CWD TSE PRION, dr. deer, shooting pen type game farms and ranchers, Texas,
TAHC, Houston Chronicle, all silent about disease ?
Outdoors: Cameras give hunters an edge over whitetail
Aimed at scrapes and rubs, monitors can help track hard-to-find mature
bucks
By John Goodspeed | December 26, 2012 | Updated: December 26, 2012 9:18pm
snip...
Other key trail camera locations are at food plots, along edges of
different vegetation or terrain and at water. He also puts a trail camera in
brush and scatters a little corn about 12 feet away.
"We get a lot more older bucks that way than we get at feeders," Kroll
said.
snip...
Greetings Mr. Goodspeed, Houston Chronicle et al,
I read your praise of dr. deer, the supposed great ‘deer czar’ from Texas.
but while he was playing dr. deer in Wisconsin, Texas fell to CWD.
I am sure with all the credentials and all the Phds dr. deer probably has,
he can say just about anything and most everyone will jump and be amazed with
his last breath. except me. he is like all the rest of the high end shooting
pens in my opinion.
I wish folks from the media would educate themselves a bit on CWD and these
game farms, and start writing about it. seems the Houston Chronicle and it’s
writers have gone mum about cwd and mad cow disease, along with other TSE prion
disease in Texas, since all have now been documented in Texas. before that, it
was like the USDA with it’s infamous ‘GOLD CARD’, I.E. BSE FREE, before that
fateful day in December of 2003, the day the TSE Prion science changed $$$
sad.
seems CWD has become a non-topic, non-concern, for everybody involved in
the industry of cervidae type shooting pen game farms, or ranches. what’s up
with that? also, since CWD has been detected in Texas, thanks to the state of
New Mexico, because let’s be perfectly honest, Texas would have never documented
and made this public, if not for the insistence of the state of New Mexico. but
it’s like it did not happen here in Texas, and with about 98% of hunting land in
Texas in Private hands, I think the true numbers of CWD are not being told, or
tested for. there is simply not enough testing on these captive shooting pen
farms and ranches. you wait until a deer shows signs or is dead, by then, it’s
much too late, and that is if, and this is a BIG IF, if the SSS policy of SHOOT,
SHOVEL, AND SHUT THE HELL UP is not used. the SSS policy is a proven mode of
disposal in TEXAS for livestock. ...
for your information Sir, for what ever that might be worth. ...
kind regards, terry
layperson
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.”
OPINION BLOG
These are just two insights into the man who has been asked to provide
analysis and recommended changes to Wisconsin’s deer management program. Kroll’s
insights are from an article entitled “Which Side of the Fence Are You On?” by
Joe Nick Patoski for a past edition of Texas Monthly.
If nothing more, the article gives an unabashed look into the mind-set that
will be providing the Wisconsin DNR with recommendations on how to change their
deer management practices. James Kroll (also known as “Deer Dr.”) was appointed
to the Wisconsin “deer czar” position last fall. He was hired by the Department
of Administration and instructed to complete a review of the state’s deer
management program.
Here’s a sample of the article:
“Game Management,” says James Kroll, driving to his high-fenced,
two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.”
Kroll, also known as Dr. Deer, is the director of the Forestry Resources
Institute of Texas at Stephen F. Austin State University, and the “management”
he is referring to is the sort practiced by the State of Texas. The 55-year-old
Kroll is the leading light in the field of private deer management as a means to
add value to the land. His belief is so absolute that some detractors refer to
him as Dr. Dough, implying that his eye is on the bottom line more than on the
natural world.
Kroll, who has been the foremost proponent of deer ranching in Texas for
more than thirty years, doesn’t mind the controversy and certainly doesn’t fade
in the heat. People who call for more public lands are “cocktail
conservationists,” he says, who are really pining for socialism. He calls
national parks “wildlife ghettos” and flatly accuses the government of gross
mismanagement. He argues that his relatively tiny acreage, marked by eight-foot
fences and posted signs warning off would-be poachers, is a better model for
keeping what’s natural natural while making money off the land.
