Friday, October 23, 2015


Mad deer disease can infect normal human brains in laboratory tests


Monday, May 8, 2000 has further information and facts on CJD. Jennifer Kelly or Amy Leska, EMS 202/463-6670 Washington, D.C.


Public health advocates are demanding that the Food and Drug Administration close loopholes in animal feed regulations to prevent the spread of U.S. mad cow-type diseases now at epidemic levels in Western deer and elk that might infect people who eat meat. In a letter sent today to the FDA, the Center for Food Safety (CFS), the Humane Farming Association, and families of U.S. victims of the human version of mad cow disease, Creutzfeldt-Jakob disease (CJD) are demanding new efforts to protect public health and food safety. The FDA was asked to respond to a legal petition filed in January 1999 that would change U.S. animal feed regulations to prevent the spread of U.S. mad cow-type diseases already occurring in deer, elk, sheep and humans, and suspected in pigs and cattle.


Under current FDA regulations animals known to be infected with mad cow-type disease such as deer and elk infected with 'chronic wasting disease' and scrapie-infected sheep, can be legally fed to pigs, chickens and pets, which in turn can be rendered and fed to cows. Billions of pounds of slaughterhouse waste in the form of rendered animal by-products are fed to US livestock every year as fat and protein supplements, despite this practice being the known route of transmission of British mad cow disease.


A fatal 'mad deer' disease called chronic wasting disease or CWD is occurring at epidemic levels in deer and elk in Western states and on game farms, CFS legal director Joseph Mendelson wrote in the letter to the FDA. This may already be claiming human lives as is suggested by the alarming appearance of unusually young victims of Creutzfeldt-Jakob disease.


*** Today at the first CJD Foundation conference in Miami, government researcher Byron W. Caughey, Ph.D., announced that in laboratory tests CWD from deer can infect human brain tissue at rate similar to British mad cow disease. In Britain 56 people have died of human mad cow disease, the death toll is climbing and some scientists suspect it will claim hundreds of thousands of lives in the decades ahead. Caughey's research on US mad deer disese was conducted at the National Institutes of Health Rocky Mountain Laboratories in Hamilton, Montana, and has not yet been published.


The most recent suspected victim of US mad deer disease is Jay Dee Whitlock II of Oklahoma, who died of CJD on April 7, 2000. Whitlock, 28, was an avid deer hunter and venison consumer. He is the second young hunter to die of CJD in the past year.


John Stauber, co-author of Mad Cow USA and a speaker at the CJD Foundation conference, said, "The announcement that US mad deer disease can infect the human brain, and that it happens at a rate similar to British mad cow disease, is extremely disturbing. A deadly human dementia might be already spreading from deer and elk into hunters in Western states, and the policies of the FDA and other agencies are completely inadequate to protect public health.


Could 'mad cow type epidemics happen in the US John Stauber, talk given 7 May 00 CJD Foundation conference Miami Center for Media & Democracy 520 University Avenue, Suite #310 Madison, WI 53703


"Three years ago Sheldon Rampton and I were finishing our book Mad Cow USA published in November of 97. In our introduction we wrote that ours is not a biology book nor a diet guide, but a "book about politics and how it operates in the real world. It explains how government officials have placed concerns for the food industry over human health and welfare. In addition to telling the story of an exotic, mysterious and frightening disease, we have written this book to report on equally dangerous legal and political trends which threaten not only our physical health, but also our fundamental democratic rights..." The title of this session asks a question: "Could 'mad cow type epidemics happen in the US.?" My answer is not only could they, but they are. Sheep scrapie arrived in the US a half century ago and thanks to government bungling is now widely spread throughout the US, with dozens of different strains. Chronic wasting disease may have begun as sheep scrapie but now it is spreading through deer and elk in western states and on game farms.


In the past two years two western state hunters under the age of 30 have died of CJD, and some of us suspect they may be human victims of a new strain of TSE in sheep, deer or elk that has begun claiming young human victims in the US.


Since 1964 researchers have suspected that transmissible mink encephalopathy TME in the US is from a hidden TSE in cattle, and the late Dr. Richard Marsh, to whom we dedicate our book, believed that he isolated that TSE in mink in Wisconsin in 1985, a year before the British strain of TSE dubbed mad cow disease was observed.


As our book was going to completion, we discovered that USDA inspectors felt they had identified a TSE in pigs way back in the the 1970s, when few researchers other than a small group in what Paul Brown calls the Club were very concerned or aware of TSE diseases.


Of course, British mad cow disease and the looming specter of hundreds of thousands of people condemned to death in the decades ahead has changed everything. Everything, that is, except public policy here in the US. For despite the fact that two Nobel prize winners in this area of research are from the US, there is a public relations cover-up of massive proportions in this country that is preventing us from effectively establishing public policies that can monitor, prevent and eventually treat TSE diseases.


Please note that I said a public relations cover-up; that's important. I suspect that if TSE diseases were spread by mosquitoes, we'd be spraying pesticides all over the US to try and irradiate sheep scrapie and chronic wasting disease. But these diseases are spread by agribusiness through animal livestock products fed to people and animals, and thus instead of putting the concerns of people first, we have see that consistently governments have put the concerns of industry first.


We've heard eminent and hard working scientists talk about TSE diseases in terms that dizzy the head of even other scientists. This is a very contentious and mysterious area of research because TSE diseases break many rules.


Luckily, my co-author and I are not experts or scientists. However, we did have the benefit of being able to interview top TSE researchers like Richard Marsh and Dr. Gajdusek, have them review parts of our manuscript, and thus deliver a book that is based on solid, sound science regarding what is known, and what is unknown, what is proven, and what is not.


From my perspective, this is the most important point and perspective to keep in mind:


For the past thirty years a massive unregulated experiment in creating new strains of TSE disease has been undertaken by the livestock industry, and we're the guinea pigs. The experiment is ongoing. The experiment began as a really neat idea: lets take the billions and billions of pounds of slaughterhouse waste, blood and offal that is produced every year from cattle and pigs and sheep and roadkill and pets and zoo animals, and let's recycle it. Let's turn it into protein fat supplements, and let's feed it back to the livestock we eat.


It seemed like a good idea. Unfortunately, what it didn't take into account was the infectious prion agent. As Dr. Gibbs has pointed out, probably every mammalian species has a TSE disease at some minute level: people, pigs, cows, sheep, mink, cats and dogs, deer, elk. Grind up the most infectious parts of millions and millions of animals, concentrate them into feed supplements, and you are creating an environment not only for spreading and amplifying existing agents such as scrapie in sheep, but also for creating an untold number of new strains of TSE.


This is especially important to grasp. In laboratory experiments, when TME or scrapie or CJD is injected into new animal species, whole new strains of TSE are created, and they can have different potential to infect new host species. The process of rendering animal waste into animal feed has been a massive and ongoing experiment in the creation of new TSEs, one of which emerged in Britain in the mid 1980s as mad cow disease, has clearly spread into humans claiming over fifty so far, and in my guess will in the years ahead be founded to have infected hundreds of thousands of Britons.


I said that this outbreak of BSE in Britain changed everything, but what really changed everything was what caused that outbreak: feeding rendered animal by-products back to animals as food.


I wish I could tell you that this practice has been stopped, but it has not. I wish I could tell you that well informed and courageous officials in the FDA, the USDA and the CDC have taken the mad bull by the horns, and are right now executing a precautionary policy to insure that what has happened in Britain does not happen in the US. Unfortunately, that is not the case.


Dr. Hansen will shortly explain why the much heralded FDA feed regulations on rendered animal by-products announced in 1997 are in many ways a farce. For instance, in the US calves are literally being weaned on cattle blood protein, and scrapie infected sheep can be used as feed for pigs which can be used as feed for cattle.


But the problem is beyond just the poor US animal feed regulations. You need look no further than your favorite vitamin and nutritional supplement stores. Right now, with the full knowledge of the FDA, the NIH, the CDC, millions of Americans are popping over the counter as glandular supplements. These unregulated products contain the most infectious parts of slaughtered animals, the very parts that make up the so-called Specified Bovine Offal that should be banned from cattle feed, such as the brain, pituitary, and glandular system. These pills are pooled, collected from hundreds of thousands of animals and taken daily by untold numbers of Americans, probably millions given the popularity of supplements.


