Infectious Prions in the Saliva and Blood of Deer with CWD

[flounder]

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

Subject: Infectious Prions in the Saliva and Blood of Deer with Chronic Wasting Disease
Date: October 5, 2006 at 1:45 pm PST
Infectious Prions in the Saliva

and Blood of Deer with Chronic

Wasting Disease


Candace K. Mathiason,1 Jenny G. Powers,3 Sallie J. Dahmes,4 David A. Osborn,5 Karl V. Miller,5

Robert J. Warren,5 Gary L. Mason,1 Sheila A. Hays,1 Jeanette Hayes-Klug,1 Davis M. Seelig,1

Margaret A. Wild,3 Lisa L. Wolfe,6 Terry R. Spraker,1,2 Michael W. Miller,6 Christina J. Sigurdson,1

Glenn C. Telling,7 Edward A. Hoover1*


A critical concern in the transmission of prion diseases, including chronic wasting disease (CWD)

of cervids, is the potential presence of prions in body fluids. To address this issue directly, we

exposed cohorts of CWD-nai¨ve deer to saliva, blood, or urine and feces from CWD-positive deer.

We found infectious prions capable of transmitting CWD in saliva (by the oral route) and in blood

(by transfusion). The results help to explain the facile transmission of CWD among cervids and

prompt caution concerning contact with body fluids in prion infections.


SNIP...


Deer cohorts 1 (blood), 2 (saliva), and 3

(urine and feces) were electively euthanized at

18 months pi to permit whole-body examination

for PrPCWD. The greatest scrutiny was directed

toward those tissues previously established

to have highest frequency of PrPCWD deposition

in infected deer and generally regarded

as the most sensitive indicators of infection—

medulla oblongata and other brainstem regions,

tonsil, and retropharyngeal lymph node. We

found unequivocal evidence of PrPCWD in brain

and lymphoid tissue of all six tonsil biopsy–

positive deer in cohorts 1 (blood) and 2 (saliva),

whereas all deer in cohorts 3 and 5 were negative

for PrPCWD in all tissues (Table 2 and

Figs. 1 and 2).

The transmission of CWD by a single blood

transfusion from two symptomatic and one

asymptomatic CWDþ donor is important in at

least three contexts: (i) It reinforces that no tissue

from CWD-infected cervids can be considered

free of prion infectivity; (ii) it poses the

possibility of hematogenous spread of CWD,

such as through insects; and (iii) it provides a

basis for seeking in vitro assays sufficiently

sensitive to demonstrate PrPCWD or alternate

prion protein conformers in blood—one of the

grails of prion biology and epidemiology.

The identification of blood-borne prion

transmission has been sought before with mixed

results (9–11). Bovine spongiform encephalopathy

and scrapie have been transmitted to naBve

sheep through the transfer of 500 ml of blood

or buffy coat white blood cells from infected

sheep (12, 13). In addition, limited but compelling

evidence argues for the transmission of variant

Creutzfeldt-Jakob disease (vCJD) through blood

from asymptomatic donors (14–16). Even in

sporadic CJD, PrPres has been found in periph-

eral organs of some patients (17). The present

work helps establish that prion diseases can be

transmitted through blood.

The presence of infectious CWD prions in

saliva may explain the facile transmission of

CWD. Cervid-to-cervid interactions (SOM text),

especially in high density and captive situations,

would be expected to facilitate salivary crosscontact

(11, 18, 19). Salivary dissemination of

prions may not be limited to CWD. Proteaseresistant

prion protein has been demonstrated in

the oral mucosa, taste buds, lingual epithelium,

vomeronasal organ, and olfactory mucosa of

hamsters infected with transmissible mink

encephalopathy (19) and ferrets infected with

CWD (20). Although no instance of CWD

transmission to humans has been detected, the

present results emphasize the prudence of using

impervious gloves during contact with saliva or

blood of cervids that may be CWD-infected.

Environmental contamination by excreta

from infected cervids has traditionally seemed

the most plausible explanation for the dissemination

of CWD (21). However, we could not

detect PrPCWD in cohort 3 deer inoculated repeatedly

with urine and feces from CWDþ deer and examined up to 18 months pi (Table 2).

