A Revolutionary Approach to Enhancing the Quality of Marengo County's Deer
Herd by introducing Record Breaking Genetics. Beginning in the Fall of 2012, the
Big Buck Project led by Tutt Land Company, will be releasing Trophy Class
Whitetail Breeder Bucks all across Marengo County in an effort to enhance the
quality of Marengo County's Whitetail Deer Herd. This ground breaking approach
to creating a positive impact on our local deer herd will provide local hunters
with a little more to look for while hunting the woods of Marengo County. As we
get closer to our first release date, we will be providing more detailed
information about the initiative and where the Big Bucks are going to be
released. Visit the link below to keep up with all current news of the Big Buck
Project.
The Big Buck Project is set to begin in the fall of 2012 in Marengo County,
Alabama. This initiative, led by Tutt Land Company, is expected to create waves
throughout the hunting industry in Alabama and beyond. Check in for updates on
this revolutionary initiative to restore “Record Book Genetics” to the local
Whitetail Population in Marengo County, Alabama.
Tutt Land Company conducted a 5 year controlled research project in Marengo
County that yielded amazing results in both herd health and quality antler
growth by introducing new trophy genetics to the native herd. Tutt Land Company
and the Big Buck Project Partners are prepared to take this research, along with
data collected from similar studies and wildlife biologists, and apply it to all
of Marengo County. We will begin the project in the fall of 2012 by purchasing
whitetail breeder bucks with 200” genetics and releasing them at various
locations throughout Marengo County. These bucks will be tagged in both ears
with highly visible tags. With enough support, this revolutionary approach will
yield amazing results throughout the whitetail population of Marengo County for
years to come.
Big Buck project intends to promote the great natural resources of Marengo
County by promoting deer management and hunter education. Positive impacts on
the Marengo County deer herd by introducing new genetics will help benefit
Marengo County by bringing attention to our natural resources and proper deer
management.
According to the Alabama Game and Fish department, it is perfectly legal to
purchase a deer from a state licensed deer breeding facility and release it on
private property.
By creating a platform to promote proper deer management and educate
hunters. Our data shows that 1 breeder buck or 1 breeder doe can impact
thousands of offspring during that deer’s lifespan. If 1 breeder buck breeds
5-10 does per year, then the math adds up to literally thousands of deer over
time that can be impacted in varying degrees from this breeder buck in a 6-10
year life span.
Big Buck Project will utilize deer from state licensed and inspected
breeder facilities and release them at various points across Marengo County as
funding levels are achieved. Currently, support from our partners and landowners
suggest that Big Buck Project may be able to achieve a sustained yearly release
of both bucks and does in large enough numbers to have a significant impact. We
currently have businesses and landowners coming on board every day.
Big Buck Project will have a positive impact on the deer hunting in Marengo
County. Results will be hard to determine during the first few years, but
sustained releases over time should yield positive results for Marengo County
hunters.
Rates for bucks and does vary greatly depending on the breeding facility
and the genetic line. Our data suggests that the average price of bucks and does
is currently between $2,000 and $20,000. Recently, a breeding doe sold for
$90,000 during a public auction in Huntsville, AL which was attended by Big Buck
Project Partners.
The landowner has every right to harvest one of these deer under current
state regulations. Big Buck Project recommends that Marengo County landowners
allow these released breeder deer to live and help provide the intended results
of improving the Marengo County deer herd.
No, this is not legal under current Alabama regulations.
All deer that will be released will be purchased from State Licensed,
Inspected, and Regulated breeding facilities in Alabama. Deer have been released
in Marengo County for over 25 years on both free range properties and in high
fence enclosures. Big Buck Project will not release a deer unless it is
delivered from a state licensed and inspected facility. Alabama’s state licensed
breeding facilities currently release thousands of deer on private properties
throughout the state and in Marengo County. This practice has been going on for
over 20 years. To date there have been no documented reports of Chronic Wasting
Disease in Alabama. Information found on the Alabama Department of Conservation
website www.outdooralabama.com :
•CWD is not known to be transmissible to humans or domestic
livestock.
•CWD is a fatal disease of white-tailed deer, mule deer, and elk.
•CWD is not known to exist in Alabama or any other southeastern
state.
•CWD will not likely be found in the Southeast unless it is transported
here.
•It is illegal to import any deer or other cervid into Alabama.
According to state wildlife officials, all deer released from state
licensed breeder facilities become state property and fall under state hunting
regulations once they are released on any property in Alabama that is not a
state licensed breeding facility.
•CWD is not known to be transmissible to humans or domestic livestock...
WRONG!
cwd transmits to deer, elk, cattle, sheep, rodents, and many scientist are
sounding the alarm for the potential transmission to humans... tss
a foolish assessment. do the southern states have some sort of cloaking
device that will protect no matter what ? I don’t think so. Texas recently was
forced to document CWD by New Mexico, finally, it’s been waltzing across the
border from New Mexico WSMR for close to a decade. I can assure you, TSE prion
disease knows NO borders, and putting restrictions on regulations by age, is
foolish...tss
•CWD will not likely be found in the Southeast unless it is transported
here. WRONG!
another foolish assessment. very foolish. as the crow flies, dream on,
because the possible routes and sources of the CWD TSE prion coming into the
Southeastern USA are many. this just more wishful thinking by an industry that
does not give a damn about the wild cervids... tss
NONE of these deer are tested for CWD, so tell me how they are proven to
be free of CWD ???
IF THSE SUPER FREAK deer, i.e. deer with quality antler growth by
introducing new trophy genetics to the native herd, are still alive when
released, still alive, when left the facilities they come from, how is there any
guarantee for them to be CWD free, free from sub-clinical CWD ???
if you think that all those deer that are brought in from who knows where,
that are live, and supposedly cwd free because of bogus assumptions, will simply
spread the cwd agent further and further, in my opinion. sub-clinical cwd is
real, and it's still spreading, by these bogus industry fed assumptions...
Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer
Long after Oral Exposure to Urine and Feces from CWD+ Deer
I will tell you, there is no proof these cervids are free of CWD. only a
myth that all animals on game farms are tested, which is totally fabricated, and
not true. the same SSS policy the USDA et al use to hide BSE in cattle, is used
on game farms i.e. shoot, shovel, and shut the hell up. also, when age
restrictions are put on CWD testing of 12 or 16 months, where we have fawns as
young as 4 and 5 months old documented with CWD, again, game farms are missing
CWD positive cervids. in my opinion, these game farms and straw bred circus
freak shows for super bucks are nothing more than a petri dish for CWD TSE prion
disease.
Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of fawns
sampled were between the ages of 5 to 9 months, though some were as young as 1
month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of
the positive fawns were taken from the core area of the CWD eradication zone
where the highest numbers of positive deer have been identified.
snip...
Dr. Langenberg noted that while the youngest CWD-positive fawns had
evidence of disease-causing prions only in lymph node tissue, several of the
older CWD-positive fawns had evidence of CWD prions in both lymph node and brain
tissues -- suggesting further progression of the disease.
snip...
Our fawn data shows that a few wild white-tailed deer may become sick from
CWD or may transmit the disease before they reach that age of 16 months."
WHILE the Texas deer czar was in Wisconsin, Texas documented it’s first
case of CWD, finally. New Mexico made them finally test there, not because I did
not tell them a time or two. But something he stated years ago, I think everyone
should read ;
Appointed by Gov. Scott Walker as the result of a campaign promise, Texas
deer biologist James Kroll, right, is shown with Walker at a meeting with
hunters in North Bristol.
Democratic legislators Thursday asked for a public hearing at which the
Texas expert hired by Gov. Scott Walker to analyze state deer management can
answer questions about his work and explain past comments he made that seemed to
favor private hunting preserves over public lands.
The legislators, minority members of the Senate and Assembly natural
resource committees, said comments by James Kroll, who was hired last year and
is being paid $125,000 to conduct his study, run counter to the history of
hunting and public lands in Wisconsin.
“Privatizing hunting is not in keeping with our state’s heritage and
tradition,” said State Rep. Fred Clark, D-Baraboo. “If this is what Dr. Kroll
believes, hunters — and all people of Wisconsin — deserve to know.”
Kroll, whose final report is due at the end of June, has called the
criticisms politically motivated, “presumably to aid in successfully removing
Gov.Walker.
“Since I am not politically motivated, did not vote for Gov. Walker, will
not be able to vote in the upcoming election, and am neither a Democrat nor
Republican, I am concerned and saddened by things being said about me and my
positions and values related to white-tailed deer,” Kroll said in a statement
last week.
In his preliminary report, Kroll was very critical of the DNR for not
listening to hunters and using bad science to estimate deer populations.
He also said DNR biologists have not done enough to work with private
landowners and, during public meetings on the initial report, recommended that
the agency should put more resources into encouraging management of deer on
private lands.
“Quite candidly,” Clark said, “the conclusions raise some serious questions
about what he will recommend.”
Kroll was also criticized by legislators at Thursday’s press conference for
widely-circulated comments that were attributed to him in a 2002 article on
Texas game farms in “Texas Monthly” magazine.
“People who call for more public lands are cocktail conservationists who
are really pining for socialism,” Kroll was quoted as saying in the article. He
also called national parks “wildlife ghettos” and accused the government of
gross mismanagement of game animals.
While he did not return a phone call Thursday, Kroll responded to the
criticisms in a statement he released last week.
Kroll said his comment about “cocktail conservationists” was aimed at
“well-meaning, wealthy individuals who support establishing a park, kicking the
native peoples off their land and then go home thinking they have done something
great.” He said he used the phrase “wildlife ghettos” to describe poorly managed
public lands.
“The unhappiness with the way whitetails have been managed in Wisconsin
came from the false idea that government always knows best, especially when they
have a computer program,” Kroll said.
Dr. Deer Wisconsin Report: Will High-Fence Bias Skew Final Plan?
Categories: Blogs, Daniel Schmidt's Whitetail Wisdom, Deer News, Featured
Tags:
antler restricitons, dan schmidt, Dr. Deer, james kroll, James Kroll
Wisconsin, qdm, quality deer management, texas hunting, wisconsin deer hunting
March 29, 2012
According to Wisconsin’s White-Tailed Deer Trustee Dr. James Kroll, people
who call for more public hunting opportunities are “pining for socialism.”
He further states, “(Public) Game management is the last bastion of
communism.”
These are just two insights into the man who has been asked to provide
analysis and recommended changes to Wisconsin’s deer management program. Kroll’s
insights are from an article entitled “Which Side of the Fence Are You On?” by
Joe Nick Patoski for a past edition of Texas Monthly. If nothing more, the
article gives an unabashed look into the mind-set that will be providing the
Wisconsin DNR with recommendations on how to change their deer management
practices. James Kroll (also known as “Deer Dr.”) was appointed to the Wisconsin
“deer czar” position last fall. He was hired by the Department of Administration
and instructed to complete a review of the state’s deer management program.
“Game Management,” says James Kroll, driving to his high-fenced,
two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.”
Kroll, also known as Dr. Deer, is the director of the Forestry Resources
Institute of Texas at Stephen F. Austin State University, and the “management”
he is referring to is the sort practiced by the State of Texas. The 55-year-old
Kroll is the leading light in the field of private deer management as a means to
add value to the land. His belief is so absolute that some detractors refer to
him as Dr. Dough, implying that his eye is on the bottom line more than on the
natural world.
Kroll, who has been the foremost proponent of deer ranching in Texas for
more than thirty years, doesn’t mind the controversy and certainly doesn’t fade
in the heat. People who call for more public lands are “cocktail
conservationists,” he says, who are really pining for socialism. He calls
national parks “wildlife ghettos” and flatly accuses the government of gross
mismanagement. He argues that his relatively tiny acreage, marked by eight-foot
fences and posted signs warning off would-be poachers, is a better model for
keeping what’s natural natural while making money off the land. A trip to South
Africa six years ago convinced Kroll that he was on the right track. There he
encountered areas of primitive, lush wildlife-rich habitats called game ranches.
They were privately owned, privately managed, and enclosed by high fences. He
noticed how most of the land outside those fences had been grazed to the nub,
used up. “Game ranches there derive their income from these animals — viewing
them, hunting them, selling their meat,” he says. “There are no losers.” At his
own ranch Kroll has set up a smaller version of the same thing. His land is
indeed lush, verdant, with pine groves, an abundance of undergrowth, wild
orchids, New Jersey tea, jack-in-the-pulpits, and other native plants. He has
also set up a full-scale breeding research center and is one of twenty Texas
deer breeders using artificial insemination to improve his herd. “We balance sex
and age ratio,” he says. “We manage habitat. We control the population and
manage for hunting. I want to leave the deer herd better than it was before we
came.” It is interesting to note that, in 2001, the State of Texas shifted its
deer management strategies toward the same leanings that Kroll has suggested for
Wisconsin. In Texas, the change was brought about via heavy lobbying from the
high-fence deer ranching industry. This pressure helped convince the Texas Parks
and Wildlife to change their regulations and allow private landowners to select
the own deer biologists.
“That has given landowners more freedom,” Kroll told Texas Monthly.
“(However,) You still have to let the state on your land to get a
wildlife-management permit.” The key difference here is that 98 percent of Texas
is comprised of private land. Wisconsin, on the other hand, consists of
approximately 34.8 million acres of land, and 25.5 percent of the state’s
638,000 gun-hunters reported hunting on public land at some point during the
season (2010, Duey, Rees).
