CWD MICHIGAN UPDATE September 5, 2008

CWD Update Chronic Wasting Disease Eradication Program Provided by the Animal Industry Division Michigan Department of Agriculture September 5, 2008

Background: The Michigan departments of Agriculture (MDA) and Natural Resources (DNR) confirmed the state’s first case of Chronic Wasting Disease (CWD) in a three-year old white-tailed deer from a privately owned cervid (POC) facility in Kent County on Monday, August 25, 2008. The state quarantined all POC facilities, prohibiting the movement of all – dead or alive – privately-owned deer, elk, or moose. Officials do not yet know how the deer may have contracted the disease. To date, there is no evidence that CWD presents a risk to humans or to animals other than cervids. MDA Actions: The state-wide quarantine on all privately owned cervid facilities is still in place. Facilities may continue to hold shooting events, but all carcasses* must be held until testing clears the animal/or the quarantine is released. A clarification to the quarantines was published and distributed to law enforcement officials, stakeholders and other interested parties. A questions and answers sheet is available under the livestock link on the www.michigan.gov/chronicwastingdisease website.

The test results from the Kent County cervid breeding facility, where the index case was confirmed, found no additional diseased deer. Epidemiologists are reviewing taxidermy records on a facility related to the index case. Taxidermy operations must be licensed and operators must follow Michigan requirements when conducting business with hunters who have harvested animals from other states. Current Michigan law prohibits the import of free-ranging deer or elk carcasses from states or provinces with CWD. Only de-boned meat, antlers, antlers attached to a scull cap cleaned of all brain and muscle tissue, hides and upper canine teeth may be brought into Michigan. A person that is notified by mail or other means, that a carcass imported into Michigan tested positive for CWD must notify the Michigan DNR.

The first tier of traces from the index facility led to five facilities: three in Kent County, one in Montcalm County, and one in Osceola County. These facilities were quarantined by MDA. Records of sales and purchases have been reviewed and have revealed that two facilities received deer from the index case. Four deer from these two facilities were 2 euthanized, samples were tested at MSU’s DCPAH and were found to be negative on Thursday, September 04, 2008. One of the five facilities in tier one, also a Kent County facility conducts a taxidermy operation on the premises. Taxidermy is of great concern because infectious prions in the bones and spinal tissue of the carcass from CWD positive states can infect deer on the facility. MDA, DNR and USDA staff are investigating the records of the taxidermy operation. The second tier investigation to this point, has quarantined four facilities in Bay, Kent, Mecosta, and Saginaw counties. These facilities only sold to the tier one facilities and did not receive anything. They are quarantined as terminal operations and any deer that die, are culled, or shot for sport must be submitted for CWD testing. POC Facilities Quarantined: All POC facilities, except those that only have reindeer, are under quarantine in Michigan until the disease investigation is complete. Epidemiologists are developing a policy for records review and release of quarantines based on management practices and risk.

Disease Surveillance Table: Index facility Depopulated Tier 1 Tier 2 1 Entire index herd tested negative 5 herds 2 trace outs (four test-negative animals) 3 trace ins 4 none of these 4 facilities trace directly to the index facility DNR Actions: The ban on all baiting and feeding of deer and elk in the Lower Peninsula is in effect. MSU’s Product Center for Agriculture Development is taking calls from bait growers/sellers. The Center is using Michigan Market Maker, an interactive mapping system that connects Agriculture processors and businesses with Michigan growers and marketers. http://mi.marketmaker.uiuc.edu/ Information on the baiting and feeding ban is available on the CWD page of the Emerging Diseases website. A mandatory deer check for hunters who take a deer within the Kent County townships of Tyrone, Solon, Nelson, Sparta, Algoma, Courtland, Alpine, Plainfield, and Cannon, is in effect for the 2008 hunting season. The deer heads will be collected and tested for CWD. All transport of live wild deer, elk, and moose is prohibited statewide, including transport for rehabilitation purposes. Education and Outreach: A town hall meeting is scheduled to take place in Kent County on September 9, 2008 at 6:30 p.m. near Grand Rapids. Representatives from MDA, USDA, DNR and MSU will be there to answer questions about CWD, quarantines and the baiting ban. An update on the disease investigation will be presented to the House of Representatives Committee on Outdoor Recreation and Natural Resources on September 9, 2008 and the Senate Natural Resources, Agriculture, and Hunting and Fishing committees on September 10, 2008. 3 Questions and Answers regarding POC facility quarantines were sent via email to legislative offices, POC facility executive directors, and DNR law enforcement. They are also posted to the MDA, and Emerging Diseases websites. A coordinated communications action plan is in place. MSU Extension, Michigan Deer and Elk Breeders, MUCC, and many other special interest groups have volunteered to assist with information distribution. Information on CWD may be found on the Michigan Emerging Diseases website at www.michigan.gov/emergingdiseases. Corrected on September 8, 2008 – changed from “meat” to “carcasses”.



http://www.michigan.gov/documents/emergingdiseases/MDA_CWD_Update_September_5_2008_final_248172_7.pdf

http://www.michigan.gov/emergingdiseases/0,1607,7-186-25806_26356---,00.html



Summary of Michigan Wildlife Chronic Wasting Disease Surveillance Updated May 1, 2008 by Michigan Department of Natural Resources, Wildlife Disease Laboratory



http://www.michigan.gov/documents/emergingdiseases/CWDTable082508_246523_7.pdf



http://www.michigan.gov/images/emergingdiseases/cwdcum1998_2002-050108_246525_7.jpg



Consumer Warning September – December 2008

The state's first case of Chronic Wasting Disease (CWD) was confirmed in a three-year old white-tailed deer from a privately owned cervid (POC) facility in Kent County on August 25, 2008. As a result, all POC facilities in Michigan were quarantined. Chronic Wasting Disease (CWD) is a fatal neurological disease that affects deer, elk and moose. Infected animals display abnormal behavior, progressive weight loss and physical debilitation. CWD is believed to be caused by infectious, self-multiplying proteins (prions). Prions are normal cell proteins whose shape has been transformed, causing CWD. To date, CWD is not known to cause or be associated with disease in humans. No increase in human prion disease has been observed in areas of the western United States where CWD has been endemic in cervid populations for decades.

However, because much is still unknown about prion diseases, the Centers for Disease Control and Prevention and the World Health Organization advise that humans do NOT consume animals that have been tested and are known to be infected with CWD. In general, people should not handle or consume wild animals that appear sick or act abnormally, regardless of the cause. CWD prions are primarily found in central nervous system tissues (e.g. brain and spinal cord) and the lymphatic system (e.g. tonsils, lymph nodes and spleen) of infected cervids. Humans should avoid the handling or consumption of these tissues. Hunters should wear disposable gloves while field dressing and de-boning meat from the carcass. Recent research has shown that CWD prions may also be found in the saliva and urine of the infected animal. Experiments conducted suggest that CWD prions can persist in the environment and may indirectly infect other susceptible animals that come into contact with the contaminated environment. The meat product you are receiving has come from a quarantined facility under surveillance for CWD. MDA recommends you take de-boned meat from the carcass, hold the meat product in a freezer and consume it only after the facility of origin receives clarification from MDA that the animal was negative for CWD.



http://www.michigan.gov/documents/emergingdiseases/Meat_-_CWD_Consumer_Warning_final_248038_7.pdf



From: TSS Subject: CWD aka MAD DEER/ELK TO HUMANS ??? Date: September 30, 2002 at 7:06 am PST

From: "Belay, Ermias" To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias" Sent: Monday, September 30, 2002 9:22 AM Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.

