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From: TSS (216-119-132-51.ipset12.wt.net)
Subject: SHEDDING LIGHT ON CHRONIC WASTING DISEASE
Date: September 13, 2004 at 7:45 pm PST

SHEDDING LIGHT ON CHRONIC WASTING DISEASE

Developed on DVD medium, this video provides hunters with detailed suggested field precautions in a CWD area, disease (prion) location using 3D animation, lymph node identification and state transportation regulations surrounding CWD. Also included in this video is a full description of how to bone out your animal in the field as well as a home processing section that allows any hunter to become self sufficient. Purchase now and get access to over 100 prime deer and elk recipes...
Details

Weight 0.35 lbs
Bulk Orders
Price: $ 9.95

http://www.aoproductions.com/custom/catalog/customer/product.php?productid=1&cat=&page=

TO see some neurosurgeon, pathologist, scientist work with
human TSE tissue in some BIO 3/4 lab suiting up for CJD
from head to toe, and then watch this movie presentation on
CWD safety, there is a big difference between the safety
precautions taken by the neurosurgeons, pathologists, scientist
and doctors working with TSEs, than the safety precautions
suggested in this movie presentation for hunters, well, good luck;-(TSS)

TSS

-------- Original Message --------
Subject: CWD and TSEs
Date: Mon, 13 Sep 2004 15:46:43 -0500
From: "Terry S. Singeltary Sr."
To: info@aoproductions.com


Greetings,

re-shedding light on cwd...

http://www.aoproductions.com

a few comments please;

CWD TO HUMANS the false assurance that it will not transmit to humans due to no epidemiological evidence, this is a false sense of security you are passing to hunters. CWD transmits to primates, humans are primates and CJD surviellance in humans in the USA is about like the surveillance of BSE/TSE in cattle (non-existance).

Field dressing and Boning out deer

WHAT about the fact the agent survives ashing to 600 degrees celsius?

WHAT about those tools (knives, saws etc), they should not be reused.

WHAT about sub-clinical CWD? this is a real threat, but goes ignored.

WHAT will CJD/CWD in humans look like?

AS implied in the Inset 25 we must not _ASSUME_ that transmission
of BSE to other species will invariably present pathology typical
of a scrapie-like disease.

snip...

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf

Gerald Wells: Report of the Visit to USA, April-May 1989

snip...

The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...

snip...

It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...

snip...

3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be _avoided_ in the US _at
all costs_...

snip...

PAGE 25

Transmission Studies

Mule deer transmissions of CWD were by intracerebral inoculation and
compared with natural cases resulted in a more rapidly
progressive clinical disease with repeated episodes of synocopy ending
in coma. One control animal became affected, it is believed through
contamination of inoculam (?saline). Further CWD transmissions were
carried out by Dick Marsh into ferret, mink and squirrel monkey.
Transmission occurred in all of these species with the shortest
incubation period in the ferret.

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

Aguzzi warns of CWD danger

The TSE family of diseases also includes chronic wasting disease (CWD)
in deer, a condition that has spread in the US in recent years (Nature
416, 569; 2002). Speaking at the Days of Molecular Medicine conference
in La Jolla in March, prion expert Adriano Aguzzi issued a strong
warning against underestimating this form of TSE.

"For more than a decade, the US has by-and-large considered mad cows
to be an exquisitely European problem. The perceived need to protect
US citizens from this alien threat has even prompted the deferral of
blood donors from Europe," he said. "Yet the threat-from-within
posed by CWD needs careful consideration, since the evidence that CWD
is less dangerous to humans than BSE is less-than-complete. Aguzzi
went on to point out that CWD is arguably the most mysterious of all
prion diseases.

