Mad deer disease can infect normal human brains in laboratory tests
Monday, May 8, 2000
www.ems.org 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."
From: Terry S. Singeltary Sr.
Sent: Friday, October 23, 2015 12:50 PM
Cc: melany@cjdfoundation.org ; lori@cjdfoundation.org ; ruthie@cjdfoundation.org ; florence@cjdfoundation.org ; cjdsurv@po.cwru.edu ; contactus@cjdsupport.org.au ; help@cjdsupport.net ; info@aienp.it ; cs-net@takenet.or.jp ; info@cjd-israel.org ; mcj-apev@wanadoo.fr ; pathology@case.edu
; info@cjdaware.com ; cjdaware@iwon.com ;
cjdaware@gmail.com ; cjdvoice@yahoogroups.com ; bloodcjd@yahoogroups.com ; CJD-L@LISTS.AEGEE.ORG
Subject: CJD FOUNDATION CREUTZFELDT JAKOB DISEASE TSE PRION
QUESTIONNAIRE UPDATE OCTOBER 2015
2015 CJD Foundation Family Conference Washington, DC July 10th-12th,
2015
USA CREUTZFELDT JAKOB DISEASE CJD TSE PRION QUESTIONNAIRE UPDATE OCTOBER
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 
kindest regards, terry
USA CREUTZFELDT JAKOB DISEASE CJD TSE PRION QUESTIONNAIRE UPDATE OCTOBER
2015
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.
also;
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
DEPARTMENT OF HEALTH AND HUMAN SERVICES
FOOD AND DRUG ADMINISTRATION CENTER FOR BIOLOGICS EVALUATION AND RESEARCH
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE
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.
1/19/01
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...
NATURAL PEANUT BUTTER STANDARDBAR
bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney...
USF (MAD COW) OINTMENT (RUB A DUB DUB, KURU ETC) ;
bovine orhic glandular extract
UTROPHIN PMG
bovine uterus PMG
VASCULIN
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
MYO-PLUS
bovine heart PMG, bovine liver, porcine stomach, bovine orchic extract,
bovine spleen, ovine spleen, bovine adrenal Cytosol extract, BOVINE BRAIN
NEUROPLEX
bovine orchic Cytosol extract, bovine spleen, BOVINE BRAIN PMG EXTRACT,
BOVINE ANTERIOR PITUITARY, bovine liver, BOVINE PITUITARY PMG EXTRACT, AND MORE
BOVINE BRAIN...
NEUROTROPHIN PMG
BOVINE BRAIN PMG
NIACINAMIDE B6 VM
bovine liver, porcine stomach, bovine spleen ovine spleen, BOVINE BRAIN
OCULOTROPHIN PMG BOVINE EYE PMG
ORCHEX
bovine liver, bovine orchic Cytosol extract, porcine stomch, bovine spleen,
ovine spleen, BOVINE BRAIN
OSTARPLEX
veal bone PMG extract, veal bone PMG extract, bovine liver, porcine
stomach, bovine adrenal, bovine spleen, ovine spleen, BOVINE BRAIN
PARAPLEX
bovine pancreas PMG extract, porcine duodenum, bovine adrenal PMG, BOVINE
PITUITARY PMG EXTRACT, bovine thyroid PMG extract
PITUITROPHIN PMG
RUMAPLEX
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
SENAPLEX
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
Correspondence
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 aol.com) 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. http://www.cfsan.fda.gov/~dms/ds-oview.html
(accessed Feb 20, 2002). 4 Pear R. Feds call for tighter control over
nutritional supplements. Organic Consumers Association, April 17, 2001. http://www.organicconsumers.org/Organic/dietsupp.cfm
(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: mailto:gomezj%40gao.gov Cc: mailto:siggerudk%40gao.gov ;
mailto:youngc1%40gao.gov ; mailto:oighotline%40gao.gov
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]
SNIP...SEE MUCH MORE HERE ;
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
*** CJD QUESTIONNAIRE
***HISTORY OF CJD FOUNDATION CREUTZFELDT JAKOB DISEASE QUESTIONNAIRE SINCE
INCEPTION***
PLEASE REMEMBER ;
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.