That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

Ermias Belay, M.D. Centers for Disease Control and Prevention

-----Original Message----- From: Sent: Sunday, September 29, 2002 10:15 AM To: [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask] Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

snip...see full text ;



http://chronic-wasting-disease.blogspot.com/2008/08/cwd-stakeholder-advisory-group.html



The meat product you are receiving has come from a quarantined facility under surveillance for CWD. MDA recommends you take de-boned meat from the carcass, hold the meat product in a freezer and consume it only after the facility of origin receives clarification from MDA that the animal was negative for CWD.<<< HOW WOULD ANYONE KNOW THIS UNLESS EVERY DEER, ELK, CERVID, ON EVERY GAME FARM IN MICHIGAN IS TESTED??? IT WOULD BE INTERESTING TO KNOW EXACTLY HOW MANY CWD TEST WERE PERFORMED IN ALL OF THE GAME FARMS IN MICHIGAN SINCE THE 1ST CASE WAS REPORTED ??? CLAIMING 'ALL CLEAR' WITHOUT PERFORMING TEST, would be foolish in my opinion. ...TSS [2] USA: (Wyoming) Date: Mon 29 Oct 2007 Source: The Courier Journal [edited]


http://www.courier-journal.com/apps/pbcs.dll/article?AID=/20071028/SPORTS09/710280596/1002/SPORTS





An Indiana hunter will be allowed to keep the head mount of a deer he killed in Wyoming that tested positive for chronic wasting disease.

The unidentified hunter knew about the CWD risk and submitted a portion of the animal to the Wyoming Game and Fish Department for testing before having the meat deboned for transport home. After the animal tested positive for CWD, Wyoming officials contacted the hunter and the Indiana Department of Natural Resources.

Indiana DNR officials disposed of the meat, but the hunter was allowed to keep the mount, according to Dr Jennifer Strasser, a veterinarian with the Indiana Board of Animal Health and a state conservation officer. "As long as the skull cap and cape are cleaned properly, the hunter can safely keep the mount," she said. The Indiana DNR (Department of Natural Resources) has tight restrictions on transporting deer, elk, and other cervids into the state. For information go to <http://www.in.gov/dnr/deerhealth/cwd.htm>.


-- communicated by: Terry S Singeltary Sr <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000295/!x-usc:mailto:flounder9@verizon.net>

[The article does not tell us if the head and cape were cleaned by the hunter or by a professional taxidermist. Neither does the article indicate how this was verified, or if it was verified. If it were done by a taxidermist then one must wonder where the taxidermist is located, in Wyoming or Indiana, or some other state. In the past Indiana had no regulations regarding disposal of offal associated with a head mount and Indiana DNR had no way to track such either. Unless something has changed, the Indiana DNR did not have a complete list of taxidermists within the state. Without such a list or regulation of how the offal for a head/cape mount are to be disposed of it is possible that CWD could have been allowed to enter the state. - Mod.TG

The US states of Wyoming and Indiana can be located on the HealthMap/ProMED-mail interactive map at <http://healthmap.org/promed?v=40,-97.6,4>. - CopyEd.MJ]



http://michigan-sportsman.com/forum/showthread.php?p=1837107



http://www.michigan-sportsman.com/forum/showthread.php?t=23313



http://www.biggamehunt.net/forums/viewtopic.php?t=7603



but the hunter was allowed to keep the mount, according to Dr. Jennifer Strasser, a veterinarian with the Indiana Board of Animal Health and a state conservation officer. "As long as the skull cap and cape are cleaned properly, the hunter can safely keep the mount," she said.? <<< i think it's foolish. in my opinion, the complete carcass should have been incinerated, including the head mount. What actions have been taken to prevent the spread of CWD? The movement of high-risk carcass parts (brain, spinal cord, lymph tissues) is a potential avenue through which CWD could be spread from infected areas. Investigations in New York indicate that the infection could have been spread by a taxidermist who accepted specimens from CWD-positive states, allowed rehabilitated fawns access to the taxidermy workshop and spread potentially infectious curing salt waste as a fence line weed killer on his deer farm. Several states, including Pennsylvania, have developed regulations to prohibit the importation of high-risk carcass parts from CWD endemic states. As of April 1, 2006 Pennsylvania's importation ban prohibits the importation of high-risk carcass parts from Colorado, Illinois, Kansas, Nebraska, New Mexico, New York (CWD containment area only), South Dakota, Utah, West Virginia (Hampshire County only), Wisconsin, Wyoming and the Canadian provinces of Alberta and Saskatchewan. Pennsylvanians hunting in CWD-positive areas should get their animals tested and should leave high-risk carcass parts in the area where the animal was hunted.


http://www.pgc.state.pa.us/pgc/cwp/view.asp?a=458&q=168948



The movement of high-risk carcass parts (brain, spinal cord, lymph tissues) is a potential avenue through which CWD could be spread from infected areas. Investigations in New York indicate that the infection could have been spread by a taxidermist who accepted specimens from CWD-positive states, allowed rehabilitated fawns access to the taxidermy workshop and spread potentially infectious curing salt waste as a fence line weed killer on his deer farm.



http://www.pgc.state.pa.us/pgc/cwp/view.asp?a=458&q=168948



http://www.pgc.state.pa.us/pgc/lib/pgc/taxidermists_cwd.pdf



http://wolftracksproductions.yuku.com/topic/874/t/Wyoming-deer-killed-by-Hoosier-had-CWD.html



Thursday, August 28, 2008

cwd, feeding, and baiting piles


http://chronic-wasting-disease.blogspot.com/2008/08/cwd-feeding-and-baiting-piles.html



Sunday, September 07, 2008

CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA


http://chronic-wasting-disease.blogspot.com/2008/09/cwd-live-test-and-political-aspects-or.html



Saturday, September 06, 2008

Chronic wasting disease in a Wisconsin white-tailed deer farm 79% INFECTION RATE


http://chronic-wasting-disease.blogspot.com/2008/09/chronic-wasting-disease-in-wisconsin.html



Monday, August 25, 2008

CWD FIRST DOCUMENTED IN MICHIGAN


http://chronic-wasting-disease.blogspot.com/2008/08/cwd-first-documented-in-michigan.html



Thursday, August 28, 2008


CWD TISSUE INFECTIVITY brain, lymph node, blood, urine, feces, antler velvet and muscle


http://chronic-wasting-disease.blogspot.com/2008/08/cwd-tissue-infectivity-brain-lymph-node.html



Wednesday, September 03, 2008

Accelerated High Fidelity Prion Amplification Within and Across Prion Species Barriers



http://chronic-wasting-disease.blogspot.com/2008/09/accelerated-high-fidelity-prion.html




P01.47

Quantifying the Species Barrier in Chronic Wasting Disease by a Novel in vitro Conversion Assay

Li, L1; Coulthart, MB2; Balachandran, A3; Chakrabartty, A4; Cashman, NR1 1University of British Columbia, Brain Research Centre, Canada; 2Public Health Agency of Canada, National Microbiology Laboratory, Canada; 3Animal Diseases Research Institute, Canada Food Inspection Agency, National Reference Laboratory for Scrapie and CWD, Canada; 4Ontario Cancer Institute and Department of Medical Biophysics, University of Toronto, Canada

Background: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy that can affect North American cervids (deer, elk, and moose). Although the risk of CWD crossing the species barrier and causing human disease is still unknown, however, definite bovine spongiform encephalopathy (BSE) transmission to humans as variant CJD (vCJD), it would seem prudent to limit the exposure of humans to CWD.

Aim: In view of the fact that BSE can be readily transmitted to non-bovid species, it is important to establish the species susceptibility range of CWD.

Methods: In vitro conversion system was performed by incubation of prions with normal brain homogenates as described before, and protease K (PK) resistant PrP was determined by immunoblotting with 6H4 monoclonal prion antibody.

Results: Our results demonstrate that PrPC from cervids (including moose) can be efficiently converted to a protease-resistant form by incubation with elk CWD prions, presumably due to sequence and structural similarities between these species. Interestingly, hamster shows a high conversion ratio by PrPCWD. Moreover, partial denaturation of substrate PrPC can apparently overcome the structural barriers between more distant species.

Conclusions: Our work correctly predicted the transmission of CWD to a wild moose. We find a species barrier for prion protein conversion between cervids and other species, however, this barrier might be overcome if the PrPC substrate has been partially denatured in a cellular environment. Such an environment might also promote CWD transmission to non-cervid species, *** including humans. Acid/GdnHCl-treated brain PrPC was a superior substrate for the in vitro conversion than PrPC treated at physiological pH. This has implications for the process by which the prion protein is converted in disease.



http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf




-------- 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: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000295/!x-usc:mailto:fdadockets@oc.fda.gov

Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

full text ;



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



Friday, August 01, 2008


Excretion of transmissible spongiform encephalopathy infectivity in urine



http://creutzfeldt-jakob-disease.blogspot.com/2008/08/excretion-of-transmissible-spongiform.html




Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease

2008 1: Vet Res. 2008 Apr 3;39(4):41

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.

snip...

