Saturday, March 10, 2012

CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow protein feed CUSTOM MADE for deer and elk

CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow protein feed CUSTOM MADE for deer and elk

Greetings QDMA et al,

some old history about game farms and cwd below, and then, what about game farms and mad cow protein feed for those big bucks $

what about tainted land and soil content ?

urine, feces ?

lichens ?

for those interested, a review of sorts. ...tss

Nebraska Dept of Agriculture and Game and Parks

On April 9, 1998, chronic wasting disease (CWD) was diagnosed in a captive elk in Nebraska.� This discovery follows the confirmation of CWD in two captive elk herds in South Dakota earlier this year.� The Nebraska elk was a 4 1/2-year old male that was among a privately owned herd of approximately 150 elk.� The health of the animal had deteriorated for about 2 months before it died.� Confirmation of CWD was made by the USDA's National Veterinary Services Laboratories in Ames, Iowa. The case history revealed that the affected elk was born on a farm on the Western Slope of the Rocky Mountains in Colorado, but it was on two additional Colorado farms before it arrived in Nebraska at 2 to 2 1/2 years of age.� One of the Colorado premises was in the known CWD-endemic region along the Eastern Slope of the Rocky Mountains in northcentral Colorado.

The Nebraska State Veterinarian's Office has quarantined the affected herd, and a hold order was placed on two additional herds in Nebraska that received animals from the affected herd.� It also has been determined that elk farmers in four states (IA, IL, TX, WI) have received elk from the infected herd, and these states were notified by the Nebraska Bureau of Animal Industry.� Additional tracing may be forthcoming because elk from the affected herd were sold through two auctions in Colorado and Missouri.� A CWD Working Group is being formed to develop Voluntary CWD Management Guidelines.� The first goals of the Nebraska Bureau of Animal Industry are:� (1) to implement a policy requiring disease reporting of animals over 16 months of age; (2) to require identification of individual animals and reporting change of ownership; and (3) to establish a data base to monitor change of ownership.

South Dakota has taken legislative action to create a CWD control program for captive cervids.� Their program calls for a 5-year quarantine with monitoring of all affected, adjacent, or exposed captive cervid herds.� Monitored herds that maintain clean status are given certificates at annual milestones for years 1 through 4 and are designated "Certified CWD Cervid Herd" after 5 years of negative surveillance.� The Cervid CWD Surveillance Identification Program includes required examination of brain tissue from all dead cervids 18 months or older, including deaths by slaughter, hunting, illness, and injury.� The South Dakota State Veterinarian has forwarded the description of his State's program to the United States Animal Health Association along with the suggestion that it should be considered as a "starting place" for developing a Model CWD Control Program.� Persons interested in this document can obtain a copy from Dr. Sam Holland, South Dakota State Veterinarian, SD Animal Industry Board, 411 South Fort Street, Pierre, South Dakota 57501-4503.�

Bad news on game farm elk Dr. Holland, South Dakota State Veterinarian 20 Dec 98 news release

Some initial SD data released by Dr. Holland, SD State Veterinarian was verified with two of his colleagues.

There are 39 game farm elk in South Dakota with confirmed chronic wasting disease in 1998, out of 179 tested (22%).

There are 4 or 5 herds involved - all are from game farm animals, none are from the fall hunt. The total number of elk studied is not yet available for wild elk. Two white-tail deer are also affected, also captive animals.

Elk disease prompts protective quarantine of Philipsburg, Hardin game farms Tue, 23 Jun 1998 (AP)

HELENA- A debilitating disease that showed up in an elk transported from a Montana game farm to Oklahoma has prompted a protective quarantine at two game farms, State Veterinarian Arnold Gertonson said Monday. One is the Kesler Game Farm near Philipsburg, where the elk was sold, and the other is near Hardin where other Kesler elk have been shipped, Gertonson said.

The infected elk was shipped two years ago, and Gertonson said it is unknown if the fatal disease was present in the elk then. "The disease has a long incubation of unknown duration," Gertonson said of chronic wasting disease. It causes deer and elk to waste away and die.

"We are taking the actions necessary at this time to protect the game farms and wild herds," Gertonson said. Gertonson said the only way to diagnose the disease is through an autopsy. He has not yet decided if any of the game farm animals in Philipsburg or Hardin will be killed for testing.

"We want to work with the game farmers as far as the economic effect, but will do what we need to protect the animals," Gertonson said. The first case in a game farm elk was identified in last December in South Dakota. Cases in wild deer were first found in Colorado in 1981 and it has since spread to southeast Wyoming.

The disease is always fatal to the animal, according to Karen Zackheim of the Department of Fish, Wildlife and Parks, but is not believed to pose a threat to humans. [This is an inaccurate and irresponsible statement, very similar to those made by MAFF in early days of BSE -- webmaster] .

A study of elk in Yellowstone County area was performed two years ago and the disease was not found, Zackheim said. [No such study has been published; the number of animals tested is unknown. It may be necessary to re-examine elk brains using newer antibody techniques. -- webmaster]

She said that area was studied because it is along a natural migration route to the infected southeastern Wyoming herd. "I really feel we do not have it in the wild in Montana," Zackheim said.

