# Mineral Blocks and Spread of CWD, TB, etc.



## Whit1 (Apr 27, 2001)

Is there any research out there that investigates whether or not the use of mineral blocks to attract deer and their subsequent use by whitetails can enhance, cause, spread CWD, TB, and/or other diseases of whitetails?


----------



## sadocf1 (Mar 10, 2002)

On p. 2 of MUCC thread "calling for end of pen raised deer", etc there is reference to this question.
CWD:Report From Ground Zero - http://www.madison.com/archives/read.php?ref=tct:2002:07:20:25569:FRONT -- AN EXCELLENT DESCRIPTION OF HOW CWD WAS INTRODUCED INTO WISCONSIN'S WILD DEER !!! It has of course been ignored by the officials because it implicates hunters rather than the deer farms. Mineral blocks, salt blocks, mineral mixtures and licks are excellent sources of TB/CWD transmission for deer and cattle. One must remember that these products are articles of commerce, a part of the livestock industry,and are protected by PRODUCT DISCRIMINATION LEGISLATION !!!!!


----------



## terry (Sep 13, 2002)

FEEDING AND BAITING OF WILDLIFE

It is accepted scientific knowledge that the artificial concentration of any species of

wildlife increases the risk of disease transmission. With CWD, the majority of experts

agree that some transmission is via body fluids such as saliva, feces and, possibly urine.

The concentration of cervids around artificially developed feeding and baiting sites

greatly increases the potential for the ingestion of contaminated food. Even in the

endemic area, CWD could spread faster through artificial concentrations of deer and/or

7

elk. Wildlife disease experts believe that artificial baiting and feeding is responsible for

bovine tuberculosis sustaining itself in Michigans deer herds. Additionally, brucellosis in

Wyoming and Montana elk herds in the Greater Yellowstone Area (GYA) have acted as a

reservoir for reinfection of domestic livestock in the area. Elk in the GYA have been

artificially fed for decades and this practice is continuing, further exacerbating the

problem. Artificial feeding is an unnatural activity, due to the repeated replacement of

food in the same location and it results in much more direct contact among deer and

contact with potentially contaminated feed and ground. The concern with unnatural

concentrations extends to the use of mineral blocks, salt blocks, protein blocks and other

similar blocks or supplements. Since baiting and feeding is one risk factor that can be

controlled, prudent management calls for a prohibition on this practice where disease

risks are of a significant concern. Food sources from normal agricultural practices such

as grain waste fields and other activities do not pose the same risk factor due to the fact

that they are not usually concentrated in a small area and are not replaced after

consumption by wildlife. ...snip





http://www.ngpc.state.ne.us/wildlife/guides/cwd/management.pdf





What about the theory that mineral deficiency or toxicity causes CWD?
Several hypotheses about the cause of CWD have received attention recently, including the theory that high body levels of manganese (Mn), in conjunction with low levels of copper (Cu), can cause the onset of CWD. Although it may be possible such environmental factors play a role in CWD development, there are no data that support the notion that changes in Mn/Cu levels cause CWD. Very little scientific evidence has been provided to support this theory. No well-designed lab studies have been carried out to test this hypothesis.

Another hypothesis is that CWD positive deer are actually suffering from cadmium (Cd) toxicity. Cd is a naturally occurring element that is found in trace quantities in the environment. Cd has no known biological function.

There is no question that deer in southwest/southeastern Wisconsin have the ability to accumulate cadmium  all animals do. And, Cd is a toxic element that can cause serious health problems. Cd concentrations have been documented in a wide variety of cervids in North America, including whitetailed deer, elk and moose. In none of these studies did Cd concentrations reach toxic levels in the liver. In fact, a review of scientific literature failed to produce a single occurrence of Cd poisoning in mammals anywhere in the world.

In Wisconsin, liver and kidney tissue from a few CWD positive game farm deer have been analyzed for Cd, along with other metals. Cd was detected in three samples and levels were far below the toxic threshold.

The distribution of CWD in Wisconsin, and across North America, would also seem to refute the notion that a mineral deficiency or toxicity is responsible for these disease outbreaks. Soil, plant and animal tissue data do not support that there is something unique about the Cu/Mn or Cd levels in these areas as compared to the rest of Wisconsin or the rest of North America.



