# Chronic Wasting Disease (cwd)



## Hamilton Reef (Jan 20, 2000)

From NRC meeting March 10

CHRONIC WASTING DISEASE (CWD)

Dr. Steve Schmitt presented the 2004 CWD Annual Report. In 2004, over 17,000 deer, 349 elk and 21 moose were tested for CWD in Michigan. No positives were detected. He described target deer as skinny deer you can walk up to. From 2002 to 2005, 181 target deer were tested. All were negative for CWD. Dr. Schmitt concluded that the surveillance data suggests that Michigan does not have a large outbreak of CWD in free-ranging deer anywhere in the state. However, there could be a small pocket of the disease somewhere in Michigan. 

Dr. Schmitt continued by reviewing the summary of CWD positive out-of-state cervids brought into the State by Michigan hunters. There were 26 CWD positive deer and 1 elk imported into Michigan. He indicated that a Wildlife Conservation Order is in place that would prohibit baiting and feeding if a CWD positive animal is found within 50 miles of the Michigan border.

It has been determined that CWD can be transmitted via CWD infected carcasses and feces from infected animals. A Wildlife Conservation Order prohibits the import of deer and elk carcasses from states and provinces that have CWD.

Chairman Byrum questioned the difference between CWD and BSE. Dr. Schmitt responded that BSE is transmitted to humans, whereas CWD is restricted to deer and elk.


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## sadocf1 (Mar 10, 2002)

"CWD can be transmitted via infected CWD carcasses - a Wildlife Conservation Order prohibits the importation of deer and elk carcasses from states and provinces that have CWD"
One of DNR Commissioners brought back the boned meat from an elk he shot in a CWD Risk Area in Colorado. A sample from the animal later proved to be positive for CWD.


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## terry (Sep 13, 2002)

> Chairman Byrum questioned the difference between CWD and BSE. Dr. Schmitt 

>responded that BSE is transmitted to humans, whereas CWD is restricted to 

>deer and elk...


YES! this is not the ordinary bug. i have wasted almost 8 years
of my life warning the gov and public of this. i have seen it in
humans, and yes, CWD transmits to primates, cattle and sheep
in the lab, transmission studies on humans have never taken place.
the next time the gov officials tells you that CWD does not transmit
to humans, please kindly ask them to show you the transmission
studies...

kind regards,
terry


Greetings New York,

CWD MEETING

I HOPE THIS MEETING STARTS OUT WITH THE TRUTH,
not the fabricated lies we are use to hearing.

SADLY, im afraid this meeting will consist of lies that CWD does not
transmit to humans (without any scientific proof or any transmission
studies to back there false statement up). IT would be much better
to just say that with what limited surveillance they have done with
human/CJD in relations to CWD transmission, they simply cannot
answer that question. THEN tell them of the transmission studies
that show CWD does transmit in the lab by inoculation,
CWD does transmit to primate, cattle and sheep. LIKE the lies
we hear about Scrapie, when we know it transmits to primates
by there NON-FORCED ORAL consumption of scrapie tainted
feed TO PRIMATE ;

1: J Infect Dis 1980 Aug;142(2):205-8


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.

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


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.

[hmmm, CWD transmission to squirrel monkey. are humans primates?TSS]

snip...

The occurrence of CWD must be viewed against the context of the
locations in which it occurred. It was an incidental and unwelcome
complication of the respective wildlife research programmes. Despite its
subsequent recognition as a new disease of cervids, therefore justifying
direct investigation, no specific research funding was forthcoming.
The USDA viewed it as a wildlife problem and consequently not their
province!

[figures...TSS]

snip...

VISIT TO USA - DR A E WRATHALL - INFO ON BSE AND SCRAPIE

1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has
successfully transmitted ovine and caprine scrapie to cattle. The
experimental results have not been published but there are plans to do
this. This work was initiated in 1978. A summary of it is:-

better cut this short, you can read full text of part 2 here;

snip...

In Reply to: In Confidence - Perceptions of unconventional slow virus
diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells


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

Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

http://www.pnas.org/cgi/content/full/041490898v1

Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471


CWD/TSEs & ENVIRONMENT CONTAMINATION

I believe it to be very irresponsible to dispose
of clinical/sub-clinial cases of CWD or any animal
with TSEs in landfills...

TSS

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 And The Environment

The LANCET
Volume 351, Number 9110 18 April 1998

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 121ÂºC is not always
sterilising. To date, the most effective heat kill requires exposure of
infectious material to steam heat at 134ÂºC for 1 h in a porous-load
autoclave.6 Exposure to dry heat even at temperatures of up to 360ÂºC for
1 h may leave a small amount of residual infectivity.7 The standard
method of incineration, heating to about 1000ÂºC 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.

snip...continued


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## terry (Sep 13, 2002)

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 360Â°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

Some unofficial information from a source on the inside looking out -

Confidential!!!!

As early as 1992-3 there had been long studies conducted on small
pastures containing scrapie infected sheep at the sheep research station
associated with the Neuropathogenesis Unit in Edinburgh, Scotland.
Whether these are documented...I don't know. But personal recounts both
heard and recorded in a daily journal indicate that leaving the pastures
free and replacing the topsoil completely at least 2 feet of thickness
each year for SEVEN years....and then when very clean (proven scrapie
free) sheep were placed on these small pastures.... the new sheep also
broke out with scrapie and passed it to offspring. I am not sure that TSE
contaminated ground could ever be free of the agent!!
A very frightening revelation!!!

