Thursday, September 10, 2009

Experimental oral transmission of CWD to red deer (Cervus elaphus elaphus): early detection and late stage distribution of protease-resistant protein

Title: Experimental oral transmission of chronic wasting disease (CWD) to red deer (Cervus elaphus elaphus): early detection and late stage distribution of protease-resistant protein (PrP-res)

Authors

Balachandran, A - CANADIAN FOOD INSPCTN AG Harrington, Noel - CANADIAN FOOD INSPCTN AG Algire, James - CANADIAN FOOD INSPCTN AG Souyrine, Andre - CANADIAN FOOD INSPCTN AG Orourke, Katherine Spraker, Terry - COLORADO ST UNIV

Submitted to: Canadian Journal of Veterinary Research Publication Type: Peer Reviewed Journal Publication Acceptance Date: December 1, 2008 Publication Date: N/A

Interpretive Summary: Farmed cervids may be exposed to the prion disorder chronic wasting disease through contact with free ranging or farmed infected Rocky Mountain elk, white tailed deer, mule deer, or moose. This is the first report of experimental transmission of chronic wasting disease to red deer, an economically important agricultural commodity in parts of North America. Brain tissue from infected Rocky Mountain elk was administered by the oral route of red deer. Deer were examined at 18 months after infection for evidence of abnormal prion protein, the marker for the disease. The abnormal protein was found throughout the brain, spinal cord and lymphoid tissues, with variable distribution in other organ systems. This finding confirms the potential susceptibility of this species to disease under natural conditions and the reliability of the current testing format for identifying the abnormal protein in the tissues routinely collected in surveillance programs. The widespread distribution of the abnormal protein in red deer indicates the potential for shedding of the agent into the environment. Technical Abstract: Chronic wasting disease CWD is the transmissible spongiform encephalopathy or prion disease of wild and farmed cervid ruminants, including Rocky Mountain elk (Cervus elaphus nelsoni), white tailed deer (Odocoileus virginianus), mule deer (Odocoileus hemionus), or moose (Alces alces). Reliable data on the susceptibility of other farmed cervid species, the distribution of the abnormal prion protein marker in brain and lymphoid tissues collected in surveillance programs, and the role of prion genotype are necessary for design of control programs for CWD in farmed cervids. In this study, red deer (Cervus elaphus elaphus) were exposed to the prion agent by oral administration of brain homogenates from infected Rocky Mountain elk. Antemortem testing was performed at 7 months post infection and the deer were euthanized when clinical disease was observed at approximately 18 months after infection. The abnormal prion protein was assayed by immunohistochemistry, enzyme linked immunosorbent assay and western blot. Abnormal prion protein was found in the spinal cord, brainstem, cerebellum, midbrain, thalamus, and cerebrum in all 4 infected red deer. Most of the lymph nodes throughout the body were positive for abnormal prion proteins. Abnromal prion protein was observed in some additional peripheral tissues in some but not all of the deer. In particular, most areas of the gastrointestinal tract were positive for abnormal prions, although the salivary glands were rarely positive. This study demonstrates the potential for oral transmission of chronic wasting disease to red deer and confirms the usefulness of the current testing methods for post mortem diagnosis of the disease in this species.

Project Team

Orourke, Katherine Knowles, Donald - Don White, Stephen Schneider, David Harrington, Robert - Bob

Publications

Publications

Related National Programs

Animal Health (103)

Related Projects

Development of Sensitive in Vitro Techniques for Prion Detection Transgenic Analysis of Chronic Wasting Disease Strains Strain Typing of Chronic Wasting Disease (Cwd) and Scrapie by Intracerebral Inoculation into Transgenic and Inbred Mouse Lines Dissemination of Abnormal Prion Protein in the Neural and Extraneural Tissues of Wild Rocky Mountain Elk



http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=228787




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

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.

snip...

These results indicate that mule deer fawns develop detectable PrP res after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node. He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings support oral exposure as a natural route of CWD infection in deer and support oral inoculation as a reasonable exposure route for experimental studies of CWD.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757



Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-L To: BSE-L

8420-20.5% Antler Developer For Deer and Game in the wild Guaranteed Analysis Ingredients / Products Feeding Directions

snip...

