disease looks like in
their brains. That will take two years."
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
==============================
*** 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.
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or
Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after gaining approval
from surrounding landowners, and confirmed that the fenced had been cut or
removed in at least four separate locations; that the fence had degraded and was
failing to maintain the enclosure around the Quarantined Premises in at least
one area; that at least three gates had been opened;and that deer tracks were
visible in and around one of the open areas in the sand on both sides of the
fence, evidencing movement of deer into the Quarantined Premises.
The overall incidence of clinical CWD in white-tailed deer was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)
CWD, spreading it around...
for the game farm industry, and their constituents, to continue to believe
that they are _NOT_, and or insinuate that they have _NEVER_ been part of the
problem, will only continue to help spread cwd. the game farming industry, from
the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet
mills, shooting pens, to large ranches, are not the only problem, but it is
painfully obvious that they have been part of the problem for decades and
decades, just spreading it around, as with transportation and or exportation and
or importation of cervids from game farming industry, and have been proven to
spread cwd. no one need to look any further than South Korea blunder ;
===========================================
spreading cwd around...
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of
farmed elk in Saskatchewan in a single epidemic. All of these herds were
depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease
eradication program. Animals, primarily over 12 mo of age, were tested for the
presence CWD prions following euthanasia. Twenty-one of the herds were linked
through movements of live animals with latent CWD from a single infected source
herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily
infected herds.
***The source herd is believed to have become infected via importation of
animals from a game farm in South Dakota where CWD was subsequently diagnosed
(7,4). A wide range in herd prevalence of CWD at the time of herd depopulation
of these herds was observed. Within-herd transmission was observed on some
farms, while the disease remained confined to the introduced animals on other
farms.
spreading cwd around...
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim,
Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research
Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion
disease in native North America deer and Rocky mountain elks. The disease is a
unique member of the transmissible spongiform encephalopathies (TSEs), which
naturally affects only a few species. CWD had been limited to USA and Canada
until 2000.
On 28 December 2000, information from the Canadian government showed that a
total of 95 elk had been exported from farms with CWD to Korea. These consisted
of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72
elk in 1997, which had been held in pre export quarantine at the “source
farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD
surveillance program was initiated by the Ministry of Agriculture and Forestry
(MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994
were impossible to identify. CWD control measures included stamping out of all
animals in the affected farm, and thorough cleaning and disinfection of the
premises. In addition, nationwide clinical surveillance of Korean native
cervids, and improved measures to ensure reporting of CWD suspect cases were
implemented.
Total of 9 elks were found to be affected. CWD was designated as a
notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and
2005.
Since February of 2005, when slaughtered elks were found to be positive,
all slaughtered cervid for human consumption at abattoirs were designated as
target of the CWD surveillance program. Currently, CWD laboratory testing is
only conducted by National Reference Laboratory on CWD, which is the Foreign
Animal Disease Division (FADD) of National Veterinary Research and Quarantine
Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the
human consumption was confirmed as positive. Consequently, all cervid – 54 elks,
41 Sika deer and 5 Albino deer – were culled and one elk was found to be
positive. Epidemiological investigations were conducted by Veterinary
Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary
services.
Epidemiologically related farms were found as 3 farms and all cervid at
these farms were culled and subjected to CWD diagnosis. Three elks and 5
crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and
confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were
linked to the importation of elks from Canada in 1994 based on circumstantial
evidences.
In December 2010, one elk was confirmed as positive at Farm 5.
Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer –
were culled and one Manchurian Sika deer and seven Sika deer were found to be
positive. This is the first report of CWD in these sub-species of deer.
Epidemiological investigations found that the owner of the Farm 2 in CWD
outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced
from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed
(species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as
negative.
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600°C. It has been assumed, without proof, that incineration totally inactivates
the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Histochemical analysis of hamster brains inoculated with the solid residue
showed typical spongiform degeneration and vacuolation. Re-inoculation of these
brains into a new cohort of hamsters led to onset of clinical scrapie symptoms
within 75 days, suggesting that the specific infectivity of the prion protein
was not changed during the biodiesel process. The biodiesel reaction cannot be
considered a viable prion decontamination method for MBM, although we observed
increased survival time of hamsters and reduced infectivity greater than 6 log
orders in the solid MBM residue. Furthermore, results from our study compare for
the first time prion detection by Western Blot versus an infectivity bioassay
for analysis of biodiesel reaction products. We could show that biochemical
analysis alone is insufficient for detection of prion infectivity after a
biodiesel process.
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative
assessment is described that estimates the amount of TSE infectivity that is
present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for
cattle and classical/atypical scrapie for sheep and lambs) and the amounts that
subsequently fall to the floor during processing at facilities that handle
specified risk material (SRM). BSE in cattle was found to contain the most oral
doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to
a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep
infected with classical and atypical scrapie, respectively. Lambs contained the
least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie
and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity
falling to the floor and entering the drains from slaughtering a whole carcass
at SRM facilities were found to be from cattle infected with BSE at rendering
and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate
plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and
collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains
are from lambs infected with classical and atypical scrapie at intermediate
plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO
ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key
inputs for the model in the companion paper published here.
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.
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Tuesday, September 15, 2015
Texas TAHC Chronic Wasting Disease Confirmed in Lavaca County Captive
White-tailed Deer; Linked to Index Herd
more positives from index herd ???
trace outs there from more cwd positives ???
I spoke with MASTER Obi-Wan Kenobi about all this.
see Obi’s reply ;
GRASSHOPPER TO MASTER Obi-Wan Kenobi CWD TEXAS CAPTIVE
‘’I see no evidence whatsoever here for a genetic link. The numbers are
statistically insignificant and co-housing in contaminated facilities would
strongly predispose to this outcome.’’
‘’if the father did have a bad amino acid variant allele, it would be
diluted to heterozygozity with a normal gene in the half the four descendants
since the father never would have survived to breeding age with two bad copies.
sort of like met/val at position 129 in humans with greatly lengthened
incubation times if prnp is propagating at all. Mutations such as repeat
expansion leading to positive dominant infection have not been documented in
cervids.’’
On 09 08 15, at 9:09 AM, Terry S. Singeltary Sr. wrote: ‘’
cwd Texas and then there were 4?
genetic link ?
He said 42 deer have been killed and tested since July 28, and three
additional positives were the result.
***He added that all four deer confirmed to have the disease were males
from the same father, which leads him to believe the problem is genetic.
the silence is deafening by the TAHC TPWD et al $$$
Friday, August 14, 2015
Carcass Management During a Mass Animal Health Emergency Draft Programmatic
Environmental Impact Statement—August 2015
Sunday, August 23, 2015
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig
and take her to the dance in Texas
Sunday, August 02, 2015
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super
ovulation, and the potential TSE Prion connection, what if?
Wednesday, July 01, 2015
TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
Thursday, August 06, 2015
WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
Friday, August 07, 2015
Texas CWD Captive, and then there were 4 ?
Thursday, August 20, 2015
*** TEXAS TAHC DEER BREEDER CWD PERMIT RULES EMERGENCY ADOPTION PREAMBLE
***
Thursday, August 20, 2015
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks
and CWD
a review since the TEXAS 84th Legislature commencing this January, deer
breeders are expected to advocate for bills that will seek to further deregulate
their industry...
Sunday, December 14, 2014
TEXAS 84th Legislature commencing this January, deer breeders are expected
to advocate for bills that will seek to further deregulate their industry
Tuesday, December 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry
TAHC TPWD CWD TSE PRION
Under Texas law, though, breeder deer belong to the state, not the
permittee. See, e.g., TEX. PARKS & WILD. CODE §§ 1.011 (“All wild animals .
. . inside the borders of this state are the property of the people of this
state.”); 43.364 (“All breeder deer . . . are under the full force of the laws
of [Texas] pertaining to deer . . . .”). While a permittee may have possession
of the breeder deer, the deer are only “held under a permit[.]” Id. § 43.351.
Nowhere do the statutes or regulations state that breeder deer become the
property of a permit holder.4 Regardless, even if they did give ownership of
breeder deer to permit holders, the Andertons were not permit holders when the
deer were killed.