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You can take that with however many grains of salt you wish, and
we can debate these issues all day long, but the bottom line,
this is not rocket-science, all one has to do is some
experiments and case studies. But for the life of me,
I don't know what they are waiting on?

Kind regards,

Terry S. Singeltary Sr.
Bacliff, Texas USA

More here:

http://www.bseinquiry.gov.uk/files/ws/s018.pdf

INCINERATION TEMPS

Requirements include:

a. after burning to the range of 800 to 1000*C to eliminate smell;

well heck, this is just typical public relations fear factor control.
do you actually think they would spend the extra costs for fuel,
for such extreme heat, just to eliminate smell, when they spread
manure all over your veg's. i think not. what they really meant were
any _TSE agents_.

b. Gas scrubbing to eliminate smoke -- though steam may be omitted;

c. Stacks to be fitted with grit arreaters;

snip...

1.2 Visual Imact

It is considered that the requirement for any carcase incinerator
disign would be to ensure that the operations relating to the reception,
storage and decepitation of diseased carcasses must not be publicly
visible and that any part of a carcase could not be removed or
interfered with by animals or birds.

full text;

http://www.bseinquiry.gov.uk/files/yb/1989/04/03006001.pdf




Perspective
Chronic Wasting Disease and Potential Transmission to Humans

Ermias D. Belay,*Comments Ryan A. Maddox,* Elizabeth S. Williams, Michael W. Miller, Pierluigi Gambetti,§ 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 §Case Western Reserve University, Cleveland, Ohio, USA

Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm

Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected in other parts of the United States. Although detection in some areas may be related to increased surveillance, introduction of CWD due to translocation or natural migration of animals may account for some new foci of infection. Increasing spread of CWD has raised concerns about the potential for increasing human exposure to the CWD agent. The foodborne transmission of bovine spongiform encephalopathy to humans indicates that the species barrier may not completely protect humans from animal prion diseases. Conversion of human prion protein by CWD-associated prions has been demonstrated in an in vitro cell-free experiment, but limited investigations have not identified strong evidence for CWD transmission to humans. More epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.

snip...

Risk for Transmission to Humans
Epidemiologic Studies

The increasing detection of CWD in a wider geographic area and the presumed foodborne transmission of BSE to humans, resulting in cases of vCJD, have raised concerns about the possible zoonotic transmission of CWD (32). In the late 1990s, such concerns were heightened by the occurrence of CJD among three patients 30 years of age who were deer hunters or ate deer and elk meat harvested by family members (Table 2). However, epidemiologic and laboratory investigations of these case-patients indicated no strong evidence for a causal link between CWD and their CJD illness (33). None of the patients were reported to have hunted deer or eaten deer meat harvested in the CWD-endemic areas of Colorado and Wyoming. Such a history in unusually young CJD patients, if present, would have supported a causal link with CWD. Moreover, the testing of brain tissues from >1,000 deer and elk harvested from areas where the patients hunted or their venison originated did not show any evidence of CWD (33). In addition, the lack of homogeneity in the clinicopathologic manifestation and codon 129 of the prion protein gene among the three patients suggested that their illnesses could not be explained by exposure to the same prion strain. In vCJD, homogeneity of the genotype at codon 129 and the clinical and pathologic phenotype were attributed to the patients' exposure to the same prion strain, the agent of BSE.

In 2001, the case of a 25-year-old man who reportedly died of a prion disease after an illness lasting &#8776;22 months was investigated (Table 2). Although this man had hunted deer only rarely, his grandfather hunted deer and elk throughout much of the 1980s and 1990s and regularly shared the venison with the case-patient's family. The grandfather primarily hunted in southeastern Wyoming, around the known CWD-endemic area. The case-patient's illness began with a seizure and progressed to fatigue, poor concentration, and depression. Memory loss, ataxia, speech abnormalities, combative behavior, and recurrent seizures also developed. Histopathologic, immunohistochemical, and Western blot testing of brain autopsy samples confirmed a prion disease diagnosis. Analysis of the prion protein gene indicated a P102L mutation coupled with valine at the polymorphic codon 129 in the mutant allele, confirming a diagnosis of Gerstmann-Sträussler-Scheinker syndrome (GSS). This case-patient was unusually young even for a person with a GSS P102L mutation. It remains unknown whether the possible exposure of the case-patient to CWD-infected venison potentially contributed to the early onset of his prion disease.

In 2001, two additional CJD patients 26 and 28 years of age were reported from a single state (Table 2) (34). The patients grew up in adjacent counties and had illness onset within several months of each other. As a result of this fact and their unusually young age, a possible environmental source of infection, including exposure to CWD-infected venison, was considered. One of the patients died after an illness lasting 56 months that was characterized by progressive aphasia, memory loss, social withdrawal, vision disturbances, and seizure activity leading to status epilepticus and induced coma. Histopathologic, immunohistochemical, and Western blot testing of brain biopsy and autopsy samples confirmed a CJD diagnosis. The patient's disease phenotype corresponded to the MM2 sporadic CJD subtype reported by Parchi et al. (35). This patient did not hunt, and family members provided no history of regularly eating venison. The patient may have occasionally eaten venison originating from the Upper Peninsula of Michigan while away from home during his college years. However, ongoing surveillance has not detected CWD in Michigan deer (36).