_animal protein_

http://www.surefed.com/deer.htm


BODE'S GAME FEED SUPPLEMENT #400 A RATION FOR DEER NET WEIGHT 50 POUNDS 22.6 KG.

snip...

_animal protein_

http://www.bodefeed.com/prod7.htm


Ingredients

__Animal Protein Products__,

http://www.bodefeed.com/prod6.htm



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Ingredients

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http://www.bodefeed.com/prod8.htm


INGREDIENTS

__Animal Protein Products__,

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http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html



===================================================


DEPARTMENT OF HEALTH & HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND DRUG ADMINISTRATION

April 9, 2001 WARNING LETTER

01-PHI-12 CERTIFIED MAIL RETURN RECEIPT REQUESTED

Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145 PHILADELPHIA DISTRICT

Tel: 215-597-4390

Dear Mr. Raymond:

Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23, 2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).

Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.

In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal. Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.

The above is not intended to be an all-inclusive list of deviations from the regulations. As a manufacturer of materials intended for animal feed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance with the law. We have enclosed a copy of FDA's Small Entity Compliance Guide to assist you with complying with the regulation... blah, blah, blah...


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



above urls dead, go here ;


http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html




Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009


http://madcowfeed.blogspot.com/2009/09/foia-request-on-feed-recall-product.html



Saturday, August 29, 2009


FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009


http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html





nation and world

Deer mystery solved Experts say a fatal brain disease is passed in feces before illness appears. By Sandra Blakeslee The New York Times Posted: 09/10/2009 01:00:00 AM MDT

Researchers are reporting that they have solved a long- standing mystery about the rapid spread of a fatal brain infection in deer, elk and moose in the Midwest and West.

The infectious agent, which leads to chronic wasting disease, is spread in the feces of infected animals long before they become ill, according to a study published online Wednesday by the journal Nature. The agent is retained in the soil, where it, along with plants, is eaten by other animals, which become infected.

The finding explains the extremely high rates of transmission among deer, said the study's lead author, Dr. Stanley B. Prusiner, director of the Institute for Neurodegenerative Diseases at the University of California, San Francisco.

First identified in deer in Colorado in 1967, the disease is found throughout 14 states and two Canadian provinces. It leads to emaciation, staggering and death.

Unlike other animals, Prusiner said, deer give off the infectious agent, a form of protein called a prion, from lymph tissue in their intestinal linings up to a year before they develop the disease. By contrast, cattle that develop the related mad cow disease do not easily shed prions into the environment but accumulate them in their brains and spinal tissues.

There is no evidence to date that humans who hunt, kill and eat deer have developed chronic wasting disease. Nor does the prion that causes it pass naturally to other animal species.

The prion diseases include Creutzfeldt-Jakob, which leads to dementia and death in humans. Each prion disease is caused by a different strain, and all strains behave somewhat differently.

In the case of chronic wasting disease, "it turns out prions exploit the oldest trick in the book used by pathogens and parasites," said Dr. Mike Miller, a veterinarian at the Colorado Division of Wildlife who is an expert on chronic wasting disease. "Fecal-oral transmission is very effective."

snip...end


http://www.denverpost.com/headlines/ci_13302683




> Deer mystery solved

i doubt this problem is solved yet. maybe one part of the puzzle, but these cervids have also been fed high protein feed for years. and the oral route is highly sufficient. and what about cwd passing from mother to baby ??? these questions have not been answered yet, and to claim ''DEER MYSTERY SOLVED'', is by far from the truth, yet, in my opinion. ...




Monday, January 05, 2009

CWD, GAME FARMS, BAITING, AND POLITICS


http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.html




nation and world

Deer mystery solved

Experts say a fatal brain disease is passed in feces before illness appears.