http://www.dnr.state.wi.us/org/land/wildlife/whealth/issues/cwd/askdnr2_04.htm



EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Scientific Steering Committee
OPINION ON
ORGANOPHOSPHATE (OP) POISONING AND
HYPOTHETICAL INVOLVEMENT IN THE ORIGIN OF BSE
Background
In its opinion on possible links between BSE and Organophosphates adopted on 25-26 June
1998 and in its opinion on Hypotheses on the origin and transmission of BSE adopted on 29-
30 November 2001 the SSC concluded that there is no scientific evidence in support of the
hypothesis of an OP origin of BSE.
The issue of organophosphate poisoning has not been dealt with by the SSC so far. The
concerns expressed in the enquiries cover mainly intoxication by occupational exposure of
shepherds and farmers to OPs upon use against ecto-parasites, especially in sheep dipping and
treatment of cattle against Warble Fly infestation. Risks from residues are addressed to a
lesser extend.
In early 2003, a large number of additional enquiries on the issue have been addressed to
European Commissions Health and Consumer Directorate General. Four of these with
substantial enclosures were by one person. Most of them are addressing both issues: chronic
organophosphate (OP) poisoning and the origin of BSE.
Information provided with the enquiries
In addition to numerous newspaper and magazine articles the enclosures to the enquiries
provide the Material Safety Data Sheet on diazinon, the OHSA Occupational Safety and
Health Guideline for Tetraethylpyrophosphate (TEPP), an US agency Hazardous Substances
Fact Sheet on crufomate, company safety information sheets, some correspondence with UK
authorities including their activities to improve safe use of these chemicals. The information
regarding claimed OP chronic poisoning of cases presented does not provide evidence, neither
for OPs being the cause for diseases nor for their exclusion (i.e., very low bloodcholinesterase
levels, provided without data or comparison with the normal distribution of
values; successful treatment of a patient for OP clearance without giving any OP data). It
C:\WINNT\Temporary Internet Files\SSC_Last_OP_Final.doc 2
seems however, that due to insufficient, non-prudent use of the safety requirements undue
exposures of shepherds and farmers have occurred.
There is no additional information on the claimed involvement of OPs in the origin of BSE.
This applies for both, the hypotheses on the direct effect of OPs as well as on their
hypothetical role for Cu-deficiency to be involved in the origin of BSE (Cu binding of prion
protein is known). New publications are mentioned in one enquiry but they have not yet been
provided. In an Internet search no recent scientifically valid publications were traceable. The
SSC had been informed that research would be launched on this hypothesis, but no
information has been provided so far on its status or on results.
Conclusions
a) As regards the involvement of organophosphates in the origin of BSE, no new scientific
information providing evidence or supporting the hypothesis by valid data became
available after the adoption of the last opinion of the SSC on this issue. Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for registration of
plant protection products and veterinary medicines  addressed in the enquiries  provide
the basis for safe use of registered compounds and their formulations. Regarding the
alleged intoxication cases reported and OP exposure it must be concluded that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R., Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar, H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and transmission of BSE. Adopted
on 29-30 November 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf



Studies on the Putative Interactions between the Organophosphorus Insecticide Phosmet and Recombinant Mouse PrP and its Implication in the BSE Epidemic
I. Shaw1, C. Berry2, E. Lane1, P. Fitzmaurice1, D. Clarke3 and A. Holden1

(1) Centre for Toxicology, University of Central Lancashire, Preston, UK 
(2) Department of Morbid Anatomy, The Royal London Hospital, London, UK 
(3) CLRC Daresbury Laboratory, Warrington, UK 


Abstract It has been suggested that exposure of cattle to the ectoparasiticide Phosmet in the 1980s caused a conformational change in the cellular prion protein (PrPC) to form the BSE prion (PrPSC), which initiated the epidemic of bovine spongiform encephalopathy (BSE). 
Recombinant mouse cellular prion (r[mouse]PrPC) was exposed to the organophosphorus pesticide Phosmet in vitro and the conformation of the prion before and after exposure was monitored using circular dichroism (CD) spectroscopy, utilizing synchrotron radiation at the Council for the Central Laboratory of the Research Councils (CLRC) facilities at Daresbury, UK. Metabolites of Phosmet, generated in situ by rat microsomes, were investigated in the same way, to determine whether they might initiate the conformational change due to their high chemical reactivity.
Our studies showed that exposure of r[mouse]PrPC to Phosmet or microsomes-generated metabolites of Phosmet did not result in the conformational change in the protein from -helix to -pleated sheet that is characteristic of the PrPC to PrPSC conversion and, therefore, Phosmet is very unlikely to have initiated the BSE epidemic by a simple direct mechanism of conformational change in the prion protein.
bovine spongiform encephalopathy - circular dichroism spectroscopy - insecticide - organophosphate - Phosmet - prion - protein conformation



http://www.springerlink.com/(bmbpjj...al,31,74;linkingpublicationresults,1:103009,1



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


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

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

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

PMID: 6997404

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



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." 
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 


continued.....