The second patient died from an illness lasting <16 months. The patient's illness began with behavioral changes, including unusual outbursts of anger and depression. Confusion, memory loss, gait disturbances, incontinence, headaches, and photophobia also developed. Western blot analysis of frozen brain biopsy tissue confirmed a prion disease diagnosis. Immunohistochemical analysis of brain tissue obtained after the patient's death showed prion deposition consistent with GSS. A prion protein gene analysis could not be performed because appropriate samples were lacking. However, prion protein gene analysis of a blood sample from one of the patient's parents indicated a GSS P102L mutation. The patient did not hunt but may have eaten venison from Michigan once when he was 12 years old. The GSS diagnosis greatly reduced the likelihood that the two patients reported from adjacent counties had disease with a common origin.

Recently, rare neurologic disorders resulting in the deaths of three men who participated in "wild game feasts" in a cabin owned by one of the decedents created concern about the possible relationship of their illnesses with CWD (Table 2) (37). Two of the patients reportedly died of CJD, and the third died from Pick's disease. More than 50 persons were identified as possibly participating in these feasts; the three patients were the only participants reported to have died of a degenerative neurologic disorder. Reanalysis of autopsy brain tissues from the three patients at the National Prion Disease Pathology Surveillance Center indicated that two of them had no evidence of a prion disease by immunohistochemical analysis. CJD was confirmed in the third patient, who had clinicopathologic, codon 129, and prion characteristics similar to the most common sporadic CJD subtype (MM1/MV1) (35). This patient participated in the feasts only once, perhaps in the mid-1980s. In addition, the investigation found no evidence that the deer and elk meat served during the feasts originated from the known CWD-endemic areas of Colorado and Wyoming.

continued ;


----------



## terry (Sep 13, 2002)

In 2003, CJD in two deer and elk hunters (54 and 66 years of age) was reported (38). The report implied that the patients had striking neuropathologic similarities and that their illness may represent a new entity in the spectrum of prion diseases. A third patient (63 years of age), who was also purported to have been a big game hunter, was subsequently reported from the same area. However, none of the three patients were reported to have eaten venison from the CWD-endemic areas of the western United States. The 66-year-old patient hunted most of his life in Washington State. Although information about the 54-year-old patient was limited, there was no evidence that he hunted in CWD-endemic areas. The third patient was not a hunter but ate venison harvested from Pennsylvania and Washington. The neuropathologic changes, Western blot profile, and genotype at codon 129 of the three patients each fit the MM1, VV1, or VV2 sporadic CJD subtype, indicating absence of phenotypic similarity among the cases or atypical neuropathologic features (35).

To date, only two nonfamilial CJD cases with a positive history of exposure to venison obtained from the known CWD-endemic areas have been reported. One of the patients was a 61-year-old woman who grew up in an area where this disease is known to be endemic, and she ate venison harvested locally. She died in 2000, and analysis of autopsy brain specimens confirmed that the patient's CJD phenotype fit the MM1 subtype, with no atypical neuropathologic features. The second patient was a 66-year-old man who was reported to have eaten venison from two deer harvested in a CWD-endemic area. Both deer tested negative for CWD, and the patient's illness was consistent with the MM1 CJD phenotype.

Despite the decades-long endemicity of CWD in Colorado and Wyoming, the incidence of CJD and the age distribution of CJD case-patients in these two states are similar to those seen in other parts of the United States. From 1979 to 2000, 67 CJD cases from Colorado and 7 from Wyoming were reported to the national multiple cause-of-death database. The average annual age-adjusted CJD death rate was 1.2 per million persons in Colorado and 0.8 in Wyoming. The proportion of CJD patients who died before age 55 in Colorado (13.4%) was similar to that of the national (10.2%). The only CJD case-patient <30 years of age in Colorado had iatrogenic CJD linked to receipt of human growth hormone injections. CJD was not reported in persons <55 years of age in Wyoming during the 22-year surveillance period.
snip...

Conclusions

The lack of evidence of a link between CWD transmission and unusual cases of CJD, despite several epidemiologic investigations, and the absence of an increase in CJD incidence in Colorado and Wyoming suggest that the risk, if any, of transmission of CWD to humans is low. Although the in vitro studies indicating inefficient conversion of human prion protein by CWD-associated prions raise the possibility of low-level transmission of CWD to humans, no human cases of prion disease with strong evidence of a link with CWD have been identified. However, the transmission of BSE to humans and the resulting vCJD indicate that, provided sufficient exposure, the species barrier may not completely protect humans from animal prion diseases. Because CWD has occurred in a limited geographic area for decades, an adequate number of people may not have been exposed to the CWD agent to result in a clinically recognizable human disease. The level and frequency of human exposure to the CWD agent may increase with the spread of CWD in the United States. Because the number of studies seeking evidence for CWD transmission to humans is limited, more epidemiologic and laboratory studies should be conducted to monitor the possibility of such transmissions. Studies involving transgenic mice expressing human and cervid prion protein are in progress to further assess the potential for the CWD agent to cause human disease. Epidemiologic studies have also been initiated to identify human cases of prion disease among persons with an increased risk for exposure to potentially CWD-infected deer or elk meat (47). If such cases are identified, laboratory data showing similarities of the etiologic agent to that of the CWD agent would strengthen the conclusion for a causal link. Surveillance for human prion diseases, particularly in areas where CWD has been detected, remains important to effectively monitor the possible transmission of CWD to humans. Because of the long incubation period associated with prion diseases, convincing negative results from epidemiologic and experimental laboratory studies would likely require years of follow-up. In the meantime, to minimize the risk for exposure to the CWD agent, hunters should consult with their state wildlife agencies to identify areas where CWD occurs and continue to follow advice provided by public health and wildlife agencies. Hunters should avoid eating meat from deer and elk that look sick or test positive for CWD. They should wear gloves when field-dressing carcasses, bone-out the meat from the animal, and minimize handling of brain and spinal cord tissues. As a precaution, hunters should avoid eating deer and elk tissues known to harbor the CWD agent (e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where CWD has been identified.
Acknowledgments
snip...END

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

SEAC Statement
18th January 2005
Position statement - Chronic wasting disease in UK deer

Introduction

1. The Food Standards Agency asked SEAC to consider the possible public and animal health implications of chronic wasting disease (CWD), in particular the level of risk posed to consumers of meat from infected animals. The committee also considered the possibility that BSE may be present in UK deer.