By Sandra BlakesleeThe New York Times


http://www.denverpost.com/headlines/ci_13302683




> Deer mystery solved


i doubt this problem is solved yet. maybe one part of the puzzle, but these cervids have also been fed high protein feed for years. and the oral route is highly sufficient. and what about cwd passing from mother to baby ??? these questions have not been answered yet, and to claim ''DEER MYSTERY SOLVED'', is by far from the truth, yet, in my opinion. ...Title: Experimental oral transmission of chronic wasting disease (CWD) to red deer (Cervus elaphus elaphus): early detection and late stage distribution of protease-resistant protein (PrP-res)


snip... see TSS full comments here ;


http://www.denverpost.com/headlines/ci_13302683




Asymptomatic deer excrete infectious prions in faeces Gültekin Tamgüney1,2, Michael W. Miller3, Lisa L. Wolfe3, Tracey M. Sirochman3, David V. Glidden4, Christina Palmer1, Azucena Lemus5, Stephen J. DeArmond1,5 & Stanley B. Prusiner1,21.Institute for Neurodegenerative Diseases, 2.Department of Neurology, University of California, San Francisco, California, 94143 USA 3.Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, Colorado, 80526 USA 4.Department of Epidemiology and Biostatistics, 5.Department of Pathology, University of California, San Francisco, California, 94143 USA Correspondence to: Stanley B. Prusiner1,2 Correspondence and requests for materials should be addressed to S.B.P. (E-mail: Email: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000130/!x-usc:mailto:stanley@ind.ucsf.edu.)Top of pageAbstractInfectious prion diseases1-scrapie of sheep2 and chronic wasting disease (CWD) of several species in the deer family3, 4-are transmitted naturally within affected host populations. Although several possible sources of contagion have been identified in excretions and secretions from symptomatic animals5, 6, 7, 8, the biological importance of these sources in sustaining epidemics remains unclear. Here we show that asymptomatic CWD-infected mule deer (Odocoileus hemionus) excrete CWD prions in their faeces long before they develop clinical signs of prion disease. Intracerebral inoculation of irradiated deer faeces into transgenic mice overexpressing cervid prion protein (PrP) revealed infectivity in 14 of 15 faecal samples collected from five deer at 7-11 months before the onset of neurological disease. Although prion concentrations in deer faeces were considerably lower than in brain tissue from the same deer collected at the end of the disease, the estimated total infectious dose excreted in faeces by an infected deer over the disease course may approximate the total contained in a brain. Prolonged faecal prion excretion by infected deer provides a plausible natural mechanism that might explain the high incidence and efficient horizontal transmission of CWD within deer herds3, 4, 9, as well as prion transmission among other susceptible cervids.


http://www.nature.com/nature/journal/vaop/ncurrent/full/nature08289.html



Wednesday, June 11, 2008

Transmission and Detection of Prions in Feces

The Journal of Infectious Diseases 2008;198:81-89 © 2008 by the Infectious Diseases Society of America. All rights reserved. 0022-1899/2008/19801-0015$15.00 DOI: 10.1086/588193


http://chronic-wasting-disease.blogspot.com/2008/06/transmission-and-detection-of-prions-in.html



http://chronic-wasting-disease.blogspot.com/2009/09/asymptomatic-deer-excrete-infectious.html





Terry S. Singeltary Sr.

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Wednesday, December 17, 2008

White-tailed Deer in Portage County Tests Positive for CWD

White-tailed Deer in Portage County Tests Positive for CWD

Posted: Dec 17, 2008 06:48 PM CST

MADISON - A second white-tailed deer has tested positive for chronic wasting disease, from a herd of deer that were euthanized in November on a Portage County hunting preserve.

The first CWD-positive deer, a 7½-year-old doe, was discovered during routine testing after it was shot in September. That discovery led to destroying the herd so the rest of the deer could be tested. The second positive deer is a 3½-year-old doe.

Wildlife specialists from the U.S. Department of Agriculture Wildlife Services shot 64 deer at Alligator Creek Whitetails LLC near Junction City, beginning Wednesday, Nov. 12, and finishing Tuesday, Nov. 18. Because the hunting preserve is made up of 119 acres of open, wooded, and tall-grass marsh lands, the shooters returned after snow fell to check for tracks to see whether any deer remained. At that time, they shot two more deer. Those CWD test results are not available yet.

The National Veterinary Services Laboratory in Ames, Iowa, confirmed the positive result after initial screening tests at the Wisconsin Veterinary Diagnostic Laboratory in Madison.