While a permittee may have possession of the breeder deer, the deer are
only “held under a permit[.]” Id. § 43.351
TITLE 4. AGRICULTURE PART 2. TEXAS ANIMAL HEALTH COMMISSION
CHAPTER 40. CHRONIC WASTING DISEASE
4 TAC §40.6
The Texas Animal Health Commission (Commission) adopts new §40.6,
concerning CWD Movement Restriction Zone, with changes to the proposed text as
published in the July 6, 2012, issue of the Texas Register (37 TexReg 5061) and
will be republished.
The new section will create a Chronic Wasting Disease (CWD) movement
restriction zone(s) in the Trans Pecos Region.
There is a task force comprised of members of affected deer and exotic
livestock associations, private veterinary practitioners, and wildlife
biologists who assisted the Texas Parks and Wildlife Department (TPWD) and
Commission staff in the development of a CWD response plan upon detection of the
disease in mule deer harvested in New Mexico within 1-2 miles of the Texas
border. They recently met and provided both agencies with recommendations on a
strategy to address the risk of exposure of CWD to susceptible species in Texas.
The recommendations follow the creation of CWD movement restriction zone(s) with
restrictions put in place to protect against the exposure and spread of CWD from
New Mexico. These recommendations are being taken in a coordinated effort by
both TPWD and the Commission.
It was recently disclosed that through CWD sampling efforts of New Mexico
Game and Fish personnel that CWD has been detected in mule deer in the southern
Sacramento Mountains and northern Hueco Mountains, in southern New Mexico. While
sample sizes are very small, it seems that the CWD prevalence may be quite high
in that location. Several of the animals sampled were located in close proximity
to the Texas border. This is significant for the state of Texas, considering
basic biology and movement patterns of susceptible species located there, such
as mule deer and elk, indicate that the animals may be moving back and forth
between Texas and New Mexico.
Prions are found ubiquitously throughout the body of an infected animal and
can be shed onto soil, where they may remain viable and able to infect other
susceptible animals for many years. Suspected additional susceptible species,
besides mule deer, white tail deer and elk, include red deer and Sika deer.
There is still no evidence that humans or domestic livestock can be infected
with CWD.
Deer populations in other states where CWD prevalence exceeds 40% have
experienced significant (>45%) population declines. As the prevalence rates
increase and geographic distribution has expanded in other states, hunters are
more likely to alter hunting behaviors which may include avoiding areas with
high CWD prevalence. This could have an adverse economic impact on local
communities dependent on hunting revenue and could affect TPWD efforts to manage
cervid populations through hunter harvest.
Considering the seemingly high CWD prevalence rate in the Sacramento and
Hueco Mountains of New Mexico, CWD may be well established in the population and
in the environment in Texas at this time. The current area of concern was
delineated as all land west of the Pecos River and IH 20, and north of IH 10 to
Ft. Hancock, and all land west and north of Ft. Hancock, and the Containment
Zone (CZ) was delineated as all land west of HWY 62-180 and HWY 54, and north of
IH 10 to Ft. Hancock, and all land west and north of Ft. Hancock. Data regarding
mule deer population parameters and mule deer movements, knowledge on elk
movements, and the geography and habitat types of the area were considered in
the delineation of these zones.
The Commission received four comments regarding adoption of the new rule,
but there is no change to the rule in response to the comments.
Two of the commenters told us to "trust experts like Dr. Dan McBride and
your advisory committee that was already prepared for this issue. We must at all
cost protect the whitetail herd in the dense areas of the Texas Hill Country
where any outbreak could lead to panic and economic collapse of these
communities where hunting dollars are vital to these communities." The
Commission appreciates the support of the task force. Another comment indicated
that "it will be tough to contain free ranging deer since they range many miles
during breeding season." The Commission agrees that is a tough aspect to fully
control the spread of the disease, but the zones were sized in order to take
that into account. Lastly, a comment indicated that "in light of the Chronic
Wasting Disease (CWD) epidemic, which has jumped the border from New Mexico into
Texas, Texas ought to reevaluate its enthusiasm for land spreading sewage sludge
bio solids on farm land, grazing ranges, hay fields and dairy pastures where
livestock and deer ingest dirt and sludge with their fodder." The Commission has
no jurisdiction over that issue and that is not something addressed in this
rule.
STATUTORY AUTHORITY
The new rule is adopted under the following statutory authority as found in
Chapter 161 of the Texas Agriculture Code. The Commission is vested by statute,
§161.041(a), with the requirement to protect all livestock, domestic animals,
and domestic fowl from disease. The Commission is authorized, by §161.041(b), to
act to eradicate or control any disease or agent of transmission for any disease
that affects livestock. If the Commission determines that a disease listed in
§161.041 of this code or an agent of transmission of one of those diseases
exists in a place in this state among livestock, or that livestock are exposed
to one of those diseases or an agent of transmission of one of those diseases,
the Commission shall establish a quarantine on the affected animals or on the
affected place. That is found in §161.061.
Section 161.054 provides that as a control measure, the Commission by rule
may regulate the movement of animals, including feral swine. The Commission may
restrict the intrastate movement of animals, including feral swine, even though
the movement of the animals is unrestricted in interstate or international
commerce. The Commission by rule may prohibit or regulate the movement of
animals, into a quarantined herd, premise, or area. In §161.048, a person is
presumed to control the animal if the person is the owner or lessee of the pen,
pasture, or other place in which the animal is located and has control of that
place; or exercises care or control over the animal. That is under §161.002.
Section 161.0541, entitled "Elk Disease Surveillance Program", provides
that the Commission by rule may establish a disease surveillance program for
elk. Section 161.007 provides that if a veterinarian employed by the Commission
determines that a communicable disease exists among livestock, domestic animals,
or domestic fowl or on certain premises or that livestock, domestic animals, or
domestic fowl have been exposed to the agency of transmission of a communicable
disease, the exposure or infection is considered to continue until the
Commission determines that the exposure or infection has been eradicated through
methods prescribed by rule of the Commission. Section 161.005 provides that the
Commission may authorize the Executive Director or another employee to sign
written instruments on behalf of the Commission. A written instrument, including
a quarantine or written notice, signed under that authority has the same force
and effect as if signed by the entire Commission.
§40.6.CWD Movement Restriction Zone.
(a) Definitions:
(1) Containment Zone (CZ)--A geographic area which would include a known
affected (quarantined) area or area within Texas where there is a high risk of
CWD existing.
(2) High Risk Zone (HRZ)--Area which serves as a buffer (surveillance) zone
separating the Containment Zone from the rest of Texas.
(3) Susceptible Species--All white-tailed deer, black-tailed deer, mule
deer, elk, or other cervid species determined to be susceptible to Chronic
Wasting Disease (CWD), which means an animal of that species has had a diagnosis
of CWD confirmed by means of an official test conducted by a laboratory approved
by USDA-APHIS.
(4) Unnatural Movement--Any artificially induced movement of a live
susceptible species or the carcass of a susceptible species.
(b) Declaration of Area Restricted for CWD. CWD has been detected in mule
deer and/or elk in the southern Sacramento Mountains and northern Hueco
Mountains of Southern New Mexico, which creates the high risk that there are
susceptible species for CWD that have been exposed or infected to CWD within the
state. Considering the seemingly high CWD prevalence rate in the Sacramento and
Hueco Mountains of New Mexico, CWD may be well established in the population and
in the environment in Texas at this time. The current area of much concern was
delineated as all land west of the Pecos River and Interstate Highway (IH) 20,
and north of IH 10 to Ft. Hancock, and all land west and north of Ft. Hancock
and the CZ was delineated as all land west of HWY 62-180 and HWY 54, and north
of IH 10 to Ft. Hancock, and all land west and north of Ft. Hancock. Data
regarding mule deer population parameters, movement patterns of mule deer and
elk in the area, and the geography and habitat of the area were considered in
the delineation of these zones.
(c) Zone Boundaries:
(1) The CZ is defined as follows: beginning in Culberson County where State
Highway 62-180 enters from New Mexico and thence in a southwesterly direction to
the intersection with State Highway 54 and thence following that in a
southwesterly direction to the intersection with IH 20 and thence following it
in a westerly direction until Ft. Hancock to State Highway 20 and thence
following it a westerly direction to Farm Road 1088 (east of Ft. Hancock), and
thence following it in a southerly direction to the Rio Grande River to where it
enters the state of New Mexico.
