Sunday, January 27, 2013

Indiana 6 deer missing from farm pose health risk to state herds

1/22/2013 11:11:00 AM

6 deer missing from farm pose health risk to state herds

Aubrey Woods, Tribune

Indiana Department of Natural Resourcescontinues to search for six ear-tagged deer in Jackson County and neighboring Bartholomew, Jennings and Scott counties. Those deer are among the 20 that escaped from a captive cervid facility — or deer farm — in 2012, a spokesman with the state Department of Natural Resources said Friday.

“Of the six, one is a buck, which had a yellow ear tag with the No. 47,” Phil Bloom said.

Bloom said the buck is the only one of the six missing deer imported from a site in Pennsylvania where deer have tested positive for chronic wasting disease.

“He has been exposed to it, but that doesn’t mean he has chronic wasting disease,” Bloom said. “There is no live test for chronic wasting disease. That can’t be determined until the deer is dead and tissue has been tested.”

Bloom said the other five deer that remain free are classified as exposed to chronic wasting disease through their association with the buck.

Of particular interest are any deer with a yellow ear tag bearing the prefix “IN 764” followed by another four numbers or any deer with a yellow ear tag and two numbers on it.

Natural Resources staff will assist in taking the deer carcass to Purdue University for testing at the Indiana Animal Disease Diagnostic Laboratory.

Of the remaining 20 that escaped from the deer farm, the owner recaptured 11 shortly after the escape.

The location and ownership of the deer farm have not been released, based on guidelines of the Indiana Board of Animal Health, but the owner is cooperating, Bloom said.

The escape occurred after a tree fell on a fence at the deer farm, Bloom said.

Of the remaining nine deer that escaped, one was struck and killed by a vehicle, a second was shot and killed by a bow hunter during archery season and a third was killed during a special deer hunting session the first weekend of January, Bloom said.

The owner of the farm continues to help search for the remaining six and has been cooperative with the state, Bloom said.

State officials believe the buck is still alive because people have reported seeing it, Bloom said.

“Although it is conceivable it may have been killed,” he said.

Hunters also may have killed some of the five missing deer and just not reported their deaths to the state as required, Bloom said.

Bloom said there are no special hunting seasons planned to find the remaining deer.

“We’re making an all-out effort to find the deer,” Bloom said.

Local hunter Chuck Brenner of Freetown said the state is being too complacent about an issue that could have long-range effects on the deer population, however.

“I’m not just a hunter,” Brenner said. “I’m a conservationist. We need to manage our herds.”

Brenner said chronic wasting disease could wipe out herds and cost the state millions of dollars down the road.

“We should hunt them down and find them whether it’s deer season or not,” Brenner said.

He said there hasn’t been much publicity about the missing deer and that local hunters could help with the search.

“They need to ask the local hunters for help,” Brenner said. “They could put out trail cameras. If nothing else, the state could put a bounty on them.”

Brenner said the deer are clearly marked and there could be a special hunt just for the six deer that are ear-tagged.

Bloom said the state wants to make sure that the deer are tracked down, tested and determined if they’ve been exposed to chronic wasting disease.

“It could have some far-reaching ramifications,” he said.

So far the disease has never been found in Indiana, which has been testing for the disease since 2002. More than 10,000 deer killed during hunts or by vehicles have been tested and the disease has not been detected, Bloom said.

The tags on those missing deer are expected to tell officials whether the animals have any possible connection with a captive facility in Pennsylvania where chronic wasting disease was confirmed this winter, Bloom said. That report made Pennsylvania the 23rd state in which it has been found.

Cervid or wild game farms in Indiana can raise deer, elk and moose for several reasons, Bloom said. The animals can be processed at a slaughterhouse and sold as meat, sold for pets or sold to high-fenced hunting reserves.