The Department of Livestock has notified other states where animals from the Kesler farm were shipped. Gertonson said the department learned of the situation late last week but is working as quickly as possible to determine if the disease is present in Montana.

Where all has CWD been found?

18 Mar 98 webmaster One of the oddest aspects of all the scientific papers on CWD is the tremendous reluctance to give the names, dates, locations, and operators of affected state fish and game and university facilities. This makes it very difficult to map where and when the disease has been seen to occur and whether there are independent foci of infection beyond Ft. Colliins/Wheatland. It is hard to believe that expert facilities do not maintain a permanent tracking record for the health and disposition of each and every individual animal. Given the failure of the two eradication schemes, this secrecy makes tracking and confinement of the disease all that much harder, which is in no one's best interest.

White blood cells, marrow, and peripheral neurons are known to be infectious (but low titre compared to CNS) in scrapie, BSE, TME, and CJD; no data is available on CWD titre by tissue type. Low titre means the disease would start amplifying but spongiform changes might be slow relative to normal life span, ie it dies of something else before becoming clinical. Animals can be highly infectious a year or more before displaying symptoms.

The following statement, while on the cautious side, is certainly consistent with current medical understanding of spongiform encephalopathies and the precautionary principle:

Val Geist, former head of the University of Calgary's environmental science department, said even the antlers are capable of carrying the disease because they contain neurological tissue including blood vessels and nerve endings. "If it (TSE) is somewhere in the tissue, I certainly wouldn't ingest any of the tissue."

There are now at least 5 known captive research facilities and at least 3 zoos and 5 game farms involved in CWD, all traceable if you want to shipments of animals out of Ft. Collins. These are:

1. Sybille Wildlife Research and Education Center, Visitor Center and Wildlife Viewing Sites - on Hwy. 34, about 28 miles SW from I25 exit south of Wheatland State of Wyoming - Game and Fish Department - Sybille Visitor Center 2362 Highway 34 Wheatland State WY 82201 Phone 307-322-2784 from 4

2. Kremmling. Colorado State University - Cooperative Extension - Grand County PO. Box 475 Kremmling State CO 80459 Phone 303-724-3436 from 1

3. Meeker. Colorado State University - Cooperative Extension - Rio Blanco County 779 Sulphur Creek Road, Box 270 City Meeker CO 81641 Phone 303-878-4093 from 1

4. Main Ft. Collins facility. State of Colorado - Division of Wildlife - Wildlife Research Center State of Colorado - Division of Wildlife - Wildlife Research Center 317 West Prospect City Fort Collins CO 80526 Phone 970-484-2836

5. Wild Animal Disease Center, CSU, Ft. Collins exchanging cervids with 4

6. Denver zoo receiving mule deer from 4

7. Toronto zoo receiving mule deer from 4

8. Wyoming zoo receiving mule deer from 1

9. South Dakota game farm receiving calf elk from 1 or 4 [?]

10. Regina, Saskatchewan game farm receiving South Dakota elk, 27 April, 1996 confirmation. from 9

11. 12 cases of CWD reported now from S. Dakota, at least 2 different herds, seemingly 3-4 game farms, from 1 and 4.

South Dakota program for cwd in captive elk works well United States Animal Health Association (703) 451-3954 For immediate release:Contact - Larry Mark

MINNEAPOLIS, Minn., Oct. 7, 1998 -- A model program for the containment and eradication of chronic wasting disease (CWD) in captive elk herds was developed and carried out in South Dakota last year in response to the diagnosis of this disease in December 1997 in a captive elk herd in South Dakota. Dr. Sam Holland, South Dakota State Veterinarian, reviewed for the USAHA committee on captive wildlife and alternative livestock a program that was put together in a short period of time and was highly successful. Dr. Holland noted that the occurrence of CWD was treated as an animal health emergency and that great pains were taken to involve all people with a stake in the issue in developing a way to deal with the disease. The group consensus was that a mandatory control program needed to be enacted with official tests and movement criteria.

To date in South Dakota, there have been three elk herds with confirmed CWD and five others that were exposed to the affected herds. The latter have been quarantined for from one to five years. The source elk herd had 30 free-ranging white-tailed deer on the property but not in the same pasture. These 30 deer were harvested and one was found positive for CWD. A surveillance program of free-ranging wildlife has been developed that includes examination of deer and elk killed by hunters....

I expected TSE to appear on commercial elk ranches after it had appeard in a Canadian zoo. When the Saskatchewan case was reported, it was claimed to be an anomaly by the Agriculture Canada PR spokesmen.

Sorry to read that there are now, a year or so later, more TSE cases on game ranches. I am aware that TSE cases in free-living elk and deer in Colorado do coincide with range lands on which scrapie was recorded.

What is fed to captive deer and elk at these game farms?

what Canadian laws and regulations apply amd are there compliance visits?

how many of these game farms/animals are there?

what rules apply to trans-shipment (especially back and forth across borders)?

what sort of records are kept on individual animals?

is there a necropsy program on 'downer' animals? l Dr. Ted Leighton responds: Most of your questions are more appropriate for me to answer than for Dr. Clarke. Health Canada has a broadening program in zoonotic disease surveillance but much of it is currently under development and re-definition. Most of your questions are about CWD in wildlife and in game farmed animals.