----------



## terry (Sep 13, 2002)

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 



Establishing the transmission of BSE to mink

44. Transmissible mink encephalopathy ("TME") is a rare disease of ranch
reared mink, first recognised in the USA. It had been assumed to be
scrapie in mink and, like BSE, outbreaks have epidemiological
features consistent with a foodborne infection, but it has never been
possible to demonstrate that scrapie infected sheep brain tissue is
pathogenic to mink by oral exposure. In an incident of TME in
Stetsonville, Wisconsin, USA in 1985 Dr Richard Marsh observed that
although the rancher fed 'dead stock', mainly in the form of cattle
carcasses, sheep tissues had never been fed. Studies in the USA of
this incident showed not only that cattle inoculated intracerebrally
with the mink brain developed a fatal spongiform encephalopathy, but
also that the cattle passaged agent remained pathogenic for
mink by either intracerebral inoculation or feeding. In the absence of
reports of a clinical disease homologous to BSE in domestic cattle,
these findings prompted the suggestion that a rare or occult
form of such a disease might exist in the USA. Comparison of the
biological properties of the BSE
12
pathogen with those of the Stetsonville isolate was therefore of
considerable interest in relation to hypotheses concerning possible
origins of BSE and potential for subclinical infection in cattle.
45. Proposals to carry out studies with mink in the USA were developed
in collaboration with, the United States Department of Agriculture
("USDA") Agricultural Research Service ("ARS") and the
Department of Veterinary Science, University of Wisconsin, Madison,
Wisconsin, USA. On 30th October, 1990 I attended a CVL/NPU BSE R&D
meeting at the NPU in Edinburgh (YB90/10.30/1.1). I reported that brain
material from BSE affected cows and a control cow (not fed meat and
bonemeal) had been sent coded to Mr Mark Robinson (USDA) for
transmission studies in mink. The studies were conducted from February
1991 under the control and principal funding of USDA-ARS. The results,
discussed at the tenth CVL/NPU BSE R&D meeting on 27th April, 1993
(YB93/4.27/1.1) indicated that mink were indeed susceptible to BSE and,
in contrast to previous attempts to transmit scrapie to the species,
were susceptible by the oral route of inoculation. The collaboration
resulted in the publication of a paper: Robinson, M.M. et al (1994)
Experimental infection of mink with bovine spongiform encephalopathy.
Journal of General Virology 75, 2151-2155 (J/JVIR /75/2151).

snip...


http://www.bseinquiry.gov.uk/files/ws/s065a.pdf

BSE TO MINK CONFIRMED

http://www.bseinquiry.gov.uk/files/yb/1993/04/27001001.pdf


1: Proc Natl Acad Sci U S A 2001 Mar 27;98(7):4142-7

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

Lasmezas CI, Fournier JG, Nouvel V, Boe H, Marce D, Lamoury F, Kopp N,
Hauw JJ, Ironside J, Bruce M, Dormont D, Deslys JP.

Commissariat a l'Energie Atomique, Service de Neurovirologie, Direction
des Sciences du Vivant/Departement de Recherche Medicale, Centre de
Recherches du Service de Sante des Armees 60-68, Fontenay-aux-Roses,
France. [email protected]

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.





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



continued...


----------



## terry (Sep 13, 2002)

CORRECT LINK TO ''BSE TO MINK CONFIRMED''

http://www.bseinquiry.gov.uk/files/yb/1993/04/27001001.pdf


Research

Environmental Sources of Prion Transmission in Mule Deer
Michael W. Miller,* Elizabeth S. Williams, N. Thompson Hobbs, and Lisa L. Wolfe*
*Colorado Division of Wildlife, Fort Collins, Colorado, USA; University of Wyoming, Laramie, Wyoming, USA; and Colorado State University, Fort Collins, Colorado, USA

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


--------------------------------------------------------------------------------

Whether transmission of the chronic wasting disease (CWD) prion among cervids requires direct interaction with infected animals has been unclear. We report that CWD can be transmitted to susceptible animals indirectly, from environments contaminated by excreta or decomposed carcasses. Under experimental conditions, mule deer (Odocoileus hemionus) became infected in two of three paddocks containing naturally infected deer, in two of three paddocks where infected deer carcasses had decomposed in situ &#8776;1.8 years earlier, and in one of three paddocks where infected deer had last resided 2.2 years earlier. Indirect transmission and environmental persistence of infectious prions will complicate efforts to control CWD and perhaps other animal prion diseases.



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







Perspective

Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams, Michael W. Miller, Pierluigi Gambetti,§ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; University of Wyoming, Laramie, Wyoming, USA; Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA

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


--------------------------------------------------------------------------------

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



snip...





