Fwd: Educate Yourself more on MADCOW!!!(another interview++++)

February 14, 2004

"Terry S. Singeltary Sr." <flounder wrote:

Fri, 13 Feb 2004 19:32:01 -0600"Terry S. Singeltary Sr." k_t723Subject: Re: A Madcow Interview(Dave Louthan) I Doubt That Any MainstreamMedia Would Print OR Air!!!-------

DAVE LOUTHAN and INSPECTOR TRENT on Pete Collins radio interview;

Wed, 11 Feb 2004 09:20:38 -0600

"Terry S. Singeltary Sr." <flounder

Bovine Spongiform Encephalopathy <BSE-L

BSE-L######## Bovine Spongiform Encephalopathy #########

DAVE LOUTHAN on Pete Collins radio interview (REALPLAYER);

"once it is boned out, it goes in a great big card board box,

and it's lost forever."

"stuff like tongue, liver, tail we sell in town with no

identity"

http://www.maddeer.org/louthan/audio/012904louthan.ram

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

-------

Re: DAVE LOUTHAN (aka mad cow killer) speaks before the Washington State Senate Ag Comm

Tue, 10 Feb 2004 09:42:10 -0600

"Terry S. Singeltary Sr." <flounder

Bovine Spongiform Encephalopathy <BSE-L

BSE-L

References:

<40203070.3000900 <402120BB.1040900 <4028106D.8020101 <40284D4A.80309 <4028E986.4080807######## Bovine Spongiform Encephalopathy #########

The guy with the gun who tried to get Dave into the green govt suv a couple

of days back has been identified as Gundar Grundberg

GUNDAR.GRUNDBERG He is listed at the USDA web site as an

employee of the Office of the Inspector General, ie within USDA but not

APHIS or FSIS

http://ds.usda.gov/ shows the listing but not a phone number.

http://www.usda.gov/oig/home.htm Phone for OIG is: (202) 720-5677

"The mission of the Office of Inspector General is to investigate

allegations of crime against the Department's programs, and to promote the

economy and efficiency of its operations, with the object of helping to

protect its programs and to ensure integrity. Maintaining the integrity of

Department programs. Helping the Department strengthen its defenses against

activities that might threaten Government facilities, production

agriculture, and the Nation¹s food supply. During the 6-month period ending

September 30, 2001 our audits and investigations yielded $32 million in

recoveries, collections, restitutions, fines, claims established, cost

avoided, and administrative penalties. Management agreed to put $78 million

to better use. We identified one-half of a million dollars in questioned

costs that cannot be recovered. Our investigations and produced 181

indictments and 172 convictions.... investigating allegations of fraud and

abuse; using preventive audit approaches, such as reviews of systems under

development; conducting audits of the adequacy and vulnerability of

management and program control systems; and auditing the adequacy of large

USDA payments, such as insurance and deficiency payments, major loans, and

retailer food stamp redemptions. "

TSS

Terry S. Singeltary Sr. wrote:

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

> #########

>

> more comments from Dave Louthan for those interested;

>

>> First a blank form that said every thing I told them was under oath

>> with penalty of perjury. Then they wanted me to right out a statement

>> absolveing Gunder Grundberg of any wrong doing and stateing the

>> NYtimes article was wrong. I told them I can't see up close to write

>> so they said they would write it and I could sign it tommorrow. They

>> quizzed me about every detail that has occured since day one but they

>> only wrote stuff down when they asked about Grundberg and the times

>

> TSS

>

> Terry S. Singeltary Sr. wrote:

>

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

>> #########

>>

>> Greetings list members,

>>

>> got a reply back from dave and an aritcle below that may be of interest

>> to some;

>>

>>> That was ugly and scarey. They griiled me for 2 hours about everything

>>> I've said and done. What that other agent did. About the inspector

>>> about the N.Y.Times article Everything They wanted me to sign some

>>> statements but I refused. They were insistant but I held fast they

>>> said they would be back tommorrow. They said 27 times we are not

>>> harrasing you we just want to talk.

>>

>> USDA vets question agency's mad cow lab

>>

>> By Steve Mitchell

>> United Press International

>> Published 2/9/2004 7:06 PM

>> View printer-friendly version

>>

>> WASHINGTON, Feb. 9 (UPI) -- The federal laboratory in Ames, Iowa, that

>> conducts all of the nation's tests for mad cow disease has a history of

>> producing ambiguous and conflicting results -- to the point where many

>> federal meat inspectors have lost confidence in it, Department of

>> Agriculture veterinarians and a deer rancher told United Press

>> International.