There are several reasons to view this negative

finding cautiously, including small sample size,

elective preclinical termination, and potential

variation in individual susceptibility that may

be associated with the 96 G/S polymorphism in

the PRNP gene (7, 22). Although no genotype

of white-tailed deer is resistant to CWD infection,

PRNP genotypes S/S or G/S at codon 96

appear to have reduced susceptibility manifest

by longer survival (7). Both deer in cohort 3

(urine and feces) were subsequently shown to

be of the PRNP 96 G/S genotype. Thus, it is

possible, although we think unlikely, that these

deer had a prolonged incubation period (918

months pi) before the amplification of PrPCWD

became detectable in tissues. Recent studies

have shown that PrPres is poorly preserved

after incubation with intestinal or fecal content

(23, 24). Further research using cervid and surrogate

cervid PrP transgenic mice (25) are indicated

to continue to address the presence of

infectious CWD prions in excreta of CWDþ deer and to provide a more substantial basis for

reconsideration of the assumption that excreta

are the chief vehicle for CWDdissemination and

transmission.

The results reported here provide a plausible

basis for the efficient transmission of CWD in

nature. We demonstrate that blood and saliva in

particular are able to transmit CWD to naBve deer

and produce incubation periods consistent with

those observed in naturally acquired infections

(3, 26). The time from exposure to first detection

of PrPCWD by tonsil biopsy was variable—as

short as 3 months but as long as 18 months (likely

underestimates due to sampling frequency).

The results also reinforce a cautious view of the

exposure risk presented by body fluids, excreta,

and all tissues from CWDþ cervids. ...



SNIP...END




http://www.sciencemag.org/






CWD AND ENVIRONMENTAL FACTORS i.e. saliva, fecal shedding and fecal-oral transmission is likely


http://p079.ezboard.com/fwolftracksproductionsfrm2.showMessage?topicID=592.topic





TSS

#################### https://lists.aegee.org/bse-l.html ####################

 

[Cowpuncher]

Do you suppose any of the North American BSE cases arose from CWD deer licking on livestock salt?

 

[PORKER]

Mad deer disease may spread with saliva

By LAURAN NEERGAARD
AP Medical Writer

Thursday October 5, 2006

Source of Article: http://www.wfaa.com/sharedcontent/health/stories/100506ccjccwNatMadDeer.c72946e.html

WASHINGTON, D.C. — Deer probably spread a brain-destroying illness called chronic wasting disease through their saliva, concludes a study that finally pins down a long-suspected culprit. The key was that Colorado researchers tested some special deer.


Chronic wasting disease is in the same family of fatal brain illnesses as mad cow disease and its human equivalent. There is no evidence that people have ever caught chronic wasting disease from infected deer or elk.


But CWD is unusual because, unlike its very hard-to-spread relatives, it seems to spread fairly easily from animal to animal.


Scientists were not sure how, primarily because studying large wild animals is a logistical nightmare. The sheer stress of researchers handling a deer caught in the wild could kill it.


Likewise, animals deliberately exposed to infections must be kept indoors so as not to spread disease, another stress for deer used to roaming.


So Colorado State University researcher Edward Hoover turned to fawns hand-raised indoors in Georgia, which has not experienced chronic wasting disease.


"This allows you to do this safely so the deer aren't freaking out," explained Hoover, who reported the first evidence of saliva's long-suspected role in Friday's edition of the journal Science. "These deer are calm and approachable."


Hoover took saliva from wild Colorado deer found dying of CWD, and squirted it into the mouths of three of the healthy tame deer - about 3 tablespoons worth.


Additional tame deer were exposed to blood, urine and feces from CWD-infected deer.


He housed the newly exposed deer in a specialized lab for up to 18 months, periodically checking tonsil tissue for signs of infection and eventually autopsying their brains.


All of the saliva-exposed deer got sick.


So did deer given a single transfusion of blood from a CWD-infected deer - not a surprise, as blood is known to transmit this disease's cousins. But it does reinforce existing warnings to hunters in states where CWD has been found to take precautions in handling their kills.


The three deer exposed to urine and feces didn't get sick. That doesn't rule out those substances, Hoover cautioned; he simply may not have tested enough animals.


Proving that saliva is able to spread CWD is important, so that scientists next can determine exactly how that happens in the wild, said Richard T. Johnson, a Johns Hopkins University neurology professor who headed a major report on prion science.


"You can move deer out of a pasture, put other deer into the pasture, and they'll come down with the disease. It's not even casual contact, it's contact with the pasture," Johnson said. "It must be something in their secretions."