According to the Wisconsin Realtors Association, more than 5.7 million
acres of this land, or 16.5 percent, is publicly owned and used for parks,
forests, trails, and natural resource protection. [Note: these statistics do not
include the public land used for roads, government buildings, military bases,
and college/school campuses.] This 5.7 million acres of public land is owned as
follows: Federal government owns approximately 1.5 million acres (4.4 percent of
the state’s land area). Almost all of the federal forestland in Wisconsin is
located in Chequamegon-Nicolet National Forest. State government owns
approximately 1.6 million acres (4.6 percent of the state’s land area). The land
is managed by two agencies, the Board of Commissioners of Public Land (who
manages lands granted by federal government) and the DNR (managing land owned by
the state). County government owns approximately 2.6 million acres (7.5 percent
of the state’s land area). Public land is located in 71 of Wisconsin’s 72
counties, with the most public land located in Bayfield County (464,673 acres).
[Note: Menominee County does not have any public land, but 98 percent of the
land is held in trust by the Menominee Tribe.] Twenty counties have more than
100,000 acres of public land, while only 12 counties have fewer than 10,000
acres. What does this all mean? My initial reaction, which is one that I
predicted when Kroll was named to the state’s deer trustee position, is that his
team’s final recommendations — if implemented — will be heavily skewed toward
the state’s larger landowners (500+ acres) and folks who own small parcels in
areas comprised mostly of private land. It is also my prediction that the final
recommendations (again, if implemented) will do little, if anything, to improve
deer herds and deer hunting on Wisconsin’s 5.7 million acres of public land.
Where does this leave the public-land hunter? “It will suck to be you,” said one
deer manager who asked to remain anonymous out of fear for his job. “The
resources and efforts will go toward improving the private land sector. This is
all about turning deer hunting away from the Public Land Doctrine and more
toward a European-style of management — like they have in Texas.” I do, of
course, hope these assumptions are wrong. As with all things in life, we should
maintain an open mind to change. Life is all about change. However, change for
the sake of change is usually a recipe for disaster. Especially when that change
is driven by something more than a sincere desire to manage public resources for
the greater good. As noted yesterday (Dr. James Kroll Report: Is That All You
Get For Your Money), I will provide more of my opinions and interpretation on
this important issue in forthcoming installments of this blog. Read his full
preliminary report here.
“Game Management,” says James Kroll, driving to his high-fenced,
two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.”
Kroll, also known as Dr. Deer, is the director of the Forestry Resources
Institute of Texas at Stephen F. Austin State University, and the “management”
he is referring to is the sort practiced by the State of Texas. The 55-year-old
Kroll is the leading light in the field of private deer management as a means to
add value to the land. His belief is so absolute that some detractors refer to
him as Dr. Dough, implying that his eye is on the bottom line more than on the
natural world.
Kroll, who has been the foremost proponent of deer ranching in Texas for
more than thirty years, doesn’t mind the controversy and certainly doesn’t fade
in the heat. People who call for more public lands are “cocktail
conservationists,” he says, who are really pining for socialism. He calls
national parks “wildlife ghettos” and flatly accuses the government of gross
mismanagement. He argues that his relatively tiny acreage, marked by eight-foot
fences and posted signs warning off would-be poachers, is a better model for
keeping what’s natural natural while making money off the land.
“It will suck to be you,” said one deer manager who asked to remain
anonymous out of fear for his job.
“The resources and efforts will go toward improving the private land
sector. This is all about turning deer hunting away from the Public Land
Doctrine and more toward a European-style of management — like they have in
Texas.”
TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT
CALLING KETTLE BLACK
Texas Animal Health Commission (TAHC) is Now Accepting Comments on Rule
Proposals for “Chronic Wasting Disease (CWD)”
Alabama captive cervid farming, testing and regulations for CWD, recipe
for disaster
FIRST OF ALL, the likelyhood of Alabama ever finding a case of CWD would
almost be impossible, considering several factors, but the biggest factor is the
low testing figures for CWD over the years. the regulatory authority over low
fence cervid game farms is a recipe for cwd disaster. the myth that game farms
test every animal, is so far out of touch with reality that it's just as well be
called a lie. these low fence game farms have not a clue. every dead animal
tested for cwd never in a million years, call it what it is, like the cattle
industry and the usda and BSE, they call it the SSS policy, shoot, shovel, and
shut the hell up. how in the world can a state claim to be seeking out cwd to
find and destroy, when you only test some 300 deer (wild and farmed), with some
1,800,000 deer in the state? i will tell you, it's a bold face lie when they
claim cwd free with said testing figures. low fence regulations is another
factor that in my opinion is wrong. hell, in my younger day i could just about
jump over an 8 foot fence, and you mean to tell me that deer are not going to
jump an 8 foot fence, i don't believe it. fencing should be double fencing, at
least 12 foot tall, with a capture or dead zone perimeter between the two
fences, big enough to disperse any potential Aerosol transmission of cwd via
dirt and dust, so any potentially tainted ground soil from said low fence game
farm, would be in that capture or dead zone between fences.
let's look at the very low cwd testing figures for Alabama, and then you
may not have to ask yourself why Alabama has not documented a case of CWD yet $
fact is, they are not looking to find it yet. kinda like Texas did, where Texas
looked in all the wrong places for a decade, before New Mexico made them test
where they would find it, and they did.
Alabama captive cervid farming industry, testing and regulations for CWD,
recipe for disaster
approximately 1,800,000 deer in Alabama in 2011, and only 311 tested for
CWD. ...
What is the Division of Wildlife and Freshwater Fisheries doing to keep CWD
from reaching our state?
The Division is currently taking several measures to help prevent CWD from
reaching our state. The State has had a regulation banning the importation of
all cervids (members of the deer family) into Alabama since 1973. Recently the
fines for violating this regulation were significantly increased. Investigations
have discovered animal movements among many of the 20 privately owned elk herds
(outside of Alabama) where CWD has been diagnosed. The movement of infected
animals very likely was the reason for the disease's spread. Halting the
movement of live captive deer and elk into and within Alabama is a major step in
preventing the disease from reaching our state.
The Division also started an active monitoring program for CWD during the
2001-02 hunting season. The number of Alabama deer tested for the presence of
CWD is as follows:
None of those deer tested positive for the disease. Plans are to continue
this testing program during the 2011-2012 season.
‘Animals from captive herds are included in the state CWD sampling program.
‘
Department of Conservation and Natural Resources. Contact: Gary Moody,
gmoody@dcnr.alabama.gov
Cervid imports have not been allowed since 1973. It is illegal to have
penned deer, several high fenced areas do exist.
Cervid imports have not been allowed since 1973.
NA - Have not allowed imports for over 30 years.
Animals from captive herds are included in the state CWD sampling program.
The Department of Agriculture is implementing a more comprehensive sampling
protocol.
Sampling began in 2001, with 90 animals being tested. In 2002-03, 440
animals were tested; 2003-04, 768 were tested; 2004-05, 745 tested; 2005-06, 798
tested;
06-07, 654 tested. Plan to continue surveillance efforts. Education efforts
have also made the public more aware of the need to report deer that may be
doing poorly or may not be acting normally. Those deer are submitted for testing
as well.
Baiting is not allowed.
Feeding is not allowed in areas of hunting.
No ban.
State wildlife officials want hunters and landowners to know Chronic
Wasting Disease (CWD) in deer has not occurred in Alabama and they hope to keep
it that way. The Alabama Department of Conservation and Natural Resources
(ADCNR) Division of Wildlife and Freshwater Fisheries (WFF) is taking several
measures to help prevent the disease from reaching the state.
Diagnostics to confirm the presence of CWD require collecting the skull and
neck vertebra from adult age class hunter harvested white-tailed deer. WFF staff
work with local clubs and deer processors to collect the necessary samples for
CWD monitoring. A minimum of 300 samples have been collected annually statewide
for the past 10 years. WFF staff expect to complete this hunting season’s
collection and monitoring by Christmas. Collected samples are sent to the State
Department of Agriculture diagnostic labs for testing and analysis. WFF
appreciates all of those that cooperated to obtain the samples.
CWD is a fatal disease affecting the central nervous system of deer and
elk. It belongs to a family of diseases known as transmissible spongiform
encephalopathies (TSEs). The disease attacks the brains of infected deer and elk
and causes animals to become emaciated (skinny), display abnormal behavior, lose
bodily functions and die. It has been found in captive and/or wild cervids
(members of the deer family) in 18 states and two Canadian provinces.
Alabama is recognized as a leader in minimizing disease risks by preventing
the importation of deer. Alabama has had a regulation banning the importation of
all cervids into Alabama since 1973. Convictions for violating the importation
ban carry a fine of $1,000-5,000 and up to 30 days in jail. Many other states
have since implemented some form of this regulation to reduce their risk of
introducing CWD.
Many Alabamians hunt outside the state and bring their harvested animals
back with them. WFF requests that these hunters take the following precautions
before bringing any harvested cervids from CWD endemic areas into the state:
• Remove the bones and package the meat; avoid cutting into the spinal cord
or removing the head; also avoid quartering the carcass with any of the spinal
column or head attached.
• Do not bring the brain, intact skull, or spinal cord back into the state.
• If you wish to take the antlers attached to the skull plate, thoroughly
scrape and clean tissue from the skull plate using a knife or brush and bleach.
Thoroughly clean all utensils afterward with bleach.
• If you are hunting in an endemic area, have the animal tested for CWD in
the state in which it was harvested.
• Finished taxidermy products, including head mounts, are not known to pose
a risk.
The ADCNR needs your support to maintain Alabama’s CWD-free status. You can
assist the WFF with its CWD monitoring program by reporting any transport of
live deer or elk on Alabama’s roads and highways. Call the Operation Game Watch
line immediately at 1-800-272-4263 if you see live deer or elk being transported
in Alabama. Contacting the Division immediately makes it more likely the deer or
elk will be intercepted before it can be released. You should also call this
number if you see a deer that exhibits clinical signs of CWD. Personnel will
contact you to obtain additional information.
The Alabama Department of Conservation and Natural Resources promotes wise
stewardship, management and enjoyment of Alabama’s natural resources through
five divisions: Marine Police, Marine Resources, State Lands, State Parks, and
Wildlife and Freshwater Fisheries. To learn more about ADCNR, visit
www.outdooralabama.com.
Deer Fact: As of 2011 the deer population in the State of Alabama is
1,800,000.
From the Field: Efficacy of detecting Chronic Wasting Disease via sampling
hunter-killed white-tailed deer
Duane R. Diefenbach, Christopher S. Rosenberry, and Robert C. Boyd
Surveillance programs for Chronic Wasting Disease (CWD) in free-ranging
cervids often use a standard of being able to detect 1% prevalence when
determining minimum sample sizes. However, 1% prevalence may represent
>10,000 infected animals in a population of 1 million, and most wildlife
managers would prefer to detect the presence of CWD when far fewer infected
animals exist. We wanted to detect the presence of CWD in white-tailed deer
(Odocoileus virginianus) in Pennsylvania when the disease was present in only 1
of 21 wildlife management units (WMUs) statewide. We used computer simulation to
estimate the probability of detecting CWD based on a sampling design to detect
the presence of CWD at 0.1% and 1.0% prevalence (23–76 and 225–762 infected
deer, respectively) using tissue samples collected from hunter-killed deer. The
probability of detection at 0.1% prevalence was <30 1.0="1.0" 2="2" 46="46" a="a" an="an" and="and" any="any" approach="approach" at="at" believe="believe" but="but" cwd="cwd" deer.="deer." deer="deer" demonstrated="demonstrated" detection="detection" div="div" essential="essential" for="for" hunter-killed="hunter-killed" importance="importance" is="is" multifaceted="multifaceted" of="of" on="on" our="our" part="part" prevalence="prevalence" probability="probability" program="program" rather="rather" reliance="reliance" results="results" sample="sample" sizes="sizes" sole="sole" statewide="statewide" surveillance="surveillance" testing="testing" than="than" that="that" the="the" was="was" we="we" with="with">
Key words Chronic Wasting Disease, Odocoileus virginianus, Pennsylvania,
prevalence, probability of detection, sample size, sampling design, white-tailed
deer
Section 1. For purposes of Sections 1 to 6, inclusive, of this act, the
following words have the following meanings:
(1) GAME ANIMAL. A species of animal designated by the Commissioner of
Conservation and Natural Resources pursuant to Section 9-2-7 of the Code of
Alabama 1975, as a game or fur-bearing animal, any game or fur-bearing animal
that exists historically and naturally in the wild within this state, or any
game animal of the species of the family Cervidae (deer) that exists within this
state in the wild as a result of the natural expansion of its range prior to the
effective date of this act which are white-tailed deer, fallow deer, and elk.
Regulation 220-2-.138 LICENSED GAME BREEDERS
All persons, firms or corporations licensed under Section 9-11-30 to engage
in the business of raising game birds, game animals, or fur bearing animals
shall:
1. Submit to the Division of Wildlife and Freshwater Fisheries an accurate
inventory of all stock and maintain a record of inventory changes caused by
births, deaths, escapes, sales, purchases or other causes; provided however,
holders of the nonindigenous game breeder option who are not engaged in the
breeding and handling of such animals may submit a good faith estimate of stock
inventory and inventory changes as to such animals.
2. Allow inspection by agents authorized by the Division of stock,
facilities and records at all reasonable times.