>>

>> The veterinarians also claim the facility -- part of the USDA and known

>> as the National Veterinary Services Laboratories -- has refused to

>> release testing results to them and has been so secretive some suspect

>> it is covering up additional mad cow cases.

>>

>> Distrust of the NVSL is so widespread among USDA veterinarians and meat

>> inspectors it limits mad cow disease surveillance "tremendously," said a

>> veterinarian with more than 25 years of experience with the agency.

>>

>> The veterinarian, who requested anonymity because he feared

>> repercussions, said many agency inspectors do not consider it worth the

>> trouble to inspect cows closely for signs of mad cow disease or to send

>> brain samples to the NVSL because there is little chance the lab will

>> issue a positive result, even if the cow is infected.

>>

>> In some instances, when USDA veterinarian inspectors have sent brains

>> from cows they suspected of having mad cow disease, NVSL staff members

>> have said they did not receive enough brain tissue or that they received

>> the wrong part of the brain, the veterinarian explained.

>>

>> The inspectors insisted they sent in the entire brain, "but that is the

>> end of the story," he added.

>>

>> The USDA's official stance is that the U.S. beef supply is free of mad

>> cow disease, or bovine spongiform encephlopathy, but the veterinarian

>> said, "Most agency veterinarians know mad cow is prevalent and epidemic

>> (in U.S. herds). We're not talking about one or two cases."

>>

>> An international panel of mad cow experts, commissioned by the USDA to

>> review the agency's response to the animal that tested positive for mad

>> cow in Washington state in December, reached a similar conclusion in a

>> report they issued last week.

>>

>> The panel said it was "probable" additional infected cows had been

>> imported from Canada and Europe, some of which had been turned into cow

>> feed and indigenously infected U.S. herds.

>>

>> The concern is humans can contract a fatal brain disease known as

>> variant Creutzfeldt-Jakob disease from eating meat contaminated with the

>> agent that causes mad cow disease.

>>

>> "The USDA has such a cohesive relationship with industry" that it wants

>> to protect the $70 billion beef industry more than consumers, the

>> veterinarian said, and noted colleagues with whom he is in close contact

>> think the agency's mad cow surveillance program "is a laughing matter."

>>

>> When asked to comment for this story, USDA spokesman Jim Rogers

>> requested UPI forward its questions about NVSL via e-mail. Although UPI

>> complied with this request, the agency did not respond.

>>

>> Stanley Hall, who owns a deer herd in Almond, Wis., has been embroiled

>> in a legal battle with the USDA since 2002 over whether one of his deer

>> tested positive for chronic-wasting disease. CWD is the deer equivalent

>> of mad cow disease and is detected using the same test.

>>

>> In September 2002 NVSL said one of Hall's deer tested positive for CWD.

>> Hall, who had retained some of the deer brain, then had it tested by

>> Beth Williams, a veterinarian and renowned CWD expert at the University

>> of Wyoming in Laramie.

>>

>> Williams concluded in her report that abnormal prions, the agent thought

>> to cause CWD, were "not detected." Williams noted, however, that the

>> sample consisted only of the caudal medulla oblongata region of the

>> brain and not the preferred obex region, meaning early infection with

>> chronic wasting disease could not be ruled out.

>>

>> Based on the conflicting results, and because he knew the brain sample

>> tested by Williams originated from his deer, Hall suspected the sample

>> tested by the USDA did not come from his deer, but rather from some

>> other animal.

>>

>> USDA officials, however, refused to release their sample for DNA

>> analysis, even though Hall has offered to pay the $80 test fee himself.

>> Hall said he thinks the USDA has refused to conduct a DNA test "because

>> it won't match" his deer.

>>

>> The USDA has not responded for more than a year to a request filed by

>> Hall's attorney, Gary Drier in Stevens Point, Wis., under the Freedom of

>> Information Act, asking for additional information about the tissue

>> sample in question and how it was processed. Under federal law, the

>> agency is required to respond to a FOIA request within 30 days.

>>

>> "There's something dirty going on in that lab in Ames," Hall said. Based

>> on the NVSL results on his deer, Wisconsin's Department of Agriculture,

>> Trade and Consumer Protection ordered Hall to kill his herd of 100-plus

>> deer, an order he is appealing.

>>

>> Dr. Lester Friedlander, a former USDA veterinarian, agreed with Hall and

>> said, "There's definitely issues" with the validity of NVSL test

>> results.

>>

>> Friedlander, who was a decorated employee during his 10 years with the

>> agency from 1985 to 1995, recounted an experience he had in 1991 when he

>> sent a tissue sample from a sick cow to NVSL and a separate sample from

>> the same cow to a USDA lab in Athens, Ga. The test results conflicted,

>> with NVSL reporting one type of cancer and the Athens lab reporting a

>> different type.