Again, this amounts to an unregulated human experiment, minus laboratory controls or knowledgeable consent, feeding humans the most infectious parts of animals, possible creating new TSEs by passaging animal TSE from pooled glandular products.


I've brought along four different bottles of the pills I'm talking about, and I've asked that they be pass around so you can look at them yourself and read the label.


Some would say that FDA's hands are tied, that thanks to lobbying by the nutritional supplement industry the FDA lacks the power to prevent sales of these glandular. Actually this points to another frightening disease rampant among otherwise good people who populate government agencies which I call BCD for Bureaucratic Cowardice Disease. FDAs hands might be tied and they can't yank these products from the market, but their mouths are not gagged and concerned officials should be speaking out loudly warning the American public that they are consuming animal brains and glands and might want to consider the potential risks.


There is a reason why scientists in agencies and universities, not to mention corporations, avoid sticking their necks out, and we need look no further than Richard Marsh, a dedicated and conservative scientist who took it upon himself to speak up in 1993 in an interview in Wisconsin's largest farm paper. Richard Marsh warned Wisconsin farmers, thousands of whom were feeding rendered cow by-products back to their cows, that given the mad cow outbreak in Britain they should, despite the reassurances from USDA that such feeding was safe, stop.


The day after that article appeared Dr. Marsh was literally called on the carpet in the office of the dean of the school of agriculture at the University of Wisconsin, and read the riot act. he was told that industry funders were threaten to sue him, sue the school, cut off money for research, and who did he think he was?


Within months the school scrambled and pulled together a symposium on the subject, which served to dismiss and marginalize Dr. Marsh's views. When Dr. Marsh died of cancer in 1997, after the British announcement that mad cow disease was killing young people, the same University had the gall to praise Dr. Marsh and his work as in the best tradition of the University. Some of us feel that the stress and abuse heaped on Dr. Marsh> from 1993 to 1997 had an impact on his health that contributed to his demise.


This is what happens to scientists who break ranks and speak out, and it is a great loss to us today because I think if Dick Marsh was still alive he would be leading the charge to confront the ignorance and the cow-towing to industry that typifies this issue.


Dr. Marsh was a colleague and contemporary of many of the researchers in this room. As Paul Brown whom he once worked with might say, he was a member of the club. But Dr. Marsh was able to make realizations that I'm afraid most of the club members haven't yet come to, and he was able to put his sense of scientific obligation to society in front of concerns about his funding, or even his personal and professional safety.


I first began investigating mad cow type diseases in the early 1990s when I was working in Wisconsin organizing farmers and consumers opposed to Monsanto's genetically engineered bovine growth hormone, the cattle equivalent of human growth hormone which when injected into cattle forced them to produce more milk. Well, its not quite that biologically simple as I'm sure any woman here who has had children can imagine.


It was brought to my attention by a retired industry veterinary researcher that in order to make the hormone work, cows need to be fed additional fat and protein supplements, and that the cheapest supplements were rendered byproducts from other cows. This veterinarian told me this was very bad because it was exactly what had cause the outbreak of BSE in Britain.


I investigated and found this was true - massive feeding of cows to cows was going on in the US, despite the fact that as early as the Fall of 1987 British epidemiology had shown that is was this practice that spread mad cow disease.


I remember one of my first meetings with Dr. Marsh. We talked about his believe that a US BSE agent, different than the British strain, was in cattle at low levels and was the cause of occasional outbreaks of TME. I know that eminent researchers in this room dispute that, but frankly Dr. Marsh never doubted it and I think the evidence and commons sense remains in his favor.


I had just been to a holistic chiropractor for my chronically bad lower back, and had been sold a bottle of adrenal gland extract which I showed to Dr. Marsh - he practically fell out of his chair and I immediately stopped taking them.


He was shocked to learn that such glandular were sold. Imagine what he might think today, that at this late stage of the game with kids in their 20s in the US dying of CJD, that these glandulars are sold without warning.


Of course, I may be taking a risk myself in saying this. After all, we are in Florida, one of 13 states in the US in which the Animal Feed Industry Association members have succeeded in lobbying into law a food product disparagement bill. I could end up like Oprah Winfrey and her guest Howard Lyman, forced to spend millions and millions of dollars (which in my case would be thousands and thousands and then bankruptcy) to convince a jury that my remarks today are based on sound science.


Having written two books in the past five years, one on political PR and the other on the politics of food, I can tell you that a major reason why there has not been more news media coverage of this issue is the multi-million dollar PR campaign and litigation threats of the food industry which we document extensively in our book.


I find it ironic that this weekend as we're meeting here President Clinton announced Saturday a new initiative to address the safety of hot dogs. Philip Brasher of the Associated Press speculates that as he is leaving office the President wants to burnish his image with food safety initiatives.


The irony is that it is under this administration that the food industry has launched an all out attack on our first amendment rights by lobbying food libel laws onto the books, and the administration has remained silent. Despite knowing of the risks of cow cannibalism since the beginning of his presidency, his administration did nothing until 1997, and as we reveal in our book and Dr. Hansen will explain, the regulations are severely inadequate.


I am circulating a letter being delivered by the Center for Food Safety urging the agency to respond to the petition filed by that group and many of the families in this room that calls on FDA to severely tighten its regulations. Yet, probably to avoid publicity, the FDA stonewalls.


A couple weeks ago I was in Washington and I attended a conference that was paid for in part by the lobbyists responsible for putting food censorships laws on the books, the Animal Feed Industry Association and the law firm of Ollsen Frank and Weeda that drafted the model bill that was then lobbied for at the state level by the American Farm Bureau. I picked up this glossy brochure in which the FDA is slapping itself on the back for its food safety initiatives. In it I read that the FDA's BSE Educational Activities have Gained an award from the vice president:


The US feed regulations and the FDA were honored with VP Al Gore's Hammer Award. Dr. Stephen F. Sundlof, the directory of FDA's Center for Veterinary Medicine, the man who since January 1999 has been unable to respond to the legal petition to close gaping loopholes in the FDA regulations stated: "thanks to the development of the BSE regulation, we can continue to say that there has not been a single case of BSE reported in the United States. Educational efforts ... will help assure that we can continue to make that claim."


In researching our books we had access to documents obtained through the Freedom on Information Act. One 1991 document of the USDA was titled "BSE Public Relations," and if someday attorneys in a class action lawsuit on behalf of CJD patients in the US are looking for a smoking gun demonstrating that concerns for industry were place over concerns for people, this is it.


(p.148-149) According to this document, the mere perception that BSE might exist in the United States could have devastating effects on our domestic markets for beef and dairy products." The report examined how the British handled their PR, and it fretted over a story in the British magazine The Economist which, quote, "could potentially create alarm among US consumers," unquote, because it reported that, quote,"many veterinarians and medical experts have come around to the belief that humans could catch the mystery brain disease."


This USDA PR document approvingly noted a quote in the Washington Post by Dr. Joseph Gibbs at NIH in 1990 saying "I don't think there is any danger in consuming British beef." Remember, this was in 1991. It had known for four years that it was feeding cows to cows that was spreading BSE in Britain. More and more were fearing that humans would die. Meanwhile, in the US, billions of pounds of cow by-products were still being fed, in fact the amount was increasing each year.


Was there no one inside the USDA or FDA who saw the lunacy, indeed the criminality, in knowing this and letting cannibalistic feeding go one in the US? Some did. The report notes that "some (USDA APHIS) staff members... argue that because there is evidence that pigs, cats, mink, deer and a variety of experimental animals may b e susceptible to trans. spongiform. encephalopathy, the only prudent policy is to not feed products that contain these agents to ANY SPECIES OF ANIMAL."


That's it. That's what we should have done then, and that's what we should be doing now, but are not. Instead we are still exposing ourselves and US livestock to a massive TSE experiment.