(2) The HRZ is defined as follows: beginning in Reeves County where the
Pecos River enters from New Mexico and meanders in a southeasterly direction as
the boundary between Reeves County and Loving and Ward Counties to the
intersection with IH 20 and thence following it in a westerly direction until
the intersection with State Highway 54 and thence following it in a
northwesterly direction until the intersection with State Highway 62-180 and
thence in a northeasterly direction to the border with the state of New Mexico
and Culberson County.
(d) Restrictions:
(1) Prohibition of Unnatural Movement of Non-Captive Susceptible Species:
(A) No susceptible species may be trapped and transported from within the
HRZ or the CZ to another location. No susceptible species may be released within
the HRZ or the CZ without participating in a monitored herd program in
accordance with the requirements of §40.3 of this chapter (relating to Herd
Status Plans for Cervidae) and having a herd with Level "C" status of five years
or higher as established through §40.3(4)(C) of this chapter or for species
under the authority of Texas Parks and Wildlife in accordance with their
applicable requirements.
(B) No part of a carcass of a susceptible species, either killed or found
dead, within the HRZ or CZ may be removed from the HRZ or CZ unless a testable
CWD sample from the carcass is collected by or provided to the Commission or
TPWD with appropriate contact information provided by the submitter.
(2) CWD monitored status within the CZ:
(A) Previously Established CWD Monitored Facilities within the CZ. Movement
of susceptible species will only be allowed for animals from previously
established facilities within the CZ that have obtained a five-year status while
in the CZ in accordance with the requirements of §40.3 of this chapter and
having a herd with Level "C" status of five years or higher as established
through §40.3(4)(C) of this chapter or for species under the authority of Texas
Parks and Wildlife in accordance with their applicable requirements.
(B) Newly Established CWD Monitored Facilities within the CZ. Susceptible
species moving into newly established facilities within the CZ will have their
status reset at zero and must be held within the facility until it has received
five-year status in accordance with the requirements of §40.3 of this chapter
and having a herd with Level "C" status of five years or higher as established
through §40.3(4)(C) of this chapter or for species under the authority of Texas
Parks and Wildlife in accordance with their applicable requirements.
(3) CWD monitored status within the HRZ:
(A) Previously Established CWD Monitored Facilities within the HRZ.
Movement of susceptible species from previously established facilities within
the HRZ is only for animals that have obtained a five-year status in accordance
with the requirements of §40.3 of this chapter and having a herd with Level "C"
status of five years or higher as established through §40.3(4)(C) of this
chapter or for species under the authority of Texas Parks and Wildlife in
accordance with their applicable requirements.
(B) Newly Established CWD Monitored Facilities within the HRZ. Susceptible
species moving into newly established facilities within the HRZ will have their
status reset to zero, and movement will be restricted until the facility has
gained five-year status in accordance with the requirements of §40.3 of this
chapter and having a herd with Level "C" status of five years or higher as
established through §40.3(4)(C) of this chapter or for species under the
authority of Texas Parks and Wildlife in accordance with their applicable
requirements.
(e) The Executive Director may authorize movement. If movement is necessary
or desirable to promote the objectives of this chapter and/or to minimize the
economic impact of the restricted susceptible species without endangering those
objectives or the health and safety of other susceptible species within the
state, the Executive Director may authorize movement in a manner that creates
minimal risk to the other susceptible animals in the state.
(f) Notice of High Risk Designation. The Executive Director shall give
notice of the restrictions by publishing notice in a newspaper published in the
county where the restrictions will be established, or by other accepted
practices or publications which circulate information in the county or counties.
This agency hereby certifies that the adoption has been reviewed by legal
counsel and found to be a valid exercise of the agency's legal authority.
Filed with the Office of the Secretary of State on September 20, 2012.
TRD-201204977
Gene Snelson
General Counsel
Texas Animal Health Commission
Effective date: October 10, 2012
Proposal publication date: July 6, 2012
For further information, please call: (512) 719-0724
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 ***
Wednesday, September 16, 2015
*** WISCONSIN CAPTIVE CERVID INDUSTRY RUNNING WILD AND ON THE LOOSE RISKING
FURTHER SPREAD OF CWD ***
TEXAS DEER CZAR SENT TO WISCONSIN TO SOLVE CWD CRISIS, WHILE ROME (TEXAS)
BURNS
Tuesday, August 11, 2015
*** Wisconsin doing what it does best, procrastinating about CWD yet again
thanks to Governor Walker
Wednesday, March 04, 2015
*** Disease sampling results provide current snapshot of CWD in Wisconsin
finding 324 positive detections statewide in 2014
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Tuesday, September 22, 2015
***Host Determinants of Prion Strain Diversity Independent of Prion Protein
Genotype***
Saturday, September 12, 2015
*** In utero transmission and tissue distribution of chronic wasting
disease-associated prions in free-ranging Rocky Mountain elk ***
Sunday, September 13, 2015
*** urine, feces, and chronic wasting disease cwd tse prion risk factors,
loading up the environment ***
Friday, August 28, 2015
*** Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical
infection ***
ARE THE TESTS INFALLIBLE?
NO!
All test methods are somewhat subjective and are constantly subject to
misinterpretation and interference. Bacteria have been known to confuse test
results. False negatives are common during the early stage of disease and false
positives are possible. Post-mortem sampling procedures and sample treatment
after collection will potentially affect results. Human errors are always
possible.
Research Looks at Test to Identify Chronic Wasting Disease in Wildlife Page
Image Dr. Ed Hoover Dr. Ed Hoover
CVMBSHTML1
A Colorado State University study is developing and evaluating a more
sensitive test for chronic wasting disease – including the potential to test for
infection in live animals, animal products, and the environment – through a
project funded by Denver-based Morris Animal Foundation. The disease, which
affects deer, moose and elk and is related to similar diseases in cattle and
sheep, is a primary concern for hunters and wildlife ranchers and now affects
wildlife in 19 states, two Canadian provinces and one Asian country. Prions are
rogue proteins that cause the family of diseases that include CWD. The diseases
are known as spongiform encephalopathies. While this Morris Animal
Foundation-funded study would be the first in several steps to develop and
evaluate a potential new test, it will look at a method that shows promise in
detecting a wider array of prions at lower levels than are currently detected.
The research into the potential test may allow detection of CWD prions in live
animals, animal products and the environment. “Developing this test may
eventually lead to a more rapid and sensitive to test for CWD,” said Dr. Ed
Hoover, a Professor in the Department of Microbiology, Immunology and Pathology.
“But, just as significantly, it may lead to a substantial gain in our
understanding of how prions spread, survive in natural habitats, and impact
animal and public health.” Currently, CWD can only be identified either by
testing brain after an animal is deceased or by surgical sampling and testing
lymphatic tissues. While researchers don’t know exactly how CWD is passed from
animal to animal, CSU scientists discovered that body fluids such as saliva,
blood, urine and feces harbor infectious prions. Animals can then be exposed by
direct contact with an infected animal or by contact with a contaminated
environment. Current tests also don’t detect all levels of or kinds of
infectious prions or prions in the environment, and the test being evaluated in
this study has the potential to be developed into a process that would detect
those prions. The test is being researched in collaboration with Dr. Byron
Caughey at the National Institutes of Health’s Rocky Mountain Laboratory in
Hamilton, Mont. Dr. Caughey’s laboratory developed the strategy for the study.
Dr. Hoover, Dr. Caughey and colleagues will focus first on determining if their
proposed test detects prions in body fluids with greater sensitivity, accuracy
and faster output than is currently possible. It is unknown why an infectious
prion from one species, such as deer or elk, can “jump” to infect another
species, and the potential risk to other species such as cattle, or even humans,
remains uncertain.
P170
Clinical Stage of Infection is Critical in the Antemortem Diagnosis of
Chronic Wasting Disease in Deer and Elk
Chris Siepker1, Nicholas Haley1, W. David Walter2, Matteo Manca3, Laura
Hoon-Hanks4, Ryan Monello5, Jenny Powers5, Justin Greenlee6 , Bruce Thomsen7 ,
Aaron Lehmkuhl7, Gordon Mitchell8, Tracy Nichols9,Byron Caughey3, Edward
Hoover4, and Juergen Richt1.