"Its horizontal spread among the wild population is exceedingly
efficient, and appears to have reached a prevalence unprecedented even
by BSE in the UK at its peak. The pathogenesis of CWD, therefore,
deserves a vigorous research effort. Europeans also need to think
about this problem, and it would be timely and appropriate to increase
CWD surveillance in Europe too." Aguzzi has secured funding from the
National Institutes of Health to investigate CWD, and the effort will
be lead by Christina Sigurdson in his department at the University of
Zurich. KAREN BIRMINGHAM, LONDON

This quote from Dr. Gambetti is especially significant since he is the
rather cautious TSE researcher under contract with the Centers for Disease
Control to examine the brains of individuals who have died of CJD.
-----------------

Pierluigi Gambetti, director of the National Prion Disease Pathology
Surveillance Center at Case Western Reserve University in Cleveland,
said all deer should be tested for chronic wasting disease before any
processing is done.

"There is no way around it," he said. "Nobody should touch that meat
unless it has been tested."
--------------------------------------

http://www.ledger-enquirer.com/mld/...ion/3954298.htm
======================================================
TSEs & ENVIRONMENT

LANCET

Volume 351, Number 9110 18 April 1998
[Previous] [Next]

BSE: the final resting place

How to dispose of dangerous waste is a question that has vexed the human
race for hundreds of years. The answer has usually been to get it out of
sight--burn it or bury it. In Periclean Athens, victims of the plague
were incinerated in funeral pyres; in 14th century Venice, a law
stipulated that Black Death corpses should be buried to a minimum depth
of 5 feet; and now, as the 20th century draws to a close, we are
challenged by everything from industrial mercury to the smouldering
reactors of decommissioned atomic submarines.

The Irish Department of Agriculture will convene an expert panel on
April 27-29 to discuss the disposal of tissues from animals with bovine
spongiform encephalopathy (BSE). Proper disposal of tissues from
infected cattle has implications for both human and animal safety.
Safety for human beings is an issue because there is now unassailable if
still indirect evidence that BSE causes infections in man in the form of
"new variant" Creutzfeld-Jakob disease (nvCJD).1-3 Safety for animals is
also an issue because BSE-affected cattle could possibly transmit
disease to species other than cattle, including sheep, the species that
was almost surely the unwitting source of the BSE epidemic.

The first matter to consider is the distribution of infectivity in the
bodies of infected animals. The brain (and more generally, the central
nervous system) is the primary target in all transmissible spongiform
encephalopathies (TSE), and it contains by far the highest concentration
of the infectious agent. In naturally occuring disease, infectivity may
reach levels of up to about one million lethal doses per gram of brain
tissue, whether the disease be kuru, CJD, scrapie, or BSE. The
infectious agent in BSE-infected cattle has so far been found only in
brain, spinal cord, cervical and thoracic dorsal root ganglia,
trigeminal ganglia, distal ileum, and bone marrow.4 However, the much
more widespread distribution of low levels of infectivity in human
beings with kuru or CJD, and in sheep and goats with scrapie, suggests
that caution is advisable in prematurely dismissing as harmless other
tissues of BSE-infected cattle.

A second consideration relates to the routes by which TSE infection can
occur. Decades of accumulated data, both natural and experimental, have
shown clearly that the most efficient method of infection is by direct
penetration of the central nervous system; penetration of peripheral
sites is less likely to transmit disease. Infection can also occur by
the oral route, and the ingestion of as little as 1 g of BSE brain
tissue can transmit disease to other cattle.5 Infection by the
respiratory route does not occur (an important consideration with
respect to incineration), and venereal infection either does not occur
or is too rare to be detected.

How can tissue infectivity be destroyed before disposal? The agents that
cause TSE have been known almost since their discovery to have awesome
resistance to methods that quickly and easily inactivate most other
pathogens. Irradiation, chemicals, and heat are the three commonest
inactivating techniques. Irradiation has proved entirely ineffective,
and only a handful of a long catalogue of chemicals have produced more
than modest reduction in infectivity. The most active of these are
concentrated solutions of sodium hypochlorite (bleach) or sodium
hydroxide (lye). As for heat, even though the agent shares with most
other pathogens the feature of being more effectively damaged by wet
heat than by dry heat, boiling has little effect, and steam heat under
pressure (autoclaving) at temperatures of 121テつコC is not always
sterilising. To date, the most effective heat kill requires exposure of
infectious material to steam heat at 134テつコC for 1 h in a porous-load
autoclave.6 Exposure to dry heat even at temperatures of up to 360テつコC for
1 h may leave a small amount of residual infectivity.7 The standard
method of incineration, heating to about 1000テつコC for at least several
seconds, has been assumed to achieve total sterilisation, but needs
experimental verification in the light of suggestions that rendered
tissue waste might find some useful purpose as a source of heating fuel.

