Monday, January 14, 2013

Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe

Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe
 
 
 
Published: Jan 13, 2013 05:36 PM Modified: Jan 13, 2013 05:38 PM
 
 
 
At last, answers to a mother’s grief Cary teen died of extremely rare disease
 
 
 
By Andrew Kenney, akenney@newsobserver.com
 
 
 
By Andrew Kenney Cary News
 
 
 
It wasn’t bacteria or a virus that plagued young Michael Mendy’s body and mind. He did not inherit his symptoms from his mother or father. Nothing toxic was in his blood. And while he was sick, Michael’s parents had no explanation.
 
 
 
“I had to figure it out. I had to find an answer. I had to find a doctor that could help him,” said Michael’s mother, Kathleen Mendy, who lives in western Cary. “You don’t think you’re going to come across something that nobody’s ever seen.”
 
 
 
But they had. Dozens of specialists and three years of suffering brought no diagnosis. Michael died a year ago, at age 16. And only then did the explanation and the terrible significance of his case emerge.
 
 
 
Doctors estimate that fewer than one in 100 million young people will share Michael’s journey. The sports nut and East Cary Middle School student was killed by a disease that mostly afflicts the elderly.
 
 
 
Michael was a heart-wrenching outlier, apparently among the youngest ever to suffer a spontaneous ravaging of the brain.
 
 
 
The onset
 
 
 
Kathleen Mendy thinks it started on Michael’s 13th birthday in 2009.
 
 
 
On that January day, another boy knocked Michael’s head to the court during a basketball game. He was playing again a minute later, his mother watching with a tinge of worry.
 
 
 
The symptoms of a years-long illness crept in that weekend, during a mother-son Super Bowl trip to Florida. That’s where she first saw Michael’s confusion, his unsure movements and his inexplicable crying.
 
 
 
It seemed at first like the troubling wake of the teen’s second concussion in three months, but that theory would erode and change. Across the next three years, in a nightmare that kept unfolding, the brawny teenager would drop almost half his body weight, spend months in the hospital, lose his speech and lay debilitated by simple infections.
 
 
 
The printed record of Michael’s hospital visits and test appointments is three and a half pages long. It documents an increasingly desperate search, listing 140 days in the hospital, 91 visits with doctors and 426 therapy appointments from 2009 to 2012.
 
 
 
“I always thought he would get better,” Kathleen Mendy said. “I used to always tell him, ‘Michael, one day you’re just going to run out of your bedroom, and you’re going to come running downstairs, and you’re going to be all better.’ ”
 
 
 
The turning point wouldn’t come.
 
 
 
While his friends went on to high school, Michael was confined to a wheelchair and fed through a tube. His care grew so intense that his mother brought on a full-time medical aide.
 
 
 
His father, divorced from his mother, drove in from Florida each time he entered the hospital, and Kathleen Mendy’s family often visited from New York.
 
 
 
Each treatment was more esoteric than the last. By the end of 2011, the Mendys had seen more than 30 doctors, medical specialists, faith healers and alternative practitioners.
 
 
 
“I tried chiropractors, reflexology, myofacial therapy,” Kathleen Mendy said. “I tried everything.”
 
 
 
‘I’m so glad I didn’t know’
 
 
 
The realization came to Kathleen Mendy on the last night of January 2012, the 22nd day that Michael spent in a UNC hospital bed.
 
 
 
He’d been kept alive in an intensive-care unit by a breathing machine while an infection took hold of his lungs. The mysterious disorder had left his body unable to respond.
 
 
 
The memory shakes Kathleen Mendy to tears. The scene sticks in her mind.
 
 
 
“Not until the night before he died, is when, honestly, it hit me,” she recalled.
 
 
 
The doctors laid a choice before his parents that night. Michael could go home with a tracheotomy and a ventilator, but they believed he’d live just a few months longer. Or doctors could remove him from life support.
 
 
 
Michael’s parents didn’t want him to suffer anymore. He died on Feb. 1, 2012.
 
 
 
Only months later would Michael’s family learn the reason for his degradation and death. An autopsy showed that the teenager died of sporadic fatal insomnia, a subtype of Creutzfeldt-Jakob Disease.
 
 
 
“I’m so glad I didn’t know what it was” before Michael died, Kathleen Mendy said. “Because then I wouldn’t have had hope.”
 
 
 
‘A descent into hell’
 
 
 
“This disease is a descent into hell,” said Florence Kranitz, president of The Creutzfeldt-Jakob Disease Foundation in New York City.
 