Copyright © 2013 The Tribune

Editor, John C. DePrez Jr.; Executive Editor, Carol Rogers; Publishers: IBRC and IAR

Long kills controversial fenced hunting bill

February 1, 2012 | Filed under: Issues,Top stories | Posted by: Lesley Weidenbener

By Lesley Weidenbener

The Statehouse File

INDIANAPOLIS – An effort to legalize fenced deer hunting is dead for this session.

Senate President Pro Tem David Long, R-Fort Wayne, said he will use a procedural move to kill House Bill 1265 and won’t allow it to be considered in the Senate in the 2012 session. “I think it is a terrible bill,” Long said. “It’s something that first of all it’s not real hunting. It fences in these animals.”

Fenced deer preserves allow hunters to pay money – sometimes thousands of dollars – to shoot deer that are sometimes bred to have larger antlers. Proponents say the preserves are large enough to give the deer plenty of opportunity to escape but critics say they violate the fair chase doctrine that dictates ethical hunting.

In 2006, the Department of Natural Resources passed rules – signed by Gov. Mitch Daniels – that made the preserves illegal. But a lawsuit essentially stopped the enforcement. The suit is still pending and four preserves are operating. HB 1265 – approved 56-40 by the House this week – would have legalized the preserves and created a licensing process for new businesses.

The bill’s author, Rep. Matt Ubelhor, R-Linton, said the preserves and the farms that provide them with deer already have a $50 million annual economic impact on the state. Ubelhor says that could increase if more preserves are permitted to operate.

But Long said Wednesday he prefers to maintain the status quo.

“The bill as it currently exists would open it wide open,” Long said. “I thought we had an understanding (in the General Assembly) that we weren’t going down that path again.”

Lesley Weidenbener is managing editor of, a news website powered by Franklin College journalism students.

Move to expand Ind. fenced deer hunting shelved

1:38 PM, Feb. 2, 2012

INDIANAPOLIS (WTW) — An attempt to legalize hunting deer and elk that are kept inside high fences has been shelved by the state Senate's leader.

The House voted 56-40 this week to approve a bill allowing the fenced hunting, but Senate President Pro Tem David Long said he thought it was a "terrible idea" and will use a procedural move to kill the proposal for this year's legislative session.

The bill would have legalized four existing shooting preserves that are now operating under an injunction issued in a lawsuit against state Department of Natural Resources rules adopted in 2006 to ban captive hunting. The bill also would have allowed more similar preserves to operate.

Long, R-Fort Wayne, said Wednesday that he believed legislators reached a tacit agreement several years ago not to intercede.

"It's not real hunting," he said. "It fences in these animals. Almost every real hunter that I talk to says it's a terrible idea and they don't support it."

Supporters say legalizing the fenced hunting preserves would be an economic boon and would provide Indiana's 400 deer farms with a place to sell their animals.

Rick Miller, president of the Indiana Deer and Elk Farmers Association, told The Journal Gazette in Fort Wayne ( that deer farmers are now selling their deer out of state, but he expects that chronic wasting disease, which is fatal to deer and elk, will eventually hit Indiana and force an end to such sales. He said Indiana's existing preserves wouldn't be enough to keep the farms in business.

"They're killing us," Miller said of the Senate action. "We are begging lawmakers to help us put it to bed one way or another."

Eleven states have full bans on captive hunting and 15 states have partial prohibitions. States surrounding Indiana do not have a ban, and shooting preserves and deer farming have boomed there.

Bill sponsor Rep. Matt Ubelhor, R-Bloomfield, said Indiana's existing preserves are large — akin to 80 city blocks — and allow deer the opportunity to elude hunters.

"It's certainly fair chase," Ubelhor said.


Tuesday, December 18, 2012

A Growing Threat How deer breeding could put public trust wildlife at risk

Wednesday, November 14, 2012



Sunday, January 06, 2013

USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.”

Sunday, January 06, 2013

USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.”