Background

2. CWD has emerged as an endemic transmissible spongiform encephalopathy (TSE) in certain captive and free-ranging species of cervid (deer) in some areas of North America. The disease is characterised by weight loss and behavioural changes in infected animals, usually over a period of weeks or months leading to death. CWD has not been found in the UK or elsewhere in Europe. No definitive or suspected cases of transmission of CWD to humans have been reported.

3. SEAC considered a review of the published, and some unpublished, research on CWD, together with surveillance data on TSEs in European cervids and information on UK cervid populations (1).

Origins

4. The origins of CWD are unknown. On the basis of epidemiological data, it is highly improbable that CWD originated from the recycling of mammalian protein in processed feed. It has been suggested that CWD may have arisen from transmission and adaptation of scrapie from sheep to cervids, as a result of a spontaneous change of endogenous prion protein (PrP) to an abnormal disease-associated form, or from an unknown source.

5. Data supporting any of these possible origins of CWD are either absent or equivocal. Although CWD could have originated from scrapie, the differing properties of the two prion diseases in strain typing bioassays, whilst limited, do not support this hypothesis. Evidence for multiple strains of CWD is equivocal. It seems most likely that CWD arose from a spontaneous change of endogenous PrP resulting in a disease-associated and laterally-transmissible form of PrP, although direct data to support this hypothesis are lacking.

Host range

6. The known natural hosts for CWD are mule deer (Odocoileus hemionus hemionus), black-tailed deer (Odocoileus hemionus columbianus), white-tailed deer (Odocoileus virginianus) and Rocky Mountain elk (Cervus elaphus nelsoni). The prevalence and geographical distribution of CWD in these species appears to be increasing in North America in a manner which is unlikely to be due simply to increased surveillance.

7. There are no direct data relating to the transmissibility of CWD to UK cervid species. However, comparison of a limited number of PrP codons indicates some homology in the endogenous PrP gene of European and North American cervid species. Thus, the possibility that UK cervids may be susceptible to CWD cannot be excluded, in particular red deer (Cervus elaphus elaphus) which are closely related to elk.

8. There is no evidence to suggest that CWD is present in UK cervids. However, because surveillance in the UK is very limited, a low level prevalence of CWD cannot be ruled out. The committee endorsed the opinion of the European Food Safety Authority on CWD surveillance in the European Union (2004) .

9. Transmission studies using parenteral routes of administration to cattle, sheep and a single goat, together with data from in vitro PrP conversion experiments, suggest that a significant barrier to CWD transmission to these species may exist. No transmission has been evident so far in an on-going oral transmission study in cattle after six years. Furthermore, no signs of infection have been observed from monitoring of cattle co-habiting areas with infected cervids, or in cattle, sheep or goats in close contact with infected cervids in research facilities. Thus, although the data are limited, there is currently no evidence to suggest that CWD can be transmitted naturally to cows, sheep or goats, and it is likely that there is a strong species barrier to such transmission.

Routes of transmission

10. Epidemiological data indicate that lateral transmission between infected and susceptible cervids occurring naturally is sufficiently effective to maintain epidemics in both captive and free-living populations. There is good evidence from studies of cervids inhabiting paddocks previously inhabited by infected animals or contaminated with infected carcases, that CWD can be transmitted laterally between animals via the environment. The precise mechanism of transmission is unclear. It is possible that the infectious agent is shed in the saliva, faeces or urine or as a result of decomposition of infected carcases and transferred to other cervids grazing the contaminated areas. It is also possible that some maternal transmission occurs.

11. There have also been suggestions that the lateral transmission of CWD may be influenced by environmental factors.

Pathogenesis

12. Information on the pathogenesis of CWD is limited. The data show that, following oral challenge, PrPCWD is first detected in the oral and gut-associated lymphoid tissues before spreading more widely within the lymphoid system and then to the brain. Involvement of the retropharyngeal lymph nodes or tonsils in the pathogenesis may not occur in some elk. At the microscopic level, the nature and distribution of the tissue lesions are similar to those found for scrapie. The available data suggest the pathogenesis of CWD is similar to scrapie.

BSE in UK deer

13. Both captive and free-ranging cervids in the UK may have been exposed to contaminated feed prior to the reinforced mammalian meat and bone meal ban instituted in 1996. A study to look at the potential susceptibility of red deer to BSE has shown no signs of transmission of the disease by the oral route, but it is at a very preliminary stage. Although a theoretical possibility exists, there is no evidence from the very limited surveillance data to suggest that BSE is present in the UK cervid population.

