# Sewing The Seeds Of Cwd Mad Deer/elk Through Feeding, Especially From Animal Protein



## terry

Greetings,

i would like to pass a bit of info. not here to argue. have been researching
this for 6 years, and i am interested in
finding the truth. i am not an anti-hunter advocate, just think there
is a lot about TSEs most of you don't
know about. i have pasted a message
below. please read the studies, and
the source of those studies, not neccessarily the boards they are 
posted to...

thank you,
kind regards,
terry 


Subject: SEWING THE SEEDS OF CWD MAD DEER/ELK THROUGH FEEDING, ESPECIALLY FROM ANIMAL PROTEIN !!!
Date: Thu, 12 Sep 2002 12:14:16 -0700
From: "Terry S. Singeltary Sr." <[email protected]>
Reply-To: Bovine Spongiform Encephalopathy <[email protected]>
To: [email protected]

######## Bovine Spongiform Encephalopathy <[email protected]> #########

CWD AND STUPID SAFETY TIP & COMMENTS TEXAS & SEWING THE SEEDS OF CWD
THROUGH ANIMAL PROTEIN? Houston Chronicle

TDH

CWD is probably not a zoonotic disease. In other words, there is
no evidence that CWD can be passed from infected animal to humans

AND

* Always thoroughly cook meat

http://www.tdh.state.tx.us/zoonosis/diseases/CWD.pdf

http://www.tdh.state.tx.us/zoonosis/

with that said, there is no evidence that it cannot, but
my opinion, there is more evidence it can, that it cannot.

AND if you plan on cooking the TSE agents out of the meat
as implied above, you had better ash it to 1000 degrees celsius.

New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°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§

* 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 § Institut Alfred
Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur
Yvette, France

Contributed by D. Carleton Gajdusek, December 22, 1999

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°C to 1,000°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°C, titers equaled or exceeded
6 log10LD50/g, and after exposure to 300°C, titers equaled or exceeded 4
log10LD50/g. Exposure to 600°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°C. These results suggest that an
inorganic molecular template with a decomposition point near 600°C is
capable of nucleating the biological replication of the scrapie agent.

snip...

http://www.pnas.org/cgi/content/full/97/7/3418

But some scientists advocate stricter measures.

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."

snip...

also, what is TEXAS stance on feeding deer and CWD risk?

but before that, lets look at a few things;

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_

Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr." <[email protected]>
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
===================================================
now, what about those 'deer scents' of 100% urine',
and the prion that is found in urine, why not just
pass the prion with the urine to other deer...

Mrs. Doe Pee Doe in Estrus
Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urine
collected at the peak of the rut, blended with Fresh Doe Urine for an
extremely effective buck enticer. Use pre-rut before the does come into
heat. Use during full rut when bucks are most active. Use during
post-rut when bucks are still actively looking for does. 1 oz.

http://www.gamecalls.net/huntingproducts/deerlures.html

ELK SCENT/SPRAY BOTTLE
*
Works anytime of the year
*
100 % Cow Elk-in-Heat urine (2oz.)
*
Economical - mix with water in spray mist bottle
*
Use wind to your advantage

Product Code WP-ESB $9.95

http://www.elkinc.com/Scent.asp

prions in urine?

[PDF] A URINE TEST FOR THE IN-VIVO DIAGNOSIS OF PRION DISEASES

http://www.sigov.si/vurs/PDF/diagnoastika-bse-urin.pdf

now, other states stance on feeding deer and CWD risk?

"Although there is no proof how CWD spreads from one deer to the next,
common sense tells many people that mouth-to-mouth contact is possibly
the culprit," Stroess said.

The feed pile or feeder presents a perfect opportunity for deer to have
mouth, nose or saliva contact with deer carrying DWD.

"Just as you and I catch a cold from someone who coughs on us or with
whom we have close contact, deer likely get some sicknesses the same
way," he said.

As of July 3, both baiting for the purpose of hunting wildlife and
feeding of wildlife became illegal in Wisconsin. This means that
backyard deer feeders, feed piles, mineral blocks, salt blocks, protein
supplement blocks and all other bait is illegal to use for any deer or
other wildlife viewing or hunting purposes.

snip...

http://www.wisinfo.com/heraldtimes/news/archive/local_5812834.shtml

Poulter said the ban on feeding is to keeping deer from congregating and
transmitting the disease to one another.