A trip to South Africa six years ago convinced Kroll that he was on the
right track. There he encountered areas of primitive, lush wildlife-rich
habitats called game ranches. They were privately owned, privately managed, and
enclosed by high fences. He noticed how most of the land outside those fences
had been grazed to the nub, used up. “Game ranches there derive their income
from these animals — viewing them, hunting them, selling their meat,” he says.
“There are no losers.”
snip...
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Mr. Goodspeed, I thought I might pass on some of this data to you about
cwd/tse/prion disease for your files. ........
kind regards, terry
any passive attempt to eradicate or contain CWD will only fail, and let the
TSE agent spread further.
it seems all dr. deer did was try and promote more game farms ;
Letter from Rep. Danou: on Dr. Deer report $$$
Letter from Rep. Danou:
Deer Czar report is only the first step Last week, Dr. James Kroll released
his 136 page report on deer management for Wisconsin.
SNIP...
Another recommendation is for the DNR to provide more assistance to private
landowners on deer management. Although he did not specifically mention setting
up private hunting preserves which exist in Kroll’s home state of Texas, I am
particularly interested in learning more about this recommendation and its
specific details for implementation. This is one recommendation that will
definitely require more personnel to implement.
SNIP...
National Wildlife Health Center
Enhanced Surveillance Strategies for Detecting and Monitoring Chronic
Wasting Disease in Free-Ranging Cervids
Open-File Report 2012–1036
snip...
Spatial Risk Factors
snip...
In addition to locations of known CWD-positive individuals, other spatial
risk factors related to CWD exposure should be considered. For example, the risk
of free-ranging animals being exposed to CWD is likely greater in areas where
captive cervid facilities have or had CWD-positive animals. Current evidence
indicates that CWD infection rates are much higher in captive facilities than in
wild populations (Keane and others, 2008), and perhaps this is driven by
environmental contamination (Miller and others, 2006). This higher rate of
infection in captive animals can increase the risk of disease exposure to
surrounding wild populations. Furthermore, movement of infectious animals,
carcasses, or other materials across the landscape, naturally or with human
assistance, likely increases the risk to uninfected populations. The frequent
movement of farmed elk (Cervus elaphus) and deer between production facilities,
the concentration of infected animals on some facilities, and the possibility of
their escape into the wild increases the risk of spreading CWD to uninfected
populations of free-ranging animals. Because the infectious prions may persist
in the environment for long periods, the introduction of either captive or
free-ranging uninfected animals into a contaminated environment could increase
their risk of infection. For example, locations from which sheep have been
removed may remain contaminated with scrapie agent for more than 15 years
(Georgsson and others, 2006). In a similar manner, translocation of cervids from
areas that have not been documented to be CWD-free could pose a risk of disease
introduction. In this situation, the risk of introduction is likely related to
the probability of infected animals being moved and their ability to spread CWD
to other susceptible animals or into the environment. Thus, surveillance on and
around cervid farms or free-ranging populations that have received animals from
known CWD areas and bordering jurisdictions with CWD-positive animals can
increase the likelihood of disease spread. Additional risk factors, such as the
presence of scrapie in sheep populations that are sympatric with deer and elk
(Greenlee and others, 2011), feeding of animal protein to cervids (Johnson,
McKenzie, and others, 2011), baiting and feeding programs (Thompson and others,
2008), or other environmental factors also may be considered, although their
roles in CWD epidemiology has not been clearly established.
The soil composition of a region may also play an important role in the
occurrence and maintenance of CWD and other TSEs (Smith and others, 2011).