>>

>> In another incident, Friedlander said he was taking photographs of cow

>> brains in the early 1990s before he sent them to NVSL for mad cow

>> testing.

>>

>> "Some of the brains were really suspicious, but the test results (from

>> NVSL) always came back negative," he said, and noted he doubted the

>> results. "But when you only have one lab (doing all the testing) who's

>> going to listen to your story?"

>>

>> The anonymous USDA veterinarian said NVSL often refuses to provide test

>> results, even to the inspector who initially requested the test. NVSL's

>> refusal to send lab reports "has been routine for the last two or three

>> years," he said. "By this time, we don't trust Ames."

>>

>> In a 1997 case, with which the veterinarian was familiar, a brain sample

>> from a cow suspected of having a brain disorder was sent to NVSL. The

>> diagnosis came back as a disease known as Progressive Ataxia. This seems

>> implausible, he said, because in the annals of veterinary medicine the

>> disorder has only been seen in the Charolais and Simmental cattle breeds

>> -- and only rarely at that -- and the cow in question was a brown and

>> white Hereford.

>>

>> Without an outside lab also conducting tests, "we are not going to have

>> a very independent analysis. It's very easy to control the results," he

>> said, and noted a pathologist at NVSL told him lab staff often do not

>> have access to all the test results from one animal.

>>

>> The international panel's report advised the USDA to decentralize its

>> mad cow testing program and permit other labs around the country to

>> conduct tests and help facilitate the rapid testing of suspect animals.

>>

>> Friedlander said decentralizing the testing would be a good start toward

>> restoring confidence in the results. Right now, he added, "Nobody is

>> actually questioning the lab" or conducting confirmation tests of the

>> results.

>>

>> --

>>

>> Steve Mitchell is UPI's medical correspondent. E-mail

>> sciencemail

>>

>> 2001-2004 United Press International

>>

>> http://www.upi.com/view.cfm?StoryID=20040209-061848-3665r

>>

>> TSS

>>

>> Terry S. Singeltary Sr. wrote:

>>

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

>>> #########

>>>

>>> Feds got Dave now! want to talk???...TSS

>>>

>>>> Everyone but the nation's press seems to know the name and emails of

>>>> the

>>>> "disappeared" inspecting vet. That would be Rodney (Rod) Thompson.

>>>> Does

>>>> anyone have a current phone number for him?

>>>>

>>>> Rod.Thompson

>>>

>>> Terry S. Singeltary Sr. wrote:

>>>

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

>>>> #########

>>>>

>>>> better quality ;

>>>>

>>>> http://www.maddeer.org/video/020304louthan2.ram

>>>>

>>>> good Tri-City Herald coverage

>>>> http://www.tri-cityherald.com/tch/local/story/4704230p-4655128c.html

>>>>

>>>> TSS

>>>>

>>>> Terry S. Singeltary Sr. wrote:

>>>>

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

>>>>> #########

>>>>>

>>>>> Dave Louthan (aka mad cow killer) speaks before the Washington State

>>>>> Senate Agriculture Committee.

>>>>>

>>>>> RealPlayer audio

>>>>>

>>>>> http://www.maddeer.org/audio/020304louthan.ram

>>>>>

>>>>> TSS

>>>>>

>>>>> ########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html

>>>>> ############

>>>>>

>>>>

>>>> ########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html

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>>>>

>>>

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BSE/TSE USA FEDERAL DOCKETS SUBMISSION...TSS Docket Management Docket: 02N-0273 - Substances Prohibited From Use in Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed Comment Number: EC -10 Accepted - Volume 2 http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html PART 2 http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html PDF]Freas, William TSS SUBMISSION File Format: PDF/Adobe Acrobat - Page 1. J Freas, William Terry S. Singeltary Sr. [flounder] Monday, January 08,200l 3:03 PM freas ...

http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf Asante/Collinge et al, that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD; http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice in Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number: EC -2 Accepted - Volume 7 http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm [PDF] Appendices to PL107-9 Inter-agency Working

Group Final Report 1-1 File Format: PDF/Adobe Acrobat - View as HTML Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of those who provided comments in response to Docket No. ... Meager 8/18/01 Terry S. Singeltary Sr ... www.aphis.usda.gov/lpa/pubs/pubs/PL107-9_Appen.pdf - Similar pages # Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] - TSS 1/27/03 (0) http://www.vegsource.com/talk/madcow/messages/9912395.html Dockets Entered On October 02, 2003 ... Dockets Entered On October 2, 2003 Table of Contents, Docket #, Title, 1978N-0301, OTC External Analgesic Drug Products, ... EMC 7, Terry S.