 
 
She saw her own husband die in 2001 of an ailment similar to Michael’s. Since then she has heard the stories of many of the 300 CJD victims her organization identifies each year, including cases of fatal insomnia.
 
 
 
“We get this phone call, and tragically it’s the same phone call over and over again,” Kranitz said. “They’ve never heard of this disease.”
 
 
 
The story she heard from Kathleen Mendy fit the profile, with one beguiling exception. Almost everyone afflicted by CJD subtypes are older than 45, except those who contract a variant of the disease genetically or through contaminated beef, which Michael had not.
 
 
 
Michael’s case quickly drew the attention of national experts, including Pierluigi Gambetti, director of the National Prion Disease Pathology Surveillance Center in Ohio. Gambetti, a pioneering researcher, examined Michael’s brain and in April identified his disease as sporadic fatal insomnia.
 
 
 
He’d later take hours to talk with Kathleen Mendy about her son’s death. Sporadic fatal insomnia and CJD, he explained, are part of the still-mysterious field of neurodegenerative diseases, including Alzheimer’s and Parkinson’s.
 
 
 
Some of these ravages of the brain, such as so-called “Mad Cow,” begin with an infection of prions, or pathogenic proteins, from the outside. CJD in the young also can be caused by prions, often transmitted during surgery.
 
 
 
Like a virus, a prion can essentially “breed.” The virus hijacks human cells, and the prion reshapes other proteins into its own mutated form. And when a prion or virus propagates enough, it can destroy its host.
 
 
 
But there’s a crucial difference: The prion also can come from within. Gambetti believes that Michael’s disease began when the boy’s brain misfolded a protein, creating a prion instead. The defect may then have multiplied out of control and ruined the delicate balance of the body.
 
 
 
It’s not uncommon for the body to make mistakes. Neurons and other cells normally catch and eliminate prions before they replicate. These defensive systems may grow weaker with age; some people may also inherit weaker defenses.
 
 
 
But Michael was a teenager, with no apparent family history of neurodegenerative diseases. Gambetti put the odds of such a case at one in 100 million in the general population; another doctor said it was one in 600 million.
 
 
 
In fact, Michael may be among the youngest ever to be affected by a neurodegenerative disease without an inherited or outside cause.
 
 
 
“We just haven’t seen this disease affect someone this young,” said John Trojanowski, a professor of geriatric medicine at the University of Pennsylvania.
 
 
 
Gambetti, who played a key role in the discovery of fatal insomnia, theorizes that Michael’s illness was random, despite the odds. It may be that, by chance or some unknown factor, Michael’s brain perfectly bred its own pathogen.
 
 
 
“The bodies of all animals are a marvel of things, in positive and negative,” Gambetti said. “They can do things striking for the good, but also for the bad.”
 
 
 
Looking to others
 
 
 
Nearly a year after Michael’s death, Kathleen Mendy finds love and support from family, friends and Compassionate Friends, a local group. But the extreme rarity of Michael’s case is isolating.
 
 
 
When she attended a CJD conference last summer with her twin sister, they met the families of people who had mostly died in middle and old age.
 
 
 
Some nights she goes up to her only child’s room. It’s lined with dozens of sports team caps and trophies. Athletes’ names are still painted on the blades of his ceiling fan, and the UNC comforter is still on his bed.
 
 
 
All that’s new is the shrine on the desk, where Michael’s photo stands near a glazed statue of praying hands.
 
 
 
“Sometimes I think I’m OK, and other times it’s like it just happened last night. It’s like a rollercoaster,” Kathleen Mendy said.
 
 
 
She may have as many logical answers now as she’ll ever get – a medical, if not a spiritual description of why Michael died.
 
 
 
She still doesn’t know what it was that made her son vulnerable. She believes Michael’s concussions triggered his illness, but his doctors haven’t confirmed the idea.
 
 
 
“I’m a little bit resolved that I’ll never hear the answer,” she said. “It would be nice to know, but if I don’t know it, it’s not what matters now.”
 
 
 
She finds hope instead in the idea that she could help others; she’s thinking of writing a book and becoming a public advocate for those who suffer with CJD.
 
 
Meanwhile, as Michael’s birthday and the first anniversary of his death approach, Gambetti and one of Michael’s former doctors are preparing to present his case to their respective medical communities. As painful as the case is, “its rarity may contribute to expand the knowledge on this terrible disease,” according to Gambetti.
 
 
 
He hopes his research will one day allow much earlier diagnosis and treatment of fatal insomnia. Such a breakthrough could key medical progress across the spectrum of prion-related diseases, which are fatal in practically all cases.
 