HAVE YOU GOT YOUR CJD QUESTIONNAIRE ASKING REAL QUESTIONS PERTAINING TO
ROUTE AND SOURCE OF THE TSE AGENT THAT KILLED YOUR LOVED ONE ???
if not, why not...
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
> 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."
Reply-To: cjdvoice@yahoogroups.com
To: cjdvoice@yahoogroups.com
CC: bloodcjd@yahoogroups.com
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
CJD FOUNDATION QUESTIONNAIRE
REPORT FOR DATA BASE OF PATIENTS WITH CREUTZFELDT--JAKOB DISEASE (CJD) OR
OTHER TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES (TSE's)
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 ______
unknown
Was an autopsy performed? yes - no - unknown
If yes, what was the result? _____
positive for__________
negative for CJD and other TSE's______
unknown
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)
___Other
___Unknown
* 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.
-4-
END
==================================================
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."
Reply-To: cjdvoice@yahoogroups.com
To: cjdvoice@yahoogroups.com
CC: bloodcjd@yahoogroups.com
CJD VICTIM
1.
NAME______________________________________
STREET___________________________________
TOWN_____________________________________
phone____________________________________
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)?
________________
address__________________
phone____________________
E. DATE OF INTERVIEW__________________________
LOCATION OF INTERVIEW_____________________
F. NAME OF INTERVIEWER________________________
2. SUBJECT INFORMATION
A. SEX___________________
B. BIRTH DATE____________
C. BIRTH PLACE___________ (country, state, county, city)
D. ETHNIC ORIGIN_________
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?________________
3. PAST MEDICAL HISTORY
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
wounds?___________________
(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)_____________________________
EYE____________________________________________
ABDOMINAL______________________________________
ORTHOPEDIC_____________________________________
OTHER__________________________________________
TONSILS OUT?___________________________________
APPENDIX OUT?__________________________________
ever received an ORGAN TRANSPLANT, including corneal or bone marrow
transplant?_____________________________________
kidney, liver, and other_______________________
C. BLOOD TRANSFUSION__________________________
TRANSFUSION OF ALBUMIN OR IMUNOGLOBULIN________
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
__________________________________________________
SUMMARY OF ABOVE RESPONSES; HAS THE SUBJECT BEEN EXPOSED TO ONE OF THE
MEDICATIONS OF BOVINE OR OVINE ORIGIN, AND OR ANY DESICCATED ANIMAL ORIGIN?
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?____
4. FAMILY HISTORY PEDIGREE
(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)
D. CONFIRMATION OF FAMILY HISTORY OF CJD OR OTHER TSE'S
(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)
DIETARY HISTORY
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)
EYE___________________
TRIPE_________________
LIVER_________________
KIDNEY_______________
SWEETBREADS_________
(pancreas)
ROAST LAMB,
LAMB COPS,
LAMB STEW,
ROAST PORK,
HAM,
BACON,
ROAST BEEF,
STEAK,
BEEF STEW,
MINCED BEEF,
VEAL,
VENISON,
CHICKEN,
BURGERS,
MEAT PIES SUCH AS PORK, VEAL, AND HAM, STEAK AND KIDNEY, CHICKEN AND
MUSHROOM,***
GOTS,
MEAT SAUSAGES,
BLACK PUDDING,
HAGGAS,
LIVER SAUSAGE OR PATE',
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)
____________________________________________________________
____________________________________________________________
____________________________________________________________
5. EXPOSURE TO ANIMALS:
A. Did the Subject every HUNT, DRESS, AND EAT DEER? ____________________
ELK_____________________
SQUIRREL_______________
OTHER__________________
(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:
CATS________________
DOGS________________
FERRETS_____________
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;
CATTLE______________
SHEEP________________
GOATS_______________
PIGS__________________
CHICKENS____________
MINK_________________
(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;
medical/pharmaceutical/nursing/dentistry_____________________________
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
__________________________________________________
MEDICAL-ENDOSCOPY WORK OF ANY TYPE
__________________________________________________
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="" wt.net=""><018601c284f7 .com="" a04a80="" a64a8c0="" newportrentalguide=""><3dc80f1a .3090808="" wt.net=""><000901c28502 .com="" a64a8c0="" fac15c00="" newportrentalguide=""><3dc81fca .1040403="" wt.net="">
Terry,
Oh no....I've gone and pissed you off (ha ha)I just find it better to
speak...so 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 ?