The CWD-positive deer had been born on the property and did not have ties to any other deer farm. The preserve was placed under quarantine immediately when the first positive test result was reported Oct. 9 to the state veterinarian's office. A quarantine means that no live deer could be moved onto or off the premises.

Areas of heavy deer traffic on the preserve will have the top soil removed and replaced to reduce the risk of contamination. Stocking deer or elk on the property is prohibited for five years, and fences must be maintained during that time to prevent free-ranging deer from entering. The herd owner will receive state and federal indemnities that pay a portion of the appraised value of the deer.

This was the first new CWD-infected herd on a Wisconsin farm since January 2005. To date, 98 farm-raised animals in Wisconsin have tested positive for CWD, including 82 on a separate Portage County operation. One of the infected animals was an elk; the rest have been white-tailed deer. More than 22,500 farm-raised deer in Wisconsin have been tested for CWD.

Chronic wasting disease is a disease that is known to affect deer, elk and moose. Prions - a particular type of protein in the brain - become malformed and create microscopic holes in the brain. The disease is always fatal. Scientists have not determined exactly what causes the malformed prions or how the disease is transmitted, but one means of transmission may be ingestion of prion-contaminated soil. When CWD was first reported in free-ranging white-tailed deer in Wisconsin in February 2002, it was the first appearance of the disease east of the Mississippi River. CWD was first found in a Wisconsin farm-raised deer in September 2002.


http://www.nbc26.com/Global/story.asp?S=9541420



THEY need to get a handle on these deer farms, or just shut them down altogether. they seem to be nothing more than a petri dish of deadly pathogens, especially CWD. i know there are folks that make a living out there in this industry, but at what expense to the wild are we willing to let money and greed go, and how far $

a few findings to ponder ;

0C7.04

North American Cervids Harbor Two Distinct CWD Strains

Authors

Angers, R. Seward, T, Napier, D., Browning, S., Miller, M., Balachandran A., McKenzie, D., Hoover, E., Telling, G. 'University of Kentucky; Colorado Division of Wildlife, Canadian Food Inspection Agency; University Of Wisconsin; Colorado State University.

Content

Despite the increasing geographic distribution and host range of CWD, little is known about the prion strain(s) responsible for distinct outbreaks of the disease. To address this we inoculated CWD-susceptible Tg(CerPrP)1536+/· mice with 29 individual prion samples from various geographic locations in North America. Upon serial passage, intrastudy incubation periods consistently diverged and clustered into two main groups with means around 210 and 290 days, with corresponding differences in neuropathology. Prion strain designations were utilized to distinguish between the two groups: Type I CWD mice succumbed to disease in the 200 day range and displayed a symmetrical pattern of vacuolation and PrPSc deposition, whereas Type II CWD mice succumbed to disease near 300 days and displayed a strikingly different pattern characterized by large local accumulations of florid plaques distributed asymmetrically. Type II CWD bears a striking resemblance to unstable parental scrapie strains such as 87A which give rise to stable, short incubation period strains such as ME7 under certain passage conditions. In agreement, the only groups of CWD-inoculated mice with unwavering incubation periods were those with Type I CWD. Additionally, following endpoint titration of a CWD sample, Type I CWD could be recovered only at the lowest dilution tested (10-1), whereas Type II CWD was detected in mice inoculated with all dilutions resulting in disease. Although strain properties are believed to be encoded in the tertiary structure of the infectious prion protein, we found no biochemical differences between Type I and Type II CWD. Our data confirm the co·existence of two distinct prion strains in CWD-infected cervids and suggest that Type II CWD is the parent strain of Type I CWD.

see page 29, and see other CWD studies ;


http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf



Sunday, November 23, 2008

PRION October 8th - 10th 2008 Book of Abstracts


http://bse-atypical.blogspot.com/2008/11/prion-october-8th-10th-2008-book-of.html



Saturday, September 06, 2008

Chronic wasting disease in a Wisconsin white-tailed deer farm 79% INFECTION RATE Contents: September 1 2008, Volume 20, Issue 5

snip...see full text ;


http://chronic-wasting-disease.blogspot.com/2008/11/commentary-crimes-hurt-essence-of.html




kind regards, terry

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