1. Department of Diagnostic Medicine and Pathobiology, Kansas State
University, Manhattan KS USA 2. United States G e o l o g i c a l Survey, P e n
n s y l v a n i a Cooperative Fish and Wildlife Research Unit, University Park
PA USA 3. TSE/Prion Biochemistry Section, Rocky Mountain Laboratories, National
Institutes of Health, Hamilton, MT USA 3. Department of MIP, Colorado State
University, Fort Collins CO USA 4. National Park Service, Wildlife Health
Branch, Fort Collins CO USA 5. Virus and Prion Research Unit, National Animal
Disease Center, ARS, USDA, Ames IA USA 6. USDA, APHIS, VS, STAS, National
Veterinary Service Laboratories, Ames IA USA 7. National and OIE Reference
Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa ON
Canada 8. National Wildlife Research Center Wildlife Services, APHIS, USDA, Fort
Collins CO USA
Chronic wasting disease (CWD) is an e f f i c i e n t l y t r a n s mi t t
e d s p o n g i f o r m encephalopathy of cervids (e.g. deer, elk, and moose),
and is the only known prion disease affecting both free-ranging wildlife and
captive animals. The antemortem detection of CWD and other prion diseases has
proven difficult, due in part to difficulties in identifying an appropriate
peripheral tissue specimen and complications with conventional test sensitivity.
At present, biopsies of the recto-
Prion2015 Program Guide 22
anal mucosal-associated lymphoid tissues (RAMALT) have shown promising
sensitivity and are not impractical to collect in live animals. Nasal brush
collections have likewise proven both sensitive and practical for identification
of prion infections in humans. In this study, we evaluated both RAMALT and nasal
brush collections by real time quaking-induced conversion (RT-QuIC), and
compared our findings to RAMALT immu n o h i s t o c h emi s t r y a s we l l a
s conventional postmortem evaluation of obex and retropharyngeal lymph node
tissues from over 700 captive and free-ranging deer and elk in areas with
endemic CWD. We correlated our results with various clinical findings, including
pathological stage of infection as determined by obex scoring, PrP genotype,
age, and sex. While the sensitivity of RAMALT RT-QuIC analyses exceeded that of
RAMALT IHC (69-80% vs. >44%) and nasal brush collections (15-30%), the
sensitivity of both biopsy and nasal brush analyses were dependent primarily on
clinical stage of disease, although PrP genotype was also an important predictor
of sample positivity. Our findings further demonstrate the potential and
limitations of antemortem sample analyses by RT-QuIC in the identification and
management of prion diseases.
========
P179
Detection of CWD prion in fecal samples by RT-QuIC
Yo Ching Cheng1, Theodore Ralph John2, Sampson Law3, Stephanie Czub4,
Sabine Gilch1 1Department of Ecosystem and Public Health, Faculty of Veterinary
Medicine, University of Calgary, Calgary, Alberta, Canada, 2Department of
Molecular Biology, University of Wyoming, Laramie, Wyoming, USA, 3Department of
Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine,
University of Calgary, Calgary, Alberta, Canada, 4Canadian Food Inspection
Agency (CFIA) Lethbridge Laboratory, Lethbridge, Alberta, Canada
Chronic wasting disease (CWD) is a prion disease which mainly affects
captive and wild cervids in North America. To date, cases in elk, mule deer,
white-tailed deer and moose h a v e b e e n r e p o r t e d . I n C W D ,
infectious prions are transported from the CNS into a wide range of peripheral
tissues, body fluids, excreta and eventually shed into the environment. In order
to detect the disease, the use of easily accessible specimens such as feces
would be a practical way for prion detection. However, those excretions and
secretions harbor relatively low concentrations of prions which challenge
current diagnosis methods. In an earlier study, we demonstrated that CWD prions
are detectable in urine collected from pre-symptomatic deer and in fecal
extracts by real-time quaking-induced conversion assay (RT-QuIC). RT-QuIC
employs minute amounts of PrPSc as a seed to initiate conformational transition
of recombinant PrP (rPrP) by vigorous intermittent shaking. In this study, we
aim to improve the detection of CWD pions in fecal extracts by RT-QuIC, and to
determine the shedding pattern in feces of elk which were challenged orally with
CWD prions in an experimental study. We u s e d m e t h a n o l p r e c i p i t
a t i o n , u l t r a c e n t r i f u g a t i o n a n d s o d i u m
phosphotungstic acid (NaPTA) precipitation to purify and to concentrate CWD
prions in feces. We found that NaPTA precipitation of fecal extracts dose not
interfere with seeding activity, but increases the sensitivity of detection. Our
data demonstrate that concentration and purification of PrPSc enhances detection
of CWD prions in feces, Prion2015 Program Guide 27 which will eventually enable
the use of RTQuIC for CWD surveillance.
=============
P200
Clinical Stage of Infection is Critical in the Antemortem Diagnosis of
Chronic Wasting Disease in Deer and Elk.
Chris Siepker1, Nicholas Haley1, W. David Walter2, Laura Hoon-Hanks7, Ryan
Monello3, Jenny Powers3, Bruce Thomsen4, Justin Greenlee4, Aaron Lehmkuhl4,
Gordon Mitchell5, Tracy Nichols6, Edward Hoover7, Juergen Richt1 1Department of
Diagnostic Medicine and Pathobiology, Kansas State University, Manhattan, KS,
USA, 2United States G e o l o g i c a l Survey, P e n n s y l v a n i a
Cooperative Fish & Wildlife Research Unit, Pennsylvania State University,
University Park, PA 16802, USA, 3National Park Service, Wildlife Health Branch,
Fort Collins, CO, USA, 4USDA, APHIS, VS, STAS, National Veterinary Service
Laboratories, Ames, IA, USA, 5National and OIE Reference Laboratory for Scrapie
and CWD Ottawa Laboratory Fallowfield Canadian Food Inspection Agency, Ottawa,
ON, Canada, 6National Wildlife Research Center Wildlife Services APHIS, USDA,
Fort Collins, CO, USA, 7Department of MIP, Colorado State University, Fort
Collins, CO, USA
Chronic wasting disease (CWD) is an e f f i c i e n t l y t r a n smi t t e
d s p o n g i f o r m encephalopathy of cervids (e.g. deer, elk, and moose), and
is the only known prion disease affecting both free-ranging wildlife and captive
animals. The antemortem detection of CWD and other prion diseases has proven
difficult, due in part to difficulties in identifying an appropriate peripheral
tissue specimen and complications with conventional test sensitivity. At
present, biopsies of the rectoanal mucosal-associated lymphoid tissues (RAMALT)
have shown promising sensitivity and are not impractical to collect in live
animals. Nasal brush collections have likewise proven both sensitive and
practical for identification of prion infections in humans. In this study, we
evaluated both RAMALT and nasal brush collections by real time quaking-induced
conversion (RT-QuIC), and compared our findings to RAMALT immu n o h i s t o c h
emi s t r y a s we l l a s conventional postmortem evaluation of obex and
retropharyngeal lymph node tissues from over 700 captive and free-ranging deer
and elk in areas with endemic CWD. We correlated our results with various
clinical findings, including pathological stage of infection as determined by
obex scoring, PrP genotype, age, and sex. While the sensitivity of RAMALT
RT-QuIC analyses exceeded that of RAMALT IHC (69-80% vs. >44%) and nasal
brush collections (15-30%), the sensitivity of both biopsy and nasal brush
analyses were dependent primarily on clinical stage of disease, although PrP
genotype was also an important predictor of sample positivity. Our findings
further demonstrate the potential and limitations of antemortem sample analyses
by RT-QuIC in the identification and management of prion diseases.
Article | Open
Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of
Prion Infection
A. Christy Wyckoff , Nathan Galloway , Crystal Meyerett-Reid , Jenny Powers
, Terry Spraker , Ryan J. Monello , Bruce Pulford , Margaret Wild , Michael
Antolin , Kurt VerCauteren & Mark Zabel
Scientific Reports 5, Article number: 8358 (2015) doi:10.1038/srep08358
Download Citation Molecular ecology | Proteins | Statistics
Received:27 June 2014Accepted:19 January 2015Published online:10 February
2015 Article Tools
Abstract
Prions are unique infectious agents that replicate without a genome and
cause neurodegenerative diseases that include chronic wasting disease (CWD) of
cervids. Immunohistochemistry (IHC) is currently considered the gold standard
for diagnosis of a prion infection but may be insensitive to early or
sub-clinical CWD that are important to understanding CWD transmission and
ecology. We assessed the potential of serial protein misfolding cyclic
amplification (sPMCA) to improve detection of CWD prior to the onset of clinical
signs. We analyzed tissue samples from free-ranging Rocky Mountain elk (Cervus
elaphus nelsoni) and used hierarchical Bayesian analysis to estimate the
specificity and sensitivity of IHC and sPMCA conditional on simultaneously
estimated disease states. Sensitivity estimates were higher for sPMCA (99.51%,
credible interval (CI) 97.15–100%) than IHC of obex (brain stem, 76.56%, CI
57.00–91.46%) or retropharyngeal lymph node (90.06%, CI 74.13–98.70%) tissues,
or both (98.99%, CI 90.01–100%). Our hierarchical Bayesian model predicts the
prevalence of prion infection in this elk population to be 18.90% (CI
15.50–32.72%), compared to previous estimates of 12.90%. Our data reveal a
previously unidentified sub-clinical prion-positive portion of the elk
population that could represent silent carriers capable of significantly
impacting CWD ecology.