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

snip...

full text ;



http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html




The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.



http://www.cjdfoundation.org/fact.html



CHRONIC WASTING DISEASE BLOG



http://chronic-wasting-disease.blogspot.com/




Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA

CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA

[QUOTE=xxxxxx]There is NO viable test for CWD on LIVE deer thus the entire herd was killed and tested.................which is also why there is a "mandatory" deer check in for any deer taken from the surrounding townships during hunting season..[/QUOTE]


http://www.michigan-sportsman.com/forum/showthread.php?t=249787&page=2



TESTING OF LYMPHOID TISSUE OBTAINED BY RECTAL BIOPSY WAS APPROVED BY USDA AS AN OFFICIAL LIVE-ANIMAL TEST ON JANUARY 11, 2008. ...

PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**



http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps



Biopsy of the rectal mucosal tissue, a site readily sampled in the restrained or chemically immobilized deer, provided an accurate diagnosis in 83% of the infected deer.



http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=218153



"The use of this new live test in the initial screening, surveillance, and monitoring of CWD will greatly aid in the management and control of the disease in the wild, as well as in captive settings," Dr. VerCauteren said.


http://www.avma.org/onlnews/javma/jul08/080715t.asp



“The key advantage to the rectal biopsy test is that it can be performed on live animals. Until now, there was no practical live test for CWD in elk,” said research wildlife biologist Dr. Kurt VerCauteren with APHIS’ Wildlife Services (WS) National Wildlife Research Center (NWRC). “With this technique we can detect CWD in animals not showing any signs of the disease and, thus, remove them so they are not left to infect other individuals and further contaminate the environment.”


http://www.aphis.usda.gov/newsroom/content/2008/05/cwdelktst.shtml



Greetings Michigan Hunters et al;

now, let's ponder a few things, shall we.

why quarantine a farm for 4 to 5 years due to an atypical TSE of foreign origin and due to potential serious animal and HUMAN health here in the USA there-from. then a few years later, discover the same damn TSE in the USA, home grown, and the same quarantine is not put in place. case in points, the mad sheep of mad river valley compared to those two atypical H-BSE cases in Texas and Alabama, and 6 cases to date of the atypical scrapie NOR-98 in six different states. why is the usda et al hiding behind some serum toxin act from decades ago, simply to NOT allow testing for BSE/TSE in the USA bovine i.e. Creekstone vs USDA ? and why is the same serum-toxin act not applying to the CWD testing in the States, with deer and elk? or does it? these are not trick questions, i really want to know. you cannot ignore these other TSEs, and the politics that surround them. well, the moderators can ;-) and that's their choice, and i will abide by whatever move they take. i am not trying to get off topic, but, these issues must not be ignored. that must not happen with CWD in Michigan. and remember, in Terms of TSE i.e. prion disease, Michigan has CWD, Scrapie, and the atypical Nor-98 scrapie, Michigan also has cattle$ remember, the first recorded case of scrapie in the US occurred on a ranch in Michigan in 1947, the year of the first TME outbreak in Wisconsin. riddle me this batman, riddle me this ???

see last link at bottome of page ; ''Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?''

kind regards, terry

xxxxxxxxxxx

Prof Collinge old findings, a key issue, the media always seems to forget about, states that BSE propagates as either variant CJD-like or sporadic CJD-like prion strains. funny how our health officials, governments, and such seem to conveniently ignore these findings, let alone the atypical TSE in cattle and sheep that do NOT look like nvCJD in the lab, but some sub-types of the sporadic CJD. all this goes ignored for one reason, and one reason only $$$ it's why the UKBSEnvCJD only theory was put forth in the first place, and it's why it is still set in stone $$$ to much science has been forth to date that proves that theory wrong.

PLEASE NOTE, the last two mad cows documented in the USA were H-type BSE, then the USDA quickly shut the testing down to a level of non-detection. it would be a miracle to find one case, from testing only 40,000 annually, from some 97,000,000 (that's 97 million head), and of that, some 37 million slaughtered, if i am not mistaken. and these cattle are cherry picked brains too, probably calves from USDA grain fed facilities, and don't think these corrupt people are not capable of doing it either. they are very capable, in fact, they did just that ;

"REDACTED is alleged to have provided possibly inaccurate test results involving diseased sheep. However, because the results were determined to be inconclusive, no actual violation was actually committed.''

snip...

Statement on Texas Cow With Central Nervous System Symptoms On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.

snip...

I would note that the sample was taken in April, at which time the protocols allowed for a preservative to be used (protocols changed in June 2005). The sample was not submitted to us until last week, because the veterinarian set aside the sample after preserving it and simply forgot to send it in. On that point, I would like to emphasize that while that time lag is not optimal, it has no implications in terms of the risk to human health. The carcass of this animal was destroyed, therefore there is absolutely no risk to human or animal health from this animal.

snip...

Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.

snip...

4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half


http://www.usda.gov/oig/webdocs/sarc070619.pdf



full text ;



http://foiamadsheepmadrivervalley.blogspot.com/2008/09/re-foia-of-declaration-of-extraordinary.html



USDA: In 9,200 cases only one type of test could be used

WASHINGTON (AP)--The U.S. Department of Agriculture acknowledged Aug. 17 that its testing options for bovine spongiform encephalopathy were limited in 9,200 cases despite its effort to expand surveillance throughout the U.S. herd.

In those cases, only one type of test was used--one that failed to detect the disease in an infected Texas cow.

The department posted the information on its website because of an inquiry from The Associated Press.

Conducted over the past 14 months, the tests have not been included in the department's running tally of BSE tests since last summer. That total reached 439,126 on Aug. 17.

"There's no secret program," the department's chief veterinarian, John Clifford, said in an interview. "There has been no hiding, I can assure you of that."

Officials intended to report the tests later in an annual report, Clifford said.

These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC.

In the Texas case, officials had declared the cow free of disease in November after an IHC test came back negative. The department's inspector general ordered an additional kind of test, which confirmed the animal was infected.

Veterinarians in remote locations have used the preservative on tissue to keep it from degrading on its way to the department's laboratory in Ames, Iowa. Officials this year asked veterinarians to stop using preservative and send fresh or chilled samples within 48 hours.

The department recently investigated a possible case of BSE that turned up in a preserved sample. Further testing ruled out the disease two weeks ago.

Scientists used two additional tests--rapid screening and Western blot--to help detect BSE in the country's second confirmed case, in a Texas cow in June. They used IHC and Western blot to confirm the first case, in a Washington state cow in December 2003.

"The IHC test is still an excellent test," Clifford said. "These are not simple tests, either."

Clifford pointed out that scientists reran the IHC several times and got conflicting results. That happened, too, with the Western blot test. Both tests are accepted by international animal health officials.

Date: 8/25/05



http://www.hpj.com/archives/2005/aug05/aug29/BSEtestoptionswerelimited.cfm



""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."

THIS WAS DONE FOR A REASON!

THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS

USDA 2003

We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip.............

Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.

Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip...

FULL TEXT;

Completely Edited Version PRION ROUNDTABLE

Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado

2005

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

CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006

The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.

The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end



http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r




CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...



http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm



PLEASE NOTE ;

179 Page 10 of 17

BSE cattle may need to be reexamined.

T. Kitamoto (Ed.) PRIONS Food and Drug Safety

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

ALSO from the International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004; Bovine spongiform encephalopathy (BSE) in Japan

snip...

