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01 Oct 2007 11:00 PM  
greetings hunters,

my name is Terry S. Singeltary Sr., aka flounder and few other alias that i should not mention. but i would kindly like to add to this discussion. i lurk here and there, but this topic i have been trying to warn for over about a decade now. i plan to retire soon, never to speak of this again, but i wish to inform you on the latest data about the Transmissible Spongiform Encephalopathies, including CWD now, before i do. no, it's not pretty, hell, neither am i, but these are the facts as i have come to know them, and you should become aware of them. yep, the old saying goes, you are more likely to die from being hit by a car. but my mother and many more did not get hit by a car, they died from cjd. cjd is increasing in the USA. i am not anti-hunter, or anti-meat, i simply want you to be aware, of facts i am sure some of you are not aware of i.e. what i call 'the rest of the story'. these are the facts to date, take them with how every many grains of salt you wish. ...


Survival of PrPSc during Simulated Wastewater Treatment Processes

Pedersen, J1; Hinckley, G1; McMahon, K2; McKenzie, D3; Aiken, JM3
1University of Wisconsin, Soil Science/Civil and Environmental Engineering,
USA; 2University of Wisconsin, Civil and Environmental Engineering, USA;
3University of Wisconsin, Comparative Biosciences, USA

Concern has been expressed that prions could enter wastewater treatment systems
through sewer and/or septic systems (e.g., necropsy laboratories, rural meat
processors, private game dressing) or through leachate from landfills that have
received TSE-contaminated material. Prions are highly resistant to degradation and
many disinfection procedures raising concern that they could survive conventional
wastewater treatment. Here, we report the results of experiments examining the
partitioning and survival of PrPSc during simulated wastewater treatment processes
including activated and mesophilic anaerobic sludge digestion. We establish that PrPSc
can be efficiently extracted from activated and anaerobic digester sludges with 1%
sodium dodecyl sulfate, 10% sodium undecyl sulfate, and 1% sodium N-lauryl
sarcosinate. Activated sludge digestion does not result in significant degradation of
PrPSc. The protein partitions strongly to the activated sludge solids and is
expected to enter biosolids treatment processes. A large fraction of PrPSc survived
simulated mesophilic anaerobic sludge digestion. Our results suggest that if prions
were to enter municipal waste water treatment systems, most of the agent
would partition to activated sludge solids, survive mesophilic anaerobic digestion, and
be present in treated biosolids. Land application of biosolids containing prions could
represent a route for their unintentional introduction into the environment. Our results
argue for excluding inputs of prions to municipal wastewater treatment facilities that
would result in unacceptable risk of prion disease transmission via contaminated
biosolids." target="_blank" rel="nofollow">" target="_blank" rel="nofollow">


Chronic Wasting Disease in a Captive White-Tailed Deer Farm

Keane, D1; Barr, D1; Bochsler, P1; Hall, M2; Gidlewski, T3; O'Rourke, K4; Spraker, T5
1University of Wisconsin, USA; 2US Department of Agriculture, USA; 3US Department
of Agriculture, USA; 4USDA ARS-ADRU, Washington |State University, USA;
5Veterinary Diagnostic Laboratory, Colorado State University, USA

A white-tailed deer farm in Portage, Wisconsin, was depopulated in January 2006,
after chronic wasting disease (CWD) had been initially discovered on the property in
September 2002. Prior to the depopulation, a total of 22 positive animals had been
removed from the property: one in 2002, six in 2003, ten in 2004, four in 2005 and one
in 2006. At the time of depopulation a total of 76 animals remained: 47 females and 29
males. Age was assessed by visual examination of teeth at the time of death and
revealed 26 adult, 8 fawn and 42 yearling animals. The following tissues were
examined by immunohistochemistry for PrPCWD using Ab99/97.6.1: obex, tonsil,
retropharyngeal, submandibular, parotid, prescapular, axillary, inguinal, prefemoral and
popliteal lymph nodes, recto-anal mucosal tissue and eye. Seventy-nine percent of
animals (sixty) were found to be positive in at least one tissue; 49 were obex positive,
58 retropharyngeal positive, 56 tonsil positive, 48 recto-anal mucosal associated
lymphoid tissue positive and 4 animals were positive for PrPCWD in the retina. Prion
genotype was determined for all animals." target="_blank" rel="nofollow">" target="_blank" rel="nofollow">