============
Overall, our data contribute to the increasing evidence that a portion of a
herd may be infected, but die from other causes while infected with PrPCWD
because of age, genetic susceptibility or other unknown factors. However, the
contribution of prions shed into the environment from this sub-clinical
population may be important and requires further investigation. The existence of
an infectious PrPCWD carrier state aligns with disease ecology theory, which
proposes balance between transmissibility and pathogenesis of a pathogen. As
such, through selection pressures from the host and external environment the
pathogen will tend towards the greatest transmissibility strategy. CWD
transmission may be more complicated than disease ecology might predict, since
prolonged persistence and indirect transmission of prions in the environment may
potentiate spread without affecting pathogenesis.
Despite the fact that prions are only protein, studies continue to point at
evolutionary behavior and selection pressures of prions which indicate that like
other pathogens, prions are capable of evolving and adapting to their
environment4,27,48,49. With increasing prevalence at the population level, as is
reported in this study, sPMCA will continue to be an important tool to
investigate CWD in wildlife.
EFFICACY OF ANTEMORTEM RECTAL BIOPSIES TO DIAGNOSE AND ESTIMATE PREVALENCE
OF CHRONIC WASTING DISEASE IN FREE-RANGING COW ELK (CERVUS ELAPHUS NELSONI)
Ryan J. Monello,1,6 Jenny G. Powers,1 N. Thompson Hobbs,2 Terry R.
Spraker,3 Katherine I. O’Rourke,4,5 and Margaret A. Wild1
1 National Park Service, Biological Resource Management Division, 1201 Oak
Ridge Drive, Suite 200, Fort Collins, Colorado 80525, USA
2 Natural Resource Ecology Laboratory and Graduate Degree Program in
Ecology, Colorado State University, Fort Collins, Colorado 80523, USA
3 Colorado State Diagnostic Laboratory, College of Veterinary Medicine,
Colorado State University, Fort Collins, Colorado 80523, USA
4 United States Department of Agriculture, Agricultural Research Service,
Animal Disease Research Unit, 3003 Animal Disease Biotechnology Facility,
Washington State University, Pullman, Washington 99164, USA
5 Current address: Department of Veterinary Microbiology and Pathology,
School of Veterinary Medicine, Washington State University, Pullman, Washington
99164, USA
6 Corresponding author (email: Ryan_Monello@nps.gov)
ABSTRACT: A reliable antemortem test is needed to understand the ecology of
chronic wasting disease (CWD) in elk (Cervus elaphus nelsoni). We measured the
ability of antemortem biopsy samples from the rectal mucosa to detect the
abnormal prion protein associated with CWD (PrPCWD), the relationship between
test results from the obex and rectal biopsies at varying stages of CWD
progression, and the prevalence of CWD in free-ranging elk from Rocky Mountain
National Park, Colorado, USA. We sampled and placed radio collars on 136 adult
female elk in the winter of 2007–08. Elk with biopsy samples found positive for
PrPCWD by immunohistochemistry (IHC) were euthanized and the obex and
retropharyngeal lymph nodes were examined with IHC. We resampled, euthanized,
and necropsied 20, 25, and 34 of the remaining study elk in each of the three
following winters, respectively. Sensitivity of rectal biopsy samples increased
in an asymptotic fashion with follicle count and was maximized at 85% (95%
credible limits [CL]560, 98) in the beginning of the study, when a greater
proportion of elk were in a detectable stage of prion infection. However,
maximum sensitivity was reduced to 72% (CL546, 94) when we included resampled
elk, ***which included recently infected elk that were initially negative using
rectal biopsies and IHC. Test results were similar between rectal biopsies and
the obex, but the earliest stages of prion infection were only detected by using
retropharyngeal lymph nodes. Minimum CWD prevalence was estimated to be 9.9%
(CL55.7, 15.7) using rectal biopsies, but this rose to 12.9%
DETECTION OF PrPCWD IN FECES FROM NATURALLY EXPOSED ROCKY MOUNTAIN ELK
(CERVUS ELAPHUS NELSONI) USING PROTEIN MISFOLDING CYCLIC AMPLIFICATION
Bruce Pulford,1 Terry R. Spraker,1 A. Christy Wyckoff,1 Crystal Meyerett,1
Heather Bender,1 Adam Ferguson,1 Brittney Wyatt,1 Krista Lockwood,1 Jenny
Powers,2 Glenn C. Telling,1 Margaret A. Wild,2 and Mark D. Zabel1,3 1 Department
of Microbiology, Immunology and Pathology, Prion Research Program, Colorado
State University, 1619 Campus Delivery, Fort Collins, Colorado 80523, USA 2
National Park Service, 1201 Oakridge Drive, Fort Collins, Colorado 80525, USA 3
Corresponding author (email: mark.zabel@colostate.edu)
snip...
Detection of PrPCWD in cervid feces may also illuminate the contribution of
fecal shedding to environmental contamination and disease transmission. For
example, cervids in the vicinity of RMNP shed nearly 1 million kg of feces each
year (Nichols et al., 2009). Based on CWD prevalence estimates in RMNP and the
surrounding region, we estimate that 2– 10% of that load contains PrPCWD
(Colorado Division of Wildlife, 2009), and that each gram of infected feces
contains 100– 5,000 pg of PrPCWD, we estimate that fecal shedding may contribute
2–500 mg of PrPCWD into this endemic region every year. The PMCA protocol
outlined here complements PrPCWD detection by IHC in several ways. Most
importantly, PMCA can detect PrPCWD in easily obtainable fecal samples that are
simple to process and assay, with sensitivity comparable to IHC. Fecal PMCA may
also be an alternative test to IHC in older cervids that have fewer rectal
lymphoid follicles present in biopsy sections (Spraker et al., 2009b). Our PMCA
data suggest that fecal prion detection is independent of follicle count in
RAMALT. Only one out of five RAMALT follicles from elk 4 was positive by IHC,
while 13 of 14 fecal samples were positive by PMCA. Conversely, seven of 10
RAMALT follicles from elk 2 were positive by IHC, while only two of 14 fecal
samples were positive by PMCA. In this case, incorporation of our scoring
system, which allows for more accurate, unbiased data interpretation by
transforming qualitative PMCA results to semiquantitative numerical scores and
analyzing their significance statistically, enabled us to designate elk 2
positive.
Disadvantages of PrPCWD detection via fecal sample PMCA include the need to
maintain a colony of transgenic cervidized mice for NBH; the time, effort, and
expense of nine rounds of PMCA; and, perhaps most importantly, the care needed
to avoid false-positive results both during sample collection and analysis. In
the field, strict attention must be given to avoid cross contamination between
animals sampled. In the laboratory, specificity of PMCA can begin to wane after
six rounds of PMCA without extraordinary efforts to prevent cross contamination,
including a dedicated clean room for NBH preparation, compulsive glovechanging,
and constant prion decontamination procedures. We found that most PMCA scores
below 50 rpu required six to nine rounds of PMCA for detection, raising
legitimate concern of false positives. Recently, new technical advances employ
paramagnetic beads to specifically capture and concentrate PrPres (Miller and
Supattapone, 2011) and teflon beads added to PMCA reactions to increase
efficiency two to three orders of magnitude per round (Gonzalez-Montalban et
al., 2011). The latter study also noted improvements in reproducibility and
specificity, due mainly to the reduced number of rounds required to detect
minute quantities of PrPres. We are currently testing these modifications to
decrease the number of PMCA rounds, thereby improving speed, efficiency,
reliability, and specificity.