The ban includes food, salt, mineral blocks, and other food products
with some exceptions. For example, bird and squirrel feeders close to
homes and incidental feeding of wildlife within active livestock
operations are exempt from the ban.

http://www.zwire.com/site/news.cfm?newsid=4994835&BRD=606&PAG=461&dept_id=172213&rfi=6

The department is banning feeding of wild deer and other wildlife in
areas where wild deer are present. The ban includes food, salt, mineral
blocks and other food products, with some exceptions. For example, bird
and squirrel feeders close to homes and incidental feeding of wildlife
within active livestock operations are exempt from the ban.

The rule also bans the importation of hunter-harvested deer and elk
carcasses into Illinois, except for deboned meat, antlers, antlers
attached to skull caps, hides, upper canine teeth, and finished
taxidermist mounts. Skull caps must be cleaned of all brain and muscle
tissue.

Officials from the state said should anyone be caught violating the
rule, they would be charged with a petty offense and fined $1,000. For
more information about the rule, visit the department's Web site at
http://dnr.state.il.us/legal/rules-status.htm.

http://www.zwire.com/site/news.cfm?newsid=5091636&BRD=1719&PAG=461&dept_id=25271&rfi=6

NOW, what has the media in TEXAS been saying about this type feeding?

here is something from the Houston Chronicle today;

PLANTING SEEDS FOR CWD, TEXAS STYLE...TSS

Sept. 11, 2002, 7:31PM

It's time to plant seeds for deer season

By SHANNON TOMPKINS
Copyright 2002 Houston Chronicle

Texas deer hunters always look for an edge -- something to increase
their chances of success or improve the health of deer haunting their lease.

That's why they spend piles of money on equipment such as
infrared-sensing cameras to monitor trails and feeders, mineral blocks
and protein pellets as supplemental feed and spend restless nights
figuring where to put a new blind.

snip...

http://www.chron.com/cs/CDA/story.hts/outdoors/1571427

TSS

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############


----------



## terry

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

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.bse.org.uk/files/yb/1989/04/03006001.pdf

GUTTING DEER/ELK AND THOSE THIN GLOVES;

Distribution of prion protein in the ileal Peyer?s patch of scrapie-free
lambs and lambs naturally and experimentally exposed to the scrapie agent

Ragna Heggebø1, Charles McL. Press1, Gjermund Gunnes1, Kai Inge Lie1,
Michael A. Tranulis2, Martha Ulvund3, Martin H. Groschup4 and Thor
Landsverk1

Department of Morphology, Genetics and Aquatic Biology1 and Department
of Biochemistry, Physiology and Nutrition2, Norwegian School of
Veterinary Science, PO Box 8146 Dep., N-0033, Oslo, Norway
Department of Sheep and Goat Research, Norwegian School of Veterinary
Science, Kyrkjevegen 332/334, 4300 Sandnes, Norway3
Federal Research Centre for Virus Diseases of Animals, Paul-Ehrlich-Str.
28, 72076 Tübingen, Germany4

Author for correspondence: Charles Press. Fax +47 22964764. e-mail
[email protected]

A sensitive immunohistochemical procedure was used to investigate the
presence of prion protein (PrP) in the ileal Peyer?s patch of
PrP-genotyped lambs, including scrapie-free lambs and lambs naturally
and experimentally exposed to the scrapie agent. The tyramide signal
amplification system was used to enhance the sensitivity of conventional
immunohistochemical procedures to show that PrP was widely distributed
in the enteric nervous plexus supplying the gut wall. In scrapie-free
lambs, PrP was also detected in scattered cells in the lamina propria
and in the dome and interfollicular areas of the Peyer?s patch. In the
follicles, staining for PrP was mainly confined to the capsule and cells
associated with vascular structures in the light central zone. In lambs
naturally exposed to the scrapie agent, staining was prominent in the
dome and neck region of the follicles and was also found to be
associated with the follicle-associated epithelium. Similar observations
were made in lambs that had received a single oral dose of
scrapie-infected brain material from sheep with a homologous and
heterologous PrP genotype 1 and 5 weeks previously. These studies show
that the ileal Peyer?s patch in young sheep may be an important site of
uptake of the scrapie agent and that the biology of this major
gut-associated lymphoid tissue may influence the susceptibility to oral
infection in sheep. Furthermore, these studies suggest that homology or
heterology between PrP genotypes or the presence of PrP genotypes seldom
associated with disease does not impede uptake of PrP.
======================================================