Is it spread through shared salt licks? Or by drooling onto grass or into streams? Studying environmental contamination by infectious proteins, called prions, that cause CWD is among Hoover's next steps.


"It's very likely they could be shedding a lot of saliva" shortly before death, noted Richard Race, a veterinarian who studies CWD at the National Institutes of Health's Rocky Mountain Laboratories. "Saliva's a good bet."

 

[bse-tester]

Do you guys recall my mentioning that having witnessed wild Elk licking captive Elk through the Game Farm/Ranch fence, we posed the question that the transmission of CWD would be an almost certainty should one of those animals be a prion carrier?? At the time, my hypothesis was challenged by some on this board as being somewhat far-fetched!! Mmmmm, appears to be something to consider now huh?

I have long been a supporter of transmission studies and the one study that needs to be completed is the oral routing of PrPsc within the wild/captive herds of Deer and Elk. If captive herds are keep behind a fence which allows the physical contact (through the fence) from wild populations, then perhaps it is time to either legislate the end of captive animal ranching or to legislate double fencing to prohibit the ability of contact between wild and captive animals.

To all those who felt that oral transmission was a farce and unlikely, it would appear now to be recognized as factual.

 

[Kathy]

The "unconventional transmissible AGENT" (UTA) involved with TSEs has been identified as the rogue metals attached to the normally copper loaded octapeptide repeats.

You wish to ignore this fact, and continue to call these diseases "infectious" rather than a toxin found in the environment.

You also forget that Dr. Vitaly Vodyanoy of Auburn University has written a paper describing the "Novel Metal Clusters" or "proteon nucleating centers PNCs) found in blood. Animals living in contaminated areas, like the thousands of acres surrounding the Rocky Flats Nuclear Weapons Facility south of Fort Collins, near Denver, which is the US' largest CWD zone, are being used in these above experiments. They are loaded with radio-active particles including plutonium.

The USA military has many test ranges which are extensively contaminated now, they can no longer use them. Even the military guys are scared to use these ranges that they have contaminated with depleted uranium - so you know it must be bad.

Researchers in France have discovered that the uranium oxide particles in water, when fed chronically over 3 to 9 months to experimental rats, entered the body via the distal ileum (small intestine) one of the specified risk materials (SRM).

Guess where the uranium preferentially concentrated.... the Peyer's patches. Just as with experimental transmission procedures with BSE.

Toxicology. 2006 Oct 29;227(3):227-239. Epub 2006 Aug 17

Absorption, accumulation and biological effects of depleted uranium in Peyer's patches of rats.

Dublineau I, Grison S, Grandcolas L, Baudelin C, Tessier C, Suhard D, Frelon S, Cossonnet C, Claraz M, Ritt J, Paquet P, Voisin P, Gourmelon P.

IRSN, Direction de la RadioProtection de l'Homme, Service de Radiobiologie et d'Epidemiologie, Laboratoire de Radiotoxicologie experimentale, IRSN, BP 17, F-92262 Fontenay-aux-Roses Cedex, France.

The digestive tract is the entry route for radionuclides following the ingestion of contaminated food and/or water wells. It was recently characterized that the small intestine was the main area of uranium absorption throughout the gastrointestinal tract. This study was designed to determine the role played by the Peyer's patches in the intestinal absorption of uranium, as well as the possible accumulation of this radionuclide in lymphoid follicles and the toxicological or pathological consequences on the Peyer's patch function subsequent to the passage and/or accumulation of uranium. Results of experiments performed in Ussing chambers indicate that the apparent permeability to uranium in the intestine was higher (10-fold) in the mucosa than in Peyer's patches ((6.21+/-1.21 to 0.55+/-0.35)x10(-6)cm/s, respectively), demonstrating that the small intestinal epithelium was the preferential pathway for the transmucosal passage of uranium. A quantitative analysis of uranium by ICP-MS following chronic contamination with depleted uranium during 3 or 9 months showed a preferential accumulation of uranium in Peyer's patches (1355% and 1266%, respectively, at 3 and 9 months) as compared with epithelium (890% and 747%, respectively, at 3 and 9 months). Uranium was also detected in the mesenteric lymph nodes ( approximately 5-fold after contamination with DU). The biological effects of this accumulation of depleted uranium after chronic contamination were investigated in Peyer's patches. There was no induction of the apoptosis pathway after chronic DU contamination in Peyer's patches. The results indicate no change in the cytokine expression (Il-10, TGF-beta, IFN-gamma, TNF-alpha, MCP-1) in Peyer's patches and in mesenteric lymph nodes, and no modification in the uptake of yeast cells by Peyer's patches. In conclusion, this study shows that the Peyer's patches were a site of retention for uranium following the chronic ingestion of this radionuclide, without any biological consequences of such accumulation on Peyer's patch functions.