Quantifying the Species Barrier in Chronic Wasting Disease by a Novel in
vitro Conversion Assay

Li, L1; Coulthart, MB2; Balachandran, A3; Chakrabartty, A4; Cashman, NR1
1University of British Columbia, Brain Research Centre, Canada; 2Public Health Agency
of Canada, National Microbiology Laboratory, Canada; 3Animal Diseases
Research Institute, Canada Food Inspection Agency, National Reference Laboratory for
Scrapie and CWD, Canada; 4Ontario Cancer Institute and Department of Medical
Biophysics, University of Toronto, Canada

Background: Chronic wasting disease (CWD) is a transmissible spongiform
encephalopathy that can affect North American cervids (deer, elk, and moose).
Although the risk of CWD crossing the species barrier and causing human
disease is still unknown, however, definite bovine spongiform encephalopathy (BSE)
transmission to humans as variant CJD (vCJD), it would seem prudent to limit
the exposure of humans to CWD.

Aim: In view of the fact that BSE can be readily transmitted to non-bovid
species, it is important to establish the species susceptibility range of

Methods: In vitro conversion system was performed by incubation of prions
with normal brain homogenates as described before, and protease K (PK) resistant
PrP was determined by immunoblotting with 6H4 monoclonal prion antibody.

Results: Our results demonstrate that PrPC from cervids (including moose)
can be efficiently converted to a protease-resistant form by incubation with elk
CWD prions, presumably due to sequence and structural similarities between these
species. Interestingly, hamster shows a high conversion ratio by PrPCWD. Moreover,
partial denaturation of substrate PrPC can apparently overcome the structural
barriers between more distant species.

Conclusions: Our work correctly predicted the transmission of CWD to a wild moose.
We find a species barrier for prion protein conversion between cervids and
other species, however, this barrier might be overcome if the PrPC substrate has
been partially denatured in a cellular environment. Such an environment might
also promote CWD transmission to non-cervid species, *** including humans.
Acid/GdnHCl-treated brain PrPC was a superior substrate for the in vitro
conversion than PrPC treated at physiological pH. This has implications for the process
by which the prion protein is converted in disease." target="_blank" rel="nofollow">" target="_blank" rel="nofollow">

Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil

Christopher J. Johnson1,2, Joel A. Pedersen3, Rick J. Chappell4, Debbie
McKenzie2, Judd M. Aiken1,2*

1 Program in Cellular and Molecular Biology, University of
Wisconsin-Madison, Madison, Wisconsin, United States of America, 2
Department of Comparative Biosciences, School of Veterinary Medicine,
University of Wisconsin-Madison, Madison, Wisconsin, United States of
America, 3 Department of Soil Science and Molecular and Environmental
Toxicology Center, University of Wisconsin-Madison, Madison, Wisconsin,
United States of America, 4 Biostatistics and Medical Informatics,
University of Wisconsin Medical School, Madison, Wisconsin, United States of

Soil may serve as an environmental reservoir for prion infectivity and
contribute to the horizontal transmission of prion diseases (transmissible
spongiform encephalopathies [TSEs]) of sheep, deer, and elk. TSE infectivity
can persist in soil for years, and we previously demonstrated that the
disease-associated form of the prion protein binds to soil particles and
prions adsorbed to the common soil mineral montmorillonite (Mte) retain
infectivity following intracerebral inoculation. Here, we assess the oral
infectivity of Mte- and soil-bound prions. We establish that prions bound to
Mte are orally bioavailable, and that, unexpectedly, binding to Mte
significantly enhances disease penetrance and reduces the incubation period
relative to unbound agent. Cox proportional hazards modeling revealed that
across the doses of TSE agent tested, Mte increased the effective infectious
titer by a factor of 680 relative to unbound agent. Oral exposure to
Mte-associated prions led to TSE development in experimental animals even at
doses too low to produce clinical symptoms in the absence of the mineral. We
tested the oral infectivity of prions bound to three whole soils differing
in texture, mineralogy, and organic carbon content and found soil- bound
prions to be orally infectious. Two of the three soils increased oral
transmission of disease, and the infectivity of agent bound to the third
organic carbon-rich soil was equivalent to that of unbound agent. Enhanced
transmissibility of soil-bound prions may explain the environmental spread
of some TSEs despite the presumably low levels shed into the environment.
Association of prions with inorganic microparticles represents a novel means
by which their oral transmission is enhanced relative to unbound agent.