Thus, TSE agents are very resistant to virtually every imaginable method
of inactivation, and those methods found to be most effective may, in
one test or another, fail to sterilise. It seems that even when most
infectious particles succumb to an inactivating process, there may
remain a small subpopulation of particles that exhibit an extraordinary
capacity to withstand inactivation, and that, with appropriate testing,
will be found to retain the ability to transmit disease. Also, almost
all available inactivation data have come from research studies done
under carefully controlled laboratory conditions, and it is always
difficult to translate these conditions to the world of commerce. Even
when the data are applied in the commercial process, the repetitive
nature of the process requires vigilance in quality control and
inspection to ensure adherence to its regulations.

The final issue that must be addressed is the "lifespan" of the
infectious agent after disposal if it has been only incompletely
inactivated beforehand. Given the extraordinary resistance of the agent
to decontamination measures, the epidemiological and experimental
evidence indicating that TSE agents may endure in nature for a long time
should come as no surprise. The first real clue to this possibility came
from the Icelandic observation that healthy sheep contracted scrapie
when they grazed on pastures that had lain unused for 3 years after
having been grazed by scrapie-infected sheep.8

Support for this observation was obtained from an experiment in which
scrapie-infected brain material was mixed with soil, placed in a
container, and then allowed to "weather" in a semi-interred state for 3
years.9 A small amount of residual infectivity was detected in the
contaminated soil, and most of the infectivity remained in the topmost
layers of soil, where the tissue had originally been placed--in other
words, there had been no significant leaching of infectivity to deeper
soil layers.

It is therefore plausible for surface or subsurface disposal of
TSE-contaminated tissue or carcasses to result in long-lasting soil
infectivity. Uncovered landfills are a favourite feeding site for
seagulls, which could disperse the infectivity.10 Other animals might do
likewise, and if the landfill site were later used for herbivore
grazing, or tilled as arable land, the potential for disease
transmission might remain. A further question concerns the risk of
contamination of the surrounding water table, or even surface
waste-water channels, by effluents and discarded solid waste from
treatment plants.

A reasonable conclusion from existing data is that there is a potential
for human infection to result from environmental contamination by
BSE-infected tissue residues. The potential cannot be quantified because
of the huge number of uncertainties and assumptions that attend each
stage of the disposal process.

On the positive side, spongiform encephalopathy can be said to be not
easily transmissible. Although the level of infectivity to which
creatures are exposed is not known, it is probably very low, since sheep
that die from scrapie, cattle that die from BSE, and human beings who
die from nvCJD represent only a small proportion of their respective
exposed populations.

Whatever risk exists is therefore extremely small, but not zero, hence
all practical steps that might reduce the risk to the smallest
acceptable level must be considered. What is practical and what is
acceptable are concepts that will be hammered out on the anvil of
politics: scientific input, such as it is, already waits in the forge. A
fairly obvious recommendation, based on the science, would be that all
material that is actually or potentially contaminated by BSE, whether
whole carcasses, rendered solids, or waste effluents, should be exposed
to lye and thoroughly incinerated under strictly inspected conditions.
Another is that the residue is buried in landfills to a depth that would
minimise any subsequent animal or human exposure, in areas that would
not intersect with any potable water-table source. Certainly, it has
been, and will continue to be, necessary in many instances to accept
less than the ideal.

Paul Brown

Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, Bethesda, MD 20892, USA

1 Will RG, Ironside JW, Zeidler M, et al. A new variant of
Creutzfeldt-Jakob disease in the UK. Lancet 1996; 347: 921-25 [PubMed].