Validation of Use of Rectoanal Mucosa-Associated Lymphoid Tissue for
Immunohistochemical Diagnosis of Chronic Wasting Disease in White-Tailed Deer
(Odocoileus virginianus)
▿ Delwyn Keane1,*, Daniel Barr1, Rebecca Osborn2, Julie Langenberg2,
Katherine O'Rourke3, David Schneider3 and Philip Bochsler1 + Author Affiliations
1University of Wisconsin, Wisconsin Veterinary Diagnostic Laboratory,
Madison, Wisconsin 2Wisconsin Department of Natural Resources, Madison,
Wisconsin 3U.S. Department of Agriculture, Agricultural Research Service, Animal
Disease Research Unit, 3003 ADBF, Pullman, Washington Next Section ABSTRACT The
examination of rectoanal mucosa-associated lymphoid tissue (RAMALT) biopsy
specimens for the diagnosis of transmissible spongiform encephalopathies has
been described in sheep, elk, and small numbers of mule and white-tailed deer.
Previous sample numbers have been too small to validate examination of this type
of tissue as a viable antemortem diagnostic test. In this study, we examined
RAMALT collected postmortem from 76 white-tailed deer removed from a farm in
Wisconsin known to be affected by chronic wasting disease (CWD) and from 210
free-ranging white-tailed deer harvested from an area in Wisconsin where the
overall prevalence of CWD among the deer was approximately 4 to 6%. The results
of immunohistochemical (IHC) staining of the RAMALT sections were compared to
the results of IHC staining of sections from the brain stem at the convergence
of the dorsal motor nucleus of the vagus nerve, sections of the medial
retropharyngeal lymph nodes (RLNs), and sections of tonsil (sections of tonsil
only from captive animals were tested). The sensitivities of the IHC staining
test with RAMALT sections were 81% for the captive animals and 91% for the
free-ranging animals.
*** False-negative results were usually associated with early infection,
indicated by a low intensity of immunostaining in the obex and/or a polymorphism
at PRNP codon 96. While the RLN remains the tissue of choice for use for the
diagnosis of CWD in white-tailed deer, the results of the present study further
support the use of RAMALTs collected antemortem as an adjunct to testing of
tonsil biopsy specimens and surveillance by necropsy for the screening of farmed
deer which have been put at risk through environmental exposure or exposure to
deer with CWD.
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy
that has been reported in free-ranging and captive Rocky Mountain elk (Cervus
elaphus nelsoni), mule deer (Odocoileus hemionus), white-tailed deer (Odocoileus
virginianus), and moose (Alces alces shirasi) in North America (1, 23, 27, 28).
Clinical signs of CWD do not appear until very late in the infection process
(11), and as the successful management of CWD appears to be dependent on the
early detection and elimination of infected individuals (8), a reliable
diagnostic test for the identification of infected animals during the early
preclinical stage is of paramount importance. Currently, diagnosis is generally
dependent on the finding of PrPCWD, the abnormal isoform of the cellular prion
protein (PrPC), in obex and/or lymphoid tissues of animals collected postmortem.
Antemortem evaluation of tonsil biopsy specimens has been shown to detect
preclinical CWD in deer (17, 26, 29), but the collection of tonsil tissue is not
a universally practical procedure for use in the field, in that it requires
general anesthesia and highly trained personnel to collect adequate samples. On
the basis of the findings of recent studies that have shown that
scrapie-associated PrP (PrPSc) is deposited in the rectoanal mucosa-associated
lymphoid tissues (RAMALTs) of infected sheep relatively early in the course of
infection and that samples from this site can be used to diagnose preclinical
scrapie in sheep (5-7), studies have been conducted with elk and deer to
evaluate the use of RAMALTs for the diagnosis of CWD (11, 21, 24, 30).
***This study was undertaken to further evaluate the use of RAMALTs for the
diagnosis of CWD in white-tailed deer from a farm known to be positive for CWD
and also in free-ranging white-tailed deer harvested in an area of Wisconsin
known to have a 4 to 6% prevalence of CWD (10) and to investigate the factors
contributing to the false-negative findings with RAMALTs from some deer with
CWD.
snip...
DISCUSSION On the basis of the results of our study, the detection of
PrPCWD in RAMALTs by IHC staining should be considered a useful tool for the
preclinical diagnosis of CWD in white-tailed deer. It was previously shown that
in white-tailed deer, the accumulation of PrPCWD occurs in the RLNs or tonsils
prior to accumulation in the obex (11) and the presence of PrPCWD in the RLNs
and tonsils is a reliable marker for the antemortem and preclinical postmortem
diagnosis of CWD (26, 29, 30). The collection of lymphatic tissues from the head
and neck of live animals is not an easy task; tonsil biopsy procedures require
general anesthesia, the tonsil is difficult to visualize, the collection of a
tonsil biopsy specimen requires experienced personnel, and the samples tend to
be small (4 or 6 mm). As a tool for the screening of free-ranging or captive
populations, this technique is not as efficient or as economical as rectal
tissue biopsy. The latter procedure can be performed without general anesthesia,
visualization of the rectal mucosa is much easier than that of the tonsil, and
larger samples can be obtained without the need for specialized equipment.
However, the diagnosis of CWD by the use of RAMALTs, as with tonsil tissues, is
dependent on the collection of adequate samples.
An adequate lymphoid tissue sample in our study was defined as one with at
least six follicles in any one section examined. ***A recent study (21)
demonstrated that similar testing of elk required 10 follicles, and higher rates
of false-negative results for sheep were observed when the samples had less than
14 follicles (7). Previous studies with tonsil biopsy specimens have defined
adequate sections as having just one follicle (29) or less than three follicles
(26) per section, so a direct comparison of the number of adequate samples
between rectal and tonsil biopsy specimens is difficult. We were unable to
obtain adequate RAMALT samples from 3 of the captive animals (3.9%) and 44 (21%)
of the free-ranging animals, even though the samples were collected postmortem.
Some of this difference may be explained by the collection technique used; the
samples from the captive animals were collected by one experienced veterinarian,
and the samples from the free-ranging animals were collected by a number of
wildlife biologists with limited training. However, the major difference is
likely explained by the number of sections of RAMALT examined for individuals in
each population. The RAMALT samples in this study were embedded with the mucosal
surface down, which requires the use of a precise sectioning technique to ensure
that the sections are not taken too shallow, in which case there will be few
lymphoid follicles and large numbers of crypts, or too deep, in which case a
large percentage of lymphoid follicles will have been lost and submucosal tissue
and muscle will be present. In the farmed deer, several sections from various
depths of the mucosa were examined in an attempt to have at least six follicles
present in a single section. This procedure was not done for animals in the wild
population, in which only one section from each animal was examined, which more
closely approximates the procedure that would be used for high-volume sampling
schemes. The number of unsuitable samples from the free-ranging population could
likely have been decreased considerably by collecting sections from various
depths of the block. This is an important aspect to keep in mind when laboratory
personnel are being trained.
In this study, the sensitivity of IHC staining of RAMALTs was approximately
80%, which is slightly lower than the estimated sensitivity of the testing of
RAMALTs for the diagnosis of scrapie in sheep (5-7). As with sheep, the
sensitivity of the test is apparently improved by the exclusion of animals with
genotypes associated with reduced PrPSc or PrPCWD accumulation, very young
animals, or animals with very early disease. In white-tailed deer, the wt/G96S
genotype is associated with a delay in the progression of CWD infection (11,
30), and the confounding effects of a prolonged early infection stage and the
PRNP genotype itself cannot be resolved for this sample set. The mechanism by
which the PRNP genotype influences the kinetics of PrPCWD deposition in the
tissues of white-tailed deer (9, 11, 15, 30) is not known. In the current study,
41/44 (93%) of the CWD-positive wt/wt deer were RAMALT positive but only 7/14
(50%) of the CWD-positive wt/G96S deer were RAMALT positive. This finding is
consistent with that of an experimental pathogenesis trial (30) in which 90%
(9/10) of the experimentally infected PRNP wt/wt deer were RAMALT positive at
342 days postinfection, although only 50% (4/8) of the wt/G96S deer were RAMALT
positive at 381 days postinfection. The use of RAMALTs for the testing of
captive herds may benefit from supplementary PRNP genotype testing to identify
deer likely to have false-negative RAMALT findings. The G96S homozygous
population and Q226K homozygous or heterozygous deer were relatively rare in the
populations examined; and there were insufficient numbers of animals of the
G96S/G96S, wt/Q226K, and G96S/Q226K genotypes in our study to determine the role
of those PRNP genotypes in the testing of RAMALTs.