Discussion These experiments address the critical question of whether soil
particle­bound prions are infectious by an environmentally relevant exposure
route, namely, oral ingestion. Oral infectivity of soil particle­bound
prions is a conditio sine qua non for soil to serve as an environmental
reservoir for TSE agent. The maintenance of infectivity and enhanced
transmissibility when TSE agent is bound to the common soil mineral Mte is
remarkable given the avidity of the PrPTSE­Mte interaction [22]. One might
expect the avid interaction of PrPTSE with Mte to result in the mineral
serving as a sink, rather than a reservoir, for TSE infectivity. Our results
demonstrate this may not be the case. Furthermore, sorption of prions to
complex whole soils did not diminish bioavailability, and in two of three
cases promoted disease transmission by the oral route of exposure. While
extrapolation of these results to environmental conditions must be made with
care, prion sorption to soil particles clearly has the potential to increase
disease transmission via the oral route and contribute to the maintenance of
TSE epizootics.

Two of three tested soils potentiated oral prion disease transmission. The
reason for increased oral transmissibility associated with some, but not
all, of the soils remains to be elucidated. One possibility is that
components responsible for enhancing oral transmissibility were present at
higher levels in the Elliot and Bluestem soils than in the Dodge soil. The
major difference between the Dodge soil and the other two soils was the
extremely high natural organic matter content of the former (34%, [22]). The
Dodge and Elliot soils contained similar levels of mixed-layer
illite/smectite, although the contribution of smectite layers was higher in
the Dodge soil (14%­16%, [22]). The organic matter present in the Dodge soil
may have obstructed access of PrPTSE to sorption sites on smectite (or other
mineral) surfaces.

The mechanism by which Mte or other soil components enhances the oral
transmissibility of particle-bound prions remains to be clarified.
Aluminosilicate minerals such as Mte do not provoke inflammation of the
intestinal lining [39]. Although such an effect is conceivable for whole
soils, soil ingestion is common in ruminants and other mammals [25]. Prion
binding to Mte or other soil components may partially protect PrPTSE from
denaturation or proteolysis in the digestive tract [22,40] allowing more
disease agent to be taken up from the gut than would otherwise be the case.
Adsorption of PrPTSE to soil or soil minerals may alter the aggregation
state of the protein, shifting the size distribution toward more infectious
prion protein particles, thereby increasing the specific titer (i.e.,
infectious units per mass of protein) [41]. In the intestine, PrPTSE
complexed with soil particles may be more readily sampled, endocytosed
(e.g., at Peyer's patches), or persorbed than unbound prions.
Aluminosilicate (as well as titanium dioxide, starch, and silica)
microparticles, similar in size to the Mte used in our experiments, readily
undergo endocytotic and persorptive uptake in the small intestine [42­44].
Enhanced translocation of the infectious agent from the gut lumen into the
body may be responsible for the observed increase in transmission

Survival analysis indicated that when bound to Mte, prions from both BH and
purified PrPTSE preparations were more orally infectious than unbound agent.
Mte addition influenced the effective titer of infected BH to a lesser
extent than purified PrPTSE. Several nonmutually exclusive factors may
explain this result: (1) other macromolecules present in BH (e.g., lipids,
nucleic acids, other proteins) compete with PrPTSE for Mte binding sites;
(2) prion protein is more aggregated in the purified PrPTSE preparation than
in BH [45], and sorption to Mte reduces PrPTSE aggregate size, increasing
specific titer [41]; and (3) sorption of macromolecules present in BH to Mte
influences mineral particle uptake in the gut by altering surface charge or
size, whereas the approximately 1,000-fold lower total protein concentration
in purified PrPTSE preparations did not produce this effect.