Singeltary Sr. Vol #: 1, ... www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm Daily Dockets Entered on 02/05/03 DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2. ... Vol#: 1. 03N-0009 Federal Preemption of State & Local Medical Device Requireme. ... www.fda.gov/ohrms/dockets/dailys/03/Feb03/020503/020503.htm Docket Management Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater Comment Number: EC -1 Accepted - Volume 1 http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html ================================================= TSS PUBLISHINGS PEER REVIEWED JOURNALS Send Post-Publication Peer Review to journal: Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Email Terry S. Singeltary: flounder I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported

that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and

needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? http://www.neurology.org/cgi/eletters/60/2/176#535 LANCET INFECTIOUS DISEASE JOURNAL Volume 3, Number 8 01 August 2003 Newsdesk Tracking spongiform encephalopathies in North America Xavier Bosch My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem. 49-year-old Singeltary is one of a number of

people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation. Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained

in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source. Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle. To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the

plausibility of CWD spreading to people has remained elusive. Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk. Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE. Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have. Norman Foster, director of the Cognitive Disorders Clinic

at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out. Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of

venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison. CDC spokesman Ermias Belay says that the CDC will not be investigating the [samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans & the data seeking evidence of CWD transmission to humans have been very limited. http://infection.thelancet.com/journal/journal.isa >>>he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.<<< actually, that quote was from a more recent article in the Journal of Neurology (see below), not the JAMA article... Full Text Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow= & HITS=10 & hits=10 & RESULTFORMAT= & fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease & searchid=1048865596978_1528 & stored_search= & FIRSTINDEX=0 & journalcode=jama BRITISH MEDICAL JOURNAL SOMETHING TO CHEW ON BMJ http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2 BMJ http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1 THE PATHOLOGICAL PROTEIN BY Philip Yam CHAPTER 14 Laying Odds Are

prion diseases more prevalent than we thought? Researchers and government officials badly underestimated the threat that mad cow disease posed when it first appeared in Britain. They didn't think bovine spongifbrm encephalopathy was a zoonosisan animal disease that can sicken people. The 1996 news that BSE could infect humans with a new form of Creutzfeldt-Jakob disease stunned the world. It also got some biomedical researchers wondering whether sporadic CJD may really be a manifestation of a zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD is? Revisiting Sporadic CJD It's not hard to get Terry Singeltary going. "I have my conspiracy theo- ries," admitted the 49-year-old Texan.1 Singeltary is probably the nation's most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with

others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union's Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous www.mad- cow.orgWeb site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that 223 224 CHAPTER 14 prions represent more of a threat than people realize, and that the gov- ernment has responded poorly to the dangers because it is more con- cerned about protecting the beef industry than people's health. Singeltary has similar inclinations, but unlike these men, he doesn't have the professional credentials behind him. He is an 11-grade dropout, a machinist who retired because of a neck injury sustained at work. But you might not know that from the vast stores of information in his mind and on his hard drive. Over the years, he has provided unac-

knowledged help to reporters around the globe, passing on files to such big-time players as The New Tork Times, Newsweek, and USA Today. His networking with journalists, activists, and concerned citizens has helped medical authorities make contact with suspected CJD victims. He has kept scientists informed with his almost daily posting of news items and research abstracts on electronic newsgroups, including the bulletin board on www.vegsource.com and the BSE-listserv run out of the University of Karlsruhe, Germany. His combative, blunt, opinion- ated style sometimes borders on obsessive ranting that earns praise from some officials and researchers but infuriates othersespecially when he repeats his conviction that "the government has lied to us, the feed industry has lied to usall over a buck." As evidence, Singeltary cites the USDA's testing approach, which targets downer cows and examined 19,900 of them in

2002. To him, the USDA should test 1 mil- lion cattle, because the incidence of BSE may be as low as one in a mil- lion, as it was in some European countries. That the U.S. does not, he thinks, is a sign that the government is really not interested in finding mad cows because of fears of an economic disaster. Singeltary got into the field of transmissible spongiform encepha- lopathy in 1997, just after his mother died of sporadic CJD. She had an especially aggressive versionthe Heidenhain variantthat first causes the patient to go blind and then to deteriorate rapidly She died just ten weeks after her symptoms began. Singeltary, who said he had watched his grandparents die of cancer, considered her death by CJD to be much, much worse: "It's something you never forget." Her uncon- trollable muscle twitching became so bad "that it took three of us to hold her one time," Singeltary recalled. "She did everything but levitate in bed and spin her head." Doctors originally diagnosed