3. By April 1 of each year, fawns of the family Cervidae born on the
premises shall be marked with an ear tag, as specified by the Division, which
identifies each animal. All other stock of the family Cervidae shall be assigned
an ear tag number and shall be marked with the corresponding tag before any sale
or transfer. Such tags shall not be transferred to or reused on other
individuals. Tags shall not be removed, except during transfer when the animal
is being released, provided the tag shall be in possession during transport.
Animals which lose tags shall be reassigned a replacement tag number and
remarked before sale or transfer.
4. Identify the location of each facility by physical address and notify
designated Division personnel of any changes in size or location of the
facility.
5. Within 24 hours of discovery notify designated Division personnel of any
escapes or deaths and allow disease testing of animals that have died.
6. Upon notification by authorized Division personnel of a documented
disease risk, not remove from any facility any animals alive or dead until
approved by authorized Division personnel.
7. For species of the family Cervidae, obtain a premises registration
number and comply with the conditions set forth in any herd health or monitoring
plan that may be designated by the Alabama Department of Agriculture and
Industries. 8. Acquire animals only from other licensed game breeders, except by
written approval from authorized Division personnel.
The Commissioner of Conservation and Natural Resources, in cooperation with
the Alabama Department of Agriculture and Industries, may order the confiscation
and destruction of any animal that is deemed to be a substantial disease risk to
other wildlife, domestic animals, or the public without compensation to the
owner of such animal. This shall not affect the authority of other state or
federal agencies with respect to confiscation, destruction or condemnation of or
compensation for such animals.
Nothing in this regulation is intended to authorize the importation into
this state of any live animal, or their eggs or embryos which is otherwise
prohibited by law or regulation.
80-3-6- .23 Requirements For Wild Animals And SimiWild Animals Imported
Into Alabama; And/Or For Intrastate Movement Or Transportation And Disease
Control Of Certain Animals. Unless entry is prohibited otherwise by law enforce
by the the Department of Conservation or other game law, in order that wild
animals, and semiwild animals maintained in captivity (to include game-breeder’s
animals pursuant to Section 9-11- 30-31), Code of Ala. 1975,) may be imported
into the state; and/or in order that such animals may be moved or transported
from place to place, the number of animals involved shall be reported to the
State Veterinarian of Alabama ten (10) days prior to such entry of movement or
transportation, and immediate opportunity for examination afforded
representatives or authorized agents to determine the health status of such
animals. Specific entry, intrastate movement or transportation requirements for
Camelids; and entry, intrastate movement or transportation and disease control
requirements for live Cervidae and semi-wild animals are as follows:
(LINES ARE DRAWN THROUGH WHAT WAS TO BE ELIMINATED FROM SAID REGULATIONS
(a )...TSS)
==================================
(a ) Camelids including llamas, alpacas, and camels, and live Cervidae
imported into the state or maintained in captivity within the state which are in
intrastate movement or transportation within the state, shall have an official
Certificate of Veterinary Inspection issued by an accredited veterinarian and
shall have a permanent approved individual identification.
===================================
All live captive Cervidae as prescribed by the State Veterinarian of
Alabama, shall be made available to test for brucellosis, tuberculosis, and any
known, or to be developed tests for chronic wasting disease (CWD). Accredited
zoos, research or exhibition or treatment and rehabilitation facilities shall
have an approved CWD monitoring program, provided that Cervids entering into the
zoos and facilities must also originate from a herd that is under an approved
CWD monitoring program; and those facilities in compliance with the provisions
of Section 9-11-(30-31), Code of Ala. 1975, shall also have an approved CWD
monitoring program to include provisions for notification of animals that have
died from unknown causes.
( b ) For the purpose of disease control, the State Veterinarian with
assistance as needed from other state agencies and landowners, shall establish
by survey, questionnaire, or by physical presence or appointed representatives a
database for locating, registering, monitoring, and testing of Cervid herds
maintained in captivity. From the development and maintenance of a monitoring
program, the State Veterinarian shall establish guidelines for the diagnosis,
prevention, and control of CWD and TB, and any other emerging animal disease,
the test results shall be confirmed through another qualified testing facility.
If a positive test is determined and confirmed, a herd plan shall be forthwith
developed and executed. ...
Substance of Proposed Action : Following the application of the Chronic
Wasting Disease Monitoring Plan, applicants must involve an accredited
veterinarian in their herd plan. The Veterinarian must state that there is no
evidence of disease among deer on the farm. Therefore there is now no longer a
need for intrastate movement Certificate of Veterinary Inspections.
STATUTORY AUTHORITY: Code of Ala. 1975, §§ 2-2-8, 2-4-1, 2-15-150,
2-15-170.
HISTORY: Filed April 19, 1982. Amended: Filed February 11, 1997; effective
March 18, 1997. Amended: Filed November 15, 2000; effective December 20, 2000.
New Rule: Filed November 6, 2003; effective December 11, 2003.
Alabama Administrative Code. Alabama Department of Agriculture and
Industries. Animal Industry. Chapter 80-3-6. Livestock Sanitary Rules
Country of Origin: United States
Agency of Origin: Alabama Department of Agriculture and Industries
National Citation: AL ADC 80-3-6-.01 - .38
Agency Citation:
Last checked by Web Center Staff: 02/11
STATUTORY AUTHORITY: Code of Ala. 1975, § 2-15-170.
HISTORY: Filed Service April 19, 1982. Amended: Filed February 21, 1990.
80-3-6-.23. Requirements For Wild Animals And Simi-Wild Animals Imported
Into Alabama; And/Or For Intrastate Movement Or Transportation And Disease
Control Of Certain Animals.
Unless entry is prohibited otherwise by law enforced by the Department of
Conservation or other game law, in order that wild animals, and semi-wild
animals maintained in captivity (to include game-breeder's animals pursuant to
Section 9-11-(30-31), Code of Ala. 1975,) may be imported into the state; and/or
in order that such animals may be moved or transported intrastate from place to
place, the number of animals involved shall be reported to the State
Veterinarian of Alabama ten (10) days prior to such entry of movement or
transportation, and immediate opportunity for examination afforded
representatives or authorized agents to determine the health status of such
animals. Specific entry, intrastate movement or transportation requirements for
Camelids; and entry, intrastate movement or transportation and disease control
requirements for live Cervidae and semi-wild animals are as follows:
(a) Camelids including llamas, alpacas, and camels, and live Cervidae
imported into the state, or maintained in captivity within the state which are
in intrastate movement or transportation within the state, shall have an
official Certificate of Veterinary Inspection issued by an accredited
veterinarian and shall have a permanent approved individual identification. All
live captive Cervidae as prescribed by the State Veterinarian of Alabama, shall
be made available to test for brucellosis, tuberculosis, and any known, or to be
developed tests for chronic wasting disease (CWD). Accredited zoos, research or
exhibition or treatment and rehabilitation facilities shall have an approved CWD
monitoring program, provided that Cervids entering into the zoos and facilities
must also originate from a herd that is under an approved CWD monitoring
program; and those facilities in compliance with the provisions of Section
9-11-(30-31), Code of Ala. 1975, shall also have an approved CWD monitoring
program to include provisions for notification of animals that have died from
unknown causes.
(b) For the purpose of disease control, the State Veterinarian with
assistance as needed from other state agencies and landowners, shall establish
by survey, questionnaire, or by physical presence or appointed representatives a
database for locating, registering, monitoring, and testing of Cervid herds
maintained in captivity. From the development and maintenance of a monitoring
program, the State Veterinarian shall establish guidelines for the diagnosis,
prevention, and control of CWD and TB, and any other emerging animal diseases.
All testing shall be as prescribed by the State Veterinarian. If a Cervid tests
positive for CWD, or TB, or any other emerging animal disease, the test results
shall be confirmed through another qualified testing facility. If a positive
test is determined and confirmed, a herd plan shall be forthwith developed and
executed.
STATUTORY AUTHORITY: Code of Ala. 1975, §§ 2-2-8, 2-4-1, 2-15-150,
2-15-170.
HISTORY: Filed April 19, 1982. Amended: Filed February 11, 1997; effective
March 18, 1997. Amended: Filed November 15, 2000; effective December 20, 2000.
New Rule: Filed November 6, 2003; effective December 11, 2003.
WITHOUT CWD testing, can someone tell me how any veterinarian is capable of
detecting sub-clinical CWD ?
Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer
Long after Oral Exposure to Urine and Feces from CWD+ Deer
Nicholas J. Haley1, Candace K. Mathiason1, Mark D. Zabel1, Glenn C.
Telling2, Edward A. Hoover1*
1 Department of Microbiology, Immunology, and Pathology, College of
Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort
Collins, Colorado, United States of America, 2 Department of Molecular Biology
and Genetics, University of Kentucky, Lexington, Kentucky, United States of
America
Abstract
Chronic wasting disease (CWD) of cervids is a prion disease distinguished
by high levels of transmissibility, wherein bodily fluids and excretions are
thought to play an important role. Using cervid bioassay and established CWD
detection methods, we have previously identified infectious prions in saliva and
blood but not urine or feces of CWD+ donors. More recently, we identified very
low concentrations of CWD prions in urine of deer by cervid PrP transgenic
(Tg[CerPrP]) mouse bioassay and serial protein misfolding cyclic amplification
(sPMCA). This finding led us to examine further our initial cervid bioassay
experiments using sPMCA.
Objectives We sought to investigate whether conventional test-negative
deer, previously exposed orally to urine and feces from CWD+ sources, may be
harboring low level CWD infection not evident in the 19 month observation
period. We further attempted to determine the peripheral PrPCWD distribution in
these animals.
Methods Various neural and lymphoid tissues from conventional test-negative
deer were reanalyzed for CWD prions by sPMCA and cervid transgenic mouse
bioassay in parallel with appropriate tissue-matched positive and negative
controls.
Results PrPCWD was detected in the tissues of orally exposed deer by both
sPMCA and Tg[CerPrP] mouse bioassay; each assay revealed very low levels of CWD
prions previously undetectable by western blot, ELISA, or IHC. Serial PMCA
analysis of individual tissues identified that obex alone was positive in 4 of 5
urine/feces exposed deer. PrPCWD was amplified from both lymphoid and neural
tissues of positive control deer but not from identical tissues of negative
control deer.
Discussion Detection of subclinical infection in deer orally exposed to
urine and feces (1) suggests that a prolonged subclinical state can exist,
necessitating observation periods in excess of two years to detect CWD
infection, and (2) illustrates the sensitive and specific application of sPMCA
in the diagnosis of low-level prion infection. Based on these results, it is
possible that low doses of prions, e.g. following oral exposure to urine and
saliva of CWD-infected deer, bypass significant amplification in the LRS,
perhaps utilizing a neural conduit between the alimentary tract and CNS, as has
been demonstrated in some other prion diseases.
Citation: Haley NJ, Mathiason CK, Zabel MD, Telling GC, Hoover EA (2009)
Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long
after Oral Exposure to Urine and Feces from CWD+ Deer. PLoS ONE 4(11): e7990.
doi:10.1371/journal.pone.0007990
Editor: Jiyan Ma, Ohio State University, United States of America
Received: September 29, 2009; Accepted: October 29, 2009; Published:
November 24, 2009
Copyright: © 2009 Haley et al. This is an open-access article distributed
under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the
original author and source are credited.
Funding: This work was supported by NIH/NCRR Ruth L. Kirschstein
Institutional T32 R07072-03 and NIH/NIAID NO1-AI-25491-02 (EAH, GCT). The
funders had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests
exist.
* E-mail: Edward.Hoover@colostate.edu
SNIP...
In summary, we provide evidence for the presence of infectious prions in
the brains of conventional prion-assay-negative deer orally exposed 19 months
earlier to urine and feces from CWD-infected donor deer. This apparent low level
of prion infection was amplified by sPMCA, confirmed by Tg[CerPrP] mouse
bioassay, and detected only in the obex region of the brain. These results
demonstrate the potential for CWD prion transmission via urine and/or feces, and
highlight the application of more sensitive assays such as sPMCA in
identification of CWD infection, pathogenesis, and prevalence.
Genetic Influence/Stocking Source
A review of data collected to date by ADWFF’s Wildlife Section shows an
undeniable influence from the original stocking source for the local deer herd.
Deer from several sources, including many from outside Alabama, were used to
restock the state.
ALABAMA DEPARTMENT OF CONSERVATION AND NATURAL RESOURCES ADMINISTRATIVE
CODE CHAPTER 220-2 GAME AND FISH DIVISION TABLE OF CONTENTS 220-2-.01 2012-2013
Hunting Seasons
Conservation Chapter 220-2
Supp. 12/31/12 2-249
snip...
Supp. 12/31/12 2-264
Madison County conservation enforcement officers kill escaped bull elk
By Jeff Dute, Press-Register
on November 04, 2011 at 10:30 AM, updated November 04, 2011 at 12:13 PM
MADISON COUNTY, Alabama -- Conservation enforcement officers in Madison
County killed a young red deer/elk hybrid bull earlier this week that had
wandered more than 80 miles north, then east from where it is suspected to have
escaped from an enclosure near Hanceville, said District I assistant supervising
wildlife biologist Mitchell Marks.
Marks said the estimated 450-pound bull's path to where it was killed north
of Huntsville was easy to track from the numerous phone calls the department
received over the last two weeks.
When no one claimed ownership, Marks said the decision to kill it was based
on concerns over the possible spread of the always-fatal deer malady chronic
wasting disease and for public safety reasons.