We previously showed that other inorganic microparticles (kaolinite and
silicon dioxide) also bind PrPTSE [22]. All three types of microparticles
are widely used food additives and are typically listed as bentonite (Mte),
kaolin (kaolinite), and silica (silicon dioxide). Microparticles are
increasingly included in Western diets. Dietary microparticles are typically
inert and considered safe for consumption by themselves, do not cause
inflammatory responses or other pathologies, even with chronic consumption,
and are often sampled in the gut and transferred from the intestinal lumen
to lymphoid tissue [39,46,47]. Our data suggest that the binding of PrPTSE
to dietary microparticles has the potential to enhance oral prion disease
transmission and warrants further investigation.

In conclusion, our results provide compelling support for the hypothesis
that soil serves as a biologically relevant reservoir of TSE infectivity.
Our data are intriguing in light of reports that naïve animals can contract
TSEs following exposure to presumably low doses of agent in the environment
[5,7­9]. We find that Mte enhances the likelihood of TSE manifestation in
cases that would otherwise remain subclinical (Figure 3B and 3C), and that
prions bound to soil are orally infectious (Figure 5). Our results
demonstrate that adsorption of TSE agent to inorganic microparticles and
certain soils alter transmission efficiency via the oral route of exposure.

snip...full text is here:


From: "Terry S. Singeltary Sr."
Subject: CWD UPDATE 88 AUGUST 31, 2007

Date: Wed, 29 Aug 2007 21:13:08 -0500
From: "Terry S. Singeltary Sr."
Subject: CWD NEW MEXICO RECORDS IT'S 19 CASE (near Texas border again);P=26079

Monitoring the Potential Transmission of Chronic Wasting Disease to Humans
Using a Hunter Registry Database in Wyoming (405 lines)
From: Terry S. Singeltary Sr.
Date: Thu, 30 Aug 2007 21:23:42 -0500;P=27654

J Biol Chem. 2007 Aug 20; : 17709374

Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a
new prion strain.


our results raise the possibility that CJD cases
classified as VV1 may include cases caused by
iatrogenic transmission of sCJD-MM1 prions or
food-borne infection by type 1 prions from animals,
e.g., chronic wasting disease prions in cervid. In fact,
two CJD-VV1 patients who hunted deer or
consumed venison have been reported (40, 41). The
results of the present study emphasize the need for
traceback studies and careful re-examination of the
biochemical properties of sCJD-VV1 prions.



Re: Colorado Surveillance Program for Chronic Wasting Disease
Transmission to Humans (TWO SUSPECT CASES)

Subject: Aspects of the Cerebellar Neuropathology in Nor98
Date: September 26, 2007 at 4:06 pm PST


Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1
1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

Nor98 is a prion disease of old sheep and goats. This atypical form of
scrapie was first described in Norway in 1998. Several features of Nor98
were shown to be different from classical scrapie including the distribution
of  disease associated prion protein (PrPd) accumulation in the brain. The
cerebellum is  generally the most affected brain area in Nor98. The study here 
presented aimed at  adding information on the neuropathology in the cerebellum 
of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. 
A panel of histochemical and immunohistochemical (IHC) stainings such as IHC 
for PrPd, synaptophysin,  glial fibrillary acidic protein, amyloid, and cell markers 
for phagocytic cells were conducted. The type of histological lesions and tissue 
reactions  were evaluated. The types of PrPd deposition were characterized. The
cerebellar cortex was regularly affected, even though there was a variation
in the severity of the lesions from case to case.
Neuropil vacuolation was more marked in the molecular layer, but affected
also the granular cell layer. There was a loss of granule cells. Punctate
deposition of PrPd was characteristic. It was morphologically and in distribution
identical with that of synaptophysin, suggesting that PrPd accumulates in
the synaptic  structures. PrPd was also observed in the granule cell layer and in the
white matter.
*** The pathology features of Nor98 in the cerebellum of the affected sheep
showed similarities with those of sporadic Creutzfeldt-Jakob disease in
humans." target="_blank" rel="nofollow">" target="_blank" rel="nofollow">

From: "Terry S. Singeltary Sr."
Sent: Tuesday, August 21, 2007 9:50 AM
Subject: TWO MORE Nor98 atypical Scrapie cases detected in USA bringing
total to 3 cases to date

Infected and Source Flocks

As of June 30, 2007, there were .....


One field case and one validation case were consistent with Nor-98 scrapie.