BSE, KURU, DENTAL AND ___CUT ABRASIONS___ from gutting a deer
perhaps;

snip...

since there was a suggestion that kuru had been transmitted
through the gums and/or gum abrasions...

snip...

http://www.bse.org.uk/files/yb/1989/04/17005001.pdf

[PDF]BSE INQUIRY Statement of behalf of the Environment Agency ...
File Format: PDF/Adobe Acrobat - View as HTML
... his Statement of March 1998 to the BSE Inquiry ... systems subject
to regular or intermittent
contamination by rapid movement of recharge water ...
www.bse.org.uk/files/ws/s490.pdf

http://www.bse.org.uk/files/ws/s490.pdf

continued...tss


----------



## terry

BSE INQUIRY

Statement of behalf of the Environment Agency
Concerning Thruxted Mill
By
Mr C. P. Young
Principal Hydrogeologist, Soil Waste and Groundwater Group
WRc plc; Medmenham, Bucks

http://www.bse.org.uk/files/ws/s490.pdf

MAD COW BOARD TSS BSE NEWS
==========================

http://www.vegsource.com/talk/madcow/index.html

CJD FOUNDATION

http://pub6.bravenet.com/forum/show.php?usernum=432758200

CJD WATCH

http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm

CJD Watch message board

http://disc.server.com/Indices/167318.html

CJD VOICE MESSAGE BOARD

http://disc.server.com/Indices/7498.html

Moms death from hvCJD

http://www.vegsource.com/talk/lyman/messages/7252.html

MANY FACES

http://www.fortunecity.com/healthclub/cpr/798/cjd.htm

'A SON'S LOVE'

http://www.fortunecity.com/healthclub/cpr/798/terry.htm

'MOMS AUTOPSY REPORT'

http://www.vegsource.com/talk/lyman/messages/7548.html

CJD/BSE aka madcow disease in the U.S., please let me count the Ways$$$

http://www.whale.to/v/cjd2.html

SOMETHING TO CHEW ON

BMJ

http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2

BMJ

http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1

TSS SHORTCUTS ''MADCOW DOCUMENTS'' PARTS 1-8

http://vegancowboy.org/TSS-Shortcut-parts1to8.htm

3681t1 02.pdf (1931)

http://www.fda.gov/ohrms/dockets/ac/01/transcripts/3681t1_02.pdf

dockets site;

http://www.fda.gov/ohrms/dockets/ac/cber01.htm

My Submission will be on the 'slides' of the Jan. 19, meeting...tss

http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2.htm

also;

Diagnosis and Reporting of Creutzfeldt-Jakob Disease T. S. Singeltary,
Sr; D. E. Kraemer; R. V. Gibbons, R. C. Holman, E. D. Belay, L. B.
Schonberger

http://jama.ama-assn.org/issues/v285n6/ffull/jlt0214-2.html

Tom from mad-cow.org/ had the last word.

http://www.mad-cow.org/00/feb01_news_mid.html#mmm

also;

GERMAN DER SPIEGEL MAGAZINE

http://www.spiegel.de/spiegel/0,1518,119306,00.html

also;

http://vegancowboy.org/schedule.htm

NEW SCIENTIST MAGAZINE 4/02/01

NEW SCIENTIST EDITORIAL PAGE 3

MAD SHEEP DISEASE?

IF THERE is one categorical pronouncement you
can safely make about prion diseases like BSE
or CJD, it is that one should not make
categorical pronouncements. "British beef is
safe" and "there is no BSE in Germany" come
to mind. Now there are two more: "scrapie is
safe", and "people don't catch sporadic CJD".
Scrapie is the most widespread prion
disease, infecting untold numbers of
sheep worldwide. Sporadic CJD is the
old-fashioned pre-BSE kind that is supposed
to happen spontaneously in unlucky people.
But a surprise observation in France suggests
some sCJD cases--though by no means all--may
be linked to scrapie after all (see p 4).