Recently, it has been shown that certain soil types can chemically bind and
increase infectivity of prion protein (PrP), creating the potential for the
protein to be maintained at the soil surface for uptake by foraging animals
(Johnson and others, 2006; Johnson and others, 2007; Polano and others, 2008;
Imrie, 2009); however, the fate of prions may be highly dependent on source of
deposition into the soil (for example, fluid or tissue; Saunders and others
2009). In addition, organic soil components (humic acids) appear to enhance the
adsorption of PrP to clay minerals and show a great affinity for the protein as
well; however, it is unclear whether the effect of the organic matter increases
or decreases infectivity (Polano and others, 2008). The importance of soil in
CWD epidemiology was reaffirmed by Walter and others (2011) who demonstrated an
8.9-percent increase in an individual’s deer’s odds of CWD infection with each
1-percent increase in soil clay content within its approximate home range in
north-central Colorado. These results suggest that some regions may have a
greater probability of maintaining and spreading CWD based solely on their
geologic and chemical attributes. Thus, the soil characteristics within an
animal’s range represent a potentially important spatial risk factor for CWD
occurrence and maintenance.
The risk of disease amplification (increasing the number of infected
animals) in a target population or location postexposure likely increases as
cervid population densities increase and predation decreases. In north-central
Colorado, the greater the area of a mule deer’s (Odocoileus hemionus)
approximate home range that contained wintering concentration areas of deer
(high deer densities) the greater the odds of individual CWD infection
(Farnsworth and others, 2006; Walter and others, 2011). The absence of predators
or harvest potentially allows infected animals a longer period when they can
transmit CWD to other animals by direct contact or indirectly through
environmental reservoirs (Wild and others, 2011). Removal of infectious animals
by harvest or other means likely reduces the rate of disease transmission and
prevalence in free-ranging cervids (Gross and Miller, 2001; Schauber and Woolf,
2003; Wasserberg and others, 2009; Habib and others, 2011), deposition of
infectious prions into the environment, and the rate of disease spread. However,
if infection rates are high and sustained, even intense selective predation of
infected individuals may not reduce the spread and persistence of CWD (Miller
and others, 2008), possibly due to the effects of indirect transmission on the
disease process (Almberg and others, 2011). Baiting or feeding, which
artificially increases concentrations of animals, may increase the chance of
disease spread through direct contact among animals or indirect contact with
environmental contamination (Thompson and others, 2008; Mathiason and others,
2009; Tamguney and others, 2009; Haley and others, 2011). Thus, variation in
density of deer or infected deer across the landscape is another important
spatial risk factor to consider when conducting disease surveillance or
monitoring (Joly and others, 2009).
snip...
Anthropogenic activities, management policies, and land use patterns within
an area may also be important considerations when designing CWD surveillance or
monitoring strategies. The amount of private land within a deer’s approximate
home range has been shown to influence CWD infection rates in Colorado
(Farnsworth and others, 2006; Walter and others, 2011). Although no causal
mechanism has been established, it is probable that private lands may act as
refugia from harvest pressure (Vieira and others, 2003), and private lands may
often occur on more moist and productive soils, providing better production and
habitat that may be selected for by cervids. In addition, these soils may be
composed of soil types that may increase the infectivity of the prions as
previously described. These conditions can concentrate animals, increase
density, and affect the age-structure of local populations, which consequently
affects disease dynamics. Management policies at multiple scales can also affect
infection risk. For example, limited or no harvest or predation of deer in urban
areas, compared to undeveloped areas, may promote higher densities of deer and
prevent the removal of infected individuals (Farnsworth and others, 2005), thus
increasing disease prevalence (Wasserberg and others, 2009). Likewise, spatially
and temporally varying harvest regulations and management strategies across a
jurisdiction affects cervid densities and population structure ( age and sex
ratios), and may create spatial variability in CWD infection risk (Gross and
Miller, 2001; Wasserberg and others, 2009; Bergman and others, 2011; Sharp and
Pastor, 2011).
snip...