Tracie
----- 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,
terry
>>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?
Tracie
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
To: BSE-L@uni-karlsruhe.de
######### 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*************
*** PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS ***
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.
==========================================
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
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.
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
R. G. WILL
1984
*** 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 ;
snip...
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
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO
2015
O35
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
E-mail: jacqueline.mikol@wanadoo.fr
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
Abstract
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.
snip...
R. BRADLEY
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.
snip...
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
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
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.
snip...
76/10.12/4.6
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)
C. J. GIBBS jun. & D. C. GAJDUSEK
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...
2001
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
CC: lcamp@BMJgroup.com
References: 001501c21099$5c8bc620$7c58d182@mfacdean1.cent.gla.ac.uk
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.
>>Email: flounder@wt.net
>>Title/position: disabled {neck injury}
>>Place of work: CJD WATCH
>>IP address: 216.119.162.85
>>Hostname: 216-119-162-85.ipset44.wt.net
>>Browser: Mozilla/5.0 (Windows; U; Win98; en-US; rv:0.9.4)
>>Gecko/20011019 Netscape6/6.2
>> >>Parent ID: 50/6/888
>>Citation:
>> 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
>>procedures.
Terry S. Singeltary Sr. >>CJD WATCH
Again, many thanks, Kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
flounder@wt.net CJD WATCH
[scroll down past article for my comments]
snip...
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 ;
2003
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 flounder@wt.net 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)
SNIP...
see more history here ;
OLYMPUS ENDOSCOPY CJD
*** 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 ***
THE BAXTER STUDY...SEE MORE HERE ;
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
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
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.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-
Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M
CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B
DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal,
JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT
Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC
LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall #
V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
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.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
16 years post mad cow feed ban August 1997
2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
17 years post mad cow feed ban August 1997
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
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.
snip...
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
*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video
Saturday, March 21, 2015
***Canada and United States Creutzfeldt Jakob TSE Prion Disease Incidence
Rates Increasing ***
CANADA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic
CJD’s). ...tss
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
SEE DECEMBER 2012 CANADA
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
===========================
*** HUMAN MAD COW DISEASE nvCJD TEXAS CASE NOT LINKED TO EUROPEAN TRAVEL
CDC ***
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 ***
*** ANOTHER UPDATE FOR THE HISTORY OF CJD IN TEXAS, THE CJD CLUSTER BACK IN
1997, AND THE 38 YEAR OLD WOMEN WHOM HAD WORKED FOR TYSON, SLAUGHTERING CATTLE,
THAT DIED WITH CJD...TSS ***
CJD NE TEXAS CLUSTER
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
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN
AND SPINAL CORD MATTER
URGENT, PLEASE NOTE ;
>>> 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
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN
AND SPINAL CORD MATTER
URGENT, PLEASE NOTE ;
>>> 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 now.how 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 doctor.now 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?
SNIP...SEE FULL TEXT ;
GLOBAL CLUSTERS OF CJD
Tuesday, July 29, 2008
Heidenhain Variant Creutzfeldt Jakob Disease Case Report
snip...
Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report
'MOM'
DIVISION OF NEUROPATHOLOGY University of Texas Medical Branch 114
McCullough Bldg. Galveston, Texas 77555-0785
FAX COVER SHEET
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):
Message:
*CONFIDENTIALITY NOTICE*
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
FINAL AUTOPSY DIAGNOSIS
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
http://www.chron.com/news/houston-texas/article/Mad-cow-disease-Could-it-be-here-2042860.php
Friday, October 09, 2015
Friday, October 09, 2015
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
*** IN STRICT CONFIDENCE ***
Singeltary comment ;
http://www.plosone.org/annotation/listThread.action?root=82860
Wednesday, September 2, 2015
*** Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses in an Alzheimer’s Disease Database
http://betaamyloidcjd.blogspot.com/2015/09/clinically-unsuspected-prion-disease.html
Wednesday, September 2, 2015
*** Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses in an Alzheimer’s Disease Database
http://betaamyloidcjd.blogspot.com/2015/09/clinically-unsuspected-prion-disease.html
Terry S. Singeltary Sr.
Terry S. Singeltary Sr.
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