Human health implications

14. Epidemiological data on possible CWD infection of humans are very limited. The possibility that clinical symptoms of CWD in humans differ from those of Creutzfeldt-Jakob Disease (CJD) cannot be excluded. There is no significant difference between the prevalence of CJD in CWD endemic areas and other areas of the world. However, because CJD surveillance in the USA is relatively recent, not all CJD cases may have been identified. Additionally, detection of a small increase in prevalence of such a rare disease is very difficult. Investigation of six cases of prion disease in young people (< 30 years of age) in the USA found no definite causal link with consumption of venison from known CWD endemic areas. The disease characteristics in these cases were indistinguishable from sporadic CJD or Gerstmann-Sträussler-Scheinker syndrome. Likewise, in a study of three hunters (> 54 years of age) diagnosed with sporadic CJD, no link with consumption of venison from CWD endemic areas was found. No causal link was found in an investigation of three men with neurological illnesses who were known to partake in wild game feasts. Only one of these subjects was found to have a prion disease and this was also indistinguishable from sporadic CJD.

15. Preliminary results from transmission experiments in transgenic mice expressing human PrP suggest the presence of a significant species barrier to transmission of CWD to humans. However, these findings must be interpreted with caution as they may not accurately predict the human situation. Data from in vitro experiments on conversion of human PrP by disease-associated forms of PrP, including PrPCWD, are equivocal.

16. The committee concluded there is no evidence of transmission of CWD to humans from consumption of venison, and that there may be significant barriers to transmission. Nevertheless, as the data are extremely limited a risk cannot be ruled out should CWD enter UK herds.

Conclusions

17. There is no evidence that CWD (or BSE) is present in the UK cervid population. However, because only limited surveillance is conducted in the cervid population, a low level prevalence of CWD cannot be ruled out. It is recommended that further surveillance of TSEs in UK cervids is conducted.

18. There is no evidence of transmission of CWD to humans from consumption of meat from infected cervids. Although epidemiological and experimental data on potential transmission of CWD are extremely limited, they suggest that there may be a significant species barrier. It would be helpful if further studies were available assessing the potential species barrier for transmission to humans.

19. Although limited, there is no evidence CWD can be transmitted to cattle, sheep or goats by natural means.

20. In summary, it appears that CWD currently poses relatively little risk to human health, or to the health of cattle, sheep or goats in the UK. Nevertheless, as a risk cannot be excluded a watching brief should be maintained.


SEAC
January 2005
http://www.seac.gov.uk/statements/state180105.htm

10:00

Chronic Wasting Disease in UK deer

Alan Harvey (FSA).Wildlife Information Network.

85/2*(pdf)

http://www.seac.gov.uk/papers/tsesdeer- final.pdf

Annex 1 (pdf)

http://www.seac.gov.uk/papers/cwdiseaseannex1.pdf

Annex 2 (pdf):

http://europa.eu.int/comm/food/fs/sc/ssc/out324_en.pdf

Annex 3 (incl. appendices) (pdf)

http://www.seac.gov.uk/papers/munrodeerrptannex3.pdf

Annex 4 (pdf)

http://www.seac.gov.uk/papers/deersurvannex4.pdf

Annex 5 (pdf):
http://www.seac.gov.uk/papers/efsa-annex 5.pdf

ALL of these false reassurances we have heard time and time again, and ALL have been proven wrong.

AS with the BSE TO HUMANS AND BSE to GOAT. IT was always it never happend under natural conditions, just in the lab, so not to worry. NOW WE HAVE TO WORRY;

http://www.jarvm.com/articles/Vol2Iss1/DEBOSSCHERE.htm

http://www.pnas.org/cgi/content/full/041490898v1

CWD TRANSMITS TO PRIMATES, COWS AND SHEEP, TRANSMISSION STUDIES HAVE NEVER BEEN DONE ON HUMANS.

I ONLY HOPE DR. SCHMITT'S CYRSTAL BALL IS CORRECT...TSS


----------



## terry (Sep 13, 2002)

-------- Original Message --------
Subject: CWD NY CONSUMPTION AND CONTACT 'DON'T TOUCH THAT ANIMAL' or 'don't worry, be happy'
Date: Sat, 9 Apr 2005 11:30:23 -0500
From: "Terry S. Singeltary Sr." <[email protected]>
Reply-To: Bovine Spongiform Encephalopathy <[email protected]>
To: [email protected]


##################### Bovine Spongiform Encephalopathy #####################

http://www.health.state.ny.us/nysdoh/zoonoses/cwd.htm


Snip..

Are there any precautions for handling, processing, or eating meat from 
deer or elk?
To minimize the risk of transmission of any infectious diseases when 
handling or processing animals, the following precautions are recommended:
· Deer or elk that are observed to be ill, or found dead, should not 
be handled and should not be eaten.
· Wear rubber gloves when field dressing carcasses.
· Wash instruments and any parts of the body exposed to animal 
tissues, blood, urine, etc. thoroughly with soap and water.
· Minimize handling brain or spinal tissues/fluids and wash hands 
thoroughly with soap and water afterward if such handling occurred. If 
these nervous tissues or fluids get into a fresh open break in a 
person's skin or the eyes, mouth, or nose, contact the local health 
department to evaluate possible rabies exposure and need for testing the 
animal for other diseases.
· Request if possible that individual animals are processed 
individually, without meat from other animals being added together.
· Although no CWD risk to humans has been identified from consumption 
of organ meat, in general consumption of organ meat (including brain, 
spinal cord, and other nervous tissue, spleen, pancreas, eyes, tonsils, 
lymph nodes) may pose a greater risk of infection with a number of 
diseases. Boning out meat, including removal of fat, connective tissue, 
and lymph nodes, should be done with animals from states with confirmed 
CWD.
· Animals testing positive for CWD should not be distributed or 
donated for human consumption.
· For more information about handling, processing, or eating meat 
from deer or elk in other states, contact those state agriculture, 
wildlife, and health agencies.
Are there any risks from deer waste or products?
Although there is no indication of human infection due to contact with 
deer waste or products related to CWD-infected deer or elk, the 
following general disease control precautions are recommended:
· Avoid contact with animal bodily waste material, and clean up 
animal waste from areas frequented by children.
· If there is skin contact with animal waste, wash the area with soap 
and water immediately.
· Deer scent products should be formulated with methods to avoid 
concerns about CWD contamination.