Demographic Risk Factors
Other demographic risk factors are less well understood. For example, there
is evidence that genetics plays a role in individual susceptibility and rate of
disease progression. Similar to other TSEs, polymorphisms of the prion protein
gene (PRNP) may moderate individual susceptibility to and progression of CWD
infection of elk, mule, and white-tailed deer (O’Rourke and others, 2004;
Spraker and others, 2004; Jewell and others, 2005; Fox and others, 2006; Hamir
and others, 2006; Goldmann, 2008; Keane and others, 2008; Perucchini and others,
2008). Therefore, it appears that certain individuals are innately at higher
risk of CWD infection based solely on their PRNP genotype. For example,
Wisconsin white-tailed deer with the PRNP genotype G96G have approximately four
times higher rate of infection and 8 months shorter survival after infection
compared to G96S deer (Robinson and others, 2012). However, unlike other TSEs,
there is no evidence that any of the PRNP genotypes in wild cervids are immune
to CWD infection.
snip...
Finally, high population density, which also can be considered a spatial
risk factor, is generally believed to create increased risk of disease
transmission through higher direct or indirect contact rates (Swinton and
others, 2001; Ramsey and others, 2002). This is the basis for population
reduction strategies used by many wildlife management agencies for CWD
management in free-ranging cervids (Williams and others, 2002; Joly and others,
2003; Williams, 2005; Joly and others, 2006). The actual transmission route of
CWD is not known, however, experimental evidence from captive cervids suggests
that CWD infection occurs via horizontal transmission through both direct and
indirect contact between susceptible and infected individuals (Miller and
Williams, 2003; Williams and Miller, 2003), and both kinds of contact can be
influenced by density. Experimental inoculation with blood, urine, feces, and
saliva from CWD-infected individuals has been shown to provide viable routes of
transmission, suggesting direct contact with any of these infectious materials
could act as a route of infection (Miller and others, 2004; Mathiason and
others, 2006; Miller and others, 2006; Trifilo and others, 2007; Safar and
others, 2008; Haley and others, 2009; Mathiason and others, 2009; Tamguney and
others, 2009; Haley and others, 2011). Indirect contact may play an important
role in transmission dynamics via environmental contamination, because the CWD
agent can persist in contaminated systems for 2 or more years (Miller and
others, 2004), and if CWD is similar to scrapie, it may persist for 15 or more
years (Georgsson and others, 2006). For captive cervids, the most likely route
of exposure is orally through foraging activities in the immediate vicinity of
fresh and decomposed carcasses or ingestion of fresh and residual excreta from
infected individuals (Miller and others, 2004; Trifilo and others, 2007; Safar
and others, 2008; Mathiason and others, 2009). However, the relative importance
of direct and indirect transmission of CWD in wild cervids has not been
determined. As previously mentioned, certain soil types can also increase oral
infectivity of TSEs, which may allow environmental contamination to be
problematic even in the presence of relatively low doses of the infective agent
(Johnson and others, 2007). Thus, it is likely density of infected cervids can
contribute to increased indirect contact rate between susceptible and infected
individuals or contact with an environmental reservoir. However, it is unclear
to what the extent density influences these processes.
snip...
When Is Enough…Enough?
Another common question is “when have I conducted enough surveillance to
confidently believe my jurisdiction is disease-free?” Bohning and Greiner (2006)
provide a statistical framework for estimating the smallest number of samples
required over multiple survey events, which need to be tested to ensure an area
is free of disease for a given design prevalence and power. Their approach is
based on a geometric distribution for waiting time (that is, the time until
first detection of disease) and was developed for surveillance of BSE. An
extension of this framework allows for heterogeneity in design prevalence, which
would be particularly useful for CWD surveillance.