Friday, August 31, 2012


Tuesday, June 05, 2012

Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012 Legislative Session

Tuesday, December 18, 2012

*** A Growing Threat How deer breeding could put public trust wildlife at risk

Tuesday, February 14, 2012

Oppose Indiana House Bill 1265 game farming cervidsOppose Indiana House Bill 1265 game farming cervids

Friday, December 14, 2012

Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012


Environmental Sources of Prion Transmission in Mule Deer

Michael W. Miller,* Elizabeth S. Williams,† N. Thompson Hobbs,‡ and Lisa L. Wolfe*

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 ≈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.


Research Article

Infectious Prions in Pre-Clinical Deer and Transmission of Chronic Wasting Disease Solely by Environmental Exposure


Key to understanding the epidemiology and pathogenesis of prion diseases, including chronic wasting disease (CWD) of cervids, is determining the mode of transmission from one individual to another. We have previously reported that saliva and blood from CWD-infected deer contain sufficient infectious prions to transmit disease upon passage into naïve deer.

Here we again use bioassays in deer to show that blood and saliva of pre-symptomatic deer contain infectious prions capable of infecting naïve deer and that naïve deer exposed only to environmental fomites from the suites of CWD-infected deer acquired CWD infection after a period of 15 months post initial exposure.

These results help to further explain the basis for the facile transmission of CWD, highlight the complexities associated with CWD transmission among cervids in their natural environment, emphasize the potential utility of blood-based testing to detect pre-clinical CWD infection, and could augur similar transmission dynamics in other prion infections.


In summary, the results reported here reconfirm that blood and saliva are sources of infectious CWD prions, consistent with previous findings [27], and further support a mechanism for efficient CWD transmission in nature. We also show that infectious prions shed into the environment by CWD+ deer are sufficient to transmit the disease to naïve deer in the absence of direct animal-to-animal contact. These observations reinforce the exposure risk associated with body fluids, excreta, and all tissues from CWD+ cervids and suggest that similar dynamics may exist in other prion infections.

March 2012

Indirect Environmental Transmission Environmental transmission of the CWD agent was reported in studies demonstrating that an infected deer carcass left in a pasture for 2 years could transmit the agent to immunologically naive deer (17). Exposure of naive deer to pasture previously inhabited by an infected deer also led to CWD transmission, as did cohabitation of naive and infected deer (17). Naive deer exposed to water, feed buckets, and bedding used by CWD-infected deer contracted the disease (18).

Epidemiologic modeling suggests that indirect environmental routes of CWD transmission also play a major role in transmission (8). Environmental transmission of scrapie is well documented, and scrapie prions may remain infectious after years in the environment (19,20; S.E. Saunders, unpub. data). Nevertheless, environmental transmission of scrapie may be less efficient than transmission by direct contact (19). Conversely, the relative efficiency of CWD transmission by direct contact versus indirect, environmental routes remains unclear, but evidence suggests environmental transmission may be a major mechanism (8). The proportion of transmission by direct versus indirect routes may vary not only between captive and free-ranging cervid populations, but also among cervid species and free-ranging habitats and ecosystems. Transmission dynamics may also vary over time as CWD prevalence and ecosystem residence times continue to increase (8).


Salivary prions in sheep and deer

Gültekin Tamgüney,1,2,† Jürgen A. Richt,3,8 Amir N. Hamir,3,9 Justin J. Greenlee,3 Michael W. Miller,4 Lisa L. Wolfe,4 Tracey M. Sirochman,4 Alan J. Young,5 David V. Glidden,6 Natrina L. Johnson,1 Kurt Giles,1,2 Stephen J. DeArmond1,7 and Stanley B. Prusiner1,2,*