Alzheimer's disease, but a postmortem neuropathological exam demanded by Singeltary revealed the true nature other death. Laying Odds 225 Classifying a disease as "sporadic" is another way for doctors to say they don't know the cause. Normal prion proteins just turn rogue in the brain for no apparent reason. The term "sporadic" is often particularly hard for the victims' families to accept, especially when the patient was previously in robust health. Maybe it was something in the water, they wonder, or in the air, or something they atethe same questions CJD researchers tried to answer decades ago. The names "sporadic CJD" and "variant CJD" also confuse the public and raise suspicions that U.S. authorities are hiding something when they say there have been no native variant CJD cases in the country. Singeltary suspected an environmental cause in his mother's demise a feeling reinforced a year later when a neighbor died of spo- radic CJD. For years, the neighbor had been taking

nutritional supple- ments that contained cow brain extracts. Researchers from the National Institutes of Health collected samples of the supplement, Singeltary recounted, and inoculated suspensions into mice. The mice remained healthywhich only means that those supplement samples tested were prion-free. Scientists have made several attempts during the past few decades to find a connection between sporadic CJD and the environment. Often, these studies take the form of asking family members about CJD vic- timstheir diet, occupation, medical history, hobbies, pets, and so forthand comparing them with non-CJD subjects. Such case-control CJD studies have produced some intriguingand sometimes contra- dictoryresults. In 1985, Carleton Gajdusek and his NIH colleagues reported a correlation between CJD and eating a lot of roast pork, ham, hot dogs, and lamb, as well as rare meats and raw oysters.2 Yet they also recognized that the findings were preliminary and that more studies were

needed. Following up, Robert Will of the U.K. National CJD Surveillance Unit and others pooled this data with those from two other case-con- trol studies on CJD (one from Japan and one from the U.K.). In particu- lar, they figured the so-called odds ratiocalculated by dividing the fre- quency of a possible factor in the patient group by the frequency of the factor in the control group. An odds ratio greater than I means that the factor may be significant. In their study, Will and his collaborators found an increase of CJD in people who have worked as health profes- sionals (odds ratio of 1.5) and people who have had contact with cows 226 CHAPTER 14 (1.7) and sheep (1.6). Unfortunately, those connections were not statisti- cally significant: The numbers of pooled patients (117) and control sub- jects (333) were so small that the researchers felt the odds ratios needed to reach 2.5 to 8 (depending on the assumptions) before they could be deemed statistically significant. The only

statistically significant corre- lations they found were between CJD and a family history of either CJD (19.1) or other psychotic disease (9.9), although the latter might simply be correlated because psychotic disease may be an early symp- tom of undiagnosed CJD.3 In contrast with earlier findings, the team concluded that there was no association between sporadic CJD and the consumption of organ meats, including brains (0.6). Although these case-control studies shed a certain amount of light on potential risk factors for CJD, it's impossible to draw firm conclu- sions. Obtaining data that produces statistically meaningful results can be difficult because of the rarity of CJD and hence the shortage of sub- jects. Human memory is quite fragile, too, so patients' families may not accurately recall the lifestyle and dietary habits of their loved ones over the course of a decade or more. Consequently, researchers must cope with data that probably contain significant biases. In a review

paper on CJD, Joe Gibbs of the NIH and Richard T.Johnson of Johns Hopkins University concluded that "the absence of geographic differences in incidence is more convincing evidence against major dietary factors, since large populations eschew pork and some consume no meat or meat products."A CJD study of lifelong vegetarians, they proposed, could produce some interesting data.4 The inconclusive results of case-control studies do not completely rule out the environment as a possible cause of CJD. "Dr. Prusiner's theory does fit much of the data of spontaneous generation of [mal- formed] PrP somewhere in the brain," Will remarkedthat is, the idea that sporadic CJD just happens by itself falls within the realm of the prion theory. Still, "it's very odd, if you look at all the forms of human prion diseases there are, all of them are transmissible in the laboratory and could be due to some sort of infectious agent."5 One of the great difficulties, he explained, is that "given that this

is a disease of an extraordinarily long incubation period, are we really confident that we can exclude childhood exposure that is transmitted from person to person, as people move around? It's difficult to be sure about that." There might a "carrier state" that leaves people healthy yet still able to Laying Odds 227 infect others. If so, "you would never be able to identify what's causing the spread of the disease," concluded Will, who hasn't stopped looking for a possible environmental link. He has some preliminary data based on studies that trace CJD victims' lives well before the time symptoms beganup to 70 years; they suggest some degree of geographic cluster- ing, but no obvious candidates for a source of infection. A Case for Undercounting The difficulty in establishing causal links in sporadic prion diseasesif there are any in the first placeunderlines the importance of thorough surveillance. The U.K. has an active program, and when a victim of CJD is reported, one of