So, in 1991 the USDA and FDA rejected this advice by some anonymous staffers, as they do today. This 1991 USDA PR report admitted that a more cautious policy would be, quote, "to prohibit the feeding of sheep and cattle-origin protein products to all ruminants, regardless of age. The advantage of this option is that it minimized the risk of BSE. The disadvantage is that the cost to the livestock and rendering industries would be substantial."


In fact, absolutely nothing of substance was done until August of 1997, when FDA announced its sham feed regulation, winner of the coveted Al Gore hammer award, designed as a PR fig leaf so that FDA can say 'we are keeping British mad cow disease out of our livestock."


Let me say that the only bright spot in this story of corporate and government collusion, irresponsibility and censorship has been a few brave souls like Richard Marsh, Richard Lacey in England, others who have bucked the tide and spoken out, and those of you who are the families and loved ones of CJD victims.


*** Through CJD Foundation and CJD Voice you have found each other, and you will eventually force responsibility onto government and industry because if you don't no one else will.


In conclusion, we need a massive commitment in the United States to address TSE diseases. We need to start by admitting the shortcomings of our failed federal feed policies and change them. We need to dedicate hundreds of millions of research dollars, if necessary, to try to eradicate scrapie in sheep, eradicate CWD in deer and in elk, and investigate, research, test and monitor for TSEs in humans and animals. We need money for research to develop treatments, because while this disease used to be rare disease, I suspect we are about to see it emerge full blown in Britain with hundreds of thousands of victims, and more and younger victims appearing in the United States, as a result of our thirty year experiment in animal cannibalism.


The leadership for this will not come from politicians in bed with the agribusiness industry. It will not come from researchers who while brilliant are stuck back in pre-BSE days, still viewing this as a rare unusual disorder. It will come from average citizens who husbands and mothers and children are dying of this bizarre class of dementia diseases in increasing numbers, and who are not afraid to demand that the right policies be implemented and funded. It is upon your shoulders that leadership falls, and so far you are doing admirably."