Snip..

http://www.health.state.ny.us/nysdoh/zoonoses/cwd.htm

OR

> Observer-Dispatch
>
> VERONA - The white-tailed deer recently diagnosed with chronic wasting 
> disease was one of the deer donated to the Verona Fire Department and 
> served at its Annual Sportsmen's Feast on Sunday, March 13, an Oneida 
> County Health Department spokesman said today.
>
> People who consumed the venison need not worry about contracting the 
> disease, spokesman Ken Fanelli said.
>
> "There's no indication whatsoever that the disease has been linked to 
> human illness of any kind," Fanelli.
>
> The deer was donated before the health department knew it had the 
> disease, according to the health department. 


http://www.uticaod.com/news/updates/update2005-04-04.htm


Don't touch that animal !

BUT, if it was served at Verona, No problem at all, Don't worry, be happy?

right... talk about 'mixed signals' ...TSS


######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########




-------- Original Message --------
Subject: Re: CASE STUDY FOR CWD TRANSMISSION TO HUMANS NOW UNDERWAY
Date: Mon, 4 Apr 2005 20:54:24 -0500
From: "Terry S. Singeltary Sr." <[email protected]>
Reply-To: Bovine Spongiform Encephalopathy <[email protected]>
To: [email protected]
References: <[email protected]>


##################### Bovine Spongiform Encephalopathy #####################

> Chronic Wasting Disease in Elk and Deer in the United States
> The importance of having strong prion disease surveillance in the 
> United States has been further
> underlined by recent reports that chronic wasting disease (CWD), an 
> endemic prion disease affecting elk
> and deer which is found in an increasing number of states in the 
> Midwest and Southwest, may be
> transmitted to humans generating a new prion disease. The World Health 
> Organization (WHO) and the
> CDC agree that there currently is insufficient evidence to establish a 
> link between human disease and
> handling or consuming CWD-infected deer. Although no human cases of 
> CWD have been identified,
> laboratory research suggests that it is theoretically possible; 
> however it is believed that the risk to humans
> is low.


THE CITY OF NEW YORK
DEPARTMENT OF HEALTH AND MENTAL HYGIENE
Michael R. Bloomberg Thomas R. Frieden, M.D., M.P.H.
Mayor Commissioner
_______________________________________________________________
nyc.gov/health
2004 Health Update #5: Surveillance for Transmissible Spongiform 
Encephalopathies,
including the Classic and Variant Forms of Creutzfeld-Jakob Disease, in 
New York City
Please distribute to colleagues in Neurology, Pathology, Internal 
Medicine, Geriatric Medicine, Infectious
Diseases, Infection Control, and Family Practice
March 16, 2004

http://www.nyc.gov/html/doh/pdf/cd/04md05.pdf

TSS


Terry S. Singeltary Sr. wrote:

> ##################### Bovine Spongiform Encephalopathy 
> #####################
>
> Officials: Diseased deer served at Verona gathering
> April 4, 2005
> updated 11:22 a.m.
>
>
> LINDA MURPHY
> Observer-Dispatch
>
> VERONA - The white-tailed deer recently diagnosed with chronic wasting 
> disease was one of the deer donated to the Verona Fire Department and 
> served at its Annual Sportsmen's Feast on Sunday, March 13, an Oneida 
> County Health Department spokesman said today.
>
> People who consumed the venison need not worry about contracting the 
> disease, spokesman Ken Fanelli said.
>
> "There's no indication whatsoever that the disease has been linked to 
> human illness of any kind," Fanelli.
>
> The deer was donated before the health department knew it had the 
> disease, according to the health department.
>
> Nonetheless, the health department wants anyone who attended the event 
> on March 13 and who may have eaten the venison to contact 798-5064. Or 
> call the New York State Health Department's toll-free information line 
> at (800) 808-1987.
>
> "We want to discuss the issue with them and to reassure them," he said.
>
> http://www.uticaod.com/news/updates/update2005-04-04.htm
>
>
> Chronic Wasting Disease and Potential Transmission to Humans
>
> Ermias D. Belay,*Comments 
> Ryan A. 
> Maddox,* Elizabeth S. Williams, Michael W. Miller,! Pierluigi 
> Gambetti,§ 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 §Case Western Reserve 
> University, Cleveland, Ohio, USA
>
> Suggested citation for this article: Belay ED, Maddox RA, Williams
> ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease
> and potential transmission to humans. Emerg Infect Dis [serial on
> the Internet]. 2004 Jun [date cited]. Available from:
> http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
>
> ------------------------------------------------------------------------
>
> Chronic wasting disease (CWD) of deer and elk is endemic in a
> tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of
> CWD have been detected in other parts of the United States. Although
> detection in some areas may be related to increased surveillance,
> introduction of CWD due to translocation or natural migration of
> animals may account for some new foci of infection. Increasing
> spread of CWD has raised concerns about the potential for increasing
> human exposure to the CWD agent. The foodborne transmission of
> bovine spongiform encephalopathy to humans indicates that the
> species barrier may not completely protect humans from animal prion
> diseases. Conversion of human prion protein by CWD-associated prions
> has been demonstrated in an in vitro cell-free experiment, but
> limited investigations have not identified strong evidence for CWD
> transmission to humans. More epidemiologic and laboratory studies
> are needed to monitor the possibility of such transmissions. ...
>
> FULL TEXT
>
> http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
>
> CWD DOES TRANSMIT TO PRIMATE, COWS AND SHEEP,
> in the lab...
>
> TSS
>
>
> ######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html 
> ##########
>