IN the February 2007 Scrapie report it only mentions ;

''One case was consistent with Nor98 scrapie.''

(please note flocks of origin were in WY, CO, AND CA. PERSONAL COMMUNCATIONS


An evaluation of scrapie surveillance in the United States


From: "Terry S. Singeltary Sr."
Reply-To: Sustainable Agriculture Network Discussion Group
Date: Fri, 2 Feb 2007 17:32:58 -0600


Date: Mon, 24 Sep 2007 21:31:55 -0500

I suggest that you all read the data out about h-BASE and sporadic CJD, GSS,
blood, and some of the other abstracts from the PRION2007. ...


USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it
today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were
''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007
11:52 PM. ...TSS

see full text 143 pages ;" target="_blank" rel="nofollow">" target="_blank" rel="nofollow">

1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...

There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.


MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?

Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9

June 2003

BY Philip Yam


Answering critics like Terry Singeltary, who feels that the U.S. under-
counts CJD, Schonberger conceded that the current surveillance system
has errors but stated that most of the errors will be confined to the older

Copyright © 2003 Published by Elsevier Ltd.

Tracking spongiform encephalopathies in North America

Xavier Bosch

Available online 29 July 2003.

Volume 3, Issue 8, August 2003, Page 463

"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."

see history of cjd questionnaire

Sent: Monday May 28, 2007


HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD
only theory

TSEs have been rampant in the USA for decades in many species, and they all
have been rendered and fed back to animals for human/animal consumption.
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 2007. With all the science to date refuting it, to
continue to validate this myth, will only spread this TSE agent through a
multitude of potential routes and sources i.e. consumption, surgical, blood,
medical, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey,
Deslys, Dormont, Gibbs, 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.

This would further have to be broken down to strain of species and then the
route of transmission would further have to be broken down. Accumulation and
Transmission are key to the threshold from sub-clinical to clinical disease,
and key to all this, is to stop the amplification and transmission of this
agent, the spreading of, no matter what strain. In my opinion, to continue
with this myth that the U.K. strain of BSE (one strain TSE in cows), and the
nv/v CJD (one strain TSE humans) and that all the rest of human TSE are just
one single strain i.e. sporadic CJD (when to date there are 6 different
phenotypes of sCJD, and growing per Gambetti et al), and that no other
animal TSE transmits to humans, to continue with this masquerade will only
continue to spread, expose, and kill, who knows how many more in the years
and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain
Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans
name added to CJD, like CJD itself, Jakob and Creutzfeldt, or
Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE,
named after another human.

WE are only kidding ourselves with the current diagnostic criteria for human
and animal TSE, especially differentiating between the nvCJD vs the sporadic
strains and then the GSS strains and also the FFI fatal familial insomnia
strains or the ones that mimics one or the other of those TSE? Tissue
infectivity and strain typing of the many variants of the human and animal
TSEs are paramount in all variants of all TSE. There must be a proper
classification that will differentiate between all these human TSE in order
to do this. With the CDI and other more sensitive testing coming about, I
only hope that my proposal will some day be taken seriously. ...

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518


CJD VOICE (voice for _all_ victims of human TSE)

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

kindest regards,
6 Point
6 Point
Send Private Message

28 Oct 2007 08:10 PM  
Wyoming deer killed by Hoosier had CWD

An Indiana hunter will be allowed to keep the head mount of a deer he killed in Wyoming that tested positive for chronic wasting disease.
The unidentified hunter knew about the CWD risk and submitted a portion of the animal to the Wyoming Game and Fish Department for testing before having the meat deboned for transport home. After the animal tested positive for CWD, Wyoming officials contacted the hunter and the Indiana Department of Natural Resources.
Indiana DNR officials disposed of the meat, but the hunter was allowed to keep the mount, according to Dr. Jennifer Strasser, a veterinarian with the Indiana Board of Animal Health and a state conservation officer.
"As long as the skull cap and cape are cleaned properly, the hunter can safely keep the mount," she said.
The Indiana DNR has tight restrictions on transporting deer, elk and other cervids into the state. For information go to
stupid is, as stupid does. ...forest gump

A ProMED-mail post

ProMED-mail, a program of the
International Society for Infectious Diseases

[1] Saskatchewan
[2] Nova Scotia: new regulation

[1] Saskatchewan
Date: Fri 26 Oct 2007
Source: The Leader-Post [edited]

The Canadian Food Inspection Agency (CFIA) has confirmed animals in a
white-tail deer herd and 2 elk hunt operations in Saskatchewan have
tested positive for chronic wasting disease (CWD).