2015 CJD Foundation Family Conference Washington, DC July 10th-12th, 2015
greetings cjd foundation et al,
the cjd questionnaire has come a long way, I knew you could do it, but still, could be much enhanced, in my opinion. for instance, adding a question about nutritional supplements containing any animal tissue. please remember, that’s all those cattle that got BSE were eating was a type of nutritional supplement containing specified risk materials, and that’s what some of these nutritional supplements were/are containing. OH, and don’t forget those mad cow candy bars. I know some folks don’t like the term mad cow. I don’t really care. it is what it is, and so am I, LOL.  carry on. I’m still here damn’t Winking smile 
kindest regards, terry
2015 CJD Foundation Family Conference Washington, DC July 10th-12th, 2015
Questionnaire Report
Creutzfeldt Jakob Disease
Cele Sardo – Emeritus Co-Founder, CJD Foundation...RIP old Friend...terry
my reasoning for adding nutritional supplements containing SRM, and concerns there from’
NOTE: everyone I tell this too gets it screwed up...MY MOTHER WAS NOT TAKING THOSE SUPPLEMENTS IPLEX (that I ever knew of). this was my neighbors mother that died exactly one year _previously_ and to the day of sporadic CJD that was diagnosed as Alzheimer’s at first. my mother died exactly a year later from the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, and exceedingly rare strains of the ever growing sporadic CJD’s. _both_ cases confirmed. ...
kind regards, terry
TSEs i.e. mad cow disease's BSE/BASE and NUTRITIONAL SUPPLEMENTS
IPLEX, made by standard process;
IPLEX - vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach.
what about potential mad cow candy bars ?
see their potential mad cow candy bar list too...
THESE are just a few of MANY of just this ONE COMPANY...TSS
Friday, January 19, 2001 snip...
17 But I think that we could exhibit some quite
18 reasonable concern about blood donors who are taking dietary
19 supplements that contain a certain amount of unspecified-
20 origin brain, brain-related, brain and pituitary material.
21 If they have done this for more than a sniff or something
22 like that, then, perhaps, they should be deferred as blood
23 donors.
24 That is probably worse than spending six months in
25 the U.K.
3681t2.rtf(845) page 501
Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice in Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number: EC -2 Accepted - Volume 7
see full text ;
2003 - 2004 Product Catalog
Standard Process Inc.
NATURAL COCOA STANDARDBAR (mad cow candy bar) (i will just list animal organs) bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney...
bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney...
bovine orhic glandular extract
bovine uterus PMG
bovine heart PMG extract, veal bone PMG extract, bovine liever, porcine duodenum, bovine adrenal Cytosol extract, bovine spleen, ovine spleen
IPLEX (neighbors mom died from CJD while taking these pills for years)
bovine eye PMG extract, veal bone PMG, bovine liver, porcine stomach, bovine adrenal, bovine kidney, bovine adrenal Cytosol extract, BOVINE BRAIN, bovine bone, veal bone meal
bovine heart PMG, bovine liver, porcine stomach, bovine orchic extract, bovine spleen, ovine spleen, bovine adrenal Cytosol extract, BOVINE BRAIN
bovine liver, porcine stomach, bovine spleen ovine spleen, BOVINE BRAIN
bovine liver, bovine orchic Cytosol extract, porcine stomch, bovine spleen, ovine spleen, BOVINE BRAIN
veal bone PMG extract, veal bone PMG extract, bovine liver, porcine stomach, bovine adrenal, bovine spleen, ovine spleen, BOVINE BRAIN
bovine pancreas PMG extract, porcine duodenum, bovine adrenal PMG, BOVINE PITUITARY PMG EXTRACT, bovine thyroid PMG extract
BOVINE BRAIN, veal bone PMG extract, bovine adrenal, bovine prostate Cytosol extract, veal bone meal, bovine liver PMG extract, bovine spleen, ovine spleen, bovine liver
bovine liver PMG extract, bovine adrenal, BOVNE BRAIN, veal bone meal, bovine kidney, bovine orchic extract, bovine spleen, ovine spleen ..........
THESE are just a few of MANY of just this ONE COMPANY.
FOR the following reason, I implore that the FDA take serious action in further protecting the consumer from the TSE agent via nutritional supplements.
Does all that e-mail spam promising sexual vitality actually hide serious risk of contracting MAD COW DISEASE?
Volume 361, Number 9368 03 May 2003
Tighter regulation needed for dietary supplements in USA
Sir--Mary Palmer and colleagues (Jan 11, p 101)1 found that dietary supplements have the potential to cause serious adverse effects. The investigators state that research on the hazards and risks of dietary supplements should be a priority. The safety of individuals who consume these products is important, and organisations such as the US Food and Drug Administration (FDA) need to take initiative by enforcing stricter regulations on supplements. Several commonly used products--for example ginkgo biloba, St John's Wort, and ephedrine--can have serious adverse effects.2 Although the FDA requires multiple studies on the safety and efficacy for pharmaceutical products before placing them on the market, standards are less robust for dietary supplements. In the USA, under the Dietary Supplement Health and Education Act (DSHEA) of 1994, supplements are subject to the same regulatory requirements as food. There are no provisions that require FDA approval for the safety or effectiveness of supplements,3 which leaves consumers and manufacturers essentially responsible for the health effects of these products. The DSHEA of 1994 needs to be revised so that dietary supplements are subject to the same regulations as pharmacological drugs. The FDA needs to review clinical studies on the safety and efficacy of dietary supplements. Organisations such as Public Citizen and the American Medical Association are already taking steps to achieve these changes. However, they face immense opposition from groups such as the National Nutritional Foods Association, the American Herbal Association, and the Council for Responsible Nutrition. To overcome such resistance, consumer organisations, health-care providers, and government agencies need to approach this subject in unison. The public needs to be able to assess the risks and benefits of dietary supplements before consuming them. Health-care providers and the more than 100 million Americans who consume these products4 should encourage the FDA to treat supplements with the stringent regulations it enforces on pharmaceutical products.
Nipa Kinariwala
700 Bolinwood Drive, Apartment 12A, Chapel Hill, NC 27514, USA (e-mail nskinari at 1 Palmer ME, Haller C, McKinney PE, et al. Adverse events associated with dietary supplements: an observational study. Lancet 2003; 361: 101-06. [Text ] 2 Cupp MJ. Herbal remedies: adverse effects and drug interactions. Am Fam Physician 1999; 59: 1239-45. [PubMed ] 3 Unites States Food and Drug Administration. Overview of dietary supplements. Jan 3, 2001. (accessed Feb 20, 2002). 4 Pear R. Feds call for tighter control over nutritional supplements. Organic Consumers Association, April 17, 2001. (accessed Feb 20, 2002).
snip...end tss letter to fda.
=================== 2013 ================
my plight with Metabolife, the GAO et al, and my submission to the BSE inquiry, about mad cow in a pill ;
Wednesday, March 20, 2013
GAO-13-244, Mar 18, 2013 Dietary Supplements FDA May Have Opportunities to Expand Its Use of Reported Health Problems to Oversee Product
From: Terry S. Singeltary Sr.
Sent: Tuesday, March 19, 2013 2:46 PM
To: Cc: ; ;
Monday, February 01, 2010
Import Alert 17-04 BSE CJD HIGH RISK TISSUES, Nutritional Supplements and Cosmetics Import Alert 17-04
Thursday, March 19, 2009
Chronic Wasting Disease Prions in Elk Antler Velvet (Nutritional Supplements and CJD)
10.3201/eid1505.081458 Suggested citation for this article: Angers RC, Seward TS, Napier D, Green M, Hoover E, Spraker T, et al. Chronic wasting disease prions in elk antler velvet. Emerg Infect Dis. 2009 May; [Epub ahead of print]
Wednesday, August 5, 2015
Federal judge enters permanent injunction against Wisconsin dietary supplement manufacturers prohibited cattle materials BSE TSE Prion
*** Singeltary Submission to BSE Inquiry on Nutritional Supplements containing SRM 1998
The Akron, Ohio-based CJD Foundation said the Center for Disease Control revised that number in October of 2004 to about one in 9,000 CJD cases per year in the population group age 55 and older.
if not, why not...
Friday, November 30, 2007
> Tracy Kedzierski followed with a report about the CJD Foundation Family Questionnaire
> which she works tirelessly at conducting.
thanks tracy, glad it finally got done. we know how 'tirelessly' you must have worked ;-)
Subject: [CJDVoice] CJD FOUNDATION QUESTIONNAIRE ???(what will they find out with this ??? )
Date: Thu, 07 Nov 2002 10:10:53 -0600
From: "Terry S. Singeltary Sr."
Greetings Voice,
i send this 'CJD Foundation Questionnaire' and ask the group, what they suppose will be found out with this ???
with this questionnaire, in my opinion, they don't want to know what/where the routes and sources of CJDs in theUSA are coming from. NO WONDER they said i was interfering with there research, there research consist of _not_ finding out anything other than how it was diagnosed.
you folksjudge for yourself. maybe i'm just being an extremist as some say???
then again, maybe not...TSS
Name of Patient*:(not required; if provided, must be with express consent of family member)
Date form filled out: / / (mm/dd/yy)
Person filling out form:
Relationship of person filling out form to patient:
Location where patient died: State: County: City:
Location where patient resided: State: County: City:
Sex of patient: male female unknown
Race of patient: white African-American -- Asian/Pacific IslanderAmerican-Indian/Alaskan Native Other (please identify:Unknown
Patient's date of birth: (mm/dd/yy)
Age of patient at onset of symptoms:
Date of patient's initial symptoms: (mm/dd/yy)
Age of patient at time of death:
Patient's date of death: (mm/dd/yy)
Duration of illness: months
Was this case referred to the National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland, Ohio? yes no unknown
If yes, by whom was this case referred? Pathologist -- Neuropathologist -- Neurologist Other Physician (please identify which kind:Unknown
Who made initial diagnosis of CJD or other TSE?
Pathologist - Neuropathologist - Neurologist Other Physician (please identify which kind: )Unknown