PMID: 16978755

With regards to BSE, the paper held up as proof that prions are absorbed in the small intestine, distal ileum, was a study by G.A. Wells et al. in which processed diseased brain tissue were inserted into the stomach of lab calves, via a drenching procedure. Prions then were identified in the Peyer's patches, "Detection of disease-specific PrP in the distal ileum of cattle exposed orally to the agent of bovine spongiform encephalopathy."

The evidence is clear that environmental exposure to these radionuclides is showing up in animals, especially those animals that graze and inhale the toxins lying on the ground, especially in sandy areas. Other mammals, including humans will and have suffered the same fate, from inhalation and ingestiong of radionuclides.

 

[flounder]

The "unconventional transmissible AGENT" (UTA) involved with TSEs has been identified as the rogue metals attached to the normally copper loaded octapeptide repeats.

You wish to ignore this fact, and continue to call these diseases "infectious" rather than a toxin found in the environment.

.........

but kathy ignores the obvious :roll:



2006

e) "Big Jim's" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;



every wonder why they are so big......mad cow protein ;

http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 7
Terry S. Singeltary Sr.
Vol #:
1


-------- 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."
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


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



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...tss

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


SNIP...FULL TEXT ;


http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm


TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
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d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;

*********************************

e) "Big Jim's" BBB Deer Ration, Big Buck Blend,
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*********************************

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g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
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i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED,
net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,
Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,
Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and
visit on June 9, 2006. FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL


END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###


http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html

 

[PORKER]

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.

You got that right Terry!!!!!!!!!!

 

[Econ101]

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.

You got that right Terry!!!!!!!!!!

Or just label it for some people who don't believe it is a problem with a discaimer on it for legal damages.

We have a few on this board who seem to want a little of it or have already consumed it and are currently mad.

 

[bse-tester]

Kathy worte:

The "unconventional transmissible AGENT" (UTA) involved with TSEs has been identified as the rogue metals attached to the normally copper loaded octapeptide repeats.

You wish to ignore this fact, and continue to call these diseases "infectious" rather than a toxin found in the environment.

So when an "infected" deer, licks another deers vulva during the rutting season and happens to transfer some PrPsc into the vaginal fluid of the female deer from its own infected saliva, is that not by its very act referred to as an infection caused by directed implantation of PrPsc via saliva thus being able to be described as an infective sharing of contaminated fluids which will bring about the growth of PrPsc within the now infected animal to a point where the numbers of the PrPsc will, by replication, bring about the death of that individual. To this end, can we therefore not classify this transferral of PrPsc as being caused by an animal that was infected and subsequently discretely sharing the infectious paticulate with a non-infected animal which, after the act occurred could be considered to be now "infected" and therefore having received an infection from an animal that was originally infected by whatever means - rogue metals, or by continuous exposure to amorous and affectionate rutting practices commonly found in wild deer?

It would be foolish to consider that rogue metals are to be the sole means by which PrPsc can develop from their normal counterparts into the isoform we call PrPsc so early in this relatively new science, even if it has some important merit. But to constantly throw out the word "infectious" is akin to closing one's eyes on potential that may well prove to be factual rather than whimsical.

The cause or at least one of the causes of the disease may well be found to rogue metals (associatively or directly) - but once the disease is manifested within the animal, do we consider the animal to be simply suffering from a lack of or abundance of a metal contaminant or, in fact, to be classified as a now infectious animal??? I consider it to be not only infected, but also infectious!! And most certainly suffering from what is now an infectious disease!

Define for me, if you will, the true meaning of the word "Infectious?"

 

[rkaiser]

It's always interesting listening to the the little stories that go along with the infectious theory Ron. The amorous deer licking a little pussy. For crying out loud, you could have stopped by saying that passing fluids infects the next animal. But good on you for continuing to try to convince the unconvincible that transmission is the way that TSE's are spread.