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

Acknowledgments. ...snip...end

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





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



Science 14 October 2005:Vol. 310. no. 5746, pp. 324 - 326DOI: 10.1126/science.1118829 

Reports 

Coincident Scrapie Infection and Nephritis Lead to Urinary Prion Excretion 

Harald Seeger,1* Mathias Heikenwalder,1* Nicolas Zeller,1 Jan Kranich,1 Petra Schwarz,1 Ariana Gaspert,2 Burkhardt Seifert,3 Gino Miele,1 Adriano Aguzzi1 


Prion infectivity is typically restricted to the central nervous and lymphatic systems of infected hosts, but chronic inflammation can expand the distribution of prions. We tested whether chronic inflammatory kidney disorders would trigger excretion of prion infectivity into urine. Urinary proteins from scrapie-infected mice with lymphocytic nephritis induced scrapie upon inoculation into noninfected indicator mice. Prionuria was found in presymptomatic scrapie-infected and in sick mice, whereas neither prionuria nor urinary PrPSc was detectable in prion-infected wild-type or PrPC-overexpressing mice, or in nephritic mice inoculated with noninfectious brain. Thus, urine may provide a vector for horizontal prion transmission, and inflammation of excretory organs may influence prion spread. 

snip... 

How do prions enter the urine? Upon extrarenalreplication, blood-borne prions may beexcreted by a defective filtration apparatus.Alternatively, prions may be produced locallyand excreted during leukocyturia. Althoughprionemia occurs in many paradigms ofperipheral prion pathogenesis (15, 16), thelatter hypothesis appears more likely, becauseprionuria was invariably associated with localprion replication within kidneys.Urine from one CJD patient was reported toelicit prion disease in mice (17, 18), but not inprimates (19). Perhaps unrecognized nephriticconditions may underlie these discrepantobservations. Inflammation-associated prionuriamay also contribute to horizontal transmissionamong sheep, deer, and elk, whose high efficiencyof lateral transmission is not understood.References and Notes...snip...end 


1 Institute of Neuropathology, University Hospital of Zürich, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland.2 Institute of Clinical Pathology, University Hospital of Zürich, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland.3 Institute of Biostatistics, University of Zürich, Sumatrastrasse 30, CH-8006 Zürich, Switzerland. * These authors contributed equally to this work. To whom correspondence should be addressed. E-mail: [email protected] 

http://www.sciencemag.org/cgi/content/abstract/310/5746/324 



kind regards,
terry


----------



## TnRidge (Aug 29, 2004)

Man that had to be the longest cut and paste post I have ever skipped over .


----------



## sadocf1 (Mar 10, 2002)

Food; "what is eaten to supply the necessary nutritive elements"
salt blocks, mineral blocks, protein blocks,all come under this description of "food" "Feeding" deer is banned in Michigan; therefor it is illegal to place these products where deer can consume them besides being a major means of disease transmission. Animals that have acesss to all the necessary nutritive elements are the animals that are healthest and less likely to be diseased, conversely animals deficient in the necessary nutritive elements are more subject to disease. Farm fields are limed and fertilized,that is why 80% of our deer are in agricultural areas. Farm crops have the nutritional elements not found in the wild.
It was only a few years ago one of our local hunters was issued a citation for hunting deer near a salt block.


----------



## Ninja (Feb 20, 2005)

sadocf1 said:


> Food; "what is eaten to supply the necessary nutritive elements"
> salt blocks, mineral blocks, protein blocks,all come under this description of "food" "Feeding" deer is banned in Michigan; therefor it is illegal to place these products where deer can consume them besides being a major means of disease transmission.
> It was only a few years ago one of our local hunters was issued a citation for hunting deer near a salt block.


Salt/Mineral blocks are legal for baiting.....what was the ticket for???


----------



## sadocf1 (Mar 10, 2002)

It has been illegal to hunt deer over a salt block for as long as I can remember (started deer hunting in 1936) It was considered unsporting.
The Hunting Guide states that "the bait must be scattered over a minimum of a 10 foot x 10 foot area." (same for recreational viewing)


----------



## Ninja (Feb 20, 2005)

sadocf1 said:


> It has been illegal to hunt deer over a salt block for as long as I can remember (started deer hunting in 1936) It was considered unsporting.
> The Hunting Guide states that "the bait must be scattered over a minimum of a 10 foot x 10 foot area." (same for recreational viewing)


It is LEGAL and does not have to be broken up.

See this thread.....includes links to the DNR site.

http://www.michigan-sportsman.com/forum/showthread.php?t=109637&highlight=mineral+blocks+baiting


----------



## Jeff Sturgis (Mar 28, 2002)

It was illegal though not that long ago. When DNR officers would complete fly overs looking for pot plants they would see the white salt blocks, which made good spots to check during the hunting season. A friend of mine received a ticket for this, and much to his surprise, even though he had owned the property for over a year...received another ticket for hunting on Sunday in Tuscola county. When those 2 tickets added to the one he received for looking at deer in his headlights while his bow was packed in his case with his gear under the cap of the pick-up he had to fight to get his license back and it cost him quite a bit of money.

Anyways, it wasn't too long ago that hunting over a salt block was illegal.


----------