1Institute for Neurodegenerative Diseases; San Francisco, CA USA; 2Department of Neurology; University of California, San Francisco, CA USA; 3National Animal Disease Center; ARS-USDA; Ames, IA USA; 4Colorado Division of Wildlife; Wildlife Research Center; Fort Collins, CO USA; 5Department of Veterinary Science; South Dakota State University; Brookings, SD USA; 6Departments of Epidemiology and Biostatistics; University of California, San Francisco, CA USA; 7Department of Pathology; University of California; San Francisco, CA USA; 8College of Veterinary Medicine; Kansas State University, Manhattan, KS USA; 9MD Anderson Cancer Center; Houston, TX USA †Current address: German Center for Neurodegenerative Diseases; Bonn, Germany

Key words: scrapie, chronic wasting disease, saliva, horizontal transmission, titers

Scrapie of sheep and chronic wasting disease (CWD) of cervids are transmissible prion diseases. Milk and placenta have been identified as sources of scrapie prions but do not explain horizontal transmission. In contrast, CWD prions have been reported in saliva, urine and feces, which are thought to be responsible for horizontal transmission. While the titers of CWD prions have been measured in feces, levels in saliva or urine are unknown. Because sheep produce ~17 L/day of saliva and scrapie prions are present in tongue and salivary glands of infected sheep, we asked if scrapie prions are shed in saliva. We inoculated transgenic (Tg) mice expressing ovine prion protein, Tg(OvPrP) mice, with saliva from seven Cheviot sheep with scrapie. Six of seven samples transmitted prions to Tg(OvPrP) mice with titers of -0.5 to 1.7 log ID50 U/ml. Similarly, inoculation of saliva samples from two mule deer with CWD transmitted prions to Tg(ElkPrP) mice with titers of -1.1 to -0.4 log ID50 U/ml. Assuming similar shedding kinetics for salivary prions as those for fecal prions of deer, we estimated the secreted salivary prion dose over a 10-mo period to be as high as 8.4 log ID50 units for sheep and 7.0 log ID50 units for deer. These estimates are similar to 7.9 log ID50 units of fecal CWD prions for deer. Because saliva is mostly swallowed, salivary prions may reinfect tissues of the gastrointestinal tract and contribute to fecal prion shedding. Salivary prions shed into the environment provide an additional mechanism for horizontal prion transmission.

Conclusions. This study documents the first aerosol transmission of CWD in deer. These results further infer that aerosolized prions facilitate CWD transmission with greater efficiency than does oral exposure to a larger prion dose. Thus exposure via the respiratory mucosa may be significant in the facile spread of CWD in deer and perhaps in prion transmission overall.


Transepithelial transport of prions across nasal cavity mucosa begins within minutes of inhalation and can continue for up to 3 h. While M cells appear to transport prions across the follicular associated epithelium, larger amounts of prions are transported between the cells of the respiratory and olfactory epithelia, where they immediately enter the lymphatic vessels in the lamina propria. Thus, inhaled prions can be spread via lymph draining the nasal cavity and have access to somatic and autonomic nerves in the lamina propria of the nasal cavity. The increased efficiency of the nasal cavity route of infection compared with the oral route may be due to the rapid and prolonged transport of prions between cells of the respiratory and olfactory epithelia.

Now that these experiments are completed we conclude that TSE infectivity is likely to survive burial for long periods of time with minimal loss of infectivity and restricted movement from the site of burial. These experiments emphasize that the environment is a viable reservoir for retaining large quantities of TSE infectivity, and reinforce the importance of risk assessment when disposing of this type of infectious material.

Friday, October 26, 2012


Friday, December 14, 2012

*** DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

Monday, November 26, 2012

Rapid Transepithelial Transport of Prions following Inhalation

Thursday, May 31, 2012

CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more


From: Glenn Lange []

Sent: Friday, May 23, 2003 4:17 PM

Subject: Docket 03D-0186; Draft Guidance for Industry (#158): Use of Material From Deer and Elk in Animal Feed

To Whom It May Concern:

May 23, 2003

As Chief of Wildlife for the Division of Fish & Wildlife of the Indiana Department of Natural Resources, I would like to comment on the FDA Docket No. 03D-0186; Draft Guidance for Industry (#158): Use of Material From Deer and Elk in Animal Feed.