I will not argue that misformed prions may be found in saliva, blood and pee, or even sex juices, however the transmission of those misformed proteins is what is in question. Too big for digestion, and definately too big for the blood brain barrier. On the other hand, rouge metals causing the misfolding of prions in saliva, blood, pee, sex juices, and even brain matter does make sense and could very well be the reason for every case of full blown TSE.

I hope that you find a simple test and make it work Ron. It is the way out of this captive North American marketplace plauging the beef producers of our two countries. You will however need people like myself who fight the multinational led govenrments of these two countries almost daily, in their quest to keep our market captive and pad the pockets of those multinationals.

Stick to testing Ron and quit trying to convince those of us who "don't need a label" Econo. I'm more concerned with the metals in my body and yours than any hokey story of catching BSE from eating beef.

 

[flounder]

It's always interesting listening to the the little stories that go along with the infectious theory Ron. The amorous deer licking a little p***y. For crying out loud, you could have stopped by saying that passing fluids infects the next animal. But good on you for continuing to try to convince the unconvincible that transmission is the way that TSE's are spread.

I will not argue that misformed prions may be found in saliva, blood and pee, or even sex juices, however the transmission of those misformed proteins is what is in question. Too big for digestion, and definately too big for the blood brain barrier. On the other hand, rouge metals causing the misfolding of prions in saliva, blood, pee, sex juices, and even brain matter does make sense and could very well be the reason for every case of full blown TSE.

I hope that you find a simple test and make it work Ron. It is the way out of this captive North American marketplace plauging the beef producers of our two countries. You will however need people like myself who fight the multinational led govenrments of these two countries almost daily, in their quest to keep our market captive and pad the pockets of those multinationals.

Stick to testing Ron and quit trying to convince those of us who "don't need a label" Econo. I'm more concerned with the metals in my body and yours than any hokey story of catching BSE from eating beef.

METALS don't cause TSE. TRANSMISSION studies prove this. METALS are just another 'hokey' excuse that some want to use to change the fact that SRMs are a major factor in the transmission and spreading of TSE. Transmission studies speak for themselves, and if you cannot understand them, it does not change the facts proven by them. BUT it does make for good BS. ...TSS

 

[rkaiser]

Terry -

METALS don't cause TSE. TRANSMISSION studies prove this. METALS are just another 'hokey' excuse that some want to use to change the fact that SRMs are a major factor in the transmission and spreading of TSE. Transmission studies speak for themselves, and if you cannot understand them, it does not change the facts proven by them. BUT it does make for good BS. ...TSS

Oh Terry - just keep posting long conveluted articles about the unproven theory of misfolded prion transmission and leave this redneck to his own ideas. Transmission studies speak at length (and I'm sure the length of articles will continue with you on board) of a theory that is accepted by yourself for reasons that I am not sure. If your goal is to rid the world of TSE's Terry admit that misfolded prion transmission is not the cause, at least not the way that you see it.

I'm sorry that you cannot understand the metal contamination problem and the fact that feed, made from animals who have BSE, could transmit metals causing prions to misfold in the unfortunate diner. Thus my beleif in removal of SRM's.

Nice to see you come out with a few of your own words Terry, even though they show your incapability to comprehend anything but the mountains of theory that you read and post.

 

[flounder]

Terry -

METALS don't cause TSE. TRANSMISSION studies prove this. METALS are just another 'hokey' excuse that some want to use to change the fact that SRMs are a major factor in the transmission and spreading of TSE. Transmission studies speak for themselves, and if you cannot understand them, it does not change the facts proven by them. BUT it does make for good BS. ...TSS

Oh Terry - just keep posting long conveluted articles about the unproven theory of misfolded prion transmission and leave this redneck to his own ideas. Transmission studies speak at length (and I'm sure the length of articles will continue with you on board) of a theory that is accepted by yourself for reasons that I am not sure. If your goal is to rid the world of TSE's Terry admit that misfolded prion transmission is not the cause, at least not the way that you see it.

I'm sorry that you cannot understand the metal contamination problem and the fact that feed, made from animals who have BSE, could transmit metals causing prions to misfold in the unfortunate diner. Thus my beleif in removal of SRM's.