With the exception of one fawn in the current study, there was no evidence
of a nonlymphocytic scrapie strain responsible for CWD comparable to the ovine
Nor98 scrapie strain (2) or of a lymphoid-sparing deposition pattern, as has
been observed in some studies of classical sheep scrapie (13, 16, 25) and in up
to 15% of elk with CWD (20). However, the deer in this study represented only a
single captive population and a sample of free-ranging animals originating from
a relatively small geographic area. The findings of this study may therefore be
limited to a single strain of CWD. The presence of multiple strains responsible
for CWD is suggested by studies with a transgenic mouse model (3). Although
additional strains responsible for CWD may be discovered as our understanding of
prion strains (4) and strain typing methodologies are refined and developed,
this and previous studies (9, 11, 12, 15) suggest that the predominant U.S.
strains result in the early deposition of PrPCWD in lymphoid tissue in most
white-tailed deer.
This study was performed by using an IHC detection method validated for use
in approved veterinary diagnostic laboratories in the United States. Adaptation
and validation of laboratory methods such as protein misfolding cyclic
amplification assay (19) or paraffin-embedded tissue immunoblotting (18) may
increase the sensitivity of diagnostic testing of RAMALTs from deer. Those
methods may also be useful adjuncts to bioassay methods (14) for estimation of
the potential of fecal shedding of prions from the gut of deer with
PrPCWD-positive tissues in the gastrointestinal tract.
The results of this study are remarkably similar to those reported from a
similar study describing the IHC detection of PrPSc in the RAMALTs of sheep with
classical scrapie (6). The sensitivity of the assay in that study was 86% with
sheep with preclinical CWD. False-negative readings were observed for young
sheep, many with scant accumulations of PrPSc in other lymphoid tissues and
older sheep with genotypes associated with prolonged incubation times and scant
lymphoid accumulation of PrPSc at all stages of infection.
The RLN is the most sensitive indicator of CWD but is suitable for use only
for analysis by necropsy. Because the sensitivity of the PrPCWD IHC assay with
RAMALTs does not appear to be as high as it is with tonsil tissues, the use of
RAMALT biopsy specimens may not be as reliable a tool as the use of tonsil
biopsy specimens for the testing of individual animals for the purpose of
movement. However, the advantages of cost and ease of sampling make testing of
RAMALTs a reasonable alternative in situations in which large numbers of live
white-tailed deer are to be tested. This study further supports the use of
RAMALTs as an alternative or adjunct to tonsil biopsy specimens, particularly
for farmed deer with potential environmental exposure or exposure to cervids
with CWD.
AGE AND REPEATED BIOPSY INFLUENCE ANTEMORTEM PRPCWD TESTING IN MULE DEER
(ODOCOILEUS HEMIONUS) IN
COLORADO, USA
Chris Geremia,1,6,7 Jennifer A. Hoeting,2 Lisa L. Wolfe,3 Nathan L.
Galloway,4 Michael F. Antolin,4 Terry R. Spraker,5 Michael W. Miller,3 and N.
Thompson Hobbs1
1 Natural Resource Ecology Laboratory, Graduate Degree Program in Ecology,
Colorado State University, Fort Collins, Colorado, 80523-1499, USA
2 Department of Statistics, Colorado State University, Fort Collins,
Colorado 80523, USA
3 Colorado Division of Parks and Wildlife, Wildlife Health Program, 4330
Laporte Avenue, Fort Collins, Colorado 80521, USA
4 Department of Biology, Colorado State University, Fort Collins, Colorado
80523-1878, USA
5 Colorado State University Diagnostics Laboratory, Colorado State
University, Fort Collins, Colorado 80523, USA
6 Current address: Yellowstone Center for Resources, P.O. Box 168,
Yellowstone National Park, Mammoth Hot Springs, Wyoming 82190, USA
7 Corresponding author (email: chris_geremia@nps.gov)
ABSTRACT: Biopsy of rectal-mucosa associated lymphoid tissue provides a
useful, but imperfect, live-animal test for chronic wasting disease (CWD) in
mule deer (Odocoileus hemionus). It is difficult and expensive to complete these
tests on free-ranging animals, and wildlife health managers will benefit from
methods that can accommodate test results of varying quality. To this end, we
developed a hierarchical Bayesian model to estimate the probability that an
individual is infected based on test results. Our model was estimated with the
use of data on 210 adult female mule deer repeatedly tested during 201022014.
The ability to identify infected individuals correctly declined with age and may
have been influenced by repeated biopsy. Fewer isolated lymphoid follicles
(where PrPCWD accumulates) were obtained in biopsies of older deer and the
proportion of follicles showing PrPCWD was reduced. A deer’s genotype in the
prion gene (PRNP) also influenced detection. At least five follicles were needed
in a biopsy to assure a 95% accurate test in PRNP genotype 225SS deer.
Key words: Bayesian, capture–mark–recapture, chronic wasting disease, mule
deer, prion, test sensitivity.
snip...
Every test sample is not the same; each individual exhibits unique
variation, and the technique for estimating CWD infection that we developed here
can account for some of these complications. Disease status becomes a
probabilistic statement conditioned on the current test result, previous disease
status, and infection and test sensitivity probabilities. Therefore, uncertainty
in sampling becomes incorporated into the placement of individuals into discrete
disease categories. This step forward allows us to make explicit probabilistic
statements 0 JOURNAL OF WILDLIFE DISEASES, VOL. 51, NO. 4, OCTOBER 2015 about
whether an individual is infected and the chance that a test result is correct.
With CWD, rather than conclude that an individual is not infected based on a
test with few follicles or decide that the test was inconclusive, we can now
state the probability that an individual is truly infected. Consequently, we can
make conclusions that ‘‘a 90% chance exists that this deer is not infected,
based on the results.’’ Surveillance and containment programs for CWD benefit
from an ability to diagnose animals correctly with the use of antemortem tests.
Our model can easily be applied to surveillance on mule deer, facilitating use
of all available samples regardless of total follicle counts. Probabilistic
estimates of the infection status of each tested individual could then be used
to provide 95% credible intervals of population prevalence that account for
differences in test quality. Our model is robust to differences in population
prevalence except when prevalence is low (e.g., ,0.02%), because the detection
and infection parameters become inestimable. When planning surveillance in areas
where disease may not occur, we recommend assuming values for the test detection
parameters to allow for estimation of population prevalence. Our approach also
has application to CWD screening for transport of wild or captive deer or
targeted culling efforts. Individuals could be identified that require
additional testing to confirm disease status with desired levels of certainty,
although our approach cannot account for misdiagnosing deer in early stages of
infection when PrPCWD is undetectable (Wolfe et al. 2002, 2007). In light of our
findings, further attention to the potential for repeated sampling to lower the
probability of detecting infection via rectal mucosa biopsy appears warranted
before such approaches are substituted for more conventional surveillance that
relies on samples collected postmortem.
The diagnostic sensitivity of rectal biopsy testing for determining CWD
infection status ranged from 63% to 100% in the 4 white-tailed deer herds in the
study. The aim of the metaanalytic modeling in the present study was to improve
the estimate of diagnostic sensitivity accuracy in a manner more broadly
applicable to future application.9,11 Thus, the pooled estimate of diagnostic
test sensitivity of rectal biopsy testing was 68% when based on the 4 herds of
the current study, which was refined to 74% (95% CLs: 60% and 85%) after
inclusion of data from 2 additional herds from a similarly conducted study (data
not shown).7
***Conversely, false-negative results should be expected from rectal biopsy
samples in generally one-fourth of all CWD-infected deer. Thus, a negative test
result based on a single rectal biopsy sample should not be interpreted as a
deer being free of CWD infection.