As a result, the CFIA has quarantined a white-tail deer herd and an
elk hunt operation in the Prince Albert area along with an elk hunt
farm in the Moose Jaw area, an agency spokeswoman said.

The most recent case was confirmed Tuesday [22 Oct 2007] in a farmed
elk herd in the Prince Albert area. However, the agency spokeswoman
said the quarantine would likely have been imposed while awaiting the
test results. Saskatchewan's 1st suspected case of CWD this year
[2007] was diagnosed earlier in the month [October 2007].

Chronic wasting disease is a progressive, fatal disease of the
nervous system of cervids such as mule deer, white-tailed deer and
elk. Black-tail deer and moose have also become infected naturally,
according to the CFIA website
( html>.)
The CFIA is also tracing the movement of animals on and off the
premises, the agency spokeswoman said, noting at this time no herds
have been culled.

The findings of CWD is not unexpected, she said. There have been
periodic findings of the disease in the deer and elk population in
the province over the last 10 years.

Communicated by:
Terry S. Singeltary Sr.

[For a general map of the region please see the HealthMap/ProMED-mail
interactive map at

The opening paragraph indicates a deer herd but the rest of the
article does not mention it. It is likely a farmed herd as
quarantining a wild herd would have a number of difficulties
associated with it. The article does not indicate if the deer herd is
in the same vicinity as the elk herd. It is implied but not stated
that it is. The website does not list either of these 2 herds. - Mod.TG]

[2] Nova Scotia: new regulation
Date: Fri 26 Oct 2007
Source: The Chronicle Herald (Nova Scotia) [edited]

Deer hunters are no longer allowed to use bottled deer urine to
attract the animals during hunting season in Nova Scotia.

The 5-week deer hunting season opens today [Fri 26 Oct 2007] with
more than 70 000 hunters eligible to take part.

A new regulation this year [2007] states that while in a wildlife
habitat, no person may possess or use a product that contains any
body part or fluid of a member of the deer family, says a Natural
Resources Department news release.

The rule is designed to prevent the introduction of the deadly
chronic wasting disease found in some deer populations in Western
Canada and the United States, the release said.

Many hunters have long relied on rags or undergrowth saturated with
bottled deer urine and placed strategically throughout deer habitat
as an attractant.

This year [2007], hunters must rely on their own cunning and perhaps
a few well-placed apples and carrots.

The season runs until 1 Dec 2007, excluding Sundays, and hunters may
bag one deer.

With the exception of 5750 people who, during a phone-in lottery,
successfully won the option of hunting an antlerless deer, only fully
antlered deer may be harvested.

Many hunters also donated some or all of their kill to Nova Scotia's
food banks last year [2006] through the Hunters Help the Hungry program.

Again this season, hunters may bring their deer to one of 17
participating meat-cutters throughout the province to donate, the release

Communicated by:

[Indeed there is limited evidence that suggests that bottled deer
urine may be a method of spreading CWD. The urine is bottled from
different sources and can come from regions that have CWD.

A map of the Nova Scotia region may be seen at
. - Mod.TG]

[see also:
Chronic wasting disease, cervids - USA (WV) 20070513.1525
Chronic wasting disease, cervids - USA: 2006 summary 20070330.1091
Chronic wasting disease, cervids - Canada (03) (AB, SK) 20070117.0227
Chronic wasting disease, cervids - Canada: (02) (SK) 20070112.0139
Chronic wasting disease, cervids - Canada: (AB) 20070105.0051
Chronic wasting disease, cervids - USA (WY) (02) 20061230.3653
Chronic wasting disease, cervids - USA (WV, IL) 20061228.3644
Chronic wasting disease, cervids - USA (CO): moose 20061110.3229
Chronic wasting disease, cervids - USA (WY) 20061013.29351
Chronic wasting disease, cervids - USA (SD) 20060616.1669
Chronic wasting disease, cervids - USA (WV) 20060430.1248
Chronic wasting disease, cervid - USA (MN) 20060316.0825
Chronic wasting disease, cervids - Canada (AB) 20060224.0604
Chronic wasting disease, cervids - USA (KS) 20060124.0237
Chronic wasting disease Update 2006: USA (IL) 20060113.0119]