"It's not believed that this animal had CWD, but since we don't know
exactly where it came from, first we have to test to make sure it doesn't," he
said. "We don't want to jeopardize our deer herd at all. Second, people in
Alabama are not used to seeing an animal of this size on our state's roads.
Something that big could be a public hazard that we want to remove."
There is no CWD test for live animals, so once it was killed, the hybrid's
head was removed and sent for testing while the carcass was buried, Marks said.
Kevin Dodd, Alabama's assistant chief of enforcement said since state
regulations only mention deer in regard to seasons and bag limits, hunters who
happen to encounter a non-native species such as the sika deer shot by a
bowhunter in Jackson County on Monday or even an elk are within their rights to
legally kill it.
"If they happen to see a sika or an elk, it's fair game as far as the law's
concerned," Dodd said. "Shoot it, drag it to the truck and have it packaged at
the processor."
As an example, Dodd said a hunter legally killed what he thought was the
biggest whitetail doe of his life near Tuscaloosa last year. The animal turned
out to be a cow elk that had escaped from an eclosure and that was twice as big
as the average whitetail female.
Alabama : Elk Escape From Killen Farm to Greenhill
Date: December 05, 2003 Source: The Associated Press
Contacts: The Associated Press
A small herd of elk escaped a game farm in Killen and made its way to
Greenhill, giving local hunters a rare chance to hunt the animal close to home.
Residents had reported seeing animals that looked like deer but were
bigger, but wildlife officials were unable to track down any of the creatures.
It wasn't until residents began hunting Tuesday that authorities realized the
animals were elk.
Wildlife officials initially were puzzled about where the animals came from
- the Smoky Mountains in eastern Tennessee is the area closest to the Shoals
where elk are known to roam freely.
Authorities seized and buried three elk shot in a field off U.S. 43 by a
hunter who did not have the landowner's permission to hunt there.
Capt. Johnny Johnson of the Division of Wildlife and Freshwater Fisheries
said elk hunted in the Greenhill area would be tested for chronic wasting
disease. The disease has been spotted in several Western states and Wisconsin,
but not in Alabama.
Wildlife and Freshwater Fisheries enforcement officer Richard Wallace
warned hunters not to eat any meat from the elk until the tests are complete.
Friday, October 26, 2012
CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT
PRODUCTS, BAITING, AND MINERAL LICKS
Friday, August 31, 2012
COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a
review
UNITED STATES ANIMAL HEALTH ASSOCIATION 115th Annual Meeting September 29-
October 5, 2011 Buffalo, New York
_________________________________________________________
RESOLUTION NUMBER: 14 APPROVED SOURCE: COMMITTEE ON CAPTIVE WILDLIFE AND
ALTERNATIVE LIVESTOCK SUBJECT MATTER: CHRONIC WASTING DISEASE FUNDING FOR
CAPTIVE CERVIDS BACKGROUND INFORMATION:
The proposed rule for Chronic Wasting Disease (CWD) Herd Certification and
Interstate Movement of Captive Cervids in farmed cervidae requires that all
farmed cervidae greater than 12 months of age that die or are slaughtered must
be tested for CWD. Farmed cervidae producers across the nation have complied
with testing requirements, in large part because laboratory costs for CWD
testing have traditionally been paid with United States Department of
Agriculture (USDA) funds. The CWD testing protocol that is recommended for
farmed cervidae is the immunohistochemistry (IHC) test using formalin fixed
samples of brain stem and retropharyngeal lymph node from each animal. It is the
most sensitive and specific test for detecting CWD. The test is expensive and
costs at least $25.00 per slide to perform at USDA approved laboratories. There
is an urgency to maintain USDA funding to cover the costs of CWD testing for
farmed cervidae. If USDA funding for CWD tests ends and farmed cervidae
producers are forced to cover the cost of such tests, there is a real
possibility that producer compliance with CWD testing requirements will
decrease. Without producer cooperation, the national CWD control program for
farmed cervidae could collapse. RESOLUTION: The United States Animal Health
Association urges the United States Department of Agriculture, Animal and Plant
Health Inspection Service, Veterinary Services to continue to provide funding to
cover the laboratory costs of testing farmed cervidae for Chronic Wasting
Disease by immunohistochemistry at all approved laboratories. INTERIM RESPONSE:
The U.S. Department of Agriculture (USDA), Animal and Plant Health Inspection
Service (APHIS), Veterinary Services (VS) recognizes the concerns of the United
States Animal Health Association (USAHA) and appreciates the opportunity to
respond. Resolution 14 / pg 2 In fiscal year 2012, the congressional
appropriation for the chronic wasting disease (CWD) program was reduced by $13.9
million, to approximately $1.9 million. Consequently, VS no longer has funds to
cover testing costs for farmed cervids. Laboratories and industry were informed
that this funding ended on December 31, 2011; all such costs must now be borne
by the producers. VS will continue to cover only confirmatory testing on any
presumptive CWD positive samples from farmed and wild cervidae at the National
Veterinary Services Laboratories. VS will direct remaining program funds to the
publication of the CWD final rule and the administrative costs associated with
implementation of the national CWD herd certification program. UNITED STATES
ANIMAL HEALTH ASSOCIATION 115th Annual Meeting September 29- October 5, 2011
Buffalo, New York
_________________________________________________________
RESOLUTION NUMBER: 15 APPROVED SOURCE: COMMITTEE ON CAPTIVE WILDLIFE AND
ALTERNATIVE LIVESTOCK SUBJECT MATTER: CHRONIC WASTING DISEASE HERD CERTIFICATION
AND INTERSTATE MOVEMENT FINAL RULE BACKGROUND INFORMATION:
Implementation of rules for Chronic Wasting Disease (CWD) that define the
CWD herd certification program (9 CFR 55 Subpart B) and requirements for
interstate movement of farmed cervidae (9 CFR 81) has been delayed since 2006.
There is an urgency to finalize these rules to ensure that CWD certification
programs are uniformly administered in all states and that all farmed cervidae
that move from state to state meet the same requirements. These rules are
critically important to the survival of the farmed cervidae industry. These
rules are needed to preserve the ability of producers to move farmed cervidae
and their products interstate and internationally without unnecessary
restrictions. RESOLUTION: The United States Animal Health Association urges the
United States Department of Agriculture, Animal and Plant Health Inspection
Service, Veterinary Services to finalize rules for Chronic Wasting Disease herd
certification programs (9 CFR 55 Subpart B) and interstate movement of farmed
cervidae (9 CFR 81). INTERIM RESPONSE: The U.S. Department of Agriculture
(USDA), Animal and Plant Health Inspection Service, Veterinary Services
appreciates your interest in the rulemaking for chronic wasting disease (CWD).
The CWD amended final rule was cleared by USDA and is in clearance in the Office
of Management and Budget (OMB). Once OMB clearance is completed, the CWD amended
rule would become effective 60 days after its publication. UNITED STATES ANIMAL
HEALTH ASSOCIATION 115th Annual Meeting September 29- October 5, 2011 Buffalo,
New York
_________________________________________________________
RESOLUTION NUMBER: 16 APPROVED SOURCE: COMMITTEE ON CAPTIVE WILDLIFE AND
ALTERNATIVE LIVESTOCK SUBJECT MATTER: LIVE ANIMAL TESTING FOR CHRONIC WASTING
DISEASE BACKGROUND INFORMATION:
Detection of Chronic Wasting Disease (CWD) in live animals is an important
component of CWD Prevention and Control Programs. With the funding decrease for
CWD indemnification, the need has increased for additional diagnostic tools to
monitor CWD positive herds and epidemiologically linked herds that may be
maintained in quarantine rather than depopulated. The use of recto-anal mucosa
associated lymphoid tissue (RAMALT) has been approved as a live animal test for
Scrapie. There have been numerous studies evaluating the sensitivity and
specificity of RAMALT in cervids. There are several additional advantages to
RAMALT sampling. There is a large amount of suitable tissue to sample and
multiple sites can be sampled allowing repeat sampling over time. RESOLUTION:
The United States Animal Health Association requests that the United States
Department of Agriculture, Animal and Plant Health Inspection Service,
Veterinary Services evaluate live animal tests, including the rectal biopsy
(RAMALT), as a live animal test for Chronic Wasting Disease. INTERIM RESPONSE:
The U.S. Department of Agriculture, Animal and Plant Health Inspection Service
(APHIS), Veterinary Services appreciates your interest in live animal tests for
chronic wasting disease (CWD). APHIS is completing analysis of a multi-year
study evaluating recto-anal mucosa associated lymphoid tissue (RAMALT) biopsy
testing as a diagnostic tool for CWD detection in captive white-tailed deer.
This is a collaborative study with APHIS Wildlife Services, Agricultural
Research Service, Canadian Food Inspection Agency, Colorado State University,
and others to evaluate the existing collective data on white-tailed deer
relative to diagnostic testing and interpretation of the immunohistochemistry
test for CWD Resolution 16 / pg 2 on rectal biopsy testing in the United States
and Canada. Currently, there is insufficient data available to evaluate this
technique on other captive Cervidae. After this analysis is completed, APHIS
will determine the applicability of RAMALT for use in a CWD Herd Certification
Program (HCP). We plan to complete this determination by September 30, 2012.
APHIS also will continue to evaluate other live animal tests for CWD, as they
are developed, to assess appropriate use in a CWD HCP.
USDA-APHIS-VS Chronic Wasting Disease National Program
Patrice N. Klein of USDA APHIS VS – National Center for Animal Health
Programs provided an update on the agency’s CWD–related activities:
CWD Rule Update: The amended final rule on chronic wasting disease (CWD) is
currently in departmental clearance. The rule will set minimum standards for
interstate movement and establish the national voluntary Herd Certification
Program (HCP). Farmed/captive cervid surveillance testing: Through FY2010, VS
conducted surveillance testing on approximately 20,000 farmed /captive cervids
by the immunohistochemistry (IHC) standard protocol. As of September 15, 2011,
approximately 19,000 farmed /captive cervids were tested by IHC for CWD with
funding to cover lab costs provided through NVSL.
Farmed/captive cervid CWD status: The CWD positive captive white-tailed
deer (WTD) herd reported in Missouri (February 2010) was indemnified and
depopulation activities were completed in June 2011. All depopulated animals
were tested for CWD and no additional CWD positive animals were found.
In FY 2011, CWD was reported in two captive elk herds in Nebraska
(December, 2010 and April 2011, respectively).
To date, 52 farmed/captive cervid herds have been identified in 11 states:
CO, KS, MI, MN, MO, MT, NE, NY, OK, SD, WI.
Thirty-nine were elk herds and 13 were WTD herds. At this time, eight CWD
positive herds remain – six elk herds in Colorado and the two elk herds in
Nebraska.
Wild Cervid surveillance: In FY 2009 funding supported surveillance in
approximately 74,330 wild cervids in 47 cooperating States. Wild cervid CWD
surveillance totals are pending for fiscal year 2010 (2010 – 2011 calendar year)
due to seasonal surveillance activities and completion of final cooperative
agreement reporting to APHIS.
In fiscal year 2011, there are 15 ‘tier 1’ States, 20 ‘tier 2’ States, and
15 ‘tier 3’ States. Two new ‘tier 1’ States, Minnesota and Maryland, were added
in fiscal year 2011 based on the new CWD detections in a free-ranging
white-tailed deer in southeastern Minnesota and in western Maryland.
Consequently, Delaware was upgraded to ‘tier 2’ status as an adjacent State to
Maryland. For FY 2011, 45 States and 32 Tribes will receive cooperative
agreement funds to complete wild cervid surveillance and other approved work
plan activities. Based on FY 2012 projected budget reductions, future
cooperative agreement funds will be eliminated.
APHIS CWD Funding: In FY2011, APHIS received approximately $15.8 million in
appropriated funding for the CWD Program. The President’s FY 2012 budget
proposes to reduce program funding for CWD by $13.9 million, leaving the program
with a request of $1.925 million to provide some level of Federal coordination
for the national herd certification program (HCP).
Consequently, APHIS is planning to amend its role in the program to one of
Federal coordination. Based on the projected FY 2012 budget, funding for CWD
cooperative agreements and indemnity funding for States and Tribes will be
eliminated. Under this scenario, the States or cervid industry producers will
likely be responsible for the costs of surveillance testing and indemnity for
appraisal, depopulation, and disposal of CWD-positive animals.
Commodity Health Line Structure: In the FY 2012 budget, livestock
commodities regulated by USDA have been organized into ‘Commodity Health Line’
structures or groupings. APHIS’ Equine, Cervid and Small Ruminant (ECSR) Health
line supports efforts to protect the health and thereby improve the quality and
productivity of the equine, cervid and small ruminant industries. Activities
supported by the ECSR Health line range from monitoring and surveillance to
investigation and response actions undertaken when health issues relevant to the
industry are identified. APHIS also maintains regulations and program standards
which guide ECSR activities at both the Federal and State/Tribal level.
The ECSR Health line funds essential activities necessary to maintain
current ECSR surveillance and program operations while providing the flexibility
to respond to new and emerging industry-specific health concerns. APHIS’ current
activities include Scrapie, Chronic Wasting Disease (CWD), Slaughter Horse
Transport, and Brucellosis/Tuberculosis in cervids. Overall, APHIS will use
funding from the ECSR Health Line Item to support Agency efforts in the
following mission areas: prevention, preparedness and communication; monitoring,
surveillance and detection; response and containment; and continuity of
business, mitigation and recovery
Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)
Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National
Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie
and CWD in inoculated deer. Interspecies transmission studies afford the
opportunity to better understand the potential host range and origins of prion
diseases. We inoculated white-tailed deer intracranially (IC) and by a natural
route of exposure (concurrent oral and intranasal inoculation) with a US scrapie
isolate. All deer inoculated by the intracranial route had evidence of PrPSc
accumulation and those necropsied after 20 months post-inoculation (PI) (3/5)
had clinical signs, spongiform encephalopathy, and widespread distribution of
PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6
months PI did not have clinical signs, but had widespread distribution of PrPSc.