"Furthermore, current studies into transmission of cases of BSE that are atypical or that develop in young cattle are expected to amplify the BSE prion" NO. Date conf. Farm Birth place and Date Age at diagnosis 8. 2003.10.6. Fukushima Tochigi 2001.10.13. 23 9. 2003.11.4. Hiroshima Hyogo 2002.1.13. 21

Test results # 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology negative b = atypical BSE case c = case of BSE in a young animal b,c, No PrPSc on IHC, and no spongiform change on histology International Symposium of Prion Diseases

held in Sendai, October 31, to November 2, 2004. Tetsuyuki Kitamoto Professor and Chairman Department of Prion Research Tohoku University School of Medicine 2-1 SeiryoAoba-ku, Sendai 980-8575, JAPAN TEL +81-22-717-8147 FAX +81-22-717-8148 e-mail; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:kitamoto@mail.tains.tohoku.ac.jp Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656 e-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:kvomi-sasaki@mail.tains.tohoku.ac.ip

================================= 9/13/2005 --------------------------------------------------------------------------------


Page 11 of 17

From: TSS () Subject: Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Date: August 26, 2005 at 10:24 am PST Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Jpn. J. Infect. Dis., 56, 221-222, 2003 Laboratory and Epidemiology Communications Atypical Proteinase K-Resistant Prion Protein (PrPres) Observed in an Apparently Healthy 23-Month-Old Holstein Steer Yoshio Yamakawa*, KenÕichi Hagiwara, Kyoko Nohtomi, Yuko Nakamura, Masahiro Nishizima ,Yoshimi Higuchi1, Yuko Sato1, Tetsutaro Sata1 and the Expert Committee for BSE Diagnosis, Ministry of Health, Labour and Welfare of Japan2 Department of Biochemistry & Cell Biology and 1Department of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640 and 2Miistry of Health, Labour and Welfare, Tokyo 100-8916 Communicated by Tetsutaro Sata (Accepted December 2, 2003) *Corresponding author: Mailing address: Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 1628640, Japan. Tel: +81-3-5285-1111, Fax: +81-3-5285-1157, E-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:yamakawa@nih.go.jp

Since October 18, 2001, 'bovine spongiform encephalopathy (BSE) examination for all cattle slaughtered at abattoirs in the country' has been mandated in Japan by the Ministry of Health, Labour and Welfare (MHLW). 'Plateria' ELISA-kit (Bio-Rad Laboratories, Hercules, Calif., USA) is routinely used at abattoirs for detecting proteinase K (PK)-resistant prion protein (PrPSc) in the obex region. Samples positive according to the ELISA screening are further subjected to Western blot (WB) and histologic and immunohistochemical examination (IHC) at the National Institute of Infectious Diseases (NIID) or Obihiro University. If PrPSc is detected either by WB or by IHC, the cattle are diagnosed as BSE. The diagnosis is approved by the Expert Committee for BSE Diagnosis, MHLW. From October 18, 2001 to September 30, 2003, approximately 2.5 million cattle were screened at abattoirs. A hundred and ten specimens positive according to ELISA were subjected to WB/IHC. Seven showed positive by both WB and IHC, all exhibiting the typical electrophoretic profile of a high content of the di-glycosylated molecular form of PrPSc (1-3) and the distinctive granular deposition of PrPSc in neuronal cells and neuropil of the dorsal nucleus of vagus. An ELISA-positive specimen from a 23 month-old Holstein steer slaughtered on September 29, 2003, in Ibaraki Prefecture (Ibaraki case) was sent to the NIID for confirmation. The animal was reportedly healthy before slaughter. The OD titer in ELISA was slightly higher than the 'cut-off' level given by the manufacturer. The histology showed no spongiform changes and IHC revealed no signal of PrPSc accumulation typical for BSE. However, WB analysis of the homogenate that was prepared from the obex region and used for ELISA revealed a small amount of PrPSc with an electrophoretic profile different from that of typical BSE-associated PrPSc (1-3). The characteristics were (i) low content of the di-glycosylated molecular form of PrPSc, (ii) a faster migration of the non-glycosylated form of PrPSc on SDS-PAGE, and (iii) less resistance against PK digestion as compared with an authentic PrPSc specimen derived from an 83-month-old Holstein (Wakayama case) (Fig. 1). Table 1 summarizes the relative amounts of three distinctive glycoforms (di-, mono, non-glycosylated) of PrPSc calculated by densitometric analysis of the blot shown in Fig. 1. As 2.5 mg wet weight obex-equivalent homogenate of the Ibaraki case (Fig. 1, lane 4) gave slightly stronger band intensities of PrPSc than an 8 mg wet weight obex-equivqlent homogenate of a typical BSE-affected Wakayama case (Fig. 1, lane 2), the amount of PrPSc accumulated in the Ibaraki case was calculated to be 1/500 - 1/1000 of the Wakayama case. In the Ibaraki case, the PrPSc bands were not detectable in the homogenates of the proximal surrounding region of the obex. These findings were consistent with the low OD value in ELISA, i.e., 0.2 -0.3 for the Ibaraki case versus over 3.0 for the Wakayama case. The DNA sequence of the PrP coding region of the Ibaraki case was the same as that appearing in the database (GenBank accession number: AJ298878). More recently, we encountered another case that resembled the Ibaraki case. It was a 21-monthold Holstein steer from Hiroshima Prefecture. WB showed typical BSE-specific PrPSc deposition though IHC did not detect positive signals of PrPSc (data not shown). Though the clinical onset of BSE is usually at around 5 years of age or later, a 20-month-old case showing the clinical signs has been reported (4). Variant forms of BSE similar to our cases, i.e., with atypical histopathological and/or biochemical phenotype, have been recently reported in Italy (5) and in France (6). Such variant BSE was not associated with mutations in the prion protein (PrP) coding region as in our case (5,6). The Ministry of Agriculture, Forestry and Fisheries of Japan (MAFF) announced a ban of feeding ruminants with meat bone meal (MBM) on September 18, 2001, and a complete ban was made on October 15 of the same year. According to the recent MAFF report, the p ous seven cases of BSE in Japan were cattle born in 1995 - 1996 and possibly fed with cross-contaminated feed. However, the two cattle in this report were born after the complete ban. Whether contaminated MBM was implicated in the present cases remains to be investigated.

REFERENCES Collinge, J., Sidle, K. C. L., Meads, J., Ironside, J. and Hill, A. F. (1996): Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature, 383, 685690. Bruce, M. E., Will, R. G., Ironside, J. W., McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. J. (1997): Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature, 389, 498-501. Hill, A. F., Desbruslais, M., Joiner, S., Sidle, K. C. L., Gowland, I. and Collinge, J. (1997): The same prion strain causes vCJD and BSE. Nature, 389, 448-450. Matravers, W., Bridgeman, J. and Smith, M.-F. (ed.)(2000): The BSE Inquiry. p. 37. vol. 16. The Stationery Office Ltd., Norwich, UK. Casalone, C., Zanusso, G., Acutis, P. L., Crescio, M. I., Corona, C., Ferrari, S., Capobianco, R., Tagliavini, F., Monaco, S. and Caramelli, M. (2003): Identification of a novel molecular and neuropathological BSE phenotype in Italy. International Conference on Prion Disease: from basic research to intervention concepts. Gasreig, Munhen, October 8-10. Bicaba, A. G., Laplanche, J. L., Ryder, S. and Baron, T. (2003): A molecular variant of bovine spongiform encephalopatie. International Conference on Prion Disease: from basic research to intervention concepts. Gasreig, Munhen, October 8-10. Asante, E. A., Linehan, J. M., Desbruslais, M., Joiner, S., Gowland, I., Wood, A. L., Welch, J., Hill, A. F., Lloyd, S. E., Wadsworth, J. D. F. and Collinge, J. (2002). BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J., 21, 6358-6366. 9/13/2005 Page 12 of 17 SEE SLIDES IN PDF FILE;


http://www.nih.go.jp/JJID/56/221.pdf



http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf




THE SEVEN SCIENTIST REPORT ***



http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf



***

WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;

Bio-Rad, TSS phone conversation 12/28/04

Finally spoke with ;

Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX

at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.

my question;

Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???

ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.

again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there. "very difficult to answer"

"very political"

"very loaded question"

outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing. said something about Dr. Houston stating; any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives? said something about ''just look at the sheep that tested IHC- but were positive''. ...