Trace-back to origin for the one CWD-positive elk detected in Canada was not possible beyond the last farm of origin prior to importation. This is becaise of a lack of an animal identification and movement registration program for game farmed elk in the USA at the time. There has not been a case of CWD in mule deer on Canadian game farms. The case was at the Toronto zoo. It is thought that the disease originated from the Colorado-Wyoming focus through importation from a captive herd subsequently found to have the disease.

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.



Wednesday, October 12, 2011

White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation

It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that 17 white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that 1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and 2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.
This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.

Author: Justin GreenleeJodi SmithRobert Kunkle Credits/Source: Veterinary Research 2011, 42:107


Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie

Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK

Key words: scrapie, evironmental persistence, sPMCA

Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.

now, I can’t say who has bought up all the mad cow protein feed, but a heck of a lot of it has been fed out, post partial, voluntary, mad cow feed ban.

could part of the CWD be caused by feeding banned mad cow protein (cows, deer, elk, sheep, goats, dogs, cats, and sometimes the circus elephant) was/is in feed for animals, for human and animal consumption.

is it the deer farmers and ranchers using the mad cow protein for those big bucks, or is it the hunters $ only ones I ever heard of using it was the farmers and ranchers. but some hunters might be using cattle feed in feed plots. which brings up another nasty topic, i.e. baiting and feeding, food plots vs apple orchids, or piles of beets, corn, etc., natural vs man made, etc. I guess that’s for another topic, but a factor of CWD control, because I don’t think we can eradicate it now. mad cow is out of the barn, like the mad deer and elk. sad, sad, sad $


IF any of you deer farmers in OHIO still using banned mad cow feed for your farm raised deer ??? if you are, I urge you to stop. ...tss

PRODUCT Product is __custom made deer feed__ packaged in 100 lb. poly bags.

The product has no labeling. Recall # V-003-5. CODE The product has no lot code.

All custom made feed purchased between June 24, 2004 and September 8, 2004. RECALLING FIRM/MANUFACTURER Farmers Elevator Co, Houston, OH, by telephone and letter dated September 27, 2004. Firm initiated recall is ongoing. REASON Feed may contain protein derived from mammalian tissues which is prohibited in ruminant feed.





Subject: ''MORE'' 'VIOLATORS' of Animal Proteins Prohibited in Ruminant Feed--U.S.A. (more and more MAD COW FEED RULES BROKEN IN U.S.A.]

Date: Tue, 24 Apr 2001 09:45:15 –0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: References: 1 , 2

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

Greetings again List Members,

''MORE'' violations and warning letters over FDA MAD COW feed ban regulations that have not been complied with since the Aug. 4, 1997 'partial' feed ban was implemented...

they implemented something, then forgot to enforce it $$$$$

another fine example letter. this one will floor you. 'Jimmy crack corn, and they don't care' no big deal, just flush those mixers with corn, then feed the corn to the deer. NOooooo problem.

these people must be brain dead???


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...

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


Date: Wed, 20 Oct 2004 14:53:56 –0500

From: "Terry S. Singeltary Sr." flounder@WT.NET

Reply-To: Bovine Spongiform Encephalopathy BSE-L@UNI-KARLSRUHE.DE


##################### 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.



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

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


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.


Date: August 6, 2006 at 6:14 pm PST

PRODUCT Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6 CODE All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.

RECALLING FIRM/MANUFACTURER Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete.

REASON The feed was manufactured from materials that may have been contaminated with mammalian protein.





Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006

Date: August 6, 2006 at 6:16 pm PST

PRODUCT a) CO-OP 32% Sinking Catfish, Recall # V-100-6; Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6; c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6; e)


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


CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6; g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6; h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6; 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".





FDA’s guidance documents, including this guidance, do not establish legally enforceable responsibilities. Instead, guidances describe the Agency’s current thinking on a topic and should be viewed only as recommendations, unless specific regulatory or statutory requirements are cited. The use of the word “should” in Agency guidances means that something is suggested or recommended, but not required.

RECALLS AND FIELD CORRECTIONS: VETMED -- CLASS IIPRODUCT & CODES: Animal feed products, packaged in 5, 25, 50, and 55 pound bags, and in bulk, intended for both ruminant and non-ruminant animals. The products are as follows: Recall # V-195-1 through V-350-1.



V-195-1 40150 B. 30% Calf Pellet V-196-1 40250 B. 16% Calf Pellet V-197-1 40350 B. 16% Calf Ration V-198-1 40450 B. 18% Calf Starter V-199-1 40600 B. 38% Dairy Pellet V-200-1 40650 B. 38% Dairy Pellet V-201-1 40750 B. 16% Dairy Feed V-202-1 40950 B. 40% Beef Pellet V-203-1 41150 B. 18% Lamb Starter Pellet V-204-1 41250 B. 39% Lamb Conc. Pellet V-205-1 41350 B. 14% Lamb & Beef Pellet V-206-1 41450 B. 16% Goat Feed V-207-1 42150 B. 32% Expectation Pellet V-208-1 42250 B. Llama & Alpaca Pellet V-209-1 42350 B. 32% Calf Grower Pellet V-210-1 42650 B. Llama & Alpaca Crums V-211-1 42750 B. 38% Hay Booster 2 V-212-1 42850 B. 25% Pasture Booster V-213-1 43100 B. 16% Grower/Dev Pellet V-214-1 43150 B. 16% Grower/Dev Pellet V-215-1 43700 WH 32% Calf Gro Pellet V-216-1 43750 WH 32% Calf Gro Pellet V-217-1 43850 B. 38% Dairy Mix V-218-1 44250 B.