2 Bruce M, Will RG, Ironside JW, et al. Transmissions to mice indicate
that 'new variant' CJD is caused by the BSE agent. Nature 1997: 389:
498-501.

3 Collinge J, Sidle KCL, Heads J, Ironside J, Hill AF. Molecular
analysis of prion strain variation and the aetiology of 'new variant'
CJD. Nature 1996; 383: 685-90 [PubMed].

4 Wells GAH, Hawkins SAC, Green RB, et al. Preliminary observations on
the pathogenesis of experimental bovine spongiform encephalopathy (BSE):
an update. Vet Rec 1998; 142: 103-06 [PubMed].

5 Collee JG, Bradley R. BSE: a decade on--part 2. Lancet 1997; 349:
715-21 [PubMed].

6 Taylor DM. Exposure to, and inactivation of, the unconventional agents
that cause transmissible degenerative encephalopathies. In: Baker HF,
Ridley RM, eds. Methods in molecular medicine: prion diseases. Totawa
NJ: Humana Press, 1996: 105-18.

7 Brown P, Liberski PP, Wolff A, Gajdusek DC. Resistance of scrapie
infectivity to steam autoclaving after formaldehyde fixation and limited
survival after ashing at 360テつーC: practical and theoretical implications,
J Infect Dis 1990; 161: 467-72 [PubMed].

8 Palsson PA. Rida (scrapie) in Iceland and its epidemiology. In:
Prusiner SB, Hadlow WJ, eds. Slow transmissible diseases of the nervous
system, vol I. New York: Academic Press, 1979: 357-66.

9 Brown P, Gajdusek DC. Survival of scrapie virus after 3 years'
interment. Lancet 1991; 337; 269-70.

10 Scrimgoeur EM, Brown P, Monaghan P. Disposal of rendered specified
offal. Vet Rec 1996; 139: 219-20 [PubMed].

http://www.thelancet.com/newlancet/sub/issues/vol351no9110/body.commentary1146.html

snip...

88. Natural decay: Infectivity persists for a long time in the
environment. A study by Palsson in 1979 showed how scrapie was
contracted by healthy sheep, after they had grazed on
land which had previously been grazed by scrapie-infected sheep, even
though the land had lain fallow for three years before the healthy sheep
were introduced. Brown also quoted an early experiment of his own
(1991), where he had buried scrapie-infected hamster brain and found
that he could still detect substantial infectivity three years later
near where the material had been placed. 89. Potential environmental
routes of infection: Brown discusses the various possible
scenarios, including surface or subsurface deposits of TSE-contaminated
material, which would lead to a build-up of long-lasting infectivity.
Birds feeding on animal remains (such as gulls visiting landfill sites)
could disperse infectivity. Other animals could become vectors if they
later grazed on contaminated land. "A further question concerns
the risk of contamination of the surrounding water table or even surface
water channels, by effluents and discarded solid wastes from treatment
plants. A reasonable conclusion is that there is a potential for human
infection to result from environmental contamination by BSE-infected
tissue residues. The potential cannot be quantified because of the huge
numbers of uncertainties and assumptions that attend each stage of the
disposal process". These comments, from a long established authority on
TSEs, closely echo my own statements which were based on a recent
examination of all the evidence. 90. Susceptibility: It is likely that
transmissibility of the disease to humans in vivo is probably low,
because sheep that die from scrapie and cattle that die from BSE are
probably a small fraction of the exposed population. However, no
definitive data are available.
91. Recommendations for disposal procedures: Brown recommends that
material which is actually or potentially contaminated by BSE should be:
1) exposed to caustic soda; 2) thoroughly incinerated under carefully
inspected conditions; and 3) that any residue should be buried in
landfill, to a depth which would minimise any subsequent animal or
human exposure, in areas that would not intersect with any potable
water-table source.
92. This review and recommendations from Brown have particular
importance. Brown is one of the world's foremost authorities on TSEs and
is a senior researcher in the US National Institutes of Health (NIH). It
is notable that such a respected authority is forthright in
acknowledging the existence of potential risks, and in identifying the
appropriate measures necessary to safeguard public health.
Paper by SM Cousens, L Linsell, PG Smith, Dr M Chandrakumar, JW
Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will, "Geographical
distribution of variant CJD in the UK (excluding Northern Ireland)".
Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41
(02/01/99)} (J/L/353/18) examined the possibility that patients with
vCJD (variant CJD) might live closer to rendering factories than would
be expected by chance. All 26 cases of vCJD in the UK with onset up to
31 st August 1998 were studied. The incubation period of vCJD is not
known but by analogy with other human TSEs could lie within the range
5-25 years. If vCJD had arisen by exposure to rendering products, such
exposure might plausibly have occurred 8-10 years before the
onset of symptoms. The authors were able to obtain the addresses of all
rendering plants in the UK which were in production in 1988. For each
case of vCJD, the distance from the place of residence on 1st January
1998 to the nearest rendering plant was calculated