Please describe the clinical neurological presentation of the illness (list the symptoms or signs):
at onset of the illness:
during the course of illness:
Was an EEG (electroencephalogram) performed? yes -- no -- unknown
If yes,
how long after onset was the EEG performed?
how many times was the EEG performed?
can you indicate the results?
- slow periodic sharp waves (PSW)
- unilateral periodic sharp waves (LSW)
- not reported
- other
Was the cerebrospinal fluid tested for the 14-3-3 protein? yes - no -unknown
If yes, what was the result? positive - negative - unknown
Was a brain biopsy performed? - yes - no - unknown
If yes, what was the result?_____
positive for__________
negative for CJD and other TSE's ______
Was an autopsy performed? yes - no - unknown
If yes, what was the result? _____
positive for__________
negative for CJD and other TSE's______
Was the neuropathology of this case consistent with new variant CJD? yes - no - unknown
What was the final diagnosis of this case?
___CJD, probably sporadic
___Familial (hereditary) CJD
___Iatrogenic (by infection) CJD;
please specify_______________
___Gerstmann-Strausster-Scheinker Syndrome (GSS)
___Fatal Familial Insomnia (FFI)
* I hereby give consent to the Creutzfeldt-Jakob Disease Foundation, Inc. to use the above information, including name of patient if supplied, in connection with activities to promote the research, education and awareness of Creutzfeldt-Jakob Disease and related transmissible spongiform encephalopathies.
Greetings again CJD Voice,
NOW, compare to the CJD questionnaire i sent through, and ask yourself why they ask me to remove this from internet? better yet, ask yourself why the CJD Foundationin fact did remove my questionnaire from their message board? what is it they are so afraid of that we may find out?
Subject: [CJDVoice] CJD QUESTIONNAIRE... updated version II...TSS
Date: Tue, 05 Nov 2002 12:52:52 -0600
From: "Terry S. Singeltary Sr."
A. What is the subjects SURNAME____________________________
B. What is the subjects status? ___________________________
(1=suspect/confirmed CJD, 2=hospital control (specifydiagnosis), 3=GP control).C. If the subject is a (suspect) case, are they alive on theday of interview?_____(yes or no or not applicable)
D. What is your (respondent's) name?_______________________
(first name, and surname)What is the relationship to (subject)? ________________
E. DATE OF INTERVIEW__________________________
LOCATION OF INTERVIEW_____________________
F. NAME OF INTERVIEWER________________________
A. SEX___________________
B. BIRTH DATE____________
C. BIRTH PLACE___________ (country, state, county, city)
E. MARITAL*DOMESTIC STATUS__________________
(If the subject is female and is/has been married) record the subjects maiden name if different
from current surname.
F. PRESENT HOME ADDRESS_________________________
(ALSO, If deceased, last home address, before subjectbecame ill?)
G. Is/was subject right or left handed?__________________
F. How many years of full-time education?________________
A. Has the Subject had dental treatment other than fillings:
e.g. extractions or root canal work?_________________
If yes, record a description of treatment; with dates;
Dentists name and address____________________________
B. Has the Subject ever had any operations, including eyeoperations or stitching of
(If yes, record the year, hospital and type of operation). _______________
(record total number of operations)
For each type of operation record the number of such operationsundergone, the year of the first such operation and the year of the lastsuch operation. When no such operations were undergone record 0 for thenumber of operations.
NEUROLOGIC (brain)_____________________________
TONSILS OUT?___________________________________
APPENDIX OUT?__________________________________
ever received an ORGAN TRANSPLANT, including corneal or bone marrow
kidney, liver, and other_______________________
C. BLOOD TRANSFUSION__________________________
BLOOD DONOR____________________________________
D. Has Subject ever been admitted to aHospital_______________________
E. Has Subject ever been to see psychiatrist
(reason andtreatment) _____________________
F. MEDICATIONS, has Subject taken any medications regularly, (if yes, record the date, name of the medication, the reason for taking it, and route of administration) prompt for prescription drugs, including insulin and type.
Prompt for hormone therapy or nutritional supplements including oral contraceptives and hormone replacement therapy:
Prompt for homeopathic/herbal therapy:
Prompt for eye drops
G. Has Subject ever been tested for allergy using needles?________________
H. Has Subject ever received a treatment involving a course ofinjections?
(If yes, record year, name of therapy, frequency, reason)
I. Has Subject been VACCINATED? _______________________________
(If yes, give name of vaccine, and route.)
J. Has Subject ever undergone lumbar puncture or electrical tests involving needles?
K. Has Subject ever undergone acupuncture? ____________________
L. Has Subject ever used drugs by needle? _____________________
M. Has Subject ever been tattooed, ear or body piercing of any kind?____
(indicating years of birth and death) Subjects grandparents,Subjects parents and parents siblings, Subject and siblings Subjects children.
A. From the genealogy, record whether the Subject has been married more than once?
B. Have any of the BLOOD relatives of the Subject included inthe Pedigree above died with dementia (or remain alive with dementia)?
C. Have any of these individuals been diagnosed as having Creutzfeldt-Jakob disease, and or any
other T.S.E.?_______________________________
(if so, give name, address, and apprx. date of illness)
(1=definite 2=probable 3=possible 4=unable to confirm 5=not a case)
E. Has Subject had social contact, through family, friends or work, with someone else who developed CJD?_____________________________
(record the persons name and the apprx. date of illness.)
F. Confirmation of social contact with case of CJD?____________
G. FOR NON-U.K. cases only, Has Subject lived in or visited theUnited Kingdom during the period 1980-1999?________________________
(if yes, record dat and duration of visits)
A. Has Subject ever been a vegetarian for a period of 1 year or more?
(if yes), during what period was Subject vegetarian, and did the Subject eat any meat or fish at all during this time? ______________
B. Does Subject have a history of any other dietary restrictions or eccentricities? (record apprx. dates and details of restrictions;
C. How many years did Subject eat school dinners?__________________
(give dates)
D. Has the Subject ever eaten animal food or petfood?
(If yes, record the types of food and dates)
E. How did/does the Subject like their steak cooked?________________
(1=well done 2=medium 3=medium-rare 4=rare 5=did not eat steak)
F. How often does/did Subject cut or chop up raw red meat or bones, in their work or in their home?_______________________________
G. (For each of the following food items) How often did Subject eat (food item)?
BRAIN_________________ (specify animal which organ came from)
STEAK TARTARE (raw minced steak with raw egg) carpaccio,
CHEESE, COWS MILK (1=drinks milk/eats breakfast cereal with milk, 2=only in tea/coffee, 3=NO)
A. Did the Subject every HUNT, DRESS, AND EAT DEER? ____________________
(if so, list location, and year, and list any specific organs that the Subject may have considered to be a delicacy).
B. Did the Subject share a home with:
C. Has the Subject worked or stayed for more than one week on a farm? (1=lived or worked, 2=stayed, 3=NO) If YES, did Subject work or help with;
(If yes), did Subject participate in: Treating cattle for Warble fly?______________
Dipping sheep?_________________________
Crop Spraying?________________________
(If the Subject took part in any of these activities), recorddates, places and details of the activity
including agentsused;
D. Has the Subject used any of the following;
BONE MEAL__________________
HOOF AND HORN____________
DRIED BLOOD________________
MANURE____________________ (if yes, record the item used and dates)
E. Has Subject ever DISSECTED ANIMAL EYES, for example at school?
6. RESIDENTIAL HISTORY (begin with the most recent residence and work backwards) From(dd/mm/yy) TO(dd/mm/yy) STREET TOWN COUNTY STATE (include zip code).
7. OCCUPATIONAL HISTORY OF SUBJECT; (begin with most recent occupation and work backwards) FROM (dd/mm/yy) TO(dd/mm/yy) NAME OF EMPLOYER TOWNDESCRIPTION OF WORK;
A. Has the Subject ever worked in farming, the meat industry,the pharmaceutical industry, or in a hospital?
B. Has the SUBJECT, their PARTNERS or PARENTS ever worked in thefollowing areas;
animal laboratories______________________________________________
pharmaceutical laboratories________________________________________
other research laboratories________________________________________
animal farming________________________________________________
veterinary medicine_____________________________________________
meat industry_________________________________________________
(BUTCHER'S/ABATTOIRS/RENDERING PLANTS, ETC) and or (catering other occupation involving animal products, including leather)?
*** NOTE ***
please include venison/sheep/lamb and the bovine to any of the above questions.
example=brain tanning deer/elk hide or any other topics that pertain to transmission of TSEs
example=antler velvet nutritional supplements
_any_ nutritional supplements??? name/ingredients
example=elk/deer brains ie/scrambled, sandwich or otherwise
COSMETICS-ie facial creams, eye make-up etc. name/brand/ingredients
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
================================================== =
Subject: Re: Tracie CJD Foundation
Date: Tue, 5 Nov 2002 15:09:29 -0500
From: "Tracie Kedzierski"
To: "Terry S. Singeltary Sr."
References: <3dc730df .8010308=""""><018601c284f7 .com="" a04a80="" a64a8c0="" newportrentalguide=""><3dc80f1a .3090808=""""><000901c28502 .com="" a64a8c0="" fac15c00="" newportrentalguide=""><3dc81fca .1040403="""">
Oh no....I've gone and pissed you off (ha ha)I just find it better to that nothing I write is misinterpreted. It is very important to me that you understand the conflict, the confusion, etc so can I call you or not? My dime ?
----- Original Message -----
From: "Terry S. Singeltary Sr."
To: "Tracie Kedzierski" S
ent: Tuesday, November 05, 2002 2:45 PM
Subject: Re: Tracie CJD Foundation