Robert Will's colleagues visits and questions the victim's family. "No one has looked for CJD systematically in the U.S.," the NIH's Paul Brown noted. "Ever."6 The U.S., through the Centers for Disease Control and Prevention, has generally maintained a more passive system, collecting information from death certificates from the National Center for Health Statistics. Because CJD is invariably fatal, mortality data is considered to be an effective means of tabulating cases. The CDC assessed the accuracy of such data by comparing the numbers with figures garnered through an active search in 1996: Teams covering five regions of the U.S. contacted the specialists involved and reviewed medical records for CJD cases between 1991 and 1995. Comparing the actively garnered data with the death certificate infor- mation showed that "we miss about 14 percent," said CDC epidemiolo- gist Lawrence Schonberger. "That's improving. Doctors are becoming more knowledgeable," thanks to increased

scientific and media atten- tion given to prion diseases.7 The active surveillance study of 1996, however, only looked at cases in which physicians attributed the deaths to CJD. Misdiagnosed patients or patients who never saw a neurologist were not tabulated thus CJD may be grossly underreported. Many neurological ailments share symptoms, especially early on. According to various studies, autopsies have found that CJD is misdiagnosed as other ills, such as dementia or Alzheimer's disease, 5 to 13 percent of the time. The CDC finds that around 50,000 Americans die from Alzheimer's each year 228 CHAPTER 14 (about 4 million have the disease, according to the Alzheimer's Association). Therefore, one could argue that thousands of CJD cases are being missed. (On the flip side, CJD could be mistakenly diagnosed as Alzheimer's disease or dementia, but the number of CJD patients is so small that they wouldn't dramatically skew the statistics for other neurological ills.) In part to address

the issue of misdiagnosis, CJD families have asked the CDC to place the disease on the national list of officially notifiable illnesses, which tends to include more contagious conditions such as AIDS, tuberculosis, hepatitis, and viral forms of encephalitis. Currently, only some states impose this requirement. CDC officials have discounted the utility of such an approach, arguing that it would duplicate the mortality data, which is more accurate than early diag- noses of CJD, anyway. Moreover, mandatory reporting of CJD cases does not necessarily guarantee the end to missed cases.8 One clue suggests that the passive system is undercounting CJD in the U.S.: racial difference. The number of black CJD victims is about 38 percent that of white victims. Rather than sporadic CJD being a one- in-a-million lottery, it's more like one-in-2.5-million for African- Americans. Access to medical care might be one reason. Schonberger recounted that the CDC had asked other countries with

substantial black populations to submit CJD figures for comparison but found that the surveillance in those countries was inadequate. "We haven't been able to find any comparable literature on this issue, so it's still up in the air," Schonberger said. On the other hand, Alzheimer's disease is more common among black people than whites, with an estimated higher prevalence ranging from 14 percent to almost 100 percent, according to a February 2002 report by the Alzheimer's Association. Are some black CJD cases being misdiagnosed as Alzheimer's? Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population. As Schonberger pointed out, no doctor would misdiagnose a 30-year-old CJD patient as having Alzheimer's. The average age of the first 100 variant CJD victims was 29; should the epidemiology of vCJD changeif older

people start coming down with itthen there would be problems. "The adequacy of our overall CJD surveillance would be Laying Odds 229 greatly reduced should the proportion of older individuals affected by variant CJD substantially increase," Schonberger explained.9 To date, only brain autopsies can confirm CJD. To encourage the necessary neuropathological studies, in 1997 the CDC helped establish the National Prion Disease Pathology Surveillance Center at Case Western Reserve University, under the directorship of Pierluigi Gambetti. But the number of brains examined has fallen far short of the number of CJD cases in the U.S.: Gambetti's lab, which receives brains based on referrals from local physicians and families, looked at only 99 sporadic CJD cases in 2000 and 138 in 2001, when about 300 each year are expected. "I'm very unhappy with the numbers," Gambetti lamented. "European countries see 100 or 90 percent of all the cases suspected. We see 30 to 40 percent."10 Most families