TSS

-------- Original Message -------- Subject: Your questions Date: Mon, 27 Dec 2004 15:58:11 -0800 From: To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:flounder@wt.net

Hi Terry:

............................................snip Let me know your phone number so I can talk to you about the Bio-Rad BSE test. Thank you

Regards

Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: =================================

END...TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########



http://madcowtesting.blogspot.com/




Executive Summary

In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.



http://www.aphis.usda.gov/lpa/issues/bse/epi-updates/bse_final_epidemiology_report.pdf




Greetings again Michigan Hunters et al ;

i know how some don't like to get political, but cwd, mad cow disease (all strains), TME, Scrapie, and cjd i.e. human and animal TSE, that's all they are are political. bush has failed us terribly, clinton before him failed us terribly, and whomever gets in office next will do the same damn thing, in terms of human and animal TSE. it was said long ago ;

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in the USA.



http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf




PLEASE NOTE, ''FANATICAL INCIDENT TO BE AVOIDED IN THE US AT ALL COSTS.''

AND they meant it. i have watched this nightmare unfold daily for over a decade. i was told long ago, by an old wise person, that the deer and elk industry, was used as a scapegoat, or was sacrificed by the USDA et al, to get the monkey off their backs i.e. livestock, commodities, and futures, i.e. global trade. mere words of wisdom i suppose, but why does the USDA et al refuse to test to find. everything they have done in the past, was done just the opposite. it's been proven. i.e. the USDA, OIE, BSE MRR policy gave birth to that. i give you this data only as history, so as to maybe not to repeat itself. who knows? you can file it away, but i dont care to debate it, there is nothing to debate in my mind, the data speaks for itself. YOU, anyone one of you do not think our Government is capable of doing such a think, i only say two words, tobacco and asbestos. decades of cover-up by big industry. i have seen it repeated time and time again, to date. and i really dont see a new regime in Washington doing anything different, from either party. the only way to do that would be to get the industry out of Washington, and this will not happen $$$

The EMBO Journal Vol. 21 No. 23 pp. 6358±6366, 2002

BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein

Emmanuel A.Asante, Jacqueline M.Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L.Wood, Julie Welch, Andrew F.Hill, Sarah E.Lloyd, Jonathan D.F.Wadsworth and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:j.collinge@prion.ucl.ac.uk Variant Creutzfeldt±Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSEderived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure. ...snip...end...TSS

Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE

Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden

Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans. ...end

USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN

18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.

snip...

64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. *** A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.

snip...



http://www.seac.gov.uk/minutes/95.pdf



AND WHAT ABOUT THOSE atypical NOR-98 scrapie cases in the USA, now documented at 6 cases in the past two years, and the risk thereof to humans as sporadic CJD ???

P03.141

Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

INFECTED AND SOURCE FLOCKS

There were 20 scrapie infected and source flocks with open statuses (Figure 3) as of April, 30, 2008. Twenty eight new infected and source flocks have been designated in FY 2008 (Figure 4); three source flocks were reported in April. ...snip

POSITIVE SCRAPIE CASES

As of April 30, 2008, 122 new scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2008 (Figure 6). Of these, 103 were field cases and 19* were Regulatory Scrapie Slaughter Surveillance (RSSS) cases (collected in FY 2008 and reported by May 20, 2008). Positive cases reported for April 2008 are depicted in Figure 7. Eighteen cases of scrapie in goats have been confirmed by NVSL since implementation of the regulatory changes in FY 2002 (Figure 8). The most recent positive goat case was confirmed in February 2008 and originated from the same herd in Michigan as the other FY 2008 goat cases. ...snip

CAPRINE SCRAPIE PREVALENCE STUDY (CSPS)

snip...

However, four positive goats have been identified this fiscal year through field investigations. One was a clinical suspect submitted for testing and the other three originated from the birth herd of the clinical case.

ANIMALS SAMPLED FOR SCRAPIE TESTING

As of April 30, 2008, 26,703 animals have been sampled for scrapie testing: 23,378 RSSS, 1,517 goats for the CSPS study, 1,466 regulatory field cases, 270 regulatory third eyelid biopsies, and 72 regulatory rectal biopsies (chart 8).

TESTING OF LYMPHOID TISSUE OBTAINED BY RECTAL BIOPSY WAS APPROVED BY USDA AS AN OFFICIAL LIVE-ANIMAL TEST ON JANUARY 11, 2008. ...

PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**



http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps



NOT to forget the 5 cases of the NOR-98 atypical scrapie documented in the USA in 2007, in five different states. WHICH pathologically looks like some sub-types of sporadic CJD, of which Stanely Prusiner warns of a public health risk ;

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.



http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf



Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)



http://www.pnas.org/cgi/content/abstract/0502296102v1



Tuesday, June 3, 2008

SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA



http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html



NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 2007



http://nor-98.blogspot.com/2008/04/seac-spongiform-encephalopathy-advisory.html



http://nor-98.blogspot.com/



Nonambulatory Cattle as a Potential Source of TSE

In this study, Wisconsin was the only State in which mink producers were reported to receive nonambulatory cows directly from dairies. However, given the small number of surveyed herds this finding is likely a result of the sampling design. Because mink producers pay a premium for nonambulatory cows, it appears reasonable that the practice of feeding nonambulatory cows to mink could occur wherever both large numbers of dairy cows and mink are found. As many as 2,157(3) nonambulatory cows per million milk cows, or a total of 9,482 nonambulatory cows, could have been fed to mink in the 7 surveyed States in 1992. Based on the sample response, only half of those cows would have had an identifiable reason for being nonambulatory. This equates to an estimated 4,741 nonambulatory cows that were, hypothetically, a potential source of TSE in the surveyed States.

(3)This estimate does not account for any nonambulatory cows received from slaughter plants.

Page 23

The five reported outbreaks of TME in the U.S. reveal no discernable trend. Assuming an average of 2,000 mink farms in the U.S. during the last 50 years, one outbreak of TME has occurred per 20,000 mink farm-years. Extrapolating from the data gathered in this study, 66,374 nonambulatory cows have been fed to mink in the 7 surveyed States since the last reported outbreak of TME in 1985. Of those, 33,187 would have had no identifiable reason for being nonambulatory and were hypothetically a potential source of TSE. Given the severity of signs and number of mink affected by TME it is unlikely that outbreaks have gone unreported. If any form Of a TSE (infectious, spontaneous, or other) occurs in U.S. cattle that is transmissible to mink in the form of TME, then it must be exceedingly rare or the conditions for its transmission must be highly specific and unusual. Nonetheless, studies are underway at the State and Federal levels to further characterize the disposition of nonambulatory cows and usage on mink farms.

snip...

An estimated 4,741 nonambulatory cows hypothetically considered to be potential sources of TSE may have been fed to mink in the 7 surveyed States in 1992. This equates to 33,187 such cows fed to mink since the last reported outbreak of TME in mink. Given this large number of nonambulatory cows fed to mink, the historic and current mink population, and the infrequent occurrence of TME, if TSE exists in cattle in the U.S. it must be very rare or transmissible to mink only under very unusual conditions.



http://downercattle.blogspot.com/2008/08/quantitative-assessment-of-possible.html



To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

•Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092

ABSTRACT

Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England.

snip...

OBSERVATIONS AND RESULTS

A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were “acting funny”, and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death.

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. ***The rancher was a “dead stock” feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.***

snip...end



http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf



Epidemiology Epidemiologic studies suggest that animals contract the disease by external exposure to the infectious agent, such as by eating contaminated feed. No evidence suggests that the TME agent spreads by contact between unrelated mink or from mother to nursing young. The disease has been identified in both genders and all color phases in animals greater than 1 year old. The first documented TME outbreak in the United States occurred in 1947 on one ranch in Wisconsin and then on a ranch in Minnesota that had received mink from the Wisconsin ranch. In 1961, TME outbreaks occurred on five ranches in Wisconsin. In Factsheet Veterinary Services February 2002 APHIS 1963, outbreaks occurred in Idaho, Minnesota, and Wisconsin. Epidemiologic data from the Minnesota and Wisconsin outbreaks trace the cases in those States to one common purchased food source.

snip...