17% Doe Pellet V-219-1 44350 B. 21% Buck Pellet V-220-1 44450

Legends Ranch Pellet V-221-1 44500

Legends 17% Breeder Pellet V-222-1 1652 B. Vitamin E-20 V-223-1 1614 B. Vitamin A-30 V-224-1 44550

Legends 17% Breeder Pellet V-225-1 44650 Legends 13.5% Rut Pellet V-226-1 44750 Deer Starter

(J) V-227-1 44940 Llama Premix (J) FSC V-228-1 45150 Empire 25% Calf Pellet V-229-1 45450 Berry Llama Pellet V-230-1 45950 50% Beef Conc. (Meal) V-231-1 46250 B. 12% Sweet Livestock V-232-1 46350 B. 1440 Bovatec Pellet V-233-1 46400 Liberty 38% Dairy Pellet V-234-1 46450 Liberty 38% Dairy Pellet V-235-1 47150 B. 14% Gold-n-Grower V-236-1 47250 B. 12% Gold-n-Conditioner V-237-1 47450 B. 18% Gold-n-Lamb V-238-1 47800 Homeworth Dairy Pellet V-239-1 47850 Homeworth Dairy Pellet V-240-1 47900 B. 36% Hi Fat Dairy Pellet V-241-1 47950 B. 36% Hi Fat Dairy Pellet V-242-1 48550 B. 16% Calf Pellet CA V-243-1 49200 Mastead Dairy Base V-244-1 49300 KLEJKA Dairy Base V-245-1 49650

Deer Premix (J) HFB V-246-1 49750 39% Lamb Premix (J) HFB V-247-1 49850 Lamb Starter Premix (J) HFB V-248-1 120850 Brood Cow Deluxe Mineral V-249-1 152850 B. A-D-E Mix


V-250-1 10150 B. Miracle Starter V-251-1 10350 B. 21% Broiler Starter V-252-1 10450 B. Pullet Grower & Developer V-253-1 10550 B. 18% Layer Breeder Pellets V-254-1 10750 B. 20% Gold Std. Laying Crum V-255-1 10950 B. 17% Complete Laying Crums V-256-1 11050 B. 16% Prosperity Layer Crums V-257-1 11100 B. 40% Poultry Concentrate V-258-1 11150 B. 40% Poultry Concentrate V-259-1 11250 B. 28% Turkey Starter Crums V-260-1 11350 20% Gig "4" Pellets V-261-1 11450 B. 16% Prosperity Layer Pellets V-262-1 11550 18% Game Bird Breeder Pellets V-263-1 11650 B. 19% Ratite Grower Diet V-264-1 11750 B. 23% Ratite Breeder Diet V-265-1 12100 B. 40% Poultry Concentrate Crums V-266-1 12550 B. 32% Base Poultry Mix V-267-1 13250 B. 28% Turkey Starter V-268-1 13450 B. 20% Poultry Grower V-269-1 14325 B. Game Bird Mix - Coarse V-270-1 20150 B. 18% Pig Starter Pellets V-271-1 20250 B. 16% Pig Grower Pellets V-272-1 20450 B. 14% Porkmaker 100 Pellets V-273-1 20550 B. 40% Gro 'Em Lean V-274-1 21850 B. 27% Hi-Fat Swine Base V-275-1 23000 Mt. Hope Hevy Hog V-276-1 30050 12% Pleasure Horse - Sweet V-277-1 30150 Alfa + Performer 10 Sweet V-278-1 30250 14% Grass + Perf Sweet V-279-1 30450 12% Wrangler - Complete V-280-1 30550 B. 12% Pleasure Horse Pellets V-281-1 30650 B. 32% Gro' N Win Pellets V-282-1 30750 12% Wrangler Cubes V-283-1 30950 18% Foal Starter V-284-1 31050 B. 14% Alfa + Dev Pellets V-285-1 31150 B. Alfa + Performer 10 Pel V-286-1 31200 Grass +Performer 14 Pel V-287-1 31250 Grass +Performer 14 Pel V-288-1 31350 12% Mustang V-289-1 31450 Endurance - 101 Extruded V-290-1 31550 B. Equine Energy - UK V-291-1 31650 B. 16% Grass + Dev Pellets V-292-1 31750 16% Grass + Dev Cubes V-293-1 31850 16% Grass + Dev Sweet V-294-1 31950 B. 11% Alfa Gro 'N Win Pel V-295-1 32050 B. Sho' Win Pellets V-296-1 32250 B. Senior Formula V-297-1 32350 Oscar Horse Mix V-298-1 32450 B. Ultimate Finish V-299-1 32550 Crossfire Horse Feed V-300-1 32650 B. Equine 16% Growth V-301-1 32750 B. Reduced Energy Formula V-302-1 32850 B. Training Formula V-303-1 32950 B. Cadence Formula V-304-1 33150 B. Track 12 Horse Feed V-305-1 33350 Spears 16% GR + Dev Cubes V-306-1 33400 B. 14% Supreme Horse Pellets V-307-1 33450 B. 14% Supreme Horse Pellets V-308-1 33650 B. Race'N Win V-309-1 33750 B. 14% Prominent Horse Feed V-310-1 33850 B. Unbeetable Horse Feed V-311-1 34750 Cargill Senior Horse V-312-1 34850 Cargill Vitality Gold V-313-1 35150 Chagrin 12% Sweet Fd V-314-1 35250 Smith Pure Pleasure V-315-1 35750 Roundup 10% Horse Pellets V-316-1 35850 12% Summerglo Horse V-317-1 36255 B. Grass +Min&VitBase - Mexico V-318-1 36850 Miller's 12% Horse Feed V-319-1 37155 B. Gro'Win Base Mix - Mexico V-320-1 38000 B. 32% Premium Mixer Pellets V-321-1 38050 B. 32% Premium Mixer Pellets V-322-1 38100 36% Maintenance Mixer Pellets V-323-1 38150 36% Maintenance Mixer Pellets V-324-1 50150 Terramycin Crumbles V-325-1 60105 16% Rabbit Pellets V-326-1 60125 16% Rabbit Pellets V-327-1 60150 B. 16% Rabbit Pellets V-328-1 60205 18% Rabbit Developer V-329-1 60250 B. 18% Rabbit Developer V-330-1 60450 B. 16% Rabbit Maintenance V-331-1 90150 B. Buckeye Scratch V-332-1 90225 Gold Standard Scratch V-333-1 90250 Gold Standard Scratch V-334-1 90350 Intermediate Scratch V-335-1 90450 B. Chick Grains V-336-1 90525 B. Shelled Corn V-337-1 90550 B. Shelled Corn V-338-1 90650 B. Cracked Corn V-339-1 90825 B. Fine Cracked Corn V-340-1 90850 B. Fine Cracked Corn V-341-1 91000 Steam Flaked Corn V-342-1 91050 Steam Flaked Corn V-343-1 91750 Oats - HP Crimped V-344-1 91850 B. HP Sweet Crimped Oats V-345-1 95550 Land O' Lakes Shelled Corn V-346-1 95650 Land O' Cracked Corn V-347-1 95850 Land O' Lakes Chick Crack V-348-1 100850 B. Alfalfa Pellets V-349-1 101850 Cooked Full Fat Soybean V-350-1 122200 Magnatone M-4-B Pels Bulk MANUFACTURER: Buckeye Feed Mills, Dalton, Ohio. RECALLED BY: Manufacturer visited local customers on April 17, 2001. On April 18 and 19, 2001, manufacturer mailed and faxed recall notices. Firm initiated recall is ongoing.