During 2002 the Indiana Department of Natural Resources, Division of Fish & Wildlife and the Indiana Board of Animal Health jointly collected approximately 3,300 White-tailed deer heads in Indiana for Chronic Wasting Disease surveillance. Approximately 1/2 of these samples were collected at deer processing plants while the bulk of the remaining samples were collected at mandatory deer checking stations. The FDA guidelines for 2002, which are very similar to the proposed guidance for 2003, prevented some processors and some deer hunters from giving us access to deer heads due to concerns about a renderer product recall if a tested head was found to be positive. The past and future guidances do not recommend a recall if the same CWD infected deer is rendered without being tested. Thus the guidance for 2003 (which would trigger a recall of rendered product if a tested animal is found to be CWD positive, section III.) does not prevent an infected deer in Indiana from going into the animal food stream, it merely interferes with our ability to collect samples to detect CWD early in an outbreak.

To further explain, our actual experience in 2002 showed that my personnel that were engaged in CWD sampling of deer at meat lockers were sometimes turned away by the plant owner, because the meat processors knew that their renderer would not accept any animal from them if some of their animals were being tested. My personnel then had to collect heads at a location where fewer heads were available than would have been the case at the initial processor. The net result was that my personnel collected fewer heads for analysis than would have been collected without the new regulation. Additionally, last fall we had cases where hunters who donated their deer heads at deer checking stations were subsequently turned away from meat processors for the same reasons. As our sample size in 2003 is reduced due to a reluctance to donate deer heads, we will not detect the disease until it has increased in the population to balance the effect of the reduction in sample size. Thus, under the guidance proposed for 2003, we will be less likely to detect the disease at an early stage than would be the case if more heads were available for testing. The reduction in our ability to detect the disease will actually increase the probability that more infected deer are rendered for a longer period of time than would be the case if we could efficiently collect a large sample of heads for analysis.

I believe that the FDA should not recall feed products that contain deer/elk from NON-ENDEMIC areas in the event that a positive is found through routine surveillance, as the proposed approach only serves to inhibit States' CWD monitoring programs. I urge the FDA to reconsider their position on this issue as stated in section III. of the proposed guidance, and not recall animal feed in the event that routine CWD surveillance on free?ranging deer/elk in non?endemic areas turns up a positive animal that has been rendered.


Glenn Lange Chief, Wildlife Section Division of Fish and Wildlife Indiana Department of Natural Resources 402 West Washington Street Room W273 Indianapolis, IN 46204 PH: 317 / 232-4080 Fax: 317 / 232 -8150

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

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

EMC 2 Indiana Department of Natural Resources Vol #: 1

-------- Original Message --------


Date: Wed, 20 Oct 2004 14:53:56 -0500

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy


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


Product is custom made deer feed packaged in 100 lb. poly bags. The product has no labeling. Recall # V-003-5.


The product has no lot code. All custom made feed purchased between June 24, 2004 and September 8, 2004.


Farmers Elevator Co, Houston, OH, by telephone and letter dated September 27, 2004. Firm initiated recall is ongoing.


Feed may contain protein derived from mammalian tissues which is prohibited in ruminant feed.


Approximately 6 tons.



################# #################

-------- 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."


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 *beep* 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 *beep* 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...


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

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.


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.



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


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


_animal protein_



_animal protein_


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.



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%


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


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


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.



April 9, 2001 WARNING LETTER


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...



Date: Sat, 25 May 2002 18:41:46 –0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy


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.


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

prions in urine?


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snip...see full text ;

-------- 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."

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

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



Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.

NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;

Wednesday, March 18, 2009

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

Saturday, December 15, 2012

Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012

Saturday, August 4, 2012

*** Final Feed Investigation Summary - California BSE Case - July 2012



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