snip...

http://www.bseinquiry.gov.uk/files/ws/s019b.pdf

infectivity surviving
ashing to 600*C is (in my opinion) degradable but infective.
based on Bown & Gajdusek, (1991), landfill and burial may be assumed to
have a reduction factor of 98% (i.e. a factor of 50) over 3 years.
CJD-infected brain-tissue remained infectious after storing at
room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is
known to remain viable after at least 30 months of desiccation (Wilson
et al, 1950). and pastures that had been grazed by scrapie-infected
sheep still appeared to be contaminated with scrapie agent three years
after they were last occupied by sheep (Palsson, 1979).

http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf

PAUL BROWN SCRAPIE SOIL TEST

http://www.bseinquiry.gov.uk/files/sc/seac07/tab03.pdf

New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600テつーC suggests an inorganic template
of replication

Paul Brown*, [dagger ] , Edward H. Rau [Dagger ] , Bruce K. Johnson*,
Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusekテつァ

* Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, and [Dagger ] Environmental
Protection Branch, Division of Safety, Office of Research Services,
National Institutes of Health, Bethesda, MD 20892; and テつァ Institut Alfred
Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur
Yvette, France

Contributed by D. Carleton Gajdusek, December 22, 1999

Abstract
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References

One-gram samples from a pool of crude brain tissue from hamsters
infected with the 263K strain of hamster-adapted scrapie agent were
placed in covered quartz-glass crucibles and exposed for either 5 or 15
min to dry heat at temperatures ranging from 150テつーC to 1,000テつーC. Residual
infectivity in the treated samples was assayed by the intracerebral
inoculation of dilution series into healthy weanling hamsters, which
were observed for 10 months; disease transmissions were verified by
Western blot testing for proteinase-resistant protein in brains from
clinically positive hamsters. Unheated control tissue contained 9.9
log10LD50/g tissue; after exposure to 150テつーC, titers equaled or exceeded
6 log10LD50/g, and after exposure to 300テつーC, titers equaled or exceeded 4
log10LD50/g. Exposure to 600テつーC completely ashed the brain samples,
which, when reconstituted with saline to their original weights,
transmitted disease to 5 of 35 inoculated hamsters. No transmissions
occurred after exposure to 1,000テつーC. These results suggest that an
inorganic molecular template with a decomposition point near 600テつーC is
capable of nucleating the biological replication of the scrapie agent.

transmissible spongiform encephalopathy | scrapie | prion | medical
waste | incineration

Introduction...snip...end


Chronic Wasting Disease and Potential Transmission to Humans

Ermias D. Belay,*Comments
Ryan A.
Maddox,* Elizabeth S. Williams, Michael W. Miller,! Pierluigi
Gambetti,ツァ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA;
University of Wyoming, Laramie, Wyoming, USA; !Colorado Division of
Wildlife, Fort Collins, Colorado, USA; and ツァCase Western Reserve
University, Cleveland, Ohio, USA

http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm


Environmental Sources of Prion Transmission in Mule Deer

Michael W. Miller,*Comments
Elizabeth S.
Williams, N. Thompson Hobbs,! and Lisa L. Wolfe*
*Colorado Division of Wildlife, Fort Collins, Colorado, USA; University
of Wyoming, Laramie, Wyoming, USA; and !Colorado State University, Fort
Collins, Colorado, USA

Suggested citation for this article: Miller MW, Williams ES, Hobbs
NT, Wolfe LL. Environmental sources of prion transmission in mule
deer. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date
cited]. Available from:
http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm

http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm

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.