For years, British authorities asserted that
BSE was harmless because it was a form of
scrapie. In fact, the only evidence scrapie
is safe is some broad-brush epidemiology, good
as far as it goes but unable to reveal
occasional risks for some people from some
sheep. Alarm bells should have rung in 1980
when researchers gave monkeys scrapie by
feeding them infected brains. But that
research, like so much other work on
prion diseases, was never followed up.
We still have little idea what BSE does
in pigs and chickens. The Queniborough
vCJD outbreak (see p 5) would be easier
to understand if we knew how much brain
we must eat to be infected. As for scrapie,
it shouldn't take a chance finding to
tell us that there may be dangerous sheep
out there.

Suspect symptoms

What if you can catch old-fashioned CJD by
eating meat from a sheep infected with
scrapie?

Exclusive from New Scientist magazine

Four years ago, Terry Singeltary watched his
mother die horribly from a degenerative brain disease.................

full text url follows
By Debora MacKenzie

Suspect Symptoms

http://www.newscientist.com/hottopics/bse/suspectsymptoms.jsp

if url dead, go here for 'SUSPECT SYMPTOMS'

you can access article here also;

you can access article here also;

http://www.organicconsumers.org/meat/scrapiecjd.cfm

http://www.vegancowboy.org/TSS-SuspectSymptoms.html

Then follow up with PNAS studies from which
new scientist article written from;

Published online before print March 20, 2001
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.041490898
Abstract of this Article
Reprint (PDF) Version of this Article
Similar articles found in:
PNAS Online
PubMed
PubMed Citation
Search Medline for articles by:
Lasmézas, C. I. || Deslys, J.-P.
Alert me when:
new articles cite this article
Download to Citation Manager
Neurobiology
Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human health
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*

* Commissariat à l'Energie Atomique, Service de Neurovirologie,
Direction des Sciences du Vivant/Département de Recherche Medicale,
Centre de Recherches du Service de Santé des Armées 60-68, Avenue du
Général Leclerc, BP 6, 92 265 Fontenay-aux-Roses Cedex, France; [Dagger
] Hôpital Neurologique Pierre Wertheimer, 59, Boulevard Pinel, 69003
Lyon, France; § Laboratoire de Neuropathologie, Hôpital de la
Salpêtrière, 83, Boulevard de l'Hôpital, 75013 Paris, France; ¶
Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital,
Crewe Road, Edinburgh EH4 2XU, United Kingdom; and [||] Institute for
Animal Health, Neuropathogenesis Unit, West Mains Road, Edinburgh EH9
3JF, United Kingdom

Edited by D. Carleton Gajdusek, Centre National de la Recherche
Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000
(received for review October 16, 2000)

Abstract
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
Conclusions
References

There is substantial scientific evidence to support the notion that
bovine spongiform encephalopathy (BSE) has contaminated human beings,
causing variant Creutzfeldt-Jakob disease (vCJD). This disease has
raised concerns about the possibility of an iatrogenic secondary
transmission to humans, because the biological properties of the
primate-adapted BSE agent are unknown. We show that (i) BSE can be
transmitted from primate to primate by intravenous route in 25 months,
and (ii) an iatrogenic transmission of vCJD to humans could be readily
recognized pathologically, whether it occurs by the central or
peripheral route. Strain typing in mice demonstrates that the BSE agent
adapts to macaques in the same way as it does to humans and confirms
that the BSE agent is responsible for vCJD not only in the United
Kingdom but also in France. 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. These data will be key in identifying the origin of
human cases of prion disease, including accidental vCJD transmission,
and could provide bases for vCJD risk assessment.

Introduction
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
Conclusions
References