QUANTITY: 2,790 tons of ruminant feed products and 14,000 tons of non-ruminant feed products. REASON: The animal feed products may contain protein derived from mammalian tissues.

PRODUCT Custom deer feed made for a Wisconsin farm.

The product was in bags holding about 40 pounds each. Recall # V-122-4. CODE 1-30-04 on the product invoice and mixing record.

RECALLING FIRM/MANUFACTURER Crivitz Feed Mill, Crivitz, WI, by telephone on February 20, 2004. Wisconsin State initiated recall is complete.

REASON The recalled deer feed contained steamed bone meal which is prohibited material in feed for ruminants.





Ruminant animals are any animals with a four-chambered stomach including cattle, sheep, goats, buffalo, elk, and deer.

-------- 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:

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...


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.



snip...see full text ;


Experimental oral transmission of chronic wasting disease to red deer (Cervus elaphus elaphus): Early detection and late stage distribution of protease-resistant prion protein

Aru Balachandran, Noel P. Harrington, James Algire, Andrei Soutyrine, Terry R. Spraker, Martin Jeffrey, Lorenzo González, Katherine I. O’Rourke

Abstract — Chronic wasting disease (CWD), an important emerging prion disease of cervids, is readily transmitted by intracerebral or oral inoculation from deer-to-deer and elk-to-elk, suggesting the latter is a natural route of exposure. Studies of host range susceptibility to oral infection, particularly of those species found in habitats where CWD currently exists are imperative. This report describes the experimental transmission of CWD to red deer following oral inoculation with infectious CWD material of elk origin. At 18 to 20 months post-inoculation, mild to moderate neurological signs and weight loss were observed and animals were euthanized and tested using 3 conventional immunological assays. The data indicate that red deer are susceptible to oral challenge and that tissues currently used for CWD diagnosis show strong abnormal prion (PrPCWD) accumulation. Widespread peripheral PrPCWD deposition involves lymphoreticular tissues, endocrine tissues, and cardiac muscle and suggests a potential source of prion infectivity, a means of horizontal transmission and carrier state.


There is a strong correlation between the presence of PrPTSE and infectivity in prion diseases. Although the epidemiologic evidence strongly suggests that CWD is not transmissible to humans, this study and others suggest caution in this regard. The finding of PrPCWD in various organs, albeit in clinical CWD, suggests that humans who consume or handle meat from CWD-infected red deer may be at risk of exposure to CWD prions. This study found that red deer tissues other than nervous and lymphoid tissue can support CWD prion replication and accumulation. As a result, the consumption or handling of meat from CWD-infected red deer will put humans at risk of exposure to CWD prions. In spite of a well-documented species barrier, a cautious approach would involve preventing such tissues from entering the animal and human food chains. Future studies will require sensitive and quantitative techniques such as bioassays in transgenic mice that assess tissue infectivity and quantitative immunoassays adapted to PrPCWD detection in peripheral tissues.