Tuesday, December 18, 2012
A Growing Threat How deer breeding could put public trust wildlife at risk
Friday, December 14, 2012
Susceptibility of domestic cats to chronic wasting disease
Friday, December 14, 2012
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005
- December 14, 2012
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
Monday, November 26, 2012
Rapid Transepithelial Transport of Prions following Inhalation
while dr. deer, the game farmer/rancher from Texas was telling Wisconsin to
take a passive approach to CWD, Texas fell to CWD.
if it had not been for the state of New Mexico, and their insistence that
CWD is and has been waltzing across Texas for a decade or more, Texas still
would have never _documented_ CWD. just like they did with mad cow disease. they
did successfully cover up one mad cow, and the second mad cow sat up on a shelf,
as a negative mad cow, even though a secret test showed it to be positive, sat
up on a shelf for 7+ months, before international scientists were demanding that
cow be retested. Thanks to the Honorable Phyllis Fong of the OIG, that cow was
finally confirmed as mad cow disease, 7+ months later, on USDA BSE confirmation
protocols that was supposed to be 48 hours.
The fact of the matter is, CWD has been waltzing across Texas for over a
decade from the WSMR at New Mexico border, and the state of Texas, in my
opinion, knew this. in my opinion, the state of Texas purposely tested the least
amount of cervids in that area for years, why, they knew it was there, and I
warned you of this in 2001, 2005, and year after year after year. now, it’s too
late. Game farms and ranchers i.e. high fence operations here in Texas are out
of control in my opinion, with the TAHC not having a clue as to the infection
rate of CWD (if any) at these high fence operations. it has been proven in the
past, they are nothing but a petri dish for CWD infection rates, with the
highest infection rate in Wisconsin at the Buckhorn Flats Game farm toping out
at 80%. TAHC actions now on CWD, as I finally applaud them, may well be much too
late, and not near enough. I pray that I am wrong. However, because of this, I
think the movement restrictions on cervids in Texas should include every region
in the state of Texas, until a very large cwd sampling over a period of 7 to 10
years. ...
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
see history of my failed attempts to get the TAHC to start testing for CWD
in far west Texas started back in 2001 – 2002 ;
Saturday, July 07, 2012
TEXAS Animal Health Commission Accepting Comments on Chronic Wasting
Disease Rule Proposal
Considering the seemingly high CWD prevalence rate in the Sacramento and
Hueco Mountains of New Mexico, CWD may be well established in the population and
in the environment in Texas at this time.
Thursday, March 29, 2012
TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT
CALLING KETTLE BLACK
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Tuesday, July 10, 2012
Dr. James C. Kroll Texas deer czar final report on Wisconsin
Thursday, December 13, 2012
HUNTERS FEELING THE HEAT Houston Chronicle December 13, 2012 OUTDOORS not
talking about CWD in Texas
Wednesday, November 07, 2012
Chronic Wasting Disease CWD, Texas, Houston Chronicle Shannon Thomkins 1998
- 2012 what happened ???
Thursday, July 12, 2012
CWD aka MAD DEER, ELK DISEASE TEXAS HOUSTON CHRONICLE Wednesday, July 11,
2012
Thursday, July 19, 2012
KANSAS NINE DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE
Friday, July 20, 2012
CWD found for first time in Iowa at hunting preserve
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).
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol
Needs To Be Revised
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
Tuesday, June 05, 2012
Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012
Legislative Session
Saturday, June 09, 2012
USDA Establishes a Herd Certification Program for Chronic Wasting Disease
in the United States
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
LANCET INFECTIOUS DISEASE JOURNAL
Volume 3, Number 8 01 August 2003
Previous
Next
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 ;
now, a few things to ponder about those said double fences that will
supposedly stop those deer from escaping.
what about water that drains from any of these game farms. surrounding
water tables etc., are the double fences going to stop the water from becoming
contaminated? where does it drain? who's drinking it?
Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic
Area
65
Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal
Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and
M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of
Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort
Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services,
United States Department of Agriculture, Fort Collins, Colorado, 80521, USA
3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA
4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory,
University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology,
Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging,
University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author-
tracy.a.nichols@aphis.usda.gov
Chronic wasting disease (CWD) is the only known transmissible spongiform
encephalopathy affecting free-ranging wildlife. Experimental and epidemiological
data indicate that CWD can be transmitted horizontally and via blood and saliva,
although the exact mode of natural transmission remains unknown. Substantial
evidence suggests that prions can persist in the environment, implicating it as
a potential prion reservoir and transmission vehicle. CWD- positive animals can
contribute to environmental prion load via biological materials including
saliva, blood, urine and feces, shedding several times their body weight in
possibly infectious excreta in their lifetime, as well as through decomposing
carcasses. Sensitivity limitations of conventional assays hamper evaluation of
environmental prion loads in water. Here we show the ability of serial protein
misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions
in spiked water samples at a 1:1 x106 , and protease-resistant prions in
environmental and municipal-processing water samples from a CWD endemic area.
Detection of CWD prions correlated with increased total organic carbon in water
runoff from melting winter snowpack. These data suggest prolonged persistence
and accumulation of prions in the environment that may promote CWD transmission.
snip...
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels. snip...end...full text at ;
what about rodents there from? 4 American rodents are susceptible to CWD to
date. are those double fences going to stop these rodents from escaping these
game farms once becoming exposed to CWD?
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 ;
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M.
Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness. Two of these cats have
developed rear limb ataxia. Although the limited data from this ongoing study
must be considered preliminary, they raise the potential for cervid-to-feline
transmission in nature. www.landesbioscience.com Prion
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 ProfessorDepartment of Chemical
EngineeringUniversity 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
Monday, January 16, 2012
9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Thursday, February 17, 2011
Environmental Sources of Scrapie Prions
Friday, December 14, 2012
IOWA Second Deer Positive for CWD at Davis County Hunting Preserve Captive
Shooting Pen
Friday, September 21, 2012
Chronic Wasting Disease CWD raises concerns about deer farms in Iowa
Tuesday, September 11, 2012
Agreement Reached with Owner to De-Populate CWD Deer at Davis County
Hunting Preserve Iowa
Wednesday, September 05, 2012
Additional Facility in Pottawatamie County Iowa Under Quarantine for CWD
after 5 deer test positive
Friday, July 20, 2012
CWD found for first time in Iowa at hunting preserve
Tuesday, December 11, 2012
PENNSYLVANIA PURPLE 4 ESCAPED CAPTIVE FOUND FREE OF CWD, what about the
deer in Louisiana ?
Sunday, December 09, 2012
Pennsylvania Sportsmen upset with agriculture’s lack of transparency on CWD
Thursday, December 06, 2012
Pennsylvania CWD Not Found in Pink 23 PA captive escapee, but where is
Purple 4 and the other escapees ?
News for Immediate Release
Wednesday, December 05, 2012
Senator Casey Urges USDA To Take Smart Steps to Implement New Measure That
Could Help Combat Chronic Wasting Disease Among Deer
From: Terry S. Singeltary Sr.
Sent: Wednesday, December 05, 2012 11:50 AM
To: Press_office@casey.senate.gov Cc: ckauffman@yorkdispatch.com ; Terry S.
Singeltary Sr.
Subject: Casey Urges USDA To Take Smart Steps to Implement New Measure That
Could Help Combat Chronic Wasting Disease Among Deer
Wednesday, November 14, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO
LOUISIANA and INDIANA
Tuesday, November 13, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD
Wednesday, November 07, 2012 PENNSYLVANIA
Second Adams County Deer Tests Positive for Chronic Wasting Disease
Friday, October 26, 2012
***CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT
PRODUCTS, BAITING, AND MINERAL LICKS
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
Pennsylvania CWD number of deer exposed and farms there from much greater
than first thought
Published: Wednesday, October 17, 2012, 10:44 PM Updated: Wednesday,
October 17, 2012, 11:33 PM
Tuesday, December 11, 2012
Wisconsin Receives Federal Approval for CWD Herd Certification Program for
Farm-raised Deer
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...