This highlights the facts that 1) prior to the onset of clinical signs PrPSc is
widely distributed in the CNS and lymphoid tissues and 2) currently used
diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical
signs. The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in white-tailed deer after IC inoculation
including early and widespread presence of PrPSc in lymphoid tissues, clinical
signs of depression and weight loss progressing to wasting, and an incubation
time of 21-23 months. Moreover, western blots (WB) done on brain material from
the obex region have a molecular profile consistent with CWD and distinct from
tissues of the cerebrum or the scrapie inoculum. However, results of microscopic
and IHC examination indicate that there are differences between the lesions
expected in CWD and those that occur in deer with scrapie: amyloid plaques were
not noted in any sections of brain examined from these deer and the pattern of
immunoreactivity by IHC was diffuse rather than plaque-like. After a natural
route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 months PI. Tissues from these deer were positive for scrapie by
IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil,
retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and
spleen. While two WB patterns have been detected in brain regions of deer
inoculated by the natural route, unlike the IC inoculated deer, the pattern
similar to the scrapie inoculum predominates.
Committee Business:
The Committee discussed and approved three resolutions regarding CWD. They
can be found in the report of the Reswolutions Committee. Essentially the
resolutions urged USDA-APHIS-VS to:
Continue to provide funding for CWD testing of captive cervids
Finalize and publish the national CWD rule for Herd Certification and
Interstate Movement
Evaluate live animal test, including rectal mucosal biopsy, for CWD in
cervids
Friday, August 24, 2012
Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting
disease within white-tailed deer (Odocoileus virginianus) herds in North America
The overall diagnostic specificity was 99.8%. Selective use of antemortem
rectal biopsy sample testing would provide valuable information during disease
investigations of CWD-suspect deer herds.
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B). SNIP... Long-term effects of CWD on cervid
populations and ecosystems remain unclear as the disease continues to spread and
prevalence increases. In captive herds, CWD might persist at high levels and
lead to complete herd destruction in the absence of human culling. Epidemiologic
modeling suggests the disease could have severe effects on free-ranging deer
populations, depending on hunting policies and environmental persistence (8,9).
CWD has been associated with large decreases in free-ranging mule deer
populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).
PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B).
Research Paper
Salivary prions in sheep and deer
Volume 6, Issue 1 January/February/March 2012
Pages 52 – 61
Thursday, November 01, 2012
PA GAME COMMISSION TO HOLD PUBLIC MEETING TO DISCUSS CWD Release #128-12
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
Friday, November 04, 2011
Elk escape from captive cervid facility in Pennsylvania near West Virginia
border West Virginia Division of Natural Resources
THE states are going to have to regulate how many farms that are allowed,
or every state in the USA will wind up being just one big private fenced in game
farm.
kind of like they did with the shrimping industry in the bays, when there
got to be too many shrimp boats, you stop issuing permits, and then lower the
exist number of permits, by not renewing them, due to reduced permits issued.
how many states have $465,000., and can quarantine and purchase there from,
each cwd said infected farm, but how many states can afford this for all the cwd
infected cervid game ranch type farms ???
11,000 game farms X $465,000., do all these game farms have insurance to
pay for this risk of infected the wild cervid herds, in each state ???
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
Form 1100-001
(R 2/11)
NATURAL RESOURCES BOARD AGENDA ITEM
SUBJECT: Information Item: Almond Deer Farm Update
FOR: DECEMBER 2011 BOARD MEETING
TUESDAY
TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief
SUMMARY:
SNIP...
2010 WISCONSIN CAPTIVE DEER ESCAPES
There were 26 reported escape incidents so far this year, this amounted to
20 actual confirmed escape incidents because 3 were previously reported, 2 were
confirmed as wild deer, and 1 incident was not confirmed. ...
snip...
Deer, elk continue to escape from state farms
Article by: DOUG SMITH , Star Tribune Updated: March 14, 2011 - 12:08 PM
Curbing chronic wasting disease remains a concern; officials are increasing
enforcement.
Almost 500 captive deer and elk have escaped from Minnesota farms over the
past five years, and 134 were never recaptured or killed.
So far this year, 17 deer have escaped, and officials are still searching
for many of those.
see ;
Friday, September 28, 2012
Stray elk renews concerns about deer farm security Minnesota
Wisconsin : 436 Deer Have Escaped From Farms to Wild
Date: March 18, 2003 Source: Milwaukee Journal Sentinel
Contacts: LEE BERGQUIST lbergquist@journalsentinel.com
State finds violations, lax record keeping at many sites, report says
A state inspection of private deer farms, prompted by the discovery of
chronic wasting disease, found that 436 white-tailed deer escaped into the wild,
officials said Tuesday
The Department of Natural Resources found that captive deer have escaped
from one-third of the state's 550 deer farms over the lifetime of the
operations. The agency also uncovered hundreds of violations and has sought a
total of 60 citations or charges against deer farm operators. These and other
findings come as state officials say they are still no closer to understanding
how the fatal deer disease got to Wisconsin.
Since the discovery a little more than a year ago, chronic wasting disease
has thrown both deer hunting and management of Wisconsin's 1.4 million deer herd
into tumult. Fewer hunters went into the woods last year, and a booming deer
population has the DNR worried that the number of whitetails could grow out of
control.
Tuesday's findings were presented to the state Department of Agriculture,
Trade and Consumer Protection. The DNR had regulated deer farms, but the
authority was transferred to the Agriculture Department on Jan. 1. Now
agriculture regulators oversee elk, deer and other captive cervids.
Solving the problem
Stricter regulations - and closer attention to the operations of game farms
- should cut down on future violations, officials from the two agencies said.
Tougher reporting requirements also will help authorities keep better track of
the movement of animals, they said. Permanent rules take effect in June, and
include tighter controls on moving animals and requiring the reporting of
escaped animals within 48 hours. There will be mandatory testing of every deer
age 16 months or older that dies.
Almost from the start of the state's battle against chronic wasting
disease, game farm operators came under scrutiny because their business involves
the buying and selling of captive deer and elk across state lines. When the
disease was first discovered here Feb. 28, 2002, Wisconsin became the first
state to have the disease east of the Mississippi River.
A representative of the deer industry said Tuesday that the DNR is trying
to shift blame for chronic wasting disease to his industry.
"The state of Wisconsin has spent a year chasing chronic wasting disease,
and they have made zero progress," said Gary Nelson, president of Whitetails of
Wisconsin. "In the past, they have essentially collected our fees and ignored
us. Now that they have discovered CWD, they are looking for someone to blame."
A DNR representative agreed that the agency could have done a better job
keeping tabs on deer farms.
"We're not pointing fingers," said Karl Brooks, a conservation warden with
the DNR. "But two things that we know for sure is that there is CWD in the wild
deer population, and we have found CWD on game farms."
CWD found on 2 farms
Seven deer have tested positive for the disease on game farms - one on a
Portage County farm and six on a Walworth County farm - since the disease was
discovered in three wild deer killed near Mount Horeb in western Dane County.
One deer that tested positive on the Walworth County farm escaped and roamed
free for six months.
Regulations have only begun to catch up to the captive deer industry, and
"unfortunately, it took CWD to get us there," said agriculture secretary Rod
Nilsestuen at a news briefing in Madison. As the DNR prepared to hand over
authority for overseeing game farms to the agriculture department, it sent 209
conservation wardens to 550 farms to collect information, attempt to pinpoint
the source of the disease and to learn whether other deer had been exposed to
it. The audit found that most farms were in compliance, but the DNR found many
violations and instances of poor record keeping. Also in numerous instances,
fences did not stop wild and captive deer from intermingling.
At least 227 farms conducted part of their business on a cash basis, making
it hard to track animal movement with financial records.
For example, both the Internal Revenue Service and the state Department of
Revenue have been contacted about a deer farm near Wild Rose in Waushara County
that is suspected of selling six large bucks for $45,000 in cash and not using
live deer shipping tags as required. The DNR found that game farm operators have
more deer in captivity than their records show, which is "due in part because
the owners of a number of large deer farm operations were unable to accurately
count the number of deer within their fences," the audit found.
Hundreds of deer escape
The DNR found a total of 671 deer that escaped farms - 436 of which were
never found - because of storm-damaged fences, gates being left open or the
animals jumping over or through fences. In one example in Kewaunee County, a
deer farmer's fence was knocked down in a summer storm. Ten deer escaped, and
the farmer told the DNR he had no intention of trying to reclaim them. The DNR
found five of the deer, killed them and cited the farmer for violation of a
regulation related to fencing.
Another deer farmer near Mishicot, in Manitowoc County, released all nine
of his whitetails last summer after he believed the discovery of chronic wasting
disease was going to drive down the market for captive deer.
The DNR found 24 instances of unlicensed deer farms and issued 19
citations. Journal Sentinel correspondent Kevin Murphy contributed to this
report.
Game Farms Inspected
A summary of the findings of the Department of Natural Resources'
inspection of 550 private white-tailed deer farms in the state: The deer farms
contained at least 16,070 deer, but the DNR believes there are more deer in
captivity than that because large deer farms are unable to accurately count
their deer. 671 deer had escaped from game farms, including 436 that were never
found.
24 farmers were unlicensed. One had been operating illegally since 1999
after he was denied a license because his deer fence did not meet minimum
specifications.
Records maintained by operators ranged from "meticulous documentation to
relying on memory." At least 227 farms conducted various portions of their deer
farm business with cash. Over the last three years, 1,222 deer died on farms for
various reasons. Disease testing was not performed nor required on the majority
of deer. Farmers reported doing business with people in 22 other states and one
© Chronic Wasting Disease Alliance
Web site development by Pyron Technologies, Inc.
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
INDIANA 20 DEER ESCAPE TROPHY BUCK GAME FARM STATE OFFICIALS FEAR CWD RISK
TO WILD
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
CWD, GAME FARMS, BAITING, AND POLITICS
AIRBORNE TRANSMISSION
In Chronic Wasting disease (CWD) of deer several careful studies have been
performed that, together with our present finding, depose in favor of airborne
transmission in this naturally occurring disease. Indeed, CWD prions can be
transmitted experimentally via aerosol and the nasal route to transgenic
cervidized mice.33 Although no anecdotal or epidemiological evidence has come
forward that airborne transmission may be important for the spread of CWD,
several lines of thought suggest that this possibility is not implausible. In
deer, prions have been detected in urine, saliva, feces and blood of diseased
animals. Moreover, it was claimed that pathological prion protein could be
recovered from the environmental water in an endemic area.34 Since all fluids
can act as sources for the generation of aerosols, any of the body fluids
mentioned above may represent the point of origin for airborne transmission of
CWD prions. In this context, also the presence of infectious prions in blood of
patients should be mentioned which was demonstrated by the transmission of vCJD
by blood transfusions.35,36 The growing body of evidence that prion transmission
can be airborne—at least under certain conditions—dictates that the release of
potentially contaminated aerosols should be avoided under all circumstances.
snip...
In conclusion, aerosols can infect mice with a surprisingly high
efficiency. Just how important a role is played by this newly recognized pathway
of spread in natural transmission is, as of now, unclear and in need of further
studies. Although it was not identified as a route of infection in
epidemiological studies thus far, the worryingly high attack rate suggests that
we would be well-advised to carefully avoid the inhalation of aerosols from
prion-containing materials. Key words: prion, prion transmission, scrapie,
chronic wasting diseases, CWD, Creutzfeldt-Jacob-disease, CJD, TSE, aerosol,
pathogens, allergens Submitted: 05/19/11 Accepted: 06/09/11 DOI:
10.4161/pri.5.3.16851 *Correspondence to: Lothar Stitz or Adriano Aguzzi; Email:
lothar.stitz@fli.bund.de or adriano.aguzzi@usz.ch
snip...see full text ;
PLEASE SEE FULL TEXT, AND AGAIN, many thanks to PLOS for open access !!!
Monday, September 17, 2012
Rapid Transepithelial Transport of Prions Following Inhalation
Thursday, December 29, 2011
Aerosols An underestimated vehicle for transmission of prion diseases?
PRION www.landesbioscience.com
please see more on Aerosols and TSE prion disease here ;
Research Paper
Salivary prions in sheep and deer
Gültekin Tamgüney, Jürgen A. Richt, Amir N. Hamir, Justin J. Greenlee,
Michael W. Miller, Lisa L. Wolfe, Tracey M. Sirochman, Alan J. Young, David V.
Glidden, Natrina L. Johnson, Kurt Giles, Stephen J. DeArmond and Stanley B.
Prusiner
Gültekin Tamgüney Institute for Neurodegenerative Diseases; Department of
Neurology; University of California, San Francisco, CA USA Jürgen A. Richt
National Animal Disease Center, ARS-USDA; Ames, IA USA Amir N. Hamir National
Animal Disease Center, ARS-USDA; Ames, IA USA Justin J. Greenlee National Animal
Disease Center, ARS-USDA; Ames, IA USA Michael W. Miller Colorado Division of
Wildlife, Wildlife Research Center; Fort Collins, CO USA Lisa L. Wolfe Colorado
Division of Wildlife, Wildlife Research Center; Fort Collins, CO USA Tracey M.