don't think about having an autopsy done (which can cost upward of $1,500 if the hospitals don't pick up the tab), and mem- bers of the support group CJD Voice have said they were too distraught to think of shipping a loved one's brain by Federal Express to Gambetti's lab. (For accurate analyses of brain tissue, the autopsy must be performed within 72 hours of death, assuming the body has been kept refrigerated.) Moreover, physicians often do not suggest an autopsy, perhaps because of liability fears should the postmortem reveal that the original diagnosis was wrong. Gambetti has been work- ing on establishing a network that would enable postmortems to be done near where the deceased person lived and without cost to the family. He is also working on advertising the existence of his surveil- lance center, via meetings and letters to neurologists, pathologists, and other specialists. Gambetti is also attempting to combat what he termed "hysteria" over the potential for infection that

has pathologists irrationally shunning CJD cases while they willingly conduct arguably riskier AIDS autopsies. "In order to make people aware, you have to keep informing them over and over and over," he said. Money is the main reason why the U.S. lags behind Europe in terms of surveillance. To adequately survey the 290 U.S. million residents, "you need a lot of money," Robert Will explained. "There was a CJD meeting of families in America in which poor old Larry {Schonberger] got attacked fairly vigorously because there wasn't proper surveillance. You could only do proper surveillance if you have adequate resources. 230 CHAPTER 14 That's the bottom line. We're very fortunate in the U.K.; we have very generous resources for CJD surveillance." Moreover, the U.K. makes feline spongifbrm encephalopathy an offi- cially notifiable disease. Domestic cats proved to be good sentinel ani- mals because they dine on the meat not fit for human consumption the parts more likely to harbor prion

infectivity. In the U.S., FSE isn't federally notifiable. And while the USDA says it has sent educational material to private veterinarians and works with vet schools,21 it's not clear just how many vets can spot FSE, which has never been reported in the U.S. Certainly, not many cat postmortems are done. The only active portion of the U.S. CJD surveillance system are the follow-up investigations conducted for victims of CJD under 55 years of age. It began in 1996, when young people in the U.K. started succumb- ing to variant CJD. Victims under 30 years of age especially arouse interest, because such cases could indicate an infection from the envi- ronment. Except for the variant CJD case in Florida, the CDC has clas- sified all of these more youthful cases of CJD as having either sporadic or familial origins. One such age cluster involved the three venison eaters that the CDC tried unsuccessfully to link to the deer-and-elk borne chronic wasting disease. A second grouping occurred

in 2002 in a pair of Michigan men. The twoone 26 years old, the other 28 did not know each other but lived in neighboring counties in Michigan and went to the same hospi- tal for diagnosis.12 The CDC's investigation turned up nothing that suggested a new form of CJD had emerged. But the increased frequency of young CJD cases is disturbing. In the 18-year period between 1979 and 1996, the U.S. had 12 cases in patients under 30, and only one of them had the sporadic form of CJD. (The other cases resulted from heredity or from transmission via contami- nated growth hormone or dura mater grafts.13) Between 1997 and 2001, five people under 30 died of sporadic CJD: the three venison eaters and the two Michigan patients. That represents a substantial blip of five young cases in five years, as opposed to only one case in 18 years. Physicians at the University of Michigan Health System who examined the two Michigan men concluded: As a result of our findings, we feel that sporadic CJD may

be more common than previously thought, that it may occur in younger indi- Laying Odds 231 viduals than currently perceived, and that some cases may go undiag- nosed due to insufficient testing. . . . We recommend that physicians everywhere begin to consider CJD in rapidly progressive neurological decline of unknown causes in people under 30 years of age, and that brain biopsy and autopsy with genetic and prion analysis be performed in all such cases.14 Pathologically, the recent bout of young casualties in the U.S. appears to be no different from CJD already seen in America. Yet theoretically it may have come from a new source of infection, based on an unex- pected result announced in late November 2002. John Collinge of the British Medical Research Council's Prion Unit found that not all trans- genic mice infected with BSE prions developed the neuropathological and molecular characteristics of variant CJD; some of the mice instead generated the molecular features of sporadic CJD.

Therefore, some CJD cases classified as sporadic may have actually been caused by BSE prions, Collinge hypothesized.15 So far, the epidemiology of CJD in the U.K. does not bear out that suppositionthere has been no substantial uptick in sporadic CJD as would be expected if BSE could paint more than one pathological picture. But the preliminary study, taken at face value, could be seen as evidence that something infectious is happening in the cases of young, sporadic CJD victims in the U.S. Another mouse study, reported in March 2002, fueled concern that prion infections may be more common than previously thought.16 Stanley Prusiner's lab found that mice infected with mouse prions accu- mulated PrPSc in their skeletal muscles, mostly in those in the hind limbs. In some mice, each gram of muscle contained some 10 million infectious doseson par with that in the brain in other experiments involving intracerebral inoculation. To some CJD researchers, this find- ing suggested that