 
 
Gambetti’s research into Michael’s case will soon yield a more immediate result too: He’ll be able to tell caregivers that sporadic fatal insomnia can strike not just the mature, but perhaps people who are just beginning their lives.

 
And with Michael’s story spreading, the next stricken family may at least know the harrowing path ahead.
 
 
 
Kenney: 919-460-2608 or twitter.com/KenneyOnCary
 
 
 
 
 
 
 
 
sporadic FFI, really $$$

 
HOW can a genetic disease, one NOT tied to any family member, how can this be a genetic disease ?
 
 
 
easy, they simply change the name to another stupid name of the same damn disease.
 
 
 
Gambetti et al must be getting paid very well for all this junk science on CJD and human TSE in the USA $$$
 
 
 
 
 
Wednesday, November 09, 2011
 
 
 
Case report Sporadic fatal insomnia in a young woman: A diagnostic challenge: Case Report TEXAS
 
 
 
HOW TO TURN A POTENTIAL MAD COW VICTIM IN THE USA, INTO A HAPPENSTANCE OF BAD LUCK, A SPONTANEOUS MUTATION FROM NOTHING.
 
 
 
OR WAS IT $$$
 
 
 
 
 
 
snip...
 
 
 
AND THAT MY FRIENDS, IS HOW YOU EXPLAIN SOMETHING AWAY INTO NOTHING. IT'S THE USDA ET AL MAD COW WAY $$$
 
 
 
how many times have we seen this happen? time and time again.
 
 
 
sporadic FFI or nvCJD Texas style ???
 
 
 
DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)
 
 
 
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 a least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the woodwork 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 a great 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.)
 
 
 
END...TSS
 
 
 
 
snip...see full text ;
 
 
 
 
 
 
 
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
 
 
 
Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
 
 
 
Date: Tue, 9 Jan 2001 16:49:00 –0800
 
 
 
From: "Terry S. Singeltary Sr."
 
 
 
Reply-To: Bovine Spongiform Encephalopathy
 
 
 
 
 
 
######### Bovine Spongiform Encephalopathy #########
 
 
 
 
 
 
 
Here we go folks. AS predicted. THIS JUST OUT ! as i predicted, more BSe. $$$
 
 
 
Tuesday, August 03, 2010
 
 
 
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein
 
 
 
 
 
 
 
 
Monday, August 9, 2010

 
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?
 
 
 
snip...see full text ;
 
 
 
 
 
 
 
 
O.K. let's compare some recent cases of this prionpathy in other countries besides Gambetti's first 10 recently, that he claims is a spontaneous event, from a genetic disorder, that is not genetic, but sporadic, that is related to no animal TSE in North America, or the world. ...
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Sunday, August 09, 2009
 
 
 
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
 
 
 
 
 
 
 
 
Tuesday, August 18, 2009
 
 
 
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
 
 
 
 
 
 
 
 
PPS POLITICAL PRION SCIENCE $$$
 
 
 
 
Creutzfeldt-Jakob Disease Surveillance in Texas
 
 
 
 
 
 
 
 
Sunday, July 11, 2010

 
CJD or prion disease 2 CASES McLennan County Texas population 230,213 both cases in their 40s
 
 
 
 
 
 
 
 
 
 
see the continuing rise of sporadic CJD in Texas here ;
 
 
 
 
 
 
 
 
 
Saturday, March 5, 2011
 
 
 
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

 
 
 
 
 
 
Sunday, August 21, 2011
 
 
 
The British disease, or a disease gone global, The TSE Prion Disease
 
 
(see video here)

 
 
 
 
 
 
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ?
 
 
 
(see video at bottom)

 
 
 
 
 
 
Sunday, September 6, 2009

 
MAD COW USA 1997
 
 
 
(SEE SECRET VIDEO)

 
 
 
 
 
 
Thursday, August 4, 2011
 
 
 
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
 
 
 
 
 
 
 
Monday, December 31, 2012
 
 
 
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State, 2006–2011-2012
 
 
 
 
 
 
 
 
Tuesday, December 25, 2012
 
 
 
CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25, 2012

 
 
 
 
 
 
Friday, November 23, 2012

 
sporadic Creutzfeldt-Jakob Disease update As at 5th November 2012 UK, USA, AND CANADA
 
 
 
 
 
 
 
 
Sunday, December 2, 2012
 
 
 
CANADA 19 cases of mad cow disease SCENARIO 4: ‘WE HAD OUR CHANCE AND WE BLEW IT’

 
 
 
 
 
 
Friday, November 23, 2012

 
sporadic Creutzfeldt-Jakob Disease update As at 5th November 2012 UK, USA, AND CANADA
 
 
 
 
 
 
 
 
Saturday, January 05, 2013
 
 
 
Immunohistochemical Detection of Disease- Associated Prion Protein in the Peripheral Nervous System in Experimental H-Type Bovine Spongiform Encephalopathy
 
 
 
 
 
 
 
 
Monday, October 10, 2011

 
EFSA Journal 2011 The European Response to BSE: A Success Story
 
 
 
snip...