Nice to see you come out with a few of your own words Terry, even though they show your incapability to comprehend anything but the mountains of theory that you read and post.

i understand metal contamination and understand that they do not cause TSE. i under transmission studies and they prove transmission of TSE. i understand that metals on their own would not be the cause of the disease but they may play a role in susceptibility. ...tss

 

[rkaiser]

How do you know that metals do not cause TSE's Terry? And why would you want to fight against something that may be the answer to a hell of a whole lot of unanswered questions surrounding TSE's?

 

[bse-tester]

Rkaiser wrote:

I will not argue that misformed prions may be found in saliva, blood and pee, or even sex juices, however the transmission of those misformed proteins is what is in question. Too big for digestion, and definately too big for the blood brain barrier. On the other hand, rouge metals causing the misfolding of prions in saliva, blood, pee, sex juices, and even brain matter does make sense and could very well be the reason for every case of full blown TSE.

Transmission seems to fit only the methods that make sense to you Randy. Too big for digestion - give your head a shake!! Too big for the blood/brain barrier - Mmm, how is the brain fed Randy?? Do not be misled into thinking that copper is the only cause - it may well be one of them and the studies surrounding metal contamination have merit as I stated. As for my little stories, well, I use them to help poor farmers who are shall we say, like you Randy - unwilling to consider the obvious but willing to accept whatever is put into their own field of view providing they control the picture.

I am not arguing against metal contamination but I am sure as heck suggesting TSE transmission through interaction between male and female deer providing they, or one of them is infected. As for trying to convince people like you, I gave up doing that years ago as it was painfully obvious that it would not happen since people who are stuck in an obvious rut will never entertain that which is already proven scientifically regardless of how they receive the information. So, keep reading the little stories Randy, you may learn more than you think you know already.

As for catching BSE Randy - that would only equate if you were Bovine! Are you a bovine Randy or do you simply think like one?? :roll: :roll: :roll:

Lastly, if I offered you some beef steak that was proven to be full of PrPsc, are you stating that you would eat it ?>????

 

[rkaiser]

bse tester -

I am not arguing against metal contamination but I am sure as heck suggesting TSE transmission through interaction between male and female deer providing they, or one of them is infected. As for trying to convince people like you, I gave up doing that years ago as it was painfully obvious that it would not happen since people who are stuck in an obvious rut will never entertain that which is already proven scientifically regardless of how they receive the information. So, keep reading the little stories Randy, you may learn more than you think you know already.

As for catching BSE Randy - that would only equate if you were Bovine! Are you a bovine Randy or do you simply think like one??

Lastly, if I offered you some beef steak that was proven to be full of PrPsc, are you stating that you would eat it ?>????

I only try to think like a cow when I am trying to manipulate them into going the way I want them too. A lot of that going around in the human world ----don't you think. Tell your little stories all you like Ron --- this human will not be manipulated by your beleifs and theories.

Show us the accepted test Ron, and I will push the hell out of it. Show us how all of your education and knowledge can lead us out of this economic mess.

As far as the steak Ron --- I'll tell you what. If you can get your hands on some BSE contaminated beef -- I'll eat it ---- at the risk of contaminating my body with whatever rouge metal caused that beast his demise. But first you have to accept my offering. A few hundred grams of strontium or barium or maybe we should test your system first and see which heavy metal would do the most damage to your personal system. Have you checked yourself out lately? What's your balance like?

Good luck Ron. And continue with the colorful stories. There are lots out there who actually beleive them. I know that you have a better chance of getting your test accepted if you follow the infectious transmission theory, so ---- you go girl.

 

[bse-tester]

Randy wrote:

As far as the steak Ron --- I'll tell you what. If you can get your hands on some BSE contaminated beef -- I'll eat it .

That statement alone tell me volumes about your knowledge of this disease.

Ignorance is bliss.

 

[rkaiser]

Volumes all right.

Convienently left off the last part of my answer, didn't you Mr. volume of knowledge.

 

[Econ101]

The way out of an unknown fear is to know it. BSE tester is trying in that regard.

If you could do a $20 test on a $200 cow and make her worth more than $220, who cares whose theory is correct? If you could take that $20 test on other animals and ship them to Japan and make that $200 cow worth more than the current $200, who cares whose theory is correct?

You are right about one thing, rkaiser, the bseconomics is bad for the cattleman and it needs a solution.

 

[Murgen]

Further to transmission theories.

In what ways do animals expell toxins from their bodies?

Urine, saliva? Does this mean that an animal that expells toxins, is still harboring the toxin?

Would they test positive after expelling the toxins?