The 1985 Stetsonville Outbreak The most recent TME outbreak occurred on one mink ranch in Stetsonville, WI, in 1985. In the herd of 7,300 adult mink, 60 percent of the animals died. Clinical signs included tail arching, incoordination, and hyperexcitability. At the most advanced stages of the disease, the animals were in trancelike states and eventually died. The outbreak lasted 5 months. Microscopic examination of sections of the brain confirmed the spongelike changes characteristic of TME. Diagnostic tests identified the prion protein. The following year, mink born during the outbreak showed no signs of TME. The late Richard Marsh, a veterinary virologist at the University of Wisconsin who studied the transmission of TME and other TSE’s, investigated this outbreak. Marsh learned that the mink were fed a diet composed of fresh meat products from “downer cattle” and commercial sources of fish, poultry, and cereal. Downer cattle are nonambulatory and cannot rise because they are affected with a condition such as a metabolic disease, broken limbs, or a central nervous system disorder. Marsh theorized that the meat from these downer cattle introduced a TSE agent to the mink in which TME resulted. Although Marsh’s hypothesis is based on speculation and anecdotal evidence, in 1993 APHIS adjusted its national BSE surveillance program to include testing downer cattle for evidence of a TSE. The brains of more than 20,141 cattle have been examined at APHIS’ National Veterinary Services Laboratories and other State diagnostic laboratories. Not a single tissue sample has revealed evidence of BSE or another TSE in cattle.



http://www.aphis.usda.gov/publications/animal_health/content/printable_version/fs_ahtme.pdf



AND as everyone knows, the rest is history, those dead-stock downers, the most high risk cattle, were NOT tested, and in FACT, was a major source of YOUR CHILDRENS SCHOOL LUNCH PROGRAM, all across the Nation. sorry, these are the most high risk cattle for TSE aka mad cow disease, and i am a bit touchy about this topic. ...sorry. ...terry

DOWNER COW SCHOOL LUNCH PROGRAM



http://downercattle.blogspot.com/



IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?

In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle and a few horses. She had never been fed.

We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.

snip...

PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986



http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf



http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf



NOW, back to those mad mink i.e. TME. let me throw a curve ball here ;

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* and Richard A. Bessen† Emerging Infectious

Transmissible mink encepholapathy (TME) is a foodborne transmissible spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant TSE has been proposed as the cause, but the precise origin of TME is unknown. To compare the phenotypes of each TSE, bovine- passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, Htype BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain lesions profi les, disease-associated prion protein brain distribution, and biochemical properties of protease-resistant prion protein, typical BSE had a distint phenotype in ovine transgenic mice compared to L-type BSE and bovine TME. The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4 mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE. Transmissible mink encephalopathy (TME) is a rare prion disease in ranch-raised mink (Mustela vison) in North America and Europe (1–4). Six outbreaks have been reported from 1947 through 1985 in North America, and several have been linked to contaminated commercial feed (1). Although contamination of feed with scrapie-infected sheep parts has been proposed as the cause of TME, the origin of the disease remains elusive. The idea that scrapie in sheep may be a source of TME infection is supported by fi ndings that scrapie-infected mink have a similar distribution of vacuolar pathologic features in the brain and the same clinical signs as mink with natural and experimental TME (5). However, mink are not susceptible to scrapie infection following oral exposure for up to 4 years postinoculation, which suggests that either the scrapie agent may not be the source of natural TME infection or that only specifi c strains of the scrapie agent are able to induce TME (6,7). Epidemiologic investigations in the Stetsonville, Wisconsin, outbreak of TME in 1985 suggested a possible cattle origin, since mink were primarily fed downer or dead dairy cattle but not sheep products (8). Experimental transmission of Stetsonville TME into cattle resulted in transmissible spongiform encephalopathy (TSE) disease with an incubation period of 18.5 months. Back passage of bovine TME into mink resulted in incubation periods of 4 and 7 months after oral or intracerebral inoculation, respectively, which was similar to that found following inoculation of Stetsonville TME into mink by these same routes (8). These fi ndings indicated that cattle are susceptible to TME, and that bovine-passaged TME did not result in a reduced pathogenicity for mink. These studies raised the question as to whether an unknown TSE in cattle was the source of TME infection in the Stetsonville outbreak. Several additional TME outbreaks in the United States have been associated with mink diet that contained downer or dead cattle (9). ...

snip...full text ;



http://www.cdc.gov/EID/content/13/12/pdfs/1887.pdf



http://transmissible-mink-encephalopathy.blogspot.com/



3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE.339 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture.340 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre.341 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle,

*** did not produce the same clinical signs of brain lesions characteristic of BSE.***



http://www.bseinquiry.gov.uk/pdf/volume2/chapter3.pdf



"the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine." <<< href="mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:http://www.vetres.org/">www.vetres.org DOI: 10.1051/vetres:2007053 c INRA, EDP Sciences, 2008 Review article

snip...

And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

snip...

Cases of atypical BSE have only been found in countries having implemented large active surveillance programs. As of 1st September 2007, 36 cases (16 H, 20 L) have been described all over the world in cattle: Belgium (1 L) [23], Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1 L) [13], Italy (3 L)18, Japan (1 L) [71], Netherlands (1 H, 2 L)19, Poland (1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23. Another H-type case has been found in a 19 year old miniature zebu in a zoological park in Switzerland [56]. It is noteworthy that atypical cases have been found in countries that did not experience classical BSE so far, like Sweden, or in which only few cases of classical BSE have been found, like Canada or the USA.

And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

full text 18 pages ;



http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/articles/vetres/pdf/2008/04/v07232.pdf



please see full text ;



http://bse-atypical.blogspot.com/2008/06/review-on-epidemiology-and-dynamics-of.html



***Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.***

Progress Report from the National Prion Disease Pathology Surveillance Center

An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD

April 3, 2008



http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45



Sunday, March 16, 2008

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE



http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html



HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008

snip...

Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...

snip...



http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html



Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate



http://organicconsumers.org/forum/index.php?showtopic=1951



http://bse-atypical.blogspot.com/2008/08/atypical-bse-base-transmitted-from.html




Sunday, August 10, 2008

A New Prionopathy OR more of the same old BSe and sporadic CJD



http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html



PLEASE NOTE THE PARTIAL AND VOLUNTARY MAD COW FEED BAN OF AUGUST 4, 1997 nothing more than ink on paper ... TSS

Wednesday, April 23, 2008

FDA Strengthens Safeguards for Consumers of Beef Issues Regulation on Animal Feeds with Added Safeguards Against BSE



http://madcowfeed.blogspot.com/



CWD, is but a small piece, of a very big puzzle. and one of the main reasons this puzzle has not been solved, is the secrecy, cover-ups, and such. you must not ignore these facts. i did not want to believe this either. for years i was naive, but the facts speak for themselves.

it goes way back ;

Wednesday, August 20, 2008

Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?

August 20, 2008



http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html



Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0006 Public Submission Title Comment from Terry S Singletary Sr Views Add Comments How To Comment

snip...

MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. and they executed Saddam for poisoning ???

go figure....

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518



http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&d=APHIS-2006-0041-0006



From: Terry S. Singeltary Sr.



To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:FREAS@CBER.FDA.GOV

Cc: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:william.freas@fda.hhs.gov ; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:rosanna.harvey@fda.hhs.gov

Sent: Friday, December 01, 2006 2:59 PM

Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION

snip...

ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear with me)

THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted blood from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.

These are the facts as i have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species. ...