muscle meat from cows might not be safe, after all, and that the measures taken in Europe to protect the food supply banning high-risk cow partsmay not be enough. Although this study may seem alarming, its implications are not as sweeping as they may appear. Only a minority of results in mouse stud- ies end up having a direct analog in humans. The skeletal muscle discov- ery warrants further examination, but it would be premature to alter food policies. Prions are different for each species, and accumulation of prions varies from species to species and from disease to disease. Furthermore, BSE cattle muscle has failed to sicken mice in bioassay 232 CHAPTER 14 work, suggesting that little or no infectious prions lurk there. What such findings truly reveal is that prion diseases are complicated and still mysterious, and trying to quantify the risks for human health is fraught with uncertainties...snip...284 pages...thanks Philip...TSS The Pathological Protein: Mad Cow, Chronic

Wasting, and Other Deadly Prion Diseases, Philip Yam Philip Yam News Editor Scientific American www.sciam.com http://www.thepathologicalprotein.com/ NEW SCIENTIST MAGAZINE 4/02/01 NEW SCIENTIST EDITORIAL PAGE 3 MAD SHEEP DISEASE? IF THERE is one categorical pronouncement you can safely make about prion diseases like BSE or CJD, it is that one should not make categorical pronouncements. "British beef is safe" and "there is no BSE in Germany" come to mind. Now there are two more: "scrapie is safe", and "people don't catch sporadic CJD". Scrapie is the most widespread prion disease, infecting untold numbers of sheep worldwide. Sporadic CJD is the old-fashioned pre-BSE kind that is supposed to happen spontaneously in unlucky people. But a surprise observation

in France suggests some sCJD cases--though by no means all--may be linked to scrapie after all (see p 4). For years, British authorities asserted that BSE was harmless because it was a form of scrapie. In fact, the only evidence scrapie is safe is some broad-brush epidemiology, good as far as it goes but unable to reveal occasional risks for some people from some sheep. Alarm bells should have rung in 1980 when researchers gave monkeys scrapie by feeding them infected brains. But that research, like so much other work on prion diseases, was never followed up. We still have little idea what BSE does in pigs and chickens. The Queniborough vCJD outbreak (see p 5) would be easier to understand if we knew how much brain we must eat to be infected. As for scrapie, it shouldn't take a chance finding to tell us that there may be dangerous sheep out there. Suspect symptoms What if you can

catch old-fashioned CJD by eating meat from a sheep infected with scrapie? Exclusive from New Scientist magazine Four years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease................. full text url follows By Debora MacKenzie Suspect Symptoms http://www.newscientist.com/hottopics/bse/suspectsymptoms.jsp if url dead, go here for 'SUSPECT SYMPTOMS' http://www.organicconsumers.org/meat/scrapiecjd.cfm http://www.vegancowboy.org/TSS-SuspectSymptoms.html USA Loch in der Mauer Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas

verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehörden sind lax. Hier klicken! <http://adserv.quality-channel.de/RealMedia/ads/click_nx.ads/www.spiegel.de/spiegel@TopLeft,Top1,Top2,TopRight,Left,Left1,Left2,Right,Right1,Middle,Middle2,Position1,Position2,Frame1,Frame2,x01,x02,x03,x04,x05,x06,x32!Middle2> So funktioniert es: Artikel kaufen <http://www.spiegel.de/extra/0,1518,180714,00.html> http://www.spiegel.de/spiegel/0,1518,119306,00.html Mad Cow: Linked to

thousands of CJD cases? By Steve Mitchell United Press International Published 12/29/2003 9:50 AM http://www.upi.com/view.cfm?StoryID=20030721-102924-4786r BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001 Tue, 9 Jan 2001 16:49:00 -0800 "Terry S. Singeltary Sr." <flounder Bovine Spongiform Encephalopathy BSE-L http://vegancowboy.org/TSS-part1of8.htm Terry S. Singeltary Sr. P.O. Box 42 Bacliff, TEXAS USA 77518 David Louthan wrote: Hi Terry, Dave Louthan here. Hey my brother and theis888 wrote:

The Man Who Slaughtered the Mad Cow on a Dreamland SpecialBoth on the Dreamland program and as a special interview available in the last slot on www.Unknowncountry.com 's Windows Media Player (reached by clicking "Listen Now" on the right side of the masthead), Whitley interviews Dave Louthan, the man who actually slaughtered the mad cow that was found last December. Dave is now a man with a mission because, as reported by the New York Times, he says that the USDA is mishandling the mad cow problem and we are in serious trouble. This is a not to be missed interview.

karl theis jr

http://groups.msn.com/exposureofthetruth

karl theis jr

http://groups.msn.com/exposureofthetruth

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