The recognition of a variant of the human transmissible spongiform
encephalopathy (TSE) Creutzfeldt-Jakob Disease (vCJD) in the U.K. in
1996 raised the major concern that it would correspond to human
infection with the agent responsible for bovine spongiform
encephalopathy (BSE; ref. 1). Transmission of BSE to macaques provided
the first experimental evidence as it produced a disease close to vCJD
in humans (2). Strain typing in inbred mice (consisting of measuring the
incubation period and establishing lesion profiles corresponding to the
strain-specific distribution of brain vacuolation) allows reliable
identification of TSE strains (3). This method, together with
biochemical methods, has revealed a single phenotype for the agents of
BSE and the British cases of vCJD (4-6). Mice expressing only the bovine
prion protein (PrP) were highly susceptible to vCJD and BSE, which
induced the same disease (7). Thus, it is now well established that BSE
has caused vCJD, probably by alimentary contamination. In this respect,
the finding of abnormal PrP labeling in the gastrointestinal tract and
lymphatic tissues of orally BSE-contaminated lemurs shows that the BSE
agent can infect primates by the oral route (8). About 1 million
contaminated cattle may have entered the human food chain, and the
future number of vCJD cases could range from 63 to 136,000 depending on
the incubation period of BSE in humans (9). Unlike sporadic CJD (sCJD)
and iatrogenic CJD (iCJD) linked to the administration of contaminated
growth hormone extracted from human hypophyses, in vCJD, the infectious
agent seems to be widely distributed in lymphoid organs, as pathological
PrP (PrPres) can be detected in tonsils, lymph nodes, spleen, and
appendix even in the preclinical phase of the disease (10, 11). This
raises a public health issue with regard to the risk of iatrogenic
transmission of vCJD through surgical instruments, grafts, blood
transfusion, or parenteral administration of biological products of
human origin. However, this risk is difficult to assess, because it
largely depends on factors such as the virulence of the BSE agent
adapted to primates and the efficiency of secondary transmission to
humans by a peripheral route such as the i.v. one. A further issue is
whether vCJD accidentally acquired from humans would be recognized. The
latter poses the question of a phenotypic variation of the BSE agent
after successive transmissions in humans: does it retain its strain
characteristics, and does it induce a pathology similar to that observed
in the previous host? A 9-year history of transmission of BSE to
primates and mice enables us today to clarify a number of these
important points.

Although BSE has mainly affected the U.K., two definite cases and one
probable case of vCJD have now been reported in France in people who
have never resided in the U.K. (12, 13). We strain-typed the first of
these cases to establish its origin. Strain typing in C57BL/6 mice of
BSE, French, and British vCJD was compared with that of BSE passaged in
nonhuman primates, thus allowing us to study the effect of serial
passages in primates. Comparisons were also made with French cases of
sCJD and iCJD and two strains of scrapie (one of French and one of U.S.
origin). Our findings provide experimental demonstration that the same
agent, namely that responsible for the cattle disease BSE, has caused
vCJD both in France and in the U.K., in line with biochemical data and
with the fact that, until 1996, about 10% of the beef consumed in France
was imported from the U.K. We found that the BSE agent in nonhuman
primates is similar to that causing vCJD in humans and tends to evolve
rapidly toward a primate-adapted variant. Furthermore, we showed that
the strain responsible for iCJD is closely related to that of one
patient with sCJD, and, more unexpectedly, that these agents were
similar to the French scrapie strain studied (but different from the
U.S. scrapie strain). This finding requires a cautious interpretation
for several reasons, not least because of the inevitably limited number
of TSE strains that can be studied by such a cumbersome method as strain
typing. Nonetheless, it also prompts reconsideration of the possibility
that, in some instances, sheep and human TSEs can share a common origin.

snip...

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

STATEMENT OF DR HELEN GRANT MD FRCP
ISSUED 13/05/1999

BSE INQUIRY

http://www.bseinquiry.gov.uk/files/ws/s410.pdf
http://www.bseinquiry.gov.uk/files/ws/s410x.pdf

http://www.bseinquiry.gov.uk/evidence/ws/ws8.htm

CWD to CJD in humans (why not?), as easy as BSE/Scrapie;

The EMBO Journal, Vol. 19, No. 17 pp. 4425-4430, 2000
© European Molecular Biology Organization

Evidence of a molecular barrier limiting
susceptibility of humans, cattle and sheep to
chronic wasting disease

G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O?Rourke3,
L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M.
Smits2
and B. Caughey1,7

1NIAID/NIH Rocky Mountain Laboratories, Hamilton, MT 59840,
3USDA/ARS/ADRU, Pullman, WA 99164-7030, 4USDA/ARS/ABADRL,
Laramie, WY 82071, 5Colorado Division of Wildlife, Wildlife Research
Center, Fort Collins, CO 80526-2097, 6Department of Veterinary Sciences,
University of Wyoming, Laramie, WY 82070, USA and 2ID-Lelystad,
Institute for Animal Science and Health, Lelystad, The Netherlands
7Corresponding author e-mail: [email protected] Received June 7, 2000;
revised July 3, 2000; accepted July 5, 2000.