> either mail me your explination or forget the it...TSS
>> Tracie Kedzierski wrote:
>> > Terry,
The only problem is that having it on our message board conflicts with the information I have on our home page about the surveillance project and the report form I send out to the families. -----it is confusing. In fact.. I'm sorry but we (The Foundation) have to pull it off. I need to talk to you about this and share a number of goals the "new" Foundation has Can I call you? Please email me your number.... Tracie
> > Original Message -----
> > From: "Terry S. Singeltary Sr." > >
To: "Tracie Kedzierski"
Sent: Tuesday, November 05, 2002 1:34 PM
Subject: Re: Tracie CJD Foundation
hi Tracie,
doing fine, thank you. about the questionnaire? by no means am i trying to step on Dr Gambetti's toes here. i think there is more to it than just reporting a case. we _must_ find the source and route of spordic CJDs, and i think a great deal of it will be from the medical/surgical arena. i just want a questionnaire made up for _all_ victims of human TSEs in the USA in _every_ state, and i want it reportable in _every_ state. i am turning the heat up. ****, i'm getting old and grey, i want to see it done before i die. will be sending this out to many media and papers and requesting them to turn the heat up on the Gov. you will be able to keep up with the ones coming through the voice and if i get some that have not come through the list, i will pass on to Dr. Gambetti if he likes. i respect Dr. Gambetti very much and would do nothing to hender his work or yours. i just think that this is too important of a matter not to have one. and i think by turning the heat up, getting to the media and pressing there buttons a bit, just might help this get done a bit faster... hope so anyway...
kindest regards,
>>Tracie Kedzierski wrote:> >>> >>>
Hi Terry,
How are you? I'm just curious about your Questionnaire ?
It just was posted on the Foundation's Message Board without any introduction... and I was a bit concerned as it may cause some confusion with the Surveillance Project I'm doing via the Foundation for Dr Gambetti. Could you let me know?
Greetings again Voice,
just what is the _new_ CJD Foundations goals witha CJD Questionnaire that asks _no_
questions about soure/route of the six variants of sporadic CJDs???
i am reminded of a few things deep throat told me years ago;
The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people......... Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie..... why???? than the UK... then would the same mechanisms that make different strains of scrapie here make different strains of BSE... if the patterns are different in sheep and mice for scrapie..... could not the BSE be different in the cattle, in the mink, in the humans....... I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........ bse..... scrapie
Scrape the damn slide and put it into mice..... wait..... chop up the mouse brain and and spinal cord........ put into some more mice..... dammit amplify the thing and start the damned research..... This is NOT rocket science... we need to use what we know and get off our butts and move.... the whining about how long everything takes..... well it takes a whole lot longer if you whine for a year and then start the research!!!
Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde..... for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year....... it is a big fat sponge... the agent continues to eat the brain ...... you can't make slides anymore because the agent has never stopped........ and the old slides that are stained with Hemolysin and Eosin...... they get holier and holier and degenerate and continue... what you looked at 6 months ago is not there........ Gambetti better be photographing every damned thing he is looking at.....
Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........ if you want to move this thing along and shake the earth.... then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........ I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........ forget any action........ it is ALL gonna be sporadic!!! And, if there is a case....... there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats.... and this may be their biggest downfall...
Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here.......... knocked me out of my chair........ you must keep pushing. If I was a power person.... I would be demanding that there be at least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the wood work as there is money to be made!!!
In short: "FIRE AT WILL"!!! for the very dumb.... who's "will"! "Will be the burden to bare if there is any coverup!"
again it was said years ago and it should be taken seriously.... BSE will NEVER be found in the US!
As for the BSE conference call... I think you did agreat service to freedom of information and making some people feign integrity... I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.
You need to watch your back........ but keep picking at them....... like a buzzard to the bone... you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)
*** Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001 ***
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
######### Bovine Spongiform Encephalopathy #########
Thursday, September 10, 2015
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
***********OCTOBER 2015*************
THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. ***We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. ***Scrapie, as recently evoked in humanized mice (Cassard, 2014), is the third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
***thus questioning the origin of human sporadic cases...
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.
***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***
From: Terry S. Singeltary Sr.
Sent: Saturday, November 15, 2014 9:29 PM
To: Terry S. Singeltary Sr.
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
July's Milwaukee Journal Sentinel article did prod state officials to ask CDC to investigate the cases of the three men who shared wild game feasts. The two men the CDC is still investigating were 55 and 66 years old. But there's also Kevin Boss, a Minnesota hunter who ate Barron County venison and died of CJD at 41. And there's Jeff Schwan, whose Michigan Tech fraternity brothers used to bring venison sausage back to the frat house. His mother, Terry, says that in May 2001, Jeff, 26, began complaining about his vision. A friend noticed misspellings in his e-mail, which was totally unlike him. Jeff began losing weight. He became irritable and withdrawn. By the end of June, he couldn't remember the four-digit code to open the garage door or when and how to feed his parents' cats. At a family gathering in July, he stuck to his parents and girlfriend, barely talking. "On the night we took him to the hospital, he was speaking like he was drunk or high and I noticed his pupils were so dilated I couldn't see the irises," his mother says. By then, Jeff was no longer able to do even simple things on his computer at work, and "in the hospital, he couldn't drink enough water." When he died on September 27, 2001, an autopsy confirmed he had sporadic CJD.
In 2000, Belay looked into three CJD cases reported by The Denver Post, two hunters who ate meat from animals killed in Wyoming and the daughter of a hunter who ate venison from a plant that processed Colorado elk. All three died of CJD before they were 30 years old. The CDC asked the USDA to kill 1,000 deer and elk in the area where the men hunted. Belay and others reported their findings in the Archives of Neurology, writing that although "circumstances suggested a link between the three cases and chronic wasting disease, they could find no 'causal' link." Which means, says Belay, "not a single one of those 1,000 deer tested positive for CWD. For all we know, these cases may be CWD. What we have now doesn't indicate a connection. That's reassuring, but it would be wrong to say it will never happen."
So far, says NIH researcher Race, the two Wisconsin cases pinpointed by the newspaper look like spontaneous CJD. "But we don't know how CWD would look in human brains. It probably would look like some garden-variety sporadic CJD." What the CDC will do with these cases and four others (three from Colorado and Schwan from Upper Michigan), Race says, is "sequence the prion protein from these people, inject it into mice and wait to see what the disease looks like in their brains. That will take two years."
CJD is so rare in people under age 30, one case in a billion (leaving out medical mishaps), that four cases under 30 is "very high," says Colorado neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in the newspaper], six cases of CJD in people associated with venison is very, very high." Only now, with Mary Riley, there are at least seven, and possibly eight, with Steve, her dining companion. "It's not critical mass that matters," however, Belay says. "One case would do it for me." The chance that two people who know each other would both contact CJD, like the two Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting disease pass into humans? We'll be able to answer that in 2022," says Race. Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. ***
Wednesday, October 07, 2015
Deer Prion Proteins Modulate the Emergence and Adaptation of Chronic Wasting Disease Strains
Saturday, October 03, 2015
J. Mikol1, S. Luccantoni-Freire1, E. Correia1, N. Lescoutra-Etchegaray1, V. Durand1, C. Dehen1, J.P. Deslys1, E. Comoy1
1Institute of Emerging Diseases and Innovative Therapies, Service of Prion Diseases, Atomic Energy Commission, 18 Route du Panorama 92265 Fontenayaux- Roses, France
Uncommon prion disease induced in macaque ten years after scrapie inoculation
Introduction: Bovine Spongiform Encephalopathy (BSE) is the single animal prion disease reputed to be zoonotic, inducing variant of Creutzfeldt-Jakob Disease (vCJD) in man, and therefore strongly conditioned the protective measures. Among different sources of animal prion diseases, we show here that after more than ten years of incubation, intracerebral injection of a sheep scrapie isolate can induce a prion disease in cynomolgus macaque, a relevant model of human situation towards several prion strains. Neuropathological studies showed classical and uncommon data.