The exact mode of transmission of CWD in nature remains unclear but is believed to involve direct animal-to-animal contact or environmental contamination. As TSE agents are extremely resistant in the environment (39), oral exposure is the most plausible pathway by which the CWD prion may be introduced to deer in nature and represents a significant obstacle to eradication of CWD from either farmed or free-ranging cervid populations. The distribution of PrPCWD in gut-associated lymphoid tissues, salivary glands, and nasal mucosa in the red deer of this study suggests potential routes of PrPCWD shedding into the environment via fluids such as saliva or feces. However, this study did not identify the point at which an animal may become infectious during the course of infection. An improved understanding of the mechanisms of shedding and transmission will be important in the future management of CWD. SNIP... In summary, this study demonstrates the potential for oral transmission of CWD to red deer and describes the pattern of PrPCWD accumulation for this species. The current surveillance testing regime for cervids would be expected to identify CWD-infected red deer should it occur in North America. These results confirm the usefulness of rapid tests such as ELISA but with generally slightly lower sensitivity when compared with IHC when testing tissues with patchy or sporadic PrPCWD deposition. The finding of PrPCWD in several extraneural tissues including cardiac muscle and the endocrine system suggests that further investigation and monitoring of the potential transmissibility to other species including humans is warranted.


(Traduit par Isabelle Vallières)

Can Vet J 2010;51:169–178

Ottawa Laboratory — Fallowfield, Canadian Food Inspection Agency, Ottawa, Ontario (Balachandran, Harrington, Algire, Soutyrine); Veterinary Diagnostic Laboratory, Colorado State University, Fort Collins, Colorado, USA (Spraker); Veterinary Laboratory Agency, Department for the Environment, Food & Rural Affairs, Lasswade, Midlothian, Scotland, United Kingdom (Jeffrey, González); Animal Disease Research Unit, Agricultural Research Service, United States Department of Agriculture, Pullman, Washington, USA (O’Rourke).

Address all correspondence to Dr. Aru Balachandran; e-mail:

Wednesday, September 08, 2010




Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5 The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region

Research Project: Transmissible Spongiform Encephalopathies: the Role of Genetics, Strain Variation, and Environmental Contamination in Disease Control

Location: Animal Diseases Research

Title: Experimental oral transmission of chronic wasting disease to red deer (Cervus elaphus elaphus): Early detection and late stage distribution of protease-resistant prion

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula

Published online January 27, 2005

As of January 1, 2004, FDA has issued 63 Warning Letters and has one court ordered Permanent Injunction since the BSE feed rule went into effect. Also, 47 firms recalled 280 products during the same time period; 12 of the recalls were in 2003.


Date: March 21, 2007 at 2:27 pm PST




Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007


Cattle feed delivered between 01/12/2007 and 01/26/2007


Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.


Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.


42,090 lbs.







The firm does not utilize a code - only shipping documentation with commodity and weights identified.


Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.


Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.


9,997,976 lbs.


ID and NV


see much more tonnage of recalled prohibited banned suspect BSE contaminated feed here ;

Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU


Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>

Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)

Sunday, February 5, 2012

February 2012 Update on Feed Enforcement Activities to Limit the Spread of BSE

The CDC just released a paper on the concern of these game farms and CWD, and also CWD to humans risk factor update.

I kindly urge you to look at the map ;

which came first, the cart or the horse ;


Captive CWD discovered 1967

Free ranging CWD discovered 1981



*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***

Saturday, February 18, 2012

Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease

CDC Volume 18, Number 3—March 2012


Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).


*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***

Saturday, February 18, 2012

Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease

CDC Volume 18, Number 3—March 2012

see much more here ;

Thursday, February 09, 2012


Saturday, February 04, 2012

Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

Tuesday, December 20, 2011


> > > The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years.

However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil.

Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. < < <


Thursday, February 09, 2012

Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

Monday, February 13, 2012

Stop White-tailed Deer Farming from Destroying Tennessee’s Priceless Wild Deer Herd oppose HB3164

Tuesday, February 14, 2012

Oppose Indiana House Bill 1265 game farming cervids

Wednesday, February 15, 2012

West Virginia Deer Farming Bill backed by deer farmers advances, why ? BE WARNED CWD

Wednesday, July 06, 2011

Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation

Oral.29: Susceptibility of Domestic Cats to CWD Infection

Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason† Colorado State University; Fort Collins, CO USA†Presenting author; Email:

Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature. Prion

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

Thursday, January 26, 2012

The Risk of Prion Zoonoses

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

Thursday, January 26, 2012

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659

Thursday, February 17, 2011

Environmental Sources of Scrapie Prions

Thursday, June 09, 2011

Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission

Chemosphere. 2012 Jan 20. [Epub ahead of print]

Soil-mediated prion transmission: Is local soil-type a key determinant of prion disease incidence?

Saunders SE, Bartz JC, Bartelt-Hunt SL.