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Transmissible Spongiform Encephalopathies Conference Agenda

Day One - 27 June 2006 | Day Two - 28 June 2006

15.00 TSE-safety of human urine-derived pharmaceuticals
Human-derived pharmaceuticals originating from urine are now receiving a
similar amount of regulatory attention as blood products. The need and the
measures taken by Ferring Pharmaceuticals and other companies to ensure the
safety of products such as urinary-derived gonadotrophins and urokinase will
be described.
Dr Peter A McAnulty, Senior Director, Non-Clinical Development, Ferring
Pharmaceuticals A/S, Denmark


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

DO A GOOGLE SEARCH ON 100% DEER/ELK SCENT AND potential spreading of CWD;

Docket Management Docket: 02N-0273 - Substances Prohibited From ... - 3
visits - Oct 5Mr. Singeltary is correct that Dr. Detwiler asked participants
to use the ..... what about those 'deer scents' of 100% urine', and the
prion that is found ...

Coincident Scrapie Infection and

Nephritis Lead to Urinary

Prion Excretion

Harald Seeger,1* Mathias Heikenwalder,1* Nicolas Zeller,1

Jan Kranich,1 Petra Schwarz,1 Ariana Gaspert,2 Burkhardt Seifert,3

Gino Miele,1 Adriano Aguzzi1.

Prion infectivity is typically restricted to the central nervous and

systems of infected hosts, but chronic inflammation can expand the
distribution of

prions. We tested whether chronic inflammatory kidney disorders would

excretion of prion infectivity into urine. Urinary proteins from

mice with lymphocytic nephritis induced scrapie upon inoculation into

indicatormice. Prionuria was found in presymptomatic scrapie-infected and in

mice, whereas neither prionuria nor urinary PrPSc was detectable in

wild-type or PrPC-overexpressing mice, or in nephritic mice inoculated with

noninfectious brain. Thus, urine may provide a vector for horizontal prion

and inflammation of excretory organs may influence prion spread.


How do prions enter the urine? Upon extrarenal

replication, blood-borne prions may be

excreted by a defective filtration apparatus.

Alternatively, prions may be produced locally

and excreted during leukocyturia. Although

prionemia occurs in many paradigms of

peripheral prion pathogenesis (15, 16), the

latter hypothesis appears more likely, because

prionuria was invariably associated with local

prion replication within kidneys.

Urine from one CJD patient was reported to

elicit prion disease in mice (17, 18), but not in

primates (19). Perhaps unrecognized nephritic

conditions may underlie these discrepant

observations. Inflammation-associated prionuria

may also contribute to horizontal transmission

among sheep, deer, and elk, whose high efficiency

of lateral transmission is not understood.

References and Notes


14 OCTOBER 2005 VOL 310 SCIENCE www.sciencemag.orgtss;f=12;t=000475;f=12;t=000475
From:         "Terry S. Singeltary Sr."
Subject:      CWD UPDATE 88 AUGUST 31, 2007

Date:         Wed, 29 Aug 2007 21:13:08 -0500
From:         "Terry S. Singeltary Sr."
Subject:      CWD NEW MEXICO RECORDS IT'S 19 CASE (near Texas border again)
Monitoring the Potential Transmission of Chronic Wasting Disease to Humans
Using a Hunter Registry Database in Wyoming (405 lines)
From: Terry S. Singeltary Sr. <[log in to unmask]>
Date: Thu, 30 Aug 2007 21:23:42 -0500

Subject: Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease
creates a new prion strain
Date: August 25, 2007 at 12:42 pm PST