Material and method: The cynomolgus macaque was intracerebrally exposed to a classical scrapie isolate issued from a naturally infected sheep flock. Upon onset of clinical signs, euthanasia was performed for ethical reasons. Classical methods of biochemistry and neuropathology were used.
Results: The three elements of the triad were present:
spongiosis was predominant in the cortex, the striatum, the cerebellum. Neuronal loss and gliosis were moderate.
The notable data were the following
(i) the brain was small, the atrophy involved mostly the temporal lobe in which axonal loss was histologically demonstrated
(ii) the spongiosis of the Purkinje cells was so intense that most of them were destroyed
(iii) there was a neuronal loss and a massive gliosis of the dorsomedialis nucleus of the thalamus
(iv) iron deposits were present in the lenticular nucleus. PrPres heavily distributed in the cortex, the basal ganglia and the cerebellum consisted in synaptic deposits and aggregates. Western Blot exhibited a type 1 PrPres in all parts of the brain.
Conclusion: We described here the successful transmission of a scrapie prion disease to a non-human primate after an extended incubation period, leading to a fatal, non-relapsing neurological disease with all the features of a prion disease. The cerebral lesional profile we observed was original in comparison to other animal prion diseases (c-BSE, L-type BSE, TME) we previously experimentally transmitted in this model.
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasized by the finding that some strains of scrapie produce lesions identical to the once which characterize the human dementias"
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the scrapie problem urgent if the sheep industry is not to suffer grievously.
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
28 Mar 01
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb...
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
28 Mar 01
Like lambs to the slaughter
31 March 2001
by Debora MacKenzie Magazine issue 2284.
FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.
As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.
"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.
But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.
People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.
But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.
Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.
Friday, January 30, 2015
*** Scrapie: a particularly persistent pathogen ***
Thursday, March 26, 2015
Increased Infectivity of Anchorless Mouse Scrapie Prions in Transgenic Mice Overexpressing Human Prion Protein
Tuesday, May 26, 2015
*** Minimise transmission risk of CJD and vCJD in healthcare settings ***
Last updated 15 May 2015
Monday, August 17, 2015
*** FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS
I told Olympus 15 years ago about these risk factors from endoscopy equipment, disinfection, even spoke with the Doctor at Olympus, this was back in 1999. I tried to tell them that they were exposing patients to dangerous pathogens such as the CJD TSE prion, because they could not properly clean them. even presented my concern to a peer review journal GUT, that was going to publish, but then it was pulled by Professor Michael Farthing et al... see ;
Something I submitted to GUT previously;
Subject: Re: gutjnl_el;21 Terry S. Singeltary Sr. (3 Jun 2002) "CJDs (all human TSEs) and Endoscopy Equipment"
Date: Thu, 20 Jun 2002 16:19:51 –0700
From: "Terry S. Singeltary Sr."
To: Professor Michael Farthing
References: 001501c21099$5c8bc620$
Greetings again Professor Farthing and BMJ,
I was curious why my small rebuttal of the article described below was not listed in this month's journal of GUT? I had thought it was going to be published, but I do not have full text access. Will it be published in the future? Regardless, I thought would pass on a more lengthy rebuttal of mine on this topic, vCJD vs sCJDs and endoscopy equipment. I don't expect it to be published, but thought you might find it interesting, i hope you don't mind and hope to hear back from someone on the questions I posed...
Here is my short submission I speak of, lengthy one to follow below that:
Date submitted: 3 Jun 2002
>> eLetter ID: gutjnl_el;21
>> >> Gut eLetter for Bramble and Ironside 50 (6): 888
>> >>Name: Terry S. Singeltary Sr.
>>Title/position: disabled {neck injury}
>>Place of work: CJD WATCH
>>IP address:
>>Browser: Mozilla/5.0 (Windows; U; Win98; en-US; rv:0.9.4)
>>Gecko/20011019 Netscape6/6.2
>> >>Parent ID: 50/6/888
>> Creutzfeldt-Jakob disease: implications for gastroenterology
>> M G Bramble and J W Ironside
>> Gut 2002; 50: 888-890 (Occasional viewpoint)
>>"CJDs (all human TSEs) and Endoscopy Equipment"
regarding your article;
Creutzfeldt-Jakob disease: implications for gastroenterology
>>I belong to several support groups for victims and relatives
>>of CJDs. Several years ago, I did a survey regarding
>>endoscopy equipment and how many victims of CJDs have
>>had any type of this procedure done. To my surprise, many
>>victims had some kind of endoscopy work done on them.
>>As this may not be a smoking gun, I think it should
>>warrant a 'red flag' of sorts, especially since data now
>>suggests a substantial TSE infectivity in the gut wall
>>of species infected with TSEs. If such transmissions
>>occur, the ramifications of spreading TSEs from
>>endoscopy equipment to the general public would be
>>horrible, and could potential amplify the transmission
>>of TSEs through other surgical procedures in that
>>persons life, due to long incubation and sub-clinical
>>infection. Science to date, has well established
>>transmission of sporadic CJDs with medical/surgical
Terry S. Singeltary Sr. >>CJD WATCH
Again, many thanks, Kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 CJD WATCH
[scroll down past article for my comments]
were not all CJDs, even nvCJD, just sporadic, until proven otherwise?
Terry S. Singeltary Sr., P.O. BOX 42, Bacliff, Texas 77518 USA
*** Professor Michael Farthing wrote: Louise Send this to Bramble (author) for a comment before we post. Michael ***
my submission, subsequently, was never published...tss
snip... see full text ;
Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr 1-24-3
Monday, December 26, 2011
Prion Uptake in the Gut: Identification of the First Uptake and Replication Sites
Friday, August 10, 2012
Incidents of Potential iatrogenic Creutzfeldt-Jakob disease (CJD) biannual update (July 2012)
see more history here ;
*** now, from all the consumption and exposure above, now think iatrogenic cjd tse prion at a hospital near you, what if?
Thursday, August 13, 2015
Iatrogenic CJD due to pituitary-derived growth hormone with genetically determined incubation times of up to 40 years
Wednesday, December 11, 2013
*** Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease ***
Tuesday, April 21, 2015
*** Transmissible Spongiform Encephalopathy Advisory Committee TSEAC MEETING SCHEDULED FOR June 1, 2015
Tuesday, August 4, 2015
*** FDA U.S. Measures to Protect Against BSE ***
P.108: Successful oral challenge of adult cattle with classical BSE
Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada
Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only. Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. We are further examining explanations for the unusual disease presentation in the third challenged animal.
10 years post mad cow feed ban August 1997
Date: March 21, 2007 at 2:27 pm PST
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
Cattle feed delivered between 01/12/2007 and 01/26/2007
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
42,090 lbs.
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
9,997,976 lbs.
ID and NV
16 years post mad cow feed ban August 1997
Sunday, December 15, 2013
17 years post mad cow feed ban August 1997
Tuesday, December 23, 2014
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain Specified Risk Materials BSE TSE Prion
Thursday, July 24, 2014
*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Posted by flounder on 03 Jul 2015 at 16:53 GMT
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
Singeltary et al
31 Jan 2015 at 20:14 GMT
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
see page 176 of 201 pages...tss
Thursday, July 24, 2014
*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations
Saturday, September 19, 2015
*** An interview with Professor John Collinge: VIDEO Director of the MRC Prion Unit Part of the Hayward Gallery's History Is Now ***
Thursday, July 30, 2015
*** Professor Lacey believes sporadic CJD itself originates from a cattle infection number of cattle farmers falling victim to Creutzfeld-Jakob Disease is much too high to be mere chance
Saturday, September 12, 2015
The Canadian Management of Bovine Spongiform Encephalopathy in Historical and Scientific Perspective, 1990-2014
>>>We propose that Canadian policies largely ignored the implicit medical nature of BSE, treating it as a purely agricultural and veterinary issue. In this way, policies to protect Canadians were often delayed and incomplete, in a manner disturbingly reminiscent of Britain’s failed management of BSE. Despite assurances to the contrary, it is premature to conclude that BSE (and with it the risk of variant Creutzfeldt-Jakob disease) is a thing of Canada’s past: BSE remains very much an issue in Canada’s present. <<<
*** Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
*** 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. ...
Thursday, October 22, 2015
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened
Sunday, October 18, 2015
*** World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research
Tuesday, October 20, 2015
*** FBI: Agroterrorism not likely, but very possible, Dr. Stephen Gold­smith FBI Laboratory Division, here's your sign
CC-Dr. Steve Goldsmith, FBI Laboratory Division
please note, I tried to forward this to the FBI, spoke with several folks at FBI headquarters, and they were not interested...just saying...terry
Transmissible Spongiform Encephalopthy TSE Prion Disease
*** Kuru Video
Kuru: The Science and The Sorcery
*** Scrapie Video
*** Human Mad Cow Video
Saturday, March 21, 2015
***Canada and United States Creutzfeldt Jakob TSE Prion Disease Incidence Rates Increasing ***
PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD) in Canada is also on a steady increase.
please see ;
> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.
CJD Deaths Reported by CJDSS1, 1994-20122
As of May 31, 2012
Deaths of Definite and Probable CJD
Year Sporadic Iatrogenic Familial GSS FFI vCJD Total