 
 
 
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
 
 
 
snip...
 
 
 
 
 
 
 
 
 
 
 
Thursday, August 12, 2010
 
 
 
Seven main threats for the future linked to prions

 
First threat
 
 
 
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

 
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

 
Second threat
 
 
 
snip...
 
 
 
 
 
 
 
IT is of my opinion, that the OIE and the USDA et al, are the soul reason, and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion diseases, including typical and atypical BSE, typical and atypical Scrapie, and all strains of CWD, and human TSE there from, spreading around the globe.
 
 
 
I have lost all confidence of this organization as a regulatory authority on animal disease, and consider it nothing more than a National Trading Brokerage for all strains of animal TSE, just to satisfy there commodity. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.
 
 
 
JUST because of low documented human body count with nvCJD and the long incubation periods, the lack of sound science being replaced by political and corporate science in relations with the fact that science has now linked some sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call for this organization to be dissolved. ...
 
 
 
 
 
Tuesday, July 17, 2012

 
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th General Session, 20 - 25 May 2012

 
 
 
 
 
 
Saturday, October 6, 2012
 
 
 
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2011 Annual Report
 
 
 
 
 
 
 
 
re-Human Prion Diseases in the United States Posted by flounder on 01 Jan 2010 at 18:11 GMT
 
 
 
I kindly disagree with your synopsis for the following reasons ;

 
 
 
 
 
 
Tuesday, November 08, 2011

 
Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011 Original Paper

 
Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.
 
 
 
 
 
 
 
 
Views & Reviews
 
 
 
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
 
 
 
Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and Lawrence B. Schonberger, MD
 
 
 
+ Author Affiliations
 
 
 
From the Division of Viral and Rickettsial Diseases (Drs. Belay and Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA; and National Prion Disease Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.

 
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600 Clifton Road, Mailstop A-39, Atlanta, GA 30333.
 
 
 
 
 
 
 
 
26 March 2003
 
 
 
Terry S. Singeltary, retired (medically) CJD WATCH

 
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
 
 
 
 
 
 
 
 
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. FREE FULL TEXT
 
 
 
 
 
 
 
2 January 2000
 
 
 
British Medical Journal
 
 
 
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

 
 
 
 
 
15 November 1999
 
 
 
British Medical Journal
 
 
 
vCJD in the USA * BSE in U.S.
 
 
 
 
 
 
 
 
 
Saturday, January 2, 2010
 
 
 
Human Prion Diseases in the United States January 1, 2010 ***FINAL***

 
 
 
 
 
14th ICID International Scientific Exchange Brochure -
 
 
 
Final Abstract Number: ISE.114
 
 
 
Session: International Scientific Exchange

 
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
 
 
 
T. Singeltary
 
 
 
Bacliff, TX, USA
 
 
 
Background:

 
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
 
 
 
Methods:
 
 
 
12 years independent research of available data
 
 
 
Results:
 
 
 
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.


 
Conclusion:
 
 
 
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
 
 
 
 
 
 
 
 
 
re-Human Prion Diseases in the United States Posted by flounder on 01 Jan 2010 at 18:11 GMT
 
 
 
I kindly disagree with your synopsis for the following reasons ;
 
 
 
 
 
 
 
Wednesday, May 16, 2012

 
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
 
 
 
Proposal ID: 29403

 
 
 
 
 
 
Monday, August 20, 2012

 
CASE REPORTS CREUTZFELDT-JAKOB DISEASE: AN UNDER-RECOGNIZED CAUSE OF DEMENTIA
 
 
 
 
 
 
 
 
Friday, October 05, 2012
 
 
 
Differential Diagnosis of Jakob-Creutzfeldt Disease
 
 
 
 
 
 
 
 
see the Duke, Pa, Yale, and Mexican study here, showing the misdiagnosis of CJD TSE prion disease as Alzheimers ;
 
 
 
 
 
 
 
 
Monday, July 23, 2012
 
 
 
The National Prion Disease Pathology Surveillance Center July 2012
 
 
 
 
 
 
 
 
TSS
layperson mom dod 12/14/97 confirmed hvCJD...

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