Department of Civil Engineering, University of Nebraska-Lincoln, Peter Kiewit Institute, Omaha, NE 68182, USA.


Prion diseases, including chronic wasting disease (CWD) and scrapie, can be transmitted via indirect environmental routes. Animals habitually ingest soil, and results from laboratory experiments demonstrate prions can bind to a wide range of soils and soil minerals, retain the ability to replicate, and remain infectious, indicating soil could serve as a reservoir for natural prion transmission and a potential prion exposure route for humans. Preliminary epidemiological modeling suggests soil texture may influence the incidence of prion disease. These results are supported by experimental work demonstrating variance in prion interactions with soil, including variance in prion soil adsorption and soil-bound prion replication with respect to soil type. Thus, local soil type may be a key determinant of prion incidence. Further experimental and epidemiological work is required to fully elucidate the dynamics of soil-mediated prion transmission, an effort that should lead to effective disease management and mitigation strategies.

Copyright © 2012 Elsevier Ltd. All rights reserved.

see much more on soil here ;

Survival and Limited Spread of TSE Infectivity after Burial

Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK

Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried. The authors gratefully acknowledge funding from DEFRA.


Degradation of Pathogenic Prion Protein and Prion Infectivity by Lichens

Christopher J. Johnson,1 James P. Bennett,1 Steven M. Biro,1,2 Cynthia M. Rodriguez,1,2 Richard A. Bessen3 and Tonie E. Rocke1 1USGS National Wildlife Health Center; 2Department of Bacteriology; University of Wisconsin, Madison; 3Department of Veterinary Molecular Biology; Montana State University; Bozeman, MT USA

Key words: prion, lichen, bioassay, protease, degradation

Few biological systems have been identified that degrade the transmissible spongiform encephalopathy (TSE)-associated form of the prion protein (PrPTSE) and TSE infectivity. Stability of the TSE agent allows scrapie and chronic wasting disease agents to persist in the environment and cause disease for years. Naturally-occurring or engineered processes that reduce infectivity in the environment could aid in limiting environmental TSE transmission. We have previously identified that species of at least three lichens, unusual, symbiotic organisms formed from a fungus and photosynthetic partner, contain a serine protease capable of degrading PrPTSE under gentle conditions. We tested the hypothesis that lichen extracts from these three species reduce TSE infectivity by treating infected brain homogenate with extracts and examining infectivity in mice. We found lichen extracts diminished TSE infectious titer by factors of 100 to 1,000 and that reductions in infectivity were not well-correlated with the extent of PrPTSE degradation observed by immunoblotting. For example, treatment of brain homogenate with Cladonia rangiferina extract caused <100-fold reduction in PrP immunoreactivity but ~1,000-fold decrease in infectivity, suggesting that some PrPTSE remaining after extract treatment was rendered uninfectious or that the lichen protease favors more infectious forms of PrPTSE. Our data also indicate that lichen species closely related to those with prion-degrading protease activity do not necessarily degrade PrPTSE. Characterization of the lichen species-specificity of PrPTSE degradation within the genera Cladonia and Usnea and comparison with known lichen phylogeny has yielded clusters of species on which to focus searches for anti-prion agents.

PPo8-14: Enzymatic Digestion of Chronic Wasting Disease Prions Bound to Soil

Samuel E. Saunders,1 Jason C. Bartz,2 Kurt C. Vercauteren3 and Shannon L. Bartelt-Hunt1 1Department of Civil Engineering; University of Nebraska-Lincoln; Peter Kiewit Institute; Omaha, Nebraska USA; 2Department of Medical Microbiology and Immunology; Creighton University; Omaha, Nebraska USA; 3USDA; Animal and Plant Health Inspection Service; Wildlife Services; National Wildlife Research Center; Fort Collins, CO USA

Chronic wasting disease (CWD) and sheep scrapie can be transmitted via indirect environmental routes, and it is known that soil can serve as a reservoir of prion infectivity. Given the strong interaction between the prion protein (PrP) and soil, we hypothesized that binding to soil enhances prion resistance to enzymatic digestion, thereby facilitating prion longevity in the environment and providing protection from host degradation. We characterized the performance of a commercially available subtilisin enzyme, the Prionzyme, to degrade soil-bound and unbound CWD and HY TME PrP as a function of pH, temperature, and treatment time. The subtilisin enzyme effectively degraded PrP adsorbed to a wide range of soils and soil minerals below the limits of detection. Signal loss occurred rapidly at high pH (12.5) and within 7 d under conditions representative of the natural environment (pH 7.4, 22°C). Serial PMCA of treated soil samples suggests a greater than 6-log decrease in infectious titer compared with controls. We observed no apparent difference in enzyme effectiveness between bound and unbound CWD PrP. Our results show that although adsorbed prions do retain relative resistance to enzymatic digestion compared with other brain homogenate proteins, they can be effectively degraded when bound to soil. Our results also suggest a topical application of a subtilisin enzyme solution may be an effective decontamination method to limit disease transmission via environmental ‘hot spots’ of prion infectivity.