1994 2 0 0 1 0 0 3
1995 3 0 0 0 0 0 3
1996 13 0 0 0 0 0 13
1997 16 0 1 1 0 0 18
1998 22 1 0 1 0 0 24
1999 26 2 2 1 0 0 31
2000 32 0 0 3 0 0 35
2001 27 0 2 1 0 0 30
2002 31 0 2 2 0 1 36
2003 27 1 1 0 0 0 29
2004 42 0 1 0 0 0 43
2005 42 0 0 2 0 0 44
2006 39 0 1 3 1 0 44
2007 35 0 0 4 0 0 39
2008 48 0 1 0 0 0 49
2009 48 0 3 2 0 0 53
2010 34 0 3 0 0 0 37
2011 37 0 2 1 0 1 41
2012 1 0 0 0 0 0 1
Total 525 4 19 22 1 2 573
1. CJDSS began in 1998
2. Data before 1998 are retrospective and partial, data from 1998 to 2008 are complete, and data for 2009 - 2012 are provisional
3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.
CJD Deaths Reported by CJDSS1, 1994-20122
As of May 31, 2012
Saturday, June 15, 2013
Canada Fraser Health Statement on Creutzfeldt-Jakob Disease outbreak
Sunday, December 14, 2014
ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD strains, TSE prion aka Mad Cow Disease United States of America Update December 14, 2014 Report
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European ***
the patient had resided in Kuwait, Russia and Lebanon. The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European ***
Creutzfeldt-Jakob Disease in Northeast Texas
J.A. Rawlings,*1 K.A. Hendricks1, O.M. Nuno1, D.A. Brown1, D.A. Evans2, Texas Department of Health, 1Austin and 2Tyler, Texas
Creutzfeldt-Jacob Disease (CJD), a transmissible spongiform encephalopathy, is caused by prions composed of proteinaceous material devoid of nucleic acid. CJD occurs sporadically (generally 1 case/1,000,000 population per year) in older patients (average age of 65) and is characterized by rapidly progressive dementia, accompanied by severe muscle spasms and incoordination. Death usually occurs within 3 to 12 months (average 7 months). CJD activity in Texas, which has a population of nearly 19 million, appeared to be typical. The statewide death rate for 1995 and 1996 was just under 1/1,000,000. In April of 1997, the Texas Department of Health became aware of an increased number of possible CJD cases in a 23-county area of NE Texas with a population of just over one million. After review of medical and pathology records, four patients were identified with definite classic CJD and three were identified with probable CJD. Dates of death for the eight patients were from April, 1996 through mid-July 1997. The patients were from 46 through 65 years of age; four were male and three were female. A case-control study to identify risks for CJD in NE Texas has been initiated.
Monday, March 29, 2010
>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas.
She left 6 Kids and a Husband.The Purpose of this web is to give information in Spanish to the Hispanic community, and to all the community who want's information about this terrible disease.- Physician Discharge Summary, Parkland Hospital, Dallas Texas Admit Date: 12/29/2009 Discharge Date: 1/20/2010 Attending Provider: Greenberg, Benjamin Morris; General Neurology Team: General Neurology Team Linda was a Hispanic female with no past medical history presents with 14 months of incresing/progressive altered mental status, generalized weakness, inability to walk, loss of appetite, inability to speak, tremor and bowel/blader incontinence. She was, in her usual state of health up until February, 2009, when her husbans notes that she began forgetting things like names and short term memories. He also noticed mild/vague personality changes such as increased aggression. In March, she was involved in a hit and run MVA,although she was not injured. The police tracked her down and ticketed her. At that time, her son deployed to Iraq with the Army and her husband assumed her mentation changes were due to stress over these two events. Also in March, she began to have weakness in her legs, making it difficult to walk. Over the next few months, her mentation and personality changes worsened, getting to a point where she could no longer recognized her children. She was eating less and less. She was losing more weight. In the last 2-3 months, she reached the point where she could not walk without an assist, then 1 month ago, she stopped talking, only making grunting/aggressive sounds when anyone came near her. She also became both bowel and bladder incontinent, having to wear diapers. Her '"tremor'" and body jerks worsened and her hands assumed a sort of permanent grip position, leading her family to put tennis balls in her hands to protect her fingers. The husband says that they have lived in Nebraska for the past 21 years. They had seen a doctor there during the summer time who prescribed her Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the medications did not help and she continued to deteriorate clinically. Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. The husband says that he does not know any fellow workers with a similar illness. He also says that she did not have any preceeding illness or travel.
Monday, March 29, 2010
>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas.
Singeltary family experience with CJD Listserve 22 May 98
Hello, my name is Terry S. Singeltary Sr. and on 12-14-97 my mother died of heidenhan variant CJD, she died a very hidious death. Next, on 12-14-96 exactly one year earlier,my neighbors' mother died from C.J.D. Ii have autopsies to confirm both cases.not to long after my mother had passed away,my neighbor called me and said that I needed to see something. He had been going through a box that he had come across of his mothers. Inside was a bottle of nutritional supplements called IPLEX; INGREDIANTS;VACUUM DRIED BOVINE BRAIN,BONE MEAL,BOVINE EYE,VEAL BONE,BOVINE LIVER POWDER,BOVINE ADRENAL,VACUUM DRIED BOVINE KIDNEY,AND VACUUM DRIED PORCINE STOMACH, it's a cow in a pill. Now this woman taking these pills,died of C.J.D.there was a big article in the Galveston Daily News about all of this. I called the Texas Dept. Of Health and they came and got the pills the next day. Julie Rawlings at the texas dept. of health told me last week that the manufacturer has clammed up on them and will not cooperate anymore. They are referring all matters to their lawyers can this be? Why doesn't the federal government intervEne?
Since the story came out in the galv. news on april 27,1998.a girl called me and told me of her father dying in late 94 or early 95 of C.J.D. in galveston. She told me that my mothers doctor was also her fathers my mothers doctor would always mention the OTHER CASE but that's as far as it went.NOW i know why,her father was a BUTCHER AT A MEAT MARKET IN GALVESTON UNTIL HE RETIRED.
Makes me wonder? Did mom ever eat any beef that had come from that meat market in the last 30 or 40 years? MADCOW is here and you can call it whatever you want to. I saw it, my mother died from it. At times she would jerk so bad it would take 3 of us to hold her down.10 weeks start to finish,and she was gone.this disease that they claim is a different disease in younger folks (nvcjd) is the same damn thing. Just because it last longer and the plaques are a little more extreme,could it not be just a more extreme case of C.J.D. any young person with any disease will last longer than a older person with the same disease, because their body and organs are much younger and healthier.
The manufacturer of IPLEX is Standard Process Inc., Palmyra, Wisconsin.1-800-558-8740. I hope you find some interest in this.if you need more details,please don't hesitate to contact me."
With thanks,
Terry S. Singeltary
Texas cluster web site 21 May 98 Mark V. Gregg 512-458-7677 fax 512-458-7616 Director, Public Health Professional Education Texas Department of Health 1100 West 49th Street T-803 Austin, Texas 78756
"We've developed a CJD Web page here at the Texas Department of Health. In addition to some general information, the page links to the CDC's CJD page as well as a 1996 issue of our biweekly morbidity and mortality newsletter, the Disease Prevention News, which is also available on the Web. Our Infectious Disease Epidemiology and Surveillance (IDEAS) Division is currently investigating what we believe to be a cluster of CJD in a small area in East Texas. The Division's number is on the Web page if you wanted to follow up with specifics."
North American Equity Research
New York
13 January 2004
BSE (Mad Cow) Update:
Do Reports of sCJD Clusters Matter?
Tuesday, July 29, 2008
Heidenhain Variant Creutzfeldt Jakob Disease Case Report
Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'
DIVISION OF NEUROPATHOLOGY University of Texas Medical Branch 114 McCullough Bldg. Galveston, Texas 77555-0785
DATE: 4-23-98
TO: Mr. Terry Singeltary @ -------
FROM: Gerald Campbell
FAX: (409) 772-5315 PHONE: (409) 772-2881
Number of Pages (including cover sheet):
This document accompanying this transmission contains confidential information belonging to the sender that is legally privileged. This information is intended only for the use of the individual or entry names above. If you are not the intended recipient, you are hereby notified that any disclosure, copying distribution, or the taking of any action in reliances on the contents of this telefaxed information is strictly prohibited. If you received this telefax in error, please notify us by telephone immediately to arrange for return of the original documents. -------------------------- Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Admitting Race: C
Attending Dr.: Date / Time Admitted : 12/14/97 1228 Copies to:
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858
Autopsy NO.: AU-97-00435
AUTOPSY INFORMATION: Occupation: Unknown Birthplace: Unknown Residence: Crystal Beach Date/Time of Death: 12/14/97 13:30 Date/Time of Autopsy: 12/15/97 15:00 Pathologist/Resident: Pencil/Fernandez Service: Private Restriction: Brain only
I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
snip...see full text ;
Mad cow disease: Could it be here?
Man's stubborn crusade attracts experts' notice By Carol Christian | August 5, 2001
An alarming presentation level II trauma center of Creutzfeldt-Jakob disease following a self-inflicted gunshot wound to the head
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Thursday, October 1, 2015
***Alzheimergate, re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy, Singeltary Submission to Nature
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014
Singeltary comment ;

Wednesday, September 2, 2015

*** Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses in an Alzheimer’s Disease Database
Terry S. Singeltary Sr.

Terry S. Singeltary Sr.