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

snip... 48 pages...



http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8



Docket APHIS-2006-0026 Docket Title Bovine Spongiform Encephalopathy; Animal Identification and Importation of Commodities Docket Type Rulemaking Document APHIS-2006-0026-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions, Identification of Ruminants and Processing and Importation of Commodities Public Submission APHIS-2006-0026-0012 Public Submission Title Comment from Terry S Singletary



http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801e47e1



Docket APHIS-2007-0033 Docket Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Docket Type Rulemaking Document APHIS-2007-0033-0001 Document Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Public Submission APHIS-2007-0033-0002.1 Public Submission Title Attachment to Singeltary comment



http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=090000648027c28e



Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2007.



http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf



i hope i have not bored anyone with all this, but you must know the history, and why we are where we are today. and where we are going in the future, in terms of Transmissible Spongiform Encephalopathy, as a whole, the bigger picture, TSEs in all species, and the ramifications thereof. NOT the infamous, bogus, UKBSEnvCJD only theory. ...

to be continued. ...

kindest regards, terry

Chronic wasting disease in a Wisconsin white-tailed deer farm 79% INFECTION RATE

Contents: September 1 2008, Volume 20, Issue 5

Journal of Veterinary Diagnostic Investigation Vol. 20 Issue 5, 698-703 Copyright © 2008 by the American Association of Veterinary Laboratory Diagnosticians

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

Case Reports

Chronic wasting disease in a Wisconsin white-tailed deer farm

Delwyn P. Keane1, Daniel J. Barr, Philip N. Bochsler, S. Mark Hall, Thomas Gidlewski, Katherine I. O'Rourke, Terry R. Spraker and Michael D. Samuel Correspondence: 1Corresponding Author: Delwyn Keane, University of Wisconsin, Wisconsin Veterinary Diagnostic Laboratory, 445 Easterday Lane, Madison, WI 53706. Delwyn.Keane@wvdl.wisc.edu

In September 2002, chronic wasting disease (CWD), a prion disorder of captive and wild cervids, was diagnosed in a white-tailed deer (Odocoileus virginianus) from a captive farm in Wisconsin. The facility was subsequently quarantined, and in January 2006 the remaining 76 deer were depopulated. Sixty animals (79%) were found to be positive by immunohistochemical staining for the abnormal prion protein (PrPCWD) in at least one tissue; the prevalence of positive staining was high even in young deer. Although none of the deer displayed clinical signs suggestive of CWD at depopulation, 49 deer had considerable accumulation of the abnormal prion in the medulla at the level of the obex. Extraneural accumulation of the abnormal protein was observed in 59 deer, with accumulation in the retropharyngeal lymph node in 58 of 59 (98%), in the tonsil in 56 of 59 (95%), and in the rectal mucosal lymphoid tissue in 48 of 58 (83%). The retina was positive in 4 deer, all with marked accumulation of prion in the obex. One deer was considered positive for PrPCWD in the brain but not in the extraneural tissue, a novel observation in white-tailed deer. The infection rate in captive deer was 20-fold higher than in wild deer. Although weakly related to infection rates in extraneural tissues, prion genotype was strongly linked to progression of prion accumulation in the obex. Antemortem testing by biopsy of recto–anal mucosal-associated lymphoid tissue (or other peripheral lymphoid tissue) may be a useful adjunct to tonsil biopsy for surveillance in captive herds at risk for CWD infection.

http://jvdi.org/cgi/content/abstract/20/5/698?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=prion&searchid=1&FIRSTINDEX=0&volume=20&issue=5&resourcetype=HWCIT


PLEASE NOTE 76 DEER WERE DEPOPULATED. SIXTY ANIMALS (79%) WERE FOUND TO BE POSITIVE BY IMMUNOHISTOCHEMICAL STAINING FOR THE ABNORMAL PRION PROTEIN (PrPCWD) IN AT LEAST ONE TISSUE; THE PREVALENCE OF POSITIVE STAINING WAS HIGH IN YOUNG DEER. ...TSS

Title: Chronic wasting disease in a Wisconsin captive white-tailed deer farm

Authors

Keane, Delwyn - U OF WIS, WIS VET DIAG LA Barr, Daniel - U OF WIS, WIS VET DIAG LA Bochsler, Philip - U OF WIS, WIS VET DIAG LA Hall, S - USDA, APHIS, VS, NVSL Gidlewski, Thomas - USDA, APHIS, VS O`rourke, Katherine Spraker, Terry - CO STATE UNIVERSITY Samuel, Michael - US GEOLOGIC SERVICE

Submitted to: Journal of Veterinary Diagnostic Investigation Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 5, 2008 Publication Date: N/A

Interpretive Summary: Chronic wasting disease is a fatal disease of deer and elk. Clinical signs, including weight loss, frequent urination, excessive thirst, and changes in behavior and gait, have been reported in mule deer and elk with this disorder. Clinical signs in captive white tailed deer are less well understood. In a previous study, a captive facility housed 200 deer, of which half were positive for the disease with no clinical signs reported. In this study, we examined 78 white tailed deer from a captive facility with a history of chronic wasting disease and no animals with clinical signs. Examination of the brain and lymph nodes demonstrated that the abnormal prion protein, a marker for disease, was observed in 60 of the deer. Biopsy of the rectal mucosa, a test that can be performed on live deer, detected 83% of the infected animals. The prion genetics of the deer was strongly linked to the rate of infection and to disease progression. The results demonstrate that clinical signs are a poor indicator of the disease in captive white tailed deer and that routine testing of live deer and comprehensive necropsy surveillance may be needed to identify infected herds. Technical Abstract: Chronic wasting disease CWD is a transmissible spongiform encephalopathy or prion disease of deer and elk in North America. All diseases in this family are characterized by long preclinical incubation periods following by a relatively short clinical course. Endpoint disease is characterized by extensive deposits of aggregates of the abnormal prion protein in the central nervous system,. In deer, the abnormal prion proteins accumulate in some peripheral lymphoid tissues early in disease and are therefore suitable for antemortem and preclinical postmortem diagnostics and for determining disease progression in infected deer. In this study, a herd of deer with previous CWD diagnoses was depopulated. No clinical suspects were identified at that time. Examination of the brain and nodes demonstrated that 79% of the deer were infected. Of the deer with abnormal prion in the peripheral lymphoid system, the retropharyngeal lymph node was the most reliable diagnostic tissue. Biopsy of the rectal mucosal tissue, a site readily sampled in the restrained or chemically immobilized deer, provided an accurate diagnosis in 83% of the infected deer. The retina in the eye of the deer was positive only in late stage cases. This study demonstrated that clinical signs are a poor indicator of disease, supports the use of the retropharyngeal lymph node as the most appropriate postmortem sample, and supports a further evaluation of the rectal mucosal tissue biopsy as an antemortem test on a herd basis.

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=218153


AN OLDER STUDY ;


Vol. 9, No. 5 May 2003

Dispatch

Chronic Wasting Disease in Free-Ranging Wisconsin White-Tailed Deer Damien O. Joly,* Christine A. Ribic,* Julie A. Langenberg,† Kerry Beheler,† Carl A. Batha,† Brian J. Dhuey,‡ Robert E. Rolley,‡ Gerald Bartelt,‡ Timothy R. Van Deelen,§; and Michael D. Samuel*¶ *United States Geological Survey-Wisconsin Cooperative Wildlife Research Unit, University of Wisconsin-Madison, Madison, Wisconsin, USA; †Wisconsin Department of Natural Resources, Madison, Wisconsin, USA; ‡Wisconsin Department of Natural Resources, Monona, Wisconsin, USA; §Wisconsin Department of Natural Resources, Rhinelander, Wisconsin, USA; and ¶United States Geological Survey–National Wildlife Health Center, Madison, Wisconsin, USA

Suggested citation for this article: Joly DO, Ribic CA, Langenberg JA, Beheler K, Batha CA, Dhuey BJ, et al. Chronic wasting disease in free-ranging Wisconsin white-tailed deer. Emerg Infect Dis [serial online] 2003 May [date cited]. Available from: URL: http://www.cdc.gov/ncidod/EID/vol9no5/02-0721.htm

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

Three White-tailed Deer shot within 5 km during the 2001 hunting season in Wisconsin tested positive for chronic wasting disease, a prion disease of cervids. Subsequent sampling within 18 km showed a 3% prevalence (n=476). This discovery represents an important range extension for chronic wasting disease into the eastern United States.