Abstract

Chronic wasting disease (CWD) is a transmissible
spongiform encephalopathy (TSE) of deer and elk,
and little is known about its transmissibility to other
species. An important factor controlling
interspecies TSE susceptibility is prion protein (PrP)
homology between the source and recipient
species/genotypes. Furthermore, the efficiency with which
the protease-resistant PrP (PrP-res) of one
species induces the in vitro conversion of the normal PrP
(PrP-sen) of another species to the
protease-resistant state correlates with the cross-species
transmissibility of TSE agents. Here we
show that the CWD-associated PrP-res (PrPCWD) of cervids
readily induces the conversion of recombinant cervid PrP-sen
molecules to the protease-resistant state in accordance
with the known transmissibility of CWD between cervids. In contrast,
PrPCWD-induced conversions of human and bovine PrP-sen were
much less efficient, and conversion of ovine PrP-sen was
intermediate. These results demonstrate a barrier at the
molecular level that should limit the susceptibility of these non-cervid
species to CWD.

snip...

Clearly, it is premature to draw firm conclusions about CWD
passing naturally into humans, cattle and sheep, but the present
results suggest that CWD transmissions to humans would be as
limited by PrP incompatibility as transmissions of BSE or sheep
scrapie to humans. Although there is no evidence that sheep
scrapie has affected humans, it is likely that BSE has caused variant
CJD in 74 people (definite and probable variant CJD cases to
date according to the UK CJD Surveillance Unit). Given the
presumably large number of people exposed to BSE infectivity,
the susceptibility of humans may still be very low compared with
cattle, which would be consistent with the relatively inefficient
conversion of human PrP-sen by PrPBSE. Nonetheless, since
humans have apparently been infected by BSE, it would seem prudent
to take reasonable measures to limit exposure of humans
(as well as sheep and cattle) to CWD infectivity as has been
recommended for other animal TSEs.

snip...

http://www.emboj.org/current.shtml

Scrapie to Humans?

http://www.ncbi.nlm.nih.gov:80/entr...eve&db=PubMed&list_uids=3915057&dopt=Abstract

My submission to federal gov. on BSE and
the 'lack of' surveillance;

https://199.132.50.48/E-Commen.nsf/($All)?OpenView

https://199.132.50.48/E-Commen.nsf/...c147d3037a26dfe285256ab000769557?OpenDocument

Houston Chronicle article Aug. 5, 2001

MAD COW DISEASE: Could It Happen Here?

'ARCHIVED'

http://www.chron.com/cs/CDA/story.hts/metropolitan/991714

go here for chronicle article;

http://www.organicconsumers.org/madcow/crusade8501.cfm

http://www.vegancowboy.org/TSS-MadCowHere.htm

thank you,
have a safe hunt,

Terry S. Singeltary Sr.


----------



## terry

ooops, one more very very critical
study.

SUB-CLINICAL/SUB-CLINICAL

those healthy looking deer may not
be so healthy. please read this study.

and don't shoot the messenger...TSS

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 £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 £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.


©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

TSS


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## Belbriette

TERRY, great thread, great posts, great Homepage !!!

The wealth of informations about prions you rendered available to all interested people is amazing : you deserve admiring congratulations for what you have accomplished !!!

Beyond CWD and hunters, your work deserve the largest interest.

I shall be watching to see how many views you will get in this Forum.

As I already posted to " sadocf1" elsewhere, I feel the thread you introduced here should also appear in the QDM and Whitetails Hunting Forums : even if many hunters who appear in these two Forums are concerned by CWD, they seem to be reluctant to come into this one : it is not easy reading ... ( at this point, I have not yet assimilated it all !!!)

Jack.


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## sadocf1

When I asked "how did game farms get infected with CWD'' ??
Terry was not afraid to supply the answer and I thank him.
Click on Links - http://www.organicconsumers.org/madcow.htm
for Terry Singletary- lots more good stuff !! Am deeply grateful, Terry's reply certainly is much, much more
than I expected or deserved.


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