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########


----------



## terry (Sep 13, 2002)

Animal protein fed to the deer
25. Available management data indicate that, except for milk (fresh, canned evaporated,
buttermilk and occasionally commercial lamb milk replacer) used in hand-rearing fawns, no
animal protein was fed to any of the deer kept in the Colorado or Wyoming research facilities.
Diets included grass, hay, other vegetation, dried high protein alfalfa hay and grain mixtures,
as well as multivitamins, salt and mineral blocks. Sources of hay and of grain mixtures used
were different for the Colorado and Wyoming facilities. Overall, it was considered that there
was no evidence of CWD being associated with feed; it was acknowledged that detailed data
on feeding was not available for the period before 1974, but it was considered probable that
management was similar (Williams & Young, 1992). ...
Annex 1 (pdf)

http://www.seac.gov.uk/papers/cwdiseaseannex1.pdf


not so ;




-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr." <[email protected]>
To: [email protected]


Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal 
Feed; Availability

Several factors on this apparent voluntary proposal disturbs me greatly,
please allow me to point them out;

1. MY first point is the failure of the partial ruminant-to-ruminant feed
ban of 8/4/97. this partial and voluntary feed ban of some ruminant
materials being fed back to cattle is terribly flawed. without the
_total_ and _mandatory_ ban of all ruminant materials being fed
back to ruminants including cattle, sheep, goat, deer, elk and mink,
chickens, fish (all farmed animals for human/animal consumption),
this half ass measure will fail terribly, as in the past decades... 

2. WHAT about sub-clinical TSE in deer and elk? with the recent
findings of deer fawns being infected with CWD, how many could
possibly be sub-clinically infected. until we have a rapid TSE test to
assure us that all deer/elk are free of disease (clinical and sub-clinical),
we must ban not only documented CWD infected deer/elk, but healthy
ones as well. it this is not done, they system will fail...

3. WE must ban not only CNS (SRMs specified risk materials),
but ALL tissues. recent new and old findings support infectivity
in the rump or ass muscle. wether it be low or high, accumulation
will play a crucial role in TSEs.

4. THERE are and have been for some time many TSEs in the
USA. TME in mink, Scrapie in Sheep and Goats, and unidentified
TSE in USA cattle. all this has been proven, but the TSE in USA
cattle has been totally ignored for decades. i will document this
data below in my references.

5. UNTIL we ban all ruminant by-products from being fed back
to ALL ruminants, until we rapid TSE test (not only deer/elk) but
cattle in sufficient numbers to find (1 million rapid TSE test in
USA cattle annually for 5 years), any partial measures such as the
ones proposed while ignoring sub-clinical TSEs and not rapid TSE
testing cattle, not closing down feed mills that continue to violate the
FDA's BSE feed regulation (21 CFR 589.2000) and not making
freely available those violations, will only continue to spread these
TSE mad cow agents in the USA. I am curious what we will
call a phenotype in a species that is mixed with who knows
how many strains of scrapie, who knows what strain or how many
strains of TSE in USA cattle, and the CWD in deer and elk (no
telling how many strains there), but all of this has been rendered
for animal feeds in the USA for decades. it will get interesting once
someone starts looking in all species, including humans here in the
USA, but this has yet to happen... 

6. IT is paramount that CJD be made reportable in every state
(especially ''sporadic'' cjd), and that a CJD Questionnaire must
be issued to every family of a victim of TSE. only checking death
certificates will not be sufficient. this has been proven as well
(see below HISTORY OF CJD -- CJD QUESTIONNAIRE)

7. WE must learn from our past mistakes, not continue to make
the same mistakes...

REFERENCES

Six white-tailed deer fawns test positive for CWD

MADISON -- Six fawns in the area of south central Wisconsin where
chronic wasting disease has been found in white-tailed deer have tested
positive for the disease, according to Department of Natural Resources
wildlife health officials. These are the youngest wild white-tailed deer
detected with chronic wasting disease (CWD) to date.

Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of
fawns sampled were between the ages of 5 to 9 months, though some were
as young as 1 month. Two of the six fawns with CWD detected were 5 to 6
months old. All six of the positive fawns were taken from the core area
of the CWD eradication zone where the highest numbers of positive deer
have been identified.

snip...

http://www.dnr.state.wi.us/org/caer/ce/news/on/2003/on20030513.htm#art4

===================================================

Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH
FINDINGS RELEVANT TO CJD AND BSE

A team of researchers led by Professor John Collinge at the Medical
Research Council Prion Unit1 report today in the Proceedings of the
National Academy of Sciences, on new evidence for the existence of a
'sub-clinical' form of BSE in mice which was unknown until now.

The scientists took a closer look at what is known as the 'species
barrier' - the main protective factor which limits the ability of
prions2 to jump from one species to infect another. They found the mice
had a 'sub-clinical' form of disease where they carried high levels of
infectivity but did not develop the clinical disease during their normal
lifespan. The idea that individuals can carry a disease and show no
clinical symptoms is not new. It is commonly seen in conventional
infectious diseases.