Errors in specificity, or false positives, can occur as a result of
cross-contamination of samples during necropsy or possibly by spontaneous
misfolding during sPMCA. We previously reported our method of sPMCA has a
specificity of 99.6% in the laboratory setting35. Negative samples used for this
sPMCA experiment were used to show specificity in our laboratory setting, but do
not account for possible necropsy contamination of the elk tissues. To remove
bias from possible necropsy-related false positives in years 2009 and 2010 we
separated “Trusted” from “Unknown” samples. Trusted samples were those found
positive by IHC (2008–2010) and all samples from 2011, when we employed
decontamination techniques at necropsy. Unknown samples are IHC-negative samples
from 2009 and 2010. sPMCA results for these samples could be true, sub-clinical
positives outside of the detection limit of IHC, or they could be false
positives resulting from contamination during sample collection at necropsy. To
maintain a conservative estimate of the specificity of sPMCA, Trusted and
Unknown samples were assumed to have independent specificity probabilities.
Errors in sensitivity, or false negatives, for either assay occurred for two
reasons: either the concentration of PrPCWD was below the detection limit of the
assay or, despite the overall presence of PrPCWD in the tissue, the exacted
portion that was assayed did not contain detectable levels of PrPCWD due to
non-homogenous distribution19,30,41,58. All estimates are reported with a 95%
Bayesian credible interval (CI).
Citation: Balachandran, A., Thomsen, B.V., Gidlewski, T., Spraker, T.R.,
Mitchell, G., Soutyrine, A., Harrington, N.P., Munger, R., Schneider, D.A.,
Orourke, K.I. 2009.
Diagnosis of preclinical CWD in farmed white-tailed deer in Canada by the
immunohistochemical examination of recto-anal mucosa- associated lymphoid tissue
(RAMALT).
NeuroPrion Workshop: New developments in TSEs of domestic and wild animals.
pg.9
Interpretive Summary: Diagnosis of prion disease [for example, scrapie in
sheep and chronic wasting disease (CWD) in elk and deer] relies upon sensitive
detection of disease-associated prion protein in the brain or tissues containing
lymph follicles. Live animal testing for scrapie disease in sheep has included
evaluation of biopsy samples of the tonsil, third eyelid and rectal mucosa.
Similarly, diagnosis of CWD in live elk has been recently accomplished through
biopsy of the rectal mucosa. This invited report to the annual NeuroPrion
meeting summarizes the diagnostic performance (test sensitivity) of various
tissue sampling sites that were collected after death. The report summarizes the
findings from two different populations of captive white-tailed deer from
Saskatchewan, Canada. The diagnostic performance of the rectal mucosa samples
were similar but lower than that achieved in two other lymphoid tissues, but
greater than that achieved in the brain. While these studies were conducted on
tissues collected after death, the findings demonstrate the comparative
potential for biopsy of the rectal mucosa in live deer not yet showing signs of
disease.
***While many factors may influence test performance in other deer
populations, these studies showed that false-negative diagnosis occurred most
often in deer presumed to be in an early stage of disease and carrying a
mutation in the prion protein gene (codon 96).
Technical Abstract: This report summarizes the comparative diagnostic
performance of postmortem rectoanal mucosa-associated lymphoid tissue (RAMALT)
sampling in two white-tailed deer farms from Saskatchewan, Canada.
*The apparent prevalence of disease in these two farms was 21% and 31%.
None of these deer were demonstrating signs consistent with CWD. The
overall tissue-specific test sensitivities were ranked:
RPLN>tonsil>RAMALT>obex. Test sensitivities in deer having at least one
PRNP G96S allele were generally lower but similarly ranked. False negative
RAMALT results were associated with early disease progression, as assessed by
PrPCWD accumulation scores in the obex, and/or the PRNP G96S allele. The
proportion of CWD-positive RAMALT follicles were generally lowest in deer early
in disease progression and/or heterozygous at PRNP codon 96. And, as expected,
variation in the proportion CWD-positive RAMALT follicles was inversely related
to the total number of observable follicles per sample. These comparisons made
on samples collected postmortem suggest general diagnostic evaluation of RAMALT
samples in white-tailed deer would have intermediate test sensitivity as
compared to evaluation of RPLN and obex.
*While many factors may influence actual test performance, early stage of
disease progression and the PRNP G96S allele are two that were associated with
lower test sensitivities.
Citation: Balachandran, A., Thomsen, B.V., Gidlewski, T., Spraker, T.R.,
Mitchell, G., Soutyrine, A., Harrington, N.P., Munger, R., Schneider, D.A.,
Orourke, K.I. 2009.
Diagnosis of preclinical CWD in farmed white-tailed deer in Canada by the
immunohistochemical examination of recto-anal mucosa- associated lymphoid tissue
(RAMALT).
NeuroPrion Workshop: New developments in TSEs of domestic and wild animals.
pg.9
Interpretive Summary: Diagnosis of prion disease [for example, scrapie in
sheep and chronic wasting disease (CWD) in elk and deer] relies upon sensitive
detection of disease-associated prion protein in the brain or tissues containing
lymph follicles. Live animal testing for scrapie disease in sheep has included
evaluation of biopsy samples of the tonsil, third eyelid and rectal mucosa.
Similarly, diagnosis of CWD in live elk has been recently accomplished through
biopsy of the rectal mucosa. This invited report to the annual NeuroPrion
meeting summarizes the diagnostic performance (test sensitivity) of various
tissue sampling sites that were collected after death. The report summarizes the
findings from two different populations of captive white-tailed deer from
Saskatchewan, Canada. The diagnostic performance of the rectal mucosa samples
were similar but lower than that achieved in two other lymphoid tissues, but
greater than that achieved in the brain. While these studies were conducted on
tissues collected after death, the findings demonstrate the comparative
potential for biopsy of the rectal mucosa in live deer not yet showing signs of
disease. While many factors may influence test performance in other deer
populations, these studies showed that false-negative diagnosis occurred most
often in deer presumed to be in an early stage of disease and carrying a
mutation in the prion protein gene (codon 96). Technical Abstract: This report
summarizes the comparative diagnostic performance of postmortem rectoanal
mucosa-associated lymphoid tissue (RAMALT) sampling in two white-tailed deer
farms from Saskatchewan, Canada. The apparent prevalence of disease in these two
farms was 21% and 31%. None of these deer were demonstrating signs consistent
with CWD. The overall tissue-specific test sensitivities were ranked:
RPLN>tonsil>RAMALT>obex. Test sensitivities in deer having at least one
PRNP G96S allele were generally lower but similarly ranked. False negative
RAMALT results were associated with early disease progression, as assessed by
PrPCWD accumulation scores in the obex, and/or the PRNP G96S allele. The
proportion of CWD-positive RAMALT follicles were generally lowest in deer early
in disease progression and/or heterozygous at PRNP codon 96. And, as expected,
variation in the proportion CWD-positive RAMALT follicles was inversely related
to the total number of observable follicles per sample. These comparisons made
on samples collected postmortem suggest general diagnostic evaluation of RAMALT
samples in white-tailed deer would have intermediate test sensitivity as
compared to evaluation of RPLN and obex. While many factors may influence actual
test performance, early stage of disease progression and the PRNP G96S allele
are two that were associated with lower test sensitivities.
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. ...
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
Monday, August 17, 2015
FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS
*** I told Olympus 15 years ago about these risk factors from endoscopy
equipment, disinfection, even spoke with the Doctor at Olympus, this was back in
1999. I tried to tell them that they were exposing patients to dangerous
pathogens such as the CJD TSE prion, because they could not properly clean them.
even presented my concern to a peer review journal GUT, that was going to
publish, but then it was pulled by Professor Michael Farthing et al... see ;
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
Alzheimergate? When miscommunication met sensationalism, or just another
cover up ?
the government has been trying to cover up that fact since the late 80s,
early 90s.
cover up, cover up, cover up at all cost, including human and animal health
$$$
AND WE ALL KNEW THIS WAS THE CASE $$$
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
*** IN STRICT CONFIDENCE ***
Singeltary comment ;
Wednesday, September 23, 2015
NIH Availability for Licensing AGENCY: [FR Doc. 2015–24117 Filed 9–22–15;
8:45 am] Detection and Discrimination of Classical and Atypical L-Type BSE
Strains by RT-QuIC
Saturday, September 19, 2015
*** An interview with Professor John Collinge: VIDEO Director of the MRC
Prion Unit Part of the Hayward Gallery's History Is Now ***
Transmissible Spongiform Encephalopthy TSE Prion Disease
*** Kuru Video
Kuru: The Science and The Sorcery
*** Scrapie Video
*** Human Mad Cow Video
*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
11:20 AM
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