Subject: Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease
creates a new prion strain
Date: August 25, 2007 at 12:42 pm PST
J Biol Chem. 2007 Aug 20; : 17709374
Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a
new prion strain.
[My paper] Atsushi Kobayashi , Masahiro Asano , Shirou Mohri , Tetsuyuki
The genotype (methionine or valine) at polymorphic codon 129 of the human
prion protein (PrP) gene and the type (type 1 or type 2) of abnormal isoform
of PrP (PrP(Sc)) are major determinants of the clinicopathological
phenotypes of sporadic Creutzfeldt-Jakob disease (sCJD). Here we found that
transmission of sCJD prions from a patient with valine homozygosity (129V/V)
and type 2 PrP(Sc) (sCJD-VV2 prions) to mice expressing human PrP with
methionine homozygosity (129M/M) generated unusual PrP(Sc) intermediate in
size between type 1 and type 2. The intermediate type PrP(Sc) was seen in
all examined dura mater graft-associated CJD cases with 129M/M and
plaque-type PrP deposits (p-dCJD). p-dCJD prions and sCJD-VV2 prions
exhibited similar transmissibility and neuropathology, and the identical
type of PrP(Sc) when inoculated into PrP-humanized mice with 129M/M or
129V/V. These findings suggest that p-dCJD could be caused by cross-sequence
transmission of sCJD-VV2 prions.


In this study, the strain-dependent traits of sCJDMM1
prions were inherited through cross-sequence
transmission without any modification. The
humanized mice with 129V/V produced type 1 PrPres
after inoculation with sCJD-MM1 prions. Because
sCJD-VV1 cases are extremely rare (at most 1-2%
of the total number of sCJD cases) and characterized
by early onset (mean age at onset: 39.3 years) (5),
our results raise the possibility that CJD cases
classified as VV1 may include cases caused by
iatrogenic transmission of sCJD-MM1 prions or
food-borne infection by type 1 prions from animals,
e.g., chronic wasting disease prions in cervid. In fact,
two CJD-VV1 patients who hunted deer or
consumed venison have been reported (40, 41). The
results of the present study emphasize the need for
traceback studies and careful re-examination of the
biochemical properties of sCJD-VV1 prions.
In conclusion, cross-sequence transmission of
sCJD-VV2 prions generates a new prion strain with
altered conformational properties and disease
phenotypes as p-dCJD prions. Furthermore, the
newly generated prions have unique transmissibility
including the traceback phenomenon. In the future, if
atypical prion strains emerge through cross-sequence
transmission, especially from animals, traceback
studies will enable us to identify the origin of the
Re: Colorado Surveillance Program for Chronic Wasting Disease
Transmission to Humans (TWO SUSPECT CASES)
Transmissible Mink Encephalopathy TME
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in
the United States

i am reminded of a few things deep throat (high ranking official at usda)
told me years ago;


The most frightening thing I have read all day is the
report of Gambetti's finding of a new strain of
sporadic cjd in young people.........Dear God,

MADCOW USDA the untold story
MADCOW USDA the untold story continued

Government Accountability Project

PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note steady increase
in  ''TYPE UNKNOWN''. ...TSS

1 Acquired in the United Kingdom; 2 Acquired in Saudi Arabia; 3 Includes 17
inconclusive and 9 pending (1 from 2006, 8
from 2007); 4 Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1
from 2001, 1 from 2003, 4 from 2004, 3
from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006,
*** 26 from 2007)
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
6 Point
6 Point
Send Private Message

29 Oct 2007 07:35 PM  

>>>but the hunter was allowed to keep the mount, according to Dr. Jennifer Strasser, a veterinarian with the Indiana Board of Animal Health and a state conservation officer. "As long as the skull cap and cape are cleaned properly, the hunter can safely keep the mount," she said.<<<


stupid is, as stupid does. forest gump.

PLEASE let me clarify this.

i understand most states allow this, but does not make it the safest way.
with the risk of the skull cap and cape NOT being cleaned properly, the risk is just to great to introduce the TSE agent to a state that has not documented it yet. why take the risk ? i think it's foolish. in my opinion, the complete carcass should have been incinerated, including the head mount.

The movement of high-risk carcass parts (brain, spinal cord, lymph tissues) is a potential avenue through which CWD could be spread from infected areas. Investigations in New York indicate that the infection could have been spread by a taxidermist who accepted specimens from CWD-positive states, allowed rehabilitated fawns access to the taxidermy workshop and spread potentially infectious curing salt waste as a fence line weed killer on his deer farm.;q=168948


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