C. & D. Captive Cervid and Law Enforcement Update (11:10 AM)- Warden
Pete Dunn gave the captive cervid farm update. 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. Approximately 30% of these escapes were caused by
gates being left open and the other 70% resulted from bad fencing or fence
related issues. The 20 actual confirmed escape incidents amounted to 77 total
animals. 50 of the escaped animals were recovered or killed and 27 were not
recovered and remain unaccounted for. Last year the CWD Committee passed a
resolution to require double gates, but this has not gone into effect yet.
Questions were raised by the committee about double fencing requirements? Pete
responded that double fencing has not been practical or accepted by the
industry. The DNR has the authority to do fence inspections. ?If a fence fails
to pass the inspection the fencing certificate can be revoked and the farmer can
be issued a citation. This year three citations and one warning have been issued
for escapes. Pete reviewed the reporting requirements for escape incidents that
these must be reported within 24 hours. The farmer then has 72 hours to recover
the animals or else it will affect the farm’s herd status and ability to move
animals. Davin proposed in the 15 year CWD Plan that the DNR take total control
and regulatory authority over all deer farm fencing. Larry Gohlke asked Pete
about the reliability for reporting escapes? Pete said that the majority of
escapes were reported by the farmer, but it is very difficult to determine when
an escape actually occurred. Pete said that they are more concerned that an
escape is reported and not that it is reported at the exact time that it
happened.
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:
Monday, January 16, 2012 9
GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD
see full text and more here ;
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Tuesday, December 18, 2012
*** A Growing Threat How deer breeding could put public trust wildlife at
risk
PLEASE NOTE, with BSE, going by OIE standards, an adequate number for
sample survey for any Country going by OIE BSE guidelines for 40,000,000 cattle,
was 433 cattle.
how did that work out for us? I will tell you, most every Country that went
by those OIE guidelines went down with BSE, including the USA. just saying, you
never can test enough. ...TSS
----- Original Message -----
From: "Terry S. Singeltary Sr."
To: BSE-L
Sent: Saturday, June 04, 2005 8:07 AM
Subject: BSE OIE CHAPTER 2.3.13 (The Weakening of a already terribly
flawwed BSE/TSE surveillance system)
##################### Bovine Spongiform Encephalopathy
#####################
Saturday, August 4, 2012
Final Feed Investigation Summary - California BSE Case - July 2012
Thursday, December 20, 2012
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe
WITH BOVINE MAD COW DISEASE
Monday, December 1, 2008
When Atypical Scrapie cross species barriers
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH
CODE
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
why do we not want to do TSE transmission studies on chimpanzees $
snip...
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
Wednesday, January 18, 2012
Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural
Scrapie Isolates Similar to CH1641 Experimental Scrapie
Journal of Neuropathology & Experimental Neurology:
February 2012 - Volume 71 - Issue 2 - p 140–147
snip...see more on scrapie and atypical scrapie here ;
Thursday, December 13, 2012
Eradication Program: Animal Identification and Recordkeeping Guide for
Sheep and Goats Veterinary Services December 2012
Veterinary Services December 2012
Saturday, December 15, 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on
attack rate and incubation period in cattle -- an update 5 December 2012
Wednesday, March 28, 2012
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion
poker goes up again $
Tuesday, December 25, 2012
CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25,
2012
Tuesday, December 18, 2012
Bioassay Studies Support the Potential for Iatrogenic Transmission of
Variant Creutzfeldt Jakob Disease through Dental Procedures
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403
we’re just kidding ourselves $$$
stupid is, as stupid does, and some times, you just can’t fix stupid $$$
RIP MOM 12/14/97 confirmed hvCJD...never forget...TSS...December 25, 2012
layperson
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
flounder9@verizon.net
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