Sirochman Colorado Division of Wildlife, Wildlife Research Center; Fort Collins,
CO USA Alan J. Young Department of Veterinary Science, South Dakota State
University; Brookings, SD USA David V. Glidden Departments of Epidemiology and
Biostatistics; University of California, San Francisco, CA USA Natrina L.
Johnson Institute for Neurodegenerative Diseases; San Francisco, CA USA Kurt
Giles Institute for Neurodegenerative Diseases; Department of Neurology;
University of California, San Francisco, CA USA Stephen J. DeArmond Institute
for Neurodegenerative Diseases; San Francisco, CA USA; Department of Pathology,
University of California; San Francisco, CA USA Stanley B. Prusiner
Corresponding author: stanley@ind.ucsf.edu Institute for Neurodegenerative
Diseases; Department of Neurology; University of California, San Francisco, CA
USA
Scrapie of sheep and chronic wasting disease (CWD) of cervids are
transmissible prion diseases. Milk and placenta have been identified as sources
of scrapie prions but do not explain horizontal transmission. In contrast, CWD
prions have been reported in saliva, urine and feces, which are thought to be
responsible for horizontal transmission. While the titers of CWD prions have
been measured in feces, levels in saliva or urine are unknown. Because sheep
produce ~17 L/day of saliva, and scrapie prions are present in tongue and
salivary glands of infected sheep, we asked if scrapie prions are shed in
saliva. We inoculated transgenic (Tg) mice expressing ovine prion protein,
Tg(OvPrP) mice, with saliva from seven Cheviot sheep with scrapie. Six of seven
samples transmitted prions to Tg(OvPrP) mice with titers of -0.5 to 1.7 log ID50
U/ml. Similarly, inoculation of saliva samples from two mule deer with CWD
transmitted prions to Tg(ElkPrP) mice with titers of -1.1 to -0.4 log ID50 U/ml.
Assuming similar shedding kinetics for salivary prions as those for fecal prions
of deer, we estimated the secreted salivary prion dose over a 10-mo period to be
as high as 8.4 log ID50 units for sheep and 7.0 log ID50 units for deer. These
estimates are similar to 7.9 log ID50 units of fecal CWD prions for deer.
Because saliva is mostly swallowed, salivary prions may reinfect tissues of the
gastrointestinal tract and contribute to fecal prion shedding. Salivary prions
shed into the environment provide an additional mechanism for horizontal prion
transmission.
ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD
Elk and Deer Use of Mineral Licks: Implications for Disease Transmission
Kurt C. VerCauteren1*, Michael J. Lavelle1, Gregory E. Phillips1, Justin W.
Fischer1, and Randal S. Stahl1 1United States Department of Agriculture, Animal
and Plant Health Inspection Service, Wildlife Services, National Wildlife
Research Center, 4101 LaPorte Avenue, Fort Collins, CO 80521-2154, USA
*Cooresponding author e-mail: kurt.c.vercauteren@aphis.usda.gov
North American cervids require and actively seek out minerals to satisfy
physiological requirements. Minerals required by free-ranging cervids exist
within natural and artificial mineral licks that commonly serve as focal sites
for cervids. Ingestion of soils contaminated with the agent that causes chronic
wasting disease (CWD) may result in risk of contracting CWD. Our objective was
to evaluate the extent and nature of use of mineral licks by CWD-susceptible
cervid species. We used animal-activated cameras to monitor use of 18 mineral
licks between 1 June and 16 October 2006 in Rocky Mountain National Park,
north-central Colorado. We also assessed mineral concentrations at mineral licks
to evaluate correlations between visitation rates and site-specific
characteristics. We collected > 400,000 images of which 991 included elk, 293
included deer, and 6 included moose. We documented elk and deer participating in
a variety of potentially risky behaviors (e.g., ingesting soil, ingesting water,
defecating, urinating) while at mineral licks. Results from the mineral analyses
combined with camera data revealed that visitation was highest at sodium-rich
mineral licks. Mineral licks may play a role in disease transmission by acting
as sites of increased interaction as well as reservoirs for deposition,
accumulation, and ingestion of disease agents.
PrPSc Detection and Infectivity in Semen from Scrapie-Infected Sheep
Richard Rubenstein1,5, Marie S Bulgin2, Binggong Chang1, Sharon
Sorensen-Melson2, Robert B Petersen3 and Giuseppe LaFauci4 + Author Affiliations
1 SUNY Downstate Medical Center, Brooklyn, NY, USA; 2 University of Idaho,
Caldwell, ID, USA; 3 Case Western Reserve University, Cleveland, OH, USA; 4 NYS
Institute for Basic Research in Developmental Disabilities, Staten Island, NY,
USA ↵5 E-mail: richard.rubenstein@downstate.edu Received 13 October 2011.
Accepted 3 February 2012. Abstract A scrapie-positive ewe was found in a flock
that had been scrapie free for 13 years, but housed adjacent to scrapie-positive
animals, separated by a wire fence. Live animal testing of the entire flock of
24 animals revealed 7 more subclinical scrapie-positive ewes. We hypothesized
that they may have contracted the disease from scrapie-positive rams used for
breeding four months prior, possibly through the semen. The genotypes of the ewe
flock were highly scrapie-susceptible and the rams were infected with the
"Caine" Scrapie Strain having a short incubation time of 4.3-14.6 mo. in sheep
with 136/171 VQ/VQ and AQ/VQ genotypes. PrPSc accumulates in a variety of
tissues in addition to the central nervous system. Although transmission of
prion diseases, or transmissible spongiform encephalopathies, has been achieved
via peripheral organ or tissue homogenates as well as by blood transfusion,
neither infectivity nor PrPSc have been found in semen from scrapie-infected
animals. Using serial protein misfolding cyclic amplification followed by a
surround optical fiber immunoassay, we demonstrate that semen from rams infected
with a short incubation time scrapie strain contains prion disease-associated
seeding activity that generated PrPSc in sPMCA. Injection of the ovinized
transgenic mouse line TgSShpPrP with semen from scrapie-infected sheep resulted
in PrPSc seeding activity in clinical and, probably as a result of the low
titer, nonclinical mouse brain. These results suggest that the transmissible
agent, or at least the seeding activity, for sheep scrapie is present in semen.
This may be a strain specific phenomenon.
Envt.18: Mother to Offspring Transmission of Chronic Wasting Disease
Candace K. Mathiason,† Amy Nalls, Kelly Anderson, Jeanette Hayes-Klug,
Jenny G. Powers, Nicholas J. Haley and Edward A. Hoover
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
We have developed a new cervid model in small Asian muntjac deer (Muntiacus
reevesi) to study potential modes of vertical transmission of chronic wasting
disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally
infected with CWD tested PrPCWD lymphoid positive by four months post infection.
Ten fawns were born to these CWD-infected doe— four of the fawns were viable,
five were non-viable and one was a first trimester fetus harvested from a
CWD-infected doe euthanized at end-stage disease. The viable fawns have been
monitored for CWD infection by immunohistochemistry and sPMCA performed on
serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in
one fawn by IHC as early as 40 days of age. Moreover, sPMCA performed on rectal
lymphoid tissue has yielded positive results on another fawn at ten days of age.
In addition, sPMCA assays have demonstrated amplifiable prions in fetal
placental or spleen tissue of three non-viable fawns and mammary tissue of the
dams.
Additional pregnancy related fluids and tissues from the doe as well as
tissue from the nonviable fawns are currently being probed for the presence of
CWD. In summary, we have employed the muntjac deer model, to demonstrate for the
first time the transmission of CWD from mother to offspring. These studies
provide the foundation to investigate the mechanisms and pathways of maternal
prion transfer.
Saturday, February 11, 2012
PrPSc Detection and Infectivity in Semen from Scrapie-Infected Sheep
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
Tuesday, January 10, 2012
ESHRE position statement concerning prion detection in urinary gonadotropin
formulations
Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Sheep
Naturally/Experimentally Infected with Scrapie and Deer with
Preclinical/Clinical Chronic Wasting Disease
▿Richard Rubenstein1,*, Binggong Chang1, Perry Gray2, Martin Piltch2, Marie
S. Bulgin3, Sharon Sorensen-Melson3 and Michael W. Miller4 + Author Affiliations
1Departments of Neurology and Physiology/Pharmacology, SUNY Downstate
Medical Center, 450 Clarkson Avenue, Brooklyn, New York 11203 2Los Alamos
National Laboratory, Los Alamos, New Mexico 87545 3University of Idaho, Caine
Veterinary Teaching and Research Center, 1020 E. Homedale Road, Caldwell, Idaho
83607 4Colorado Division of Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, Colorado 80526-2097
ABSTRACT
Prion diseases, also known as transmissible spongiform encephalopathies,
are fatal neurodegenerative disorders. Low levels of infectious agent and
limited, infrequent success of disease transmissibility and PrPSc detection have
been reported with urine from experimentally infected clinical cervids and
rodents. We report the detection of prion disease-associated seeding activity
(PASA) in urine from naturally and orally infected sheep with clinical scrapie
agent and orally infected preclinical and infected white-tailed deer with
clinical chronic wasting disease (CWD). This is the first report on PASA
detection of PrPSc from the urine of naturally or preclinical prion-diseased
ovine or cervids. Detection was achieved by using the surround optical fiber
immunoassay (SOFIA) to measure the products of limited serial protein misfolding
cyclic amplification (sPMCA). Conversion of PrPC to PrPSc was not influenced by
the presence of poly(A) during sPMCA or by the homogeneity of the PrP genotypes
between the PrPC source and urine donor animals. Analysis of the sPMCA-SOFIA
data resembled a linear, rather than an exponential, course. Compared to
uninfected animals, there was a 2- to 4-log increase of proteinase K-sensitive,
light chain immunoglobulin G (IgG) fragments in scrapie-infected sheep but not
in infected CWD-infected deer. The higher-than-normal range of IgG levels found
in the naturally and experimentally infected clinical scrapie-infected sheep
were independent of their genotypes. Although analysis of urine samples
throughout the course of infection would be necessary to determine the
usefulness of altered IgG levels as a disease biomarker, detection of PrPSc from
PASA in urine points to its potential value for antemortem diagnosis of prion
diseases.
FOOTNOTES
Received 13 May 2011. Accepted 14 June 2011. ↵*Corresponding author.
Mailing address: Downstate Medical Center, Departments of Neurology and
Physiology/Pharmacology, Box 1213, 450 Clarkson Avenue, Brooklyn, NY 11203.
Phone: (718) 270-2019. Fax: (718) 270-2459. E-mail:
richard.rubenstein@downstate.edu. ↵▿ Published ahead of print on 29 June 2011.
Copyright © 2011, American Society for Microbiology. All Rights Reserved.
Sunday, July 03, 2011
Prion Disease Detection, PMCA Kinetics, and IgG in Urine from
Naturally/Experimentally Infected Scrapie Sheep and Preclinical/Clinical CWD
Deer
Thursday, June 09, 2011
Detection of CWD prions in salivary, urinary, and intestinal tissues of
deer: potential mechanisms of prion shedding and transmission
CHRONIC WASTING DISEASE: A MODEL FOR PRION TRANSMISSION VIA SALIVA AND
URINE
Sunday, December 06, 2009
Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer
Long after Oral Exposure to Urine and Feces from CWD+ Deer
Wednesday, March 18, 2009
Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse
Bioassay
*** Tuesday, September 02, 2008
Detection of infectious prions in urine (Soto et al Available online 13
August 2008.)
-------- Original Message --------
Subject: MAD DEER FEED BAN WARNING LETTER RECALL 6 TONS DISTRIBUTED USA
Date: Wed, 20 Oct 2004 14:53:56 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@UNI-KARLSRUHE.DE
##################### Bovine Spongiform Encephalopathy
#####################
PRODUCT
Product is custom made deer feed packaged in 100 lb. poly bags. The product
has no labeling. Recall # V-003-5.
CODE
The product has no lot code. All custom made feed purchased between June
24, 2004 and September 8, 2004.
RECALLING FIRM/MANUFACTURER
Farmers Elevator Co, Houston, OH, by telephone and letter dated September
27, 2004. Firm initiated recall is ongoing.
REASON
Feed may contain protein derived from mammalian tissues which is prohibited
in ruminant feed.
VOLUME OF PRODUCT IN COMMERCE
Approximately 6 tons.
DISTRIBUTION OH.
END OF ENFORCEMENT REPORT FOR October 20, 2004
################# BSE-L-subscribe-request@uni-karlsruhe.de
#################
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material
From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov
Greetings FDA,
i would kindly like to comment on;
Docket 03D-0186
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed; Availability
Several factors on this apparent voluntary proposal disturbs me greatly,
please allow me to point them out;
1. MY first point is the failure of the partial ruminant-to-ruminant feed
ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials
being fed back to cattle is terribly flawed. without the _total_ and _mandatory_
ban of all ruminant materials being fed back to ruminants including cattle,
sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for
human/animal consumption), this half ass measure will fail terribly, as in the
past decades...
2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of
deer fawns being infected with CWD, how many could possibly be sub-clinically
infected. until we have a rapid TSE test to assure us that all deer/elk are free
of disease (clinical and sub-clinical), we must ban not only documented CWD
infected deer/elk, but healthy ones as well. it this is not done, they system
will fail...