Detection of PrPCWD in Rocky Mountain Elk Feces Using Protein Misfolding Cyclic Amplification

Bruce E Pulford,1 Terry Spraker,1 Jenny Powers,2 Margaret Wild2 and Mark D. Zabel1 1Department of Microbiology; Immunology and Pathology; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; 2Biological Resource Management Division; United States National Park Service; CO, USA

Key words: CWD, feces, PMCA, elk

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy affecting cervids, including mule and white-tailed deer (Odocoileus hemionus and virginianus), elk (Cervus elaphus nelsoni) and moose (Alces alces shirasi). The method of CWD transmission between hosts is unclear, though there is evidence that feces excreted by infected animals may play a role. Recently, CWD prions was detected in feces using bioassays in cervidized mice, which took many months to produce results. In this study, we use a more rapid procedure, protein misfolding cyclic amplification (PMCA), to test elk feces for the presence of PK-resistant cervid PrP (PrPCWD). Feces were collected from symptomatic and asymptomatic elk in several northern Colorado locations, homogenized, mixed with normal brain homogenate from Tg5037 mice (expressing cervid PrP) and subjected to up to 9 rounds of PMCA (1 round = 40 secs sonication/30 mins at 70% maximum power, 24 hours). Western blots were used to detect PrPCWD using BAR-224 anti-PrP antibody. Rectal and CNS tissue from the elk were IHC-labeled and examined for the presence of PrPCWD. Fecal samples from symptomatic and asymptomatic elk that tested positive by IHC showed characteristic PrPCWD bands on western blots following PMCA. In addition, PMCA detected PrPCWD in 25% of fecal samples from IHC-negative animals. These data suggest that PMCA may (1) prove useful as a non-invasive method to supplement or even replace IHC testing of cervids for CWD, and (2) identify additional asymptomatic carriers of CWD, the prevalence of which may be underestimated using IHC.


Detection of CWD Prions in Salivary and Urinary Tissues of Deer: Potential Mechanisms of Pathogenesis and Prion Shedding

Nicholas J. Haley,1 Candace K. Mathiason,1 Glenn C. Telling2 and Edward A. Hoover1 1Department of Microbiology, Immunology and Pathology; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; Fort Collins, Colorado USA; 2Department of Molecular Biology and Genetics; University of Kentucky; Lexington, Kentucky USA

Key words: chronic wasting disease, transmission, PMCA, pathogenesis, excretion, urine, saliva, salivary gland, urinary bladder, kidney, blood

Saliva and urine are thought to play an important role in the transmission and pathogenesis of chronic wasting disease (CWD) in captive and free-ranging cervids. We have previously identified PrPCWD in a variety of excreta using serial PMCA (sPMCA) and bioassay; however the source of infectious prions in urine and saliva has yet to be identified. In the present study, we applied sPMCA to tissues associated with saliva and urine production and excretion in an effort to seek proximal sources of prion shedding. Oropharyngeal and urogenital tissues, along with blood and obex from CWD-exposed cervids (comprising over 300 individual samples) were analyzed blindly in duplicate and scored based on apparent CWD burden. PrPCWD was detected by three rounds of sPMCA in tissues associated with saliva and urine production and excretion, notably salivary gland and urinary bladder; whereas blood samples from the same animals and concurrent negative controls (n = 116 of 117) remained negative. Route of inoculation and CNS burden appeared to play an important role in terminal prion distribution, in that IV-inoculated animals and those with increasing CNS levels of PrPCWD had higher and more widely distributed accumulation in excretory tissues. PMCA identification of PrPCWD in oropharyngeal and urogenital tissues—in the absence of detection by conventional methods—may indicate the presence of protease- sensitive infectious prions in excretory tissues not revealed by assays employing PK digestion or other means to remove PrPC reactivity. Thus, evaluation of peripheral tissues via sPMCA may allow additional insights into prion transmission, trafficking and pathogenesis.


Identification of Renal Origin for CWD Urinary Prion Excretion in Deer

Davis M. Seelig,1 Nicholas J. Haley,1 Jan P. Langeveld and Edward A. Hoover1 1Colorado State University; Department of Microbiology, Immunology and Pathology; Fort Collins, CO USA; 2Central Institute for Animal Disease Control (CIDC-Lelystad); Lelystad, The Netherlands

Chronic wasting disease (CWD) is an efficiently transmitted prion disease of cervids. Although bioassays have confirmed the presence of infectious prions in urine and other body fluids of infected deer, origin and mechanisms of prion transfer to and shedding in excreta remains unknown. To address these questions, we have developed enhanced immunohistochemistry (IHC) methods employing tyramide signal amplification (TSA) on formalin-fixed, paraffin-embedded (FFPE) tissues of n = 20 CWD-infected white-tailed deer. Using these methods we have demonstrated PrPCWD present granular to clumped aggregates both within the cytoplasm of renal tubule cells and in the interstitium. Cytoplasmic PrPCWD aggregates were detected most commonly in proximal convoluted tubule epithelial cells. PrPCWD was not identified in the lower urinary tract (ureters or bladder) of any CWD-infected animal. In summary, we present evidence for PrPCWD accumulation within the renal tubule cells, which may identify a proximate tissue source and explain the manner by which infectious prions are excreted in the urine of infected deer, thereby leading to the high degree of direct and indirect horizontal transmission of chronic wasting disease.

Friday, February 25, 2011

Soil clay content underlies prion infection odds Soil clay content underlies prion infection odds

kind regards, terry

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