Chronic wasting disease (CWD) is degenerative and usually considered to be fatal in White-tailed Deer (Odocoileus virginianus), Mule Deer (O. hemionus), and Elk (Cervus elaphus) associated with the presence of transmissible protease-resistant prion proteins (PrPcwd) (1,2). Although the transmission route of PrPcwd is unknown, it may be transmitted in deer and elk by direct contact or indirectly from the environment (1,2). In experiments, clinical signs have appeared as early as 15 months after exposure (1) and include weight loss, anorexia, repetitive behaviors, hyperesthesia, and intractability. Signs progress to severe emaciation, extreme behavioral changes, excessive salivation, tremors, and mild ataxia (1,2). CWD was first recognized in captive Mule Deer in Colorado (3) and subsequently described in the free-ranging cervid populations of Colorado and Wyoming (1); prevalence in these disease-endemic areas varies spatially and among the three sympatric cervid species (4). Before its discovery in Wisconsin, CWD was detected in captive cervid farms in Colorado, Nebraska, South Dakota, Oklahoma, Kansas, Montana (USA), as well as Alberta, Saskatchewan (Canada), and South Korea (1). Apart from the contiguous areas of Colorado, Wyoming, and Nebraska, CWD had previously only been detected in two free-ranging Mule Deer from Saskatchewan, one Mule Deer from South Dakota, and in a number of Mule Deer from the western slopes region of Colorado (1). Previously, no cases of CWD were reported east of the Mississippi; however, subsequent to our research, CWD-positive cervids were found in Minnesota (captive Elk), Wisconsin (captive White-tailed Deer and Elk), and Illinois (free-ranging White-tailed Deer). Further, west of the Mississippi, the following CWD-positive animals have been found: Mule Deer in New Mexico and Utah; free-ranging Mule and White-tailed Deer in Saskatchewan, Canada; and captive Elk and White-tailed Deer in Alberta, Canada.

The Study In autumn of 1999 and 2000, the Wisconsin Department of Natural Resources (WDNR) submitted to the National Veterinary Services Laboratories (NVSL) (Ames, Iowa) brain material (obex) from 657 hunter-killed White-tailed Deer registered at hunter check stations across the state. None came from the study area we describe. Samples were tested for CWD prion by immunohistochemistry (IHC) (5). Prion was not detected in any samples. However, 3 of 445 White-tailed Deer shot in autumn of 2001 were positive for CWD. These deer were males, 2.5 years of age, and were shot within 5 km in south-central Wisconsin. WDNR subsequently conducted a sampling program to assess the distribution and prevalence of CWD in the vicinity of these three positive deer. We report the results of this sampling program.

Samples were collected from 500 adult (>1 year of age) White-tailed Deer within an approximate 18-km radius, and all samples were tested for CWD. Deer were submitted by hunters who were issued scientific collection permits, collected at roadside after vehicular collison, or collected by WDNR or U.S. Department of Agriculture sharpshooters. Data from collected deer included the geographic location based on the Wisconsin Public Land Survey System (township-range-section), sex, and age (estimated by using tooth eruption and tooth wear patterns [6]). Location of kill was indicated on a map by hunters during interviews by DNR staff. Samples of brain stem (obex) and retropharyngeal lymphatic tissue were fixed in 10% buffered formalin and submitted to NVSL for testing using IHC. We considered a deer to be CWD positive if either obex or retropharyngeal samples were IHC positive (1).

We used the spatial scan statistic provided by Kulldorff and Nagarwalla (7) (program SaTScan available from: URL: http://www3.cancer.gov/prevention/bb/satscan.html) to assess the presence and location of CWD clusters within the surveillance area. Location data were collected to the survey unit “section” (approximately 2.6 km2). We pooled locations into 4X4 section quadrats for analysis to compensate for sections from which no deer were collected. In a separate analysis, sex and age were assessed as predictors of CWD status by using logistic regression (function glm in program R v. 1.5.0; available from: URL: http://www.r-project.org) (8). Model selection uncertainty was incorporated into the odds ratio (OR) estimates by using model averaging (9).

Results and Discussion

From March 2 to April 9, 2002, samples were collected from 505 deer; however, 29 deer were not included in the analysis because of sample autolysis, inappropriate tissue submission, or lack of availability of appropriate tissues (e.g., deer with no intact cranium or those shot in the head). Of the remaining 476 deer (87 males, 386 females, and 3 for which sex was not recorded), 15 (3.2%; 95% confidence limit [CI] 1.7% to 5.1%) were IHC positive, 11 in both obex and retropharyngeal lymph node samples and 4 from lymph nodes only. We inferred that deer that were only lymph node positive were in the earlier states of infection (1). Estimated prevalence varied spatially within the surveillance area. A cluster of higher than expected prevalence was detected in the north-central region of the sampling area (prevalence 9.4%; 95% CI 5.0% to 16.0%; p=0.003; n=127) (Figure).

Prevalence did not vary by sex (males: 3.4%, 95% CI 0.1% to 9.7%, n=87; females: 3.1%, 95% CI 1.6% to 5.3%, n=386; male vs. female OR 1.1, 95% CI 0.56 to 2.19), a pattern consistent with Mule Deer sampled in Colorado and Wyoming (4). Increasing prevalence with age was suggested, although we could not distinguish whether the OR differed from 1 (OR 1.13, 95% CI 0.93 to 1.39). We had a small sample (n=32) of older animals (>5 years of age), which weakened our ability to detect an increase in prevalence with age statistically. Miller et al. (4) found that CWD prevalence increased with age in male Mule Deer and then abruptly declined in older age classes. We did not have a sufficient sample size to evaluate a sex difference in prevalence by age.

The known range of CWD was extended by its detection in Wisconsin, which is the first report of the disease east of the Mississippi River. Although we do not know how the free-ranging deer population of Wisconsin became affected by CWD, the most commonly suggested hypothesis is that CWD in Wisconsin may have emerged through importing of an affected cervid. The current enzootic of CWD in free-ranging deer and elk is paralleled by an enzootic in the captive cervid industry, and the relationship between CWD-affected elk farms and recent (2000–2002) diagnoses of CWD in free-ranging deer in Nebraska, South Dakota, and Saskatchewan remains under investigation (1). Elk were imported to Wisconsin from CWD-affected herds in Colorado during the 1990s, and recently (September and October 2002) captive White-tailed Deer were found to be positive on two separate farms in central and southern Wisconsin (10). Furthermore, during epidemiologic investigations of these positive farms, WDNR discovered that deer had escaped in March 2002 from one of these farms, one of which was later shot and found to be CWD positive (9). We stress that these positive captive deer are likely not the source of CWD in this free-ranging White-tailed Deer outbreak because of the captive deer’s distance from the area where the CWD-positive free-ranging deer are (approximately 130 km). No direct evidence exists that CWD came to Wisconsin by the captive cervid industry. However, further investigation on possible links between CWD cases in captive and free-ranging cervids in Wisconsin is ongoing.

Conclusions The state of Wisconsin is undertaking an integrated research, surveillance, and management program to determine the distribution of CWD in the Wisconsin free-ranging deer population and eventually eliminating the disease from the known affected area of south-central Wisconsin (10,11). As of March 2003, a total of 39,636 deer had been sampled statewide for CWD as part of this surveillance and management program (data are available from: URL: http://www.dnr.state.wi.us/org/land/wildlife/whealth/issues/CWD/). Computer simulation of CWD dynamics in western cervid populations (12) indicated that CWD could severely reduce deer numbers. Disease transmission may occur at a greater rate and consequently have a larger impact on the population in the eastern United States, where White-tailed Deer densities are typically an order of magnitude larger than western deer and elk populations (e.g., deer densities in the CWD-affected area are estimated to be currently >20 deer per km2) (WDNR, unpub. data). Deer and deer-related activities, such as hunting, wildlife viewing, and other social factors, are an important component of the Wisconsin culture and economy (approximately $1 billion/year) (13), prompting an aggressive research and management strategy to combat CWD in Wisconsin’s free-ranging deer population.

Acknowledgments

http://www.cdc.gov/ncidod/EID/vol9no5/02-0721.htm


Monday, August 25, 2008 CWD FIRST DOCUMENTED IN MICHIGAN

http://chronic-wasting-disease.blogspot.com/2008/08/cwd-first-documented-in-michigan.html


Wednesday, September 03, 2008 Accelerated High Fidelity Prion Amplification Within and Across Prion Species Barriers

http://chronic-wasting-disease.blogspot.com/2008/09/accelerated-high-fidelity-prion.html


CHRONIC WASTING DISEASE

http://chronic-wasting-disease.blogspot.com/


TSS