3. WE must ban not only CNS (SRMs specified risk materials), but ALL
tissues. recent new and old findings support infectivity in the rump or ass
muscle. wether it be low or high, accumulation will play a crucial role in TSEs.
4. THERE are and have been for some time many TSEs in the USA. TME in mink,
Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has
been proven, but the TSE in USA cattle has been totally ignored for decades. i
will document this data below in my references.
5. UNTIL we ban all ruminant by-products from being fed back to ALL
ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient
numbers to find (1 million rapid TSE test in USA cattle annually for 5 years),
any partial measures such as the ones proposed while ignoring sub-clinical TSEs
and not rapid TSE testing cattle, not closing down feed mills that continue to
violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely
available those violations, will only continue to spread these TSE mad cow
agents in the USA. I am curious what we will call a phenotype in a species that
is mixed with who knows how many strains of scrapie, who knows what strain or
how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling
how many strains there), but all of this has been rendered for animal feeds in
the USA for decades. it will get interesting once someone starts looking in all
species, including humans here in the USA, but this has yet to happen...
6. IT is paramount that CJD be made reportable in every state (especially
''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family
of a victim of TSE. only checking death certificates will not be sufficient.
this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)
7. WE must learn from our past mistakes, not continue to make the same
mistakes...
snip...
Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry
R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1
Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road,
University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife,
Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097,
USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake
Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit,
Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall,
Washington State University, Pullman, WA 99164-7030, USA5
Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail
ehoover@lamar.colostate.edu
Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain
homogenate prepared from mule deer with naturally occurring chronic wasting
disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns
were necropsied and examined for PrP res, the abnormal prion protein isoform, at
10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an
immunohistochemistry assay modified to enhance sensitivity. PrPres was detected
in alimentary-tract-associated lymphoid tissues (one or more of the following:
retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as
early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.).
No PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural tissue
of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue
treatment with formic acid, proteinase K and hydrated autoclaving prior to
immunohistochemical staining with monoclonal antibody F89/160.1.5. These results
indicate that CWD PrP res can be detected in lymphoid tissues draining the
alimentary tract within a few weeks after oral exposure to infectious prions and
may reflect the initial pathway of CWD infection in deer. The rapid infection of
deer fawns following exposure by the most plausible natural route is consistent
with the efficient horizontal transmission of CWD in nature and enables
accelerated studies of transmission and pathogenesis in the native species.
snip...
These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the earliest
post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the
oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal
Peyer's patches and ileocaecal lymph nodes), which probably received the highest
initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and
spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of
nine sheep had infectivity in the retropharyngeal lymph node. He concluded that
the tissue distribution suggested primary infection via the gastrointestinal
tract. The tissue distribution of PrPres in the early stages of infection in the
fawns is strikingly similar to that seen in naturally infected sheep with
scrapie. These findings support oral exposure as a natural route of CWD
infection in deer and support oral inoculation as a reasonable exposure route
for experimental studies of CWD.
snip...
===================================
now, just what is in that deer feed? _ANIMAL PROTEIN_
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 –0700
From: "Terry S. Singeltary Sr."
Reply-To: BSE-L To: BSE-L
8420-20.5% Antler Developer For Deer and Game in the wild Guaranteed
Analysis Ingredients / Products Feeding Directions
snip...
_animal protein_
BODE'S GAME FEED SUPPLEMENT #400 A RATION FOR DEER NET WEIGHT 50 POUNDS
22.6 KG.
snip...
_animal protein_
Ingredients
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage
Products, Roughage Products 15%, Molasses Products, __Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Pyosphate, Salt, Calcium Carbonate, Vitamin A
Acetate with D-activated Animal Sterol (source of Vitamin D3), Vitamin E
Supplement, Vitamin B12 Supplement, Riboflavin Supplement, Niacin Supplement,
Calcium Panothenate, Choline Chloride, Folic Acid, Menadione Soduim Bisulfite
Complex, Pyridoxine Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous
Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum, Artificial
Flavors added.
===================================
MORE ANIMAL PROTEIN PRODUCTS FOR DEER
Bode's #1 Game Pellets A RATION FOR DEER F3153
GUARANTEED ANALYSIS Crude Protein (Min) 16% Crude Fat (Min) 2.0% Crude
Fiber (Max) 19% Calcium (Ca) (Min) 1.25% Calcium (Ca) (Max) 1.75% Phosphorus (P)
(Min) 1.0% Salt (Min) .30% Salt (Max) .70%
Ingredients
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage
Products, Roughage Products, 15% Molasses Products, __Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Phosphate, Salt, Calcium Carbonate, Vitamin A
Acetate with D-activated Animal Sterol (source of Vitamin D3) Vitamin E
Supplement, Vitamin B12 Supplement, Roboflavin Supplement, Niacin Supplement,
Calcium Pantothenate, Choline Chloride, Folic Acid, Menadione Sodium Bisulfite
Complex, Pyridoxine Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous
Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum, Artificial
Flavors added.
FEEDING DIRECTIONS Feed as Creep Feed with Normal Diet
INGREDIENTS
Grain Products, Roughage Products (not more than 35%), Processed Grain
By-Products, Plant Protein Products, Forage Products, __Animal Protein
Products__, L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium Phosphate,
Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic Copper Chloride,
Manganese Sulfate, Manganous Oxide, Sodium Selenite, Zinc Sulfate, Zinc Oxide,
Sodium Selenite, Potassium Iodide, Ethylenediamine Dihydriodide, Vitamin E
Supplement, Vitamin A Supplement, Vitamin D3 Supplement, Mineral Oil, Mold
Inhibitor, Calcium Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium
Bisulfite Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,
Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate
DIRECTIONS FOR USE
Deer Builder Pellets is designed to be fed to deer under range conditions
or deer that require higher levels of protein. Feed to deer during gestation,
fawning, lactation, antler growth and pre-rut, all phases which require a higher
level of nutrition. Provide adequate amounts of good quality roughage and fresh
water at all times.
==================================================
DEPARTMENT OF HEALTH & HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND
DRUG ADMINISTRATION
April 9, 2001 WARNING LETTER
01-PHI-12 CERTIFIED MAIL RETURN RECEIPT REQUESTED
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy
Lake, PA 16145 PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:
Food and Drug Administration Investigator Gregory E. Beichner conducted an
inspection of your animal feed manufacturing operation, located in Sandy Lake,
Pennsylvania, on March 23, 2001, and determined that your firm manufactures
animal feeds including feeds containing prohibited materials. The inspection
found significant deviations from the requirements set forth in Title 21, code
of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant
Feed. The regulation is intended to prevent the establishment and amplification
of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being
manufactured at this facility to be misbranded within the meaning of Section
403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found failure to label your swine feed with the required
cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests
that the statement be distinguished by different type-size or color or other
means of highlighting the statement so that it is easily noticed by a purchaser.
In addition, we note that you are using approximately 140 pounds of cracked
corn to flush your mixer used in the manufacture of animal feeds containing
prohibited material. This flushed material is fed to wild game including deer, a
ruminant animal. Feed material which may potentially contain prohibited material
should not be fed to ruminant animals which may become part of the food chain.
The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal feed use,
you are responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance with the law. We have enclosed
a copy of FDA's Small Entity Compliance Guide to assist you with complying with
the regulation... blah, blah, blah...
==================================
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 –0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
now, what about those 'deer scents' of 100% urine', and the prion that is
found in urine, why not just pass the prion with the urine to other deer...
Mrs. Doe Pee Doe in Estrus Model FDE1 Mrs. Doe Pee's Doe in Estrus is made
from Estrus urine collected at the peak of the rut, blended with Fresh Doe Urine
for an extremely effective buck enticer. Use pre-rut before the does come into
heat. Use during full rut when bucks are most active. Use during post-rut when
bucks are still actively looking for does. 1 oz.
www.gamecalls.net/hunting...lures.html
ELK SCENT/SPRAY BOTTLE
Works anytime of the year *
100 % Cow Elk-in-Heat urine (2oz.) *
Economical - mix with water in spray mist bottle *
Use wind to your advantage
Product Code WP-ESB $9.95
www.elkinc.com/Scent.asp
prions in urine?
DEER & ELK URINE, LURES & SCENT CONTROL DEPARTMENT by MRS.DOE PEE'S
Main Index
The Turkey Pro Sez... "Premium, fresh, top-quality, pure 100% undiluted
deer lures from Mrs. Doe Pee really work. I won't trust anything else when I'm
after big bucks. Sam Collora, owner of the company, proved how well his products
work when he bagged this monster buck in
1996.............snip......end........CWD
snip...
REFERENCES
snip...see full text ;
-------- Original Message --------
see full text ;
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material
From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer
and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 –0500
EMC 1 Terry S. Singeltary Sr. Vol #: 1
PLEASE SEE FULL TEXT SUBMISSION ;
CWD TO HUMAN TRANSMISSION, never say never !!!
Envt.06:
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2
Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6
and Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food
Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS
USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa,
ON Canada
†Presenting author; Email: emmanuel.comoy@cea.fr
The constant increase of chronic wasting disease (CWD) incidence in North
America raises a question about their zoonotic potential. A recent publication
showed their transmissibility to new-world monkeys, but no transmission to
old-world monkeys, which are phylogenetically closer to humans, has so far been
reported. Moreover, several studies have failed to transmit CWD to transgenic
mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the
only animal prion disease for which a zoonotic potential has been proven. We
described the transmission of the atypical BSE-L strain of BSE to cynomolgus
monkeys, suggesting a weak cattle-to-primate species barrier. We observed the
same phenomenon with a cattleadapted strain of TME (Transmissible Mink
Encephalopathy). Since cattle experimentally exposed to CWD strains have also
developed spongiform encephalopathies, we inoculated brain tissue from
CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice
overexpressing bovine or human PrP. Since CWD prion strains are highly
lymphotropic, suggesting an adaptation of these agents after peripheral
exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid
brains using the oral route. Nearly four years post-exposure, monkeys exposed to
CWD-related prion strains remain asymptomatic. In contrast, bovinized and
humanized transgenic mice showed signs of infection, suggesting that CWD-related
prion strains may be capable of crossing the cattle-to-primate species barrier.
Comparisons with transmission results and incubation periods obtained after
exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted
TME) will also be presented, in order to evaluate the respective risks of each
strain.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2
Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch
Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and
Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany
†Presenting author; Email: dausm@rki.de
Chronic wasting disease (CWD) is a contagious, rapidly spreading
transmissible spongiform encephalopathy (TSE) occurring in cervids in North
America. Despite efficient horizontal transmission of CWD among cervids natural
transmission of the disease to other species has not yet been observed. Here, we
report a direct biochemical demonstration of pathological prion protein PrPTSE
and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected
cervids. The presence of PrPTSE was detected by Western- and postfixed frozen
tissue blotting, while the seeding activity of PrPTSE was revealed by protein
misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal
muscles of CWD-infected WTD was estimated to be approximately 2000- to
10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE
was located in muscle- associated nerve fascicles but not, in detectable
amounts, in myocytes. The presence and seeding activity of PrPTSE in skeletal
muscle from CWD-infected cervids suggests prevention of such tissue in the human
diet as a precautionary measure for food safety, pending on further
clarification of whether CWD may be transmissible to humans.
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER
AND ELK ;
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.
NOR IS THE FDA recalling this CWD positive elk meat for the well being of
the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat
derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS
AND FIELD CORRECTIONS: FOODS CLASS II
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
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 ;
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
*** 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.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS Interspecies
transmission studies afford the opportunity to better understand the potential
host range and origins of prion diseases. Previous experiments demonstrated that
white-tailed deer are susceptible to sheep-derived scrapie by intracranial
inoculation. The purpose of this study was to determine susceptibility of
white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were
inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a
10% (wt/vol) brain homogenate derived from a sheep clinically affected with
scrapie. Non-inoculated deer were maintained as negative controls. All deer were
observed daily for clinical signs. Deer were euthanized and necropsied when
neurologic disease was evident, and tissues were examined for abnormal prion
protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal
was euthanized 15 months post-inoculation (MPI) due to an injury. At that time,
examination of obex and lymphoid tissues by IHC was positive, but WB of obex and
colliculus were negative. Remaining deer developed clinical signs of wasting and
mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer
were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity
included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node,
Peyer’s patches, and spleen. This work demonstrates for the first time that
white-tailed deer are susceptible to sheep scrapie by potential natural routes
of inoculation. In-depth analysis of tissues will be done to determine
similarities between scrapie in deer after intracranial and oral/intranasal
inoculation and chronic wasting disease resulting from similar routes of
inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in
white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A.
Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel
J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary
Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI
53706, USA 2US Geological Survey, National Wildlife Health Center, 6006
Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural
Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary
Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author
email: cjohnson@svm.vetmed.wisc.edu
We intracerebrally challenged four species of native North American rodents
that inhabit locations undergoing cervid chronic wasting disease (CWD)
epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed
mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles
(Myodes gapperi). The inocula were prepared from the brains of hunter-harvested
white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles
proved to be most susceptible, with a median incubation period of 272 days.
Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the
brains of all challenged meadow voles. Subsequent passages in meadow voles lead
to a significant reduction in incubation period. The disease progression in
red-backed voles, which are very closely related to the European bank vole (M.
glareolus) which have been demonstrated to be sensitive to a number of TSEs, was
slower than in meadow voles with a median incubation period of 351 days. We
sequenced the meadow vole and red-backed vole Prnp genes and found three amino
acid (AA) differences outside of the signal and GPI anchor sequences. Of these
differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is
particularly intriguing due its postulated involvement in "rigid loop" structure
and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5
years post-inoculation, but appear to be exhibiting a high degree of disease
penetrance. White-footed mice have an even longer incubation period but are also
showing high penetrance. Second passage experiments show significant shortening
of incubation periods. Meadow voles in particular appear to be interesting lab
models for CWD. These rodents scavenge carrion, and are an important food source
for many predator species. Furthermore, these rodents enter human and domestic
livestock food chains by accidental inclusion in grain and forage. Further
investigation of these species as potential hosts, bridge species, and
reservoirs of CWD is required.
please see ;
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
----- Original Message -----
From: David Colby To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor
Department of Chemical Engineering University of Delaware
===========END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION
CONGRESS SEPTEMBER 8-11 2010
AS THE CROW FLIES, SO DOES CWD
these studies are most disturbing to me, for the risk factor they pose of
something scientist have been concerned about for decades, the survival of the
TSE prion agent through the digestive tract, even if the carrier does not get
the TSE prion disease, by the TSE prion agent surviving the digestive track,
things like chickens, pigs, and other species, that ARE still legally able to
consume animal protein, thus, these animals that are legally able to consume
these products, are then rendered back to livestock that ARE BANNED FROM SAID
ANIMAL PROTEIN, thus, if the TSE prion agent has survived the digestive track,
you then are putting the TSE prions that are banned back into the human and
animal food chain, via feed. the late great TSE prion scientist Joe Gibbs said
it long ago ;
BRITISH MEDICAL JOURNAL
US scientists develop a possible test for BSE
15 November 1999
Terry S. Singeltary Sr.
“I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive
the digestinal track. So you have stopped nothing.”
Subject: Re: Hello Dr. Gibbs........... Date: Wed, 29 Nov 2000 14:14:18
–0500 From: "Clarence J. Gibbs, Jr., Ph.D." To: "Terry S. Singeltary Sr."
References: 3a254430.9fb97284@wt.net
Hi Terry:
xxx E Stret N.E., Washington, D. C. 20002. Better shrimp and oysters than
cards!!!! Have a happy holiday and thanks for all the information you bring to
the screen.
Joe Gibbs
==========
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009
Some tributes to research colleagues and other contributors to our
knowledge about kuru
I placed on the board my tribute to my colleague Clarence Joseph Gibbs Jr,
entitled ‘In celebration of Joe Gibbs’, written to honour Joe at a ceremony at
the National Institutes of Health (NIH) in Bethesda, Maryland soon after his
death on 16 February 2001, aged 76 years. I include extracts of it here. ...
please see full text ;
PUBMED search TSE prion science Gibbs JC
SO, my point here is not to be too worried about a crow dropping a TSE
prion bomb in your eye, or dropping a TSE prion load and causing an outbreak of
CWD any bigger than what we have in the USA already, bbbut, this study brings
forth evidence that we should not be rendering pigs, chickens, and such, that
have been fed banned ruminant protein, back to ruminants, or anything else i.e.
dogs and cats i.e. pets, or fish, in my opinion... tss
American crows (Corvus brachyrhynchos) and potential spreading of CWD
through feces of digested infectious carcases
Wednesday, October 17, 2012
Prion Remains Infectious after Passage through Digestive System of American
Crows (Corvus brachyrhynchos)
NOW, just what about big bird and the TSE prion ???
Chronic wasting disease (CWD), first identified in Wisconsin in 2002, is an
infectious transmissible spongiform encephalopathy (TSE) afflicting members of
the taxonomic family Cervidae, and causes neurodegeneration and ultimately
death. As a proxy for mortality or harvest of CWD-infected deer, we placed
disease-free white-tailed deer (Odocoileus virginianus) carcasses and gut piles
in the environment and monitored scavenger activity and carcass removal from
September to April in 2003 through 2005.
We recorded 14 species of scavenging mammals (six species of visitors), and
eight species of scavenging birds (14 species of visitors). Prominent scavengers
included American crows (Corvus brachyrhynchos), raccoons (Procyon lotor), and
Virginia opossums (Didelphis virginiana).
We found no evidence that deer directly consumed conspecific remains, but
they visited carcasses and gut piles.
Domestic dogs (Canis familiaris), cats (Felis sylvestris catus), and cows
(Bos spp.) either scavenged or visited carcass sites, which may have increased
exposure risk of CWD to humans and human food supplies.
Deer carcasses persisted for a median of 18 to 101 days, while gut piles
lasted for a median of three days. Habitat did not influence carcass
consumption/decomposition, but mammalian and avian scavenger activity and higher
temperatures (proxy for microbial and arthropod activity) were associated with
greater rates of carcass removal.
Our findings suggest that infected deer carcasses can function as an
environmental source of CWD prions to mammalian and avian scavengers. We discuss
the implications of these results in a broader context of CWD spread, and
suggest preemptive management strategies for mitigating impacts of CWD
contaminated deer remains in the environment....
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO
CAMELUS) - SPONGIFORM ENCEPHALOPATHY
4.21 Three cases of SE’s with an unknown infectious agent have been
reported in ostriches (Struthio Camellus) in two zoos in north west Germany
(Schoon @ Brunckhorst, 1999, Verh ber Erkeg Zootiere 33:309-314). These birds
showed protracted central nervous symptoms with ataxia, disturbances of balance
and uncoordinated feeding behaviour. The diet of these birds had included
poultry meat meal, some of which came from cattle emergency slaughter cases.
SE1806
TRANSMISSION STUDIES OF BSE TO DOMESTIC FOWL BY ORAL EXPOSURE TO BRAIN
HOMOGENATE
1 challenged cock bird was necropsied (41 months p.i.) following a period
of ataxia, tremor, limb abduction and other neurological signs.
Histopathological examination failed to reveal any significant lesions of the
central or peripheral nervous systems...
1 other challenged cock bird is also showing ataxia (43 months p.i.).
snip...
94/01.19/7.1
A notification of Spongiform Encephalopathy was introduced in October 1996
in respect of ungulates, poultry and any other animal.
4.23 MAFF have carried out their own transmission experiments with hens. In
these experiments, some of the chickens exposed to the BSE agent showed
neurological symptoms. However MAFF have not so far published details of the
symptoms seen in chickens. Examination of brains from these chickens did not
show the typical pathology seen in other SE’s. 4.24 A farmer in Kent in November
1996 noticed that one of his 20 free range hens, the oldest, aged about 30
months was having difficulty entering its den and appeared frightened and tended
to lose its balance when excited. Having previously experienced BSE cattle on
his farm, he took particular notice of the bird and continued to observe it over
the following weeks. It lost weight, its balance deteriorated and characteristic
tremors developed which were closely associated with the muscles required for
standing. In its attempts to maintain its balance it would claw the ground more
than usual and the ataxia progressively developed in the wings and legs, later
taking a typical form of paralysis with a clumsy involuntary jerky motion.
Violent tremors of the entire body, particularly the legs, became common,
sparked off by the slightest provocation. This is similar to that seen in many
BSE cases where any excitement may result in posterior ataxia, often with
dropping of the pelvis, kicking and a general nervousness. Three other farmers
and a bird breeder from the UK are known to have reported having hens with
similar symptoms. The bird breeder who has been exhibiting his birds for show
purposes for 20 years noticed birds having difficulty getting on to their perch
and holding there for any length of time without falling. Even though the bird
was eating normally, he noticed a weight loss of more than a pound in a bird the
original weight of which was 5 pounds. 4.25 Histological examination of the
brain revealed degenerative pathological changes in hens with a minimal
vacuolation. The presence of PrP immunostaining of the brain sections revealed
PrP-sc positive plaques and this must be regarded as very strong evidence to
demonstrate that the hens had been incubating Spongiform Encephalopathy.
OPINION on : NECROPHAGOUS BIRDS AS POSSIBLE TRANSMITTERS OF TSE/BSE ADOPTED
BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 7-8 NOVEMBER 2002
OPINION
1. Necrophagous birds as possible transmitters of BSE. The SSC considers
that the evaluation of necrophagous birds as possible transmitters of BSE,
should theoretically be approached from a broader perspective of mammals and
birds which prey on, or are carrion eaters (scavengers) of mammalian species.
Thus, carnivorous and omnivorous mammals, birds of prey (vultures, falcons,
eagles, hawks etc.), carrion eating birds (crows, magpies etc.) in general could
be considered possible vectors of transmission and/or spread of TSE infectivity
in the environment. In view also of the occurrence of Chronic Wasting Disease
(CWD) in various deer species it should not be accepted that domestic cattle and
sheep are necessarily the only source of TSE agent exposure for carnivorous
species. While some information is available on the susceptibility of
wild/exotic/zoo animals to natural or experimental infection with certain TSE
agents, nothing is known of the possibility of occurrence of TSE in wild animal
populations, other than among the species of deer affected by CWD in the
USA.
1 The carrion birds are animals whose diet regularly or occasionally
includes the consumption of carcasses, including possibly TSE infected ruminant
carcasses.
C:\WINNT\Profiles\bredagi.000\Desktop\Necrophagous_OPINION_0209_FINAL.doc
snip...
skroll down to the bottom ;
Date: Mon, 11 Jun 2001 16:24:51 –0700
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs
'THE AUTOPSY'
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
LANCET INFECTIOUS DISEASE JOURNAL
Volume 3, Number 8 01 August 2003
Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.
49-year-old Singeltary is one of a number of people who have remained
largely unsatisfied after being told that a close relative died from a rapidly
progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease
(CJD). So he decided to gather hundreds of documents on transmissible spongiform
encephalopathies (TSE) and realised that if Britons could get variant CJD from
bovine spongiform encephalopathy (BSE), Americans might get a similar disorder
from chronic wasting disease (CWD)the relative of mad cow disease seen among
deer and elk in the USA. Although his feverish search did not lead him to the
smoking gun linking CWD to a similar disease in North American people, it did
uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the
occurrence of CJD and CWD in the USA. Only a few states have made CJD
reportable. Human and animal TSEs should be reportable nationwide and
internationally, he complained in a letter to the Journal of the American
Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue
to expect us to still believe that the 85% plus of all CJD cases which are
sporadic are all spontaneous, without route or source.
Until recently, CWD was thought to be confined to the wild in a small
region in Colorado. But since early 2002, it has been reported in other areas,
including Wisconsin, South Dakota, and the Canadian province of Saskatchewan.
Indeed, the occurrence of CWD in states that were not endemic previously
increased concern about a widespread outbreak and possible transmission to
people and cattle.
To date, experimental studies have proven that the CWD agent can be
transmitted to cattle by intracerebral inoculation and that it can cross the
mucous membranes of the digestive tract to initiate infection in lymphoid tissue
before invasion of the central nervous system. Yet the plausibility of CWD
spreading to people has remained elusive.
Getting data on TSEs in the USA from the government is like pulling teeth,
Singeltary argues. You get it when they want you to have it, and only what they
want you to have.
SNIP...FULL TEXT ;
see old CWD low fence captive cervid herds data here ;
Bad news on game farm elk Dr. Holland, South Dakota State Veterinarian 20
Dec 98 news release
Some initial SD data released by Dr. Holland, SD State Veterinarian was
verified with two of his colleagues. There are 39 game farm elk in South Dakota
with confirmed chronic wasting disease in 1998, out of 179 tested (22%). There
are 4 or 5 herds involved - all are from game farm animals, none are from the
fall hunt. The total number of elk studied is not yet available for wild elk.
Two white-tail deer are also affected, also captive animals.
19 Mar 98 -- 14 facilities where CWD has been found
Elk disease prompts protective quarantine of Philipsburg, Hardin game
farms Tue, 23 Jun 1998 (AP)
Saturday, October 6, 2012
*** TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE
SPONGIFORM ENCEPHALOPATHIES 2011 Annual Report
Monday, September 3, 2012
2012 JAPAN BANS DEER AND ELK MEAT AND ALLOWS SOME BEEF PRODUCTS, what about
TSE prion concerns ?
Tuesday, June 05, 2012
Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012
Legislative Session
Letters|February 14, 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Terry S. Singeltary,
Sr
Copyright 2001 American Medical Association. All Rights Reserved.
Applicable FARS/DFARS Restrictions Apply to Government Use.
JAMA. 2001;285(6):733-734.
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North
America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember,
the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been
documented in North America, along with the typical scrapie's, and atypical
Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these
TSE in different species have been rendered and fed to food producing animals
for humans and animals in North America (TSE in cats and dogs ?), and that the
trading of these TSEs via animals and products via the USA and Canada has been
immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances
and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD
only theory in 2009. With all the science to date refuting it, to continue to
validate this old myth, will only spread this TSE agent through a multitude of
potential routes and sources i.e. consumption, medical i.e., surgical, blood,
dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and
the urgent need to make all human TSE in the USA a reportable disease, in every
state, of every age group, and to make this mandatory immediately without
further delay. The ramifications of not doing so will only allow this agent to
spread further in the medical, dental, surgical arena's. Restricting the
reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO
age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al
and many more, that the world of TSE Transmissible Spongiform Encephalopathy is
far from an exact science, but there is enough proven science to date that this
myth should be put to rest once and for all, and that we move forward with a new
classification for human and animal TSE that would properly identify the
infected species, the source species, and then the route.
CJD Singeltary submission to PLOS ;
No competing interests declared.
see full text ;
kind regards, terry
layperson
30>
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