Researchers tried to infect laboratory mice with hamster prions3 called
Sc237 and found that the mice showed no apparent signs of disease.
However, on closer inspection they found that the mice had high levels
of mouse prions in their brains. This was surprising because it has
always been assumed that hamster prions could not cause the disease in
mice, even when injected directly into the brain.

In addition the researchers showed that this new sub-clinical infection
could be easily passed on when injected into healthy mice and hamsters.

The height of the species barrier varies widely between different
combinations of animals and also varies with the type or strain of
prions. While some barriers are quite small (for instance BSE easily
infects mice), other combinations of strain and species show a seemingly
impenetrable barrier. Traditionally, the particular barrier studied here
was assumed to be robust.

Professor John Collinge said: "These results have a number of important
implications. They suggest that we should re-think how we measure
species barriers in the laboratory, and that we should not assume that
just because one species appears resistant to a strain of prions they
have been exposed to, that they do not silently carry the infection.
This research raises the possibility, which has been mentioned before,
that apparently healthy cattle could harbour, but never show signs of, BSE.

"This is a timely and unexpected result, increasing what we know about
prion disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected
material getting into the food chain and for those considering how best
to safeguard health and reduce the risk that theoretically, prion
disease could be contracted through medical and surgical procedures."

ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS
SET BY THE JOURNAL.

FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011
(OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR
PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO
TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30
ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE
MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE
DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE
ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009
(OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF
UK TIME.

NOTES FOR EDITORS

Professor Collinge is a consultant neurologist and Director of the newly
formed MRC Prion Unit based at The Imperial College School of Medicine
at St Mary's Hospital. He is also a member of the UK Government's
Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit
is was set up in 1999, and its work includes molecular genetic studies
of human prion disease and transgenic modelling of human prion diseases.

Prions are unique infectious agents that cause fatal brain diseases such
as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad
cow disease) in animals. In some circumstances prions from one species
of animals can infect another and it is clear that BSE has done this to
cause the disease variant CJD in the UK and France. It remains unclear
how large an epidemic of variant CJD will occur over the years ahead.

The strain of prion used here to infect the mice is the Sc237 strain
(also known as 263K) which infects hamsters, and until now was assumed
not to infect mice.

This research was funded by the Medical Research Council and Wellcome Trust.

The Medical Research Council (MRC) is a national organisation funded by
the UK tax-payer. Its business is medical research aimed at improving
human health; everyone stands to benefit from the outputs. The research
it supports and the scientists it trains meet the needs of the health
services, the pharmaceutical and other health-related industries and the
academic world. MRC has funded work which has led to some of the most
significant discoveries and achievements in medicine in the UK. About
half of the MRC's expenditure of Â£345 million is invested in over 50 of
its Institutes and Units, where it employs its own research staff. The
remaining half goes in the form of grant support and training awards to
individuals and teams in universities and medical schools.

The Wellcome Trust is the world's largest medical research charity with
a spend of some Â£600 million in the current financial year 1999/2000.
The Wellcome Trust supports more than 5,000 researchers, at 400
locations, in 42 different countries to promote and foster research with
the aim of improving human and animal health. As well as funding major
initiatives in the public understanding of science, the Wellcome Trust
is the country's leading supporter of research into the history of medicine.

Â©2002 Medical Research Council
Data Protection policy | Contact the MRC

http://www.mrc.ac.uk/index/public_i...blic-press_releases_2000/public-mrc-43-00.htm

======================================

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
[email protected]

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a
brain homogenate prepared from mule deer with naturally occurring
chronic wasting disease (CWD), a prion-induced transmissible spongiform
encephalopathy. Fawns were necropsied and examined for PrP res, the
abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days
post-inoculation (p.i.) using an immunohistochemistry assay modified to
enhance sensitivity. PrPres was detected in alimentary-tract-associated
lymphoid tissues (one or more of the following: retropharyngeal lymph
node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42
days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No
PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural
tissue of any fawn. PrPres-specific staining was markedly enhanced by
sequential tissue treatment with formic acid, proteinase K and hydrated
autoclaving prior to immunohistochemical staining with monoclonal
antibody F89/160.1.5. These results indicate that CWD PrP res can be
detected in lymphoid tissues draining the alimentary tract within a few
weeks after oral exposure to infectious prions and may reflect the
initial pathway of CWD infection in deer. The rapid infection of deer
fawns following exposure by the most plausible natural route is
consistent with the efficient horizontal transmission of CWD in nature
and enables accelerated studies of transmission and pathogenesis in the
native species.

snip...

These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the
earliest post-exposure period, CWD PrPres was traced to the lymphoid
tissues draining the oral and intestinal mucosa (i.e. the
retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and
ileocaecal lymph nodes), which probably received the highest initial
exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum
and spleen in a 10-month-old naturally infected lamb by mouse bioassay.
Eight of nine sheep had infectivity in the retropharyngeal lymph node.
He concluded that the tissue distribution suggested primary infection
via the gastrointestinal tract. The tissue distribution of PrPres in the
early stages of infection in the fawns is strikingly similar to that
seen in naturally infected sheep with scrapie. These findings support
oral exposure as a natural route of CWD infection in deer and support
oral inoculation as a reasonable exposure route for experimental studies
of CWD.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757
===================================

now, just what is in that deer feed? _ANIMAL PROTEIN_

continued...


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## terry (Sep 13, 2002)

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... blah, blah, blah...

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


snip...

thank you,
I am sincerely,

Terry S. Singeltary SR.
P.O. Box 42
Bacliff, TEXAS USA 77518
CJD WATCH


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