Part of the problem seems to stem from the US surveillance system. CJD

is only reported in those areas known to be endemic foci of CWD.

Moreover, US authorities have been criticised for not having performed

enough prionic tests in farm deer and elk.

Although in November last year the US Food and Drug Administration

issued a directive to state public-health and agriculture officials

prohibiting material from CWD-positive animals from being used as an

ingredient in feed for any animal species, epidemiological control and

research in the USA has been quite different from the situation in the

UK and Europe regarding BSE.

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.

Norman Foster, director of the Cognitive Disorders Clinic at the

University of Michigan (Ann Arbor, MI, USA), says that current

surveillance of prion disease in people in the USA is inadequate to

detect whether CWD is occurring in human beings; adding that, the

cases that we know about are reassuring, because they do not suggest the

appearance of a new variant of CJD in the USA or atypical features in

patients that might be exposed to CWD. However, until we establish a

system that identifies and analyses a high proportion of suspected prion

disease cases we will not know for sure. The USA should develop a

system modelled on that established in the UK, he points out.


Ali Samii, a neurologist at Seattle VA Medical Center who recently

reported the cases of three hunterstwo of whom were friendswho died

from pathologically confirmed CJD, says that at present there are

insufficient data to claim transmission of CWD into humans; adding that

[only] by asking [the questions of venison consumption and deer/elk

hunting] in every case can we collect suspect cases and look into the

plausibility of transmission further. Samii argues that by making both

doctors and hunters more aware of the possibility of prions spreading

through eating venison, doctors treating hunters with dementia can

consider a possible prion disease, and doctors treating CJD patients

will know to ask whether they ate venison.


CDC spokesman Ermias Belay says that the CDC will not be investigating

the [Samii] cases because there is no evidence that the men ate

CWD-infected meat. He notes that although the likelihood of CWD

jumping the species barrier to infect humans cannot be ruled out 100%

and that [we] cannot be 100% sure that CWD does not exist in humans&

the data seeking evidence of CWD transmission to humans have been very

limited.


http://infection.thelancet.com/journal/journal.isa


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.<<<


actually, that quote was from a more recent article in the Journal of

Neurology (see below), not the JAMA article...


Full Text

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

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

http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama

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_

http://www.surefed.com/deer.htm

BODE'S GAME FEED SUPPLEMENT #400
A RATION FOR DEER
NET WEIGHT 50 POUNDS
22.6 KG.

snip...

_animal protein_

http://www.bodefeed.com/prod7.htm

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.

http://www.bodefeed.com/prod6.htm
===================================

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

http://www.bodefeed.com/prod8.htm

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.

http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html
===================================================

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...

http://www.fda.gov/foi/warning_letters/g1115d.pdf


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


Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References

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...

Oral exposure is the most plausible pathway by which the CWD prion may be introduced to deer in nature. Consequently, we chose this means of inoculation in an attempt to demonstrate the feasibility of CWD transmission by this route and to study early lymphoid tissue tropism of the PrPres in deer. Each deer was repeatedly exposed to a known infectious CWD inoculum over a 5-day-period because recent results with scrapie in hamsters indicate repeated oral exposure increases the incidence of infection (Diringer et al., 1998 ). Because mice are relatively resistant to CWD (M. Bruce, personal communication) precluding bioassay, and because several studies have shown that PrPres strongly correlates with disease (McKinley et al., 1983 ; Race et al. , 1998 ), we employed an enhanced immunostaining method (formic acid, proteinase K and hydrated autoclaving) to detect PrPres in situ. Formic acid and hydrated autoclaving have been previously described for PrPres epitope exposure prior to immunohistochemistry (IHC) (Miller et al., 1994 ; van Keulen et al., 1995 ). Using these methods, we demonstrate PrPres in regional lymph nodes as early as 6 weeks after oral exposure of deer fawns to the CWD agent.

snip...

Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References

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...

full text;

http://vir.sgmjournals.org/cgi/content/full/80/10/2757?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&titleabstract=Oral+Transmission+And+Early+Lymphoid+Tropism+Of+Chronic+Wasting+Disease&fulltext=Oral+Transmission+And+Early+Lymphoid+Tropism+Of+Chronic+Wasting+Disease&searchid=1056118413058_454&stored_search=&FIRSTINDEX=0&search_url=http%3A%2F%2Fvir.sgmjournals.org%2Fcgi%2Fsearch&journalcode=vir

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus)
that were exposed to the infectious agents only by their nonforced
consumption of known infectious tissues. The asymptomatic incubation
period in the one monkey exposed to the virus of kuru was 36 months;
that in the two monkeys exposed to the virus of Creutzfeldt-Jakob
disease was 23 and 27 months, respectively; and that in the two monkeys
exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the
monkeys failed to reveal signs or oral lesions. One additional monkey
similarly exposed to kuru has remained asymptomatic during the 39 months
that it has been under observation.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


1: Dev Biol Stand 1993;80:9-13

Transmission of human spongiform encephalopathies to experimental
animals: comparison of the chimpanzee and squirrel monkey.

Asher DM, Gibbs CJ Jr, Sulima MP, Bacote A, Amyx H, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, NIH, Bethesda, MD 20992.

The agents of kuru and Creutzfeldt-Jakob disease have been consistently
transmitted from patients with those diseases to chimpanzees and
squirrel monkeys, as well as to other new-world primates, with average
incubation periods of two or three years. No other animals have been
found so consistently susceptible to the agents in human tissues. More
rapid and convenient assays for the infectious agents would greatly
facilitate research on the spongiform encephalopathies of humans.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8270119&dopt=Abstract

Aguzzi warns of CWD danger

The TSE family of diseases also includes chronic wasting disease (CWD)
in deer, a condition that has spread in the US in recent years (Nature
416, 569; 2002). Speaking at the Days of Molecular Medicine conference
in La Jolla in March, prion expert Adriano Aguzzi issued a strong
warning against underestimating this form of TSE.

"For more than a decade, the US has by-and-large considered mad cows
to be an exquisitely European problem. The perceived need to protect
US citizens from this alien threat has even prompted the deferral of
blood donors from Europe," he said. "Yet the threat-from-within
posed by CWD needs careful consideration, since the evidence that CWD
is less dangerous to humans than BSE is less-than-complete. Aguzzi
went on to point out that CWD is arguably the most mysterious of all
prion diseases.

"Its horizontal spread among the wild population is exceedingly
efficient, and appears to have reached a prevalence unprecedented even
by BSE in the UK at its peak. The pathogenesis of CWD, therefore,
deserves a vigorous research effort. Europeans also need to think
about this problem, and it would be timely and appropriate to increase
CWD surveillance in Europe too." Aguzzi has secured funding from the
National Institutes of Health to investigate CWD, and the effort will
be lead by Christina Sigurdson in his department at the University of
Zurich. KAREN BIRMINGHAM, LONDON

This quote from Dr. Gambetti is especially significant since he is the
rather cautious TSE researcher under contract with the Centers for Disease
Control to examine the brains of individuals who have died of CJD.
-----------------

Pierluigi Gambetti, director of the National Prion Disease Pathology
Surveillance Center at Case Western Reserve University in Cleveland,
said all deer should be tested for chronic wasting disease before any
processing is done.

"There is no way around it," he said. "Nobody should touch that meat
unless it has been tested."
--------------------------------------

TSS



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