Saturday, January 17, 2015

Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease


Greetings Honorable Governor Herbert Sir and Utah Government officials et al, 
in reply to ;
“I have known and been a friend of the Lockhart family for 25 years and I am terribly saddened by the news of Becky’s sudden and unexpected passing.
Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease CJD TSE Prion
Becky Lockhart, Utah’s first female House speaker, dies
Posted 2:14 pm, January 17, 2015, by Ben Winslow, Tiffany DeMasters, Andrew Klay and Mark Green, Updated at 05:42pm, January 17, 2015
See the two videos above for a report on Lockhart’s passing as well as a segment detailing her life and influence in Utah politics.
SALT LAKE CITY — Becky Lockhart, the first woman Speaker of the House in Utah, died Saturday at age 46, her family confirmed.
In a statement, the Lockhart family said she passed away at her Provo home around noon surrounded by friends and family. Lockhart died “from an unrecoverable and extremely rare neurodegenerative brain disease,” the family said.
“She was at peace and surrounded by her family,” said family spokesman Sen. Curt Bramble in the statement. “It’s a credit to world-class doctors and Becky’s indomitable spirit that they were able to have these past days together with her. The outpouring of prayers and positive thoughts continue to help sustain the family, and they thank everyone for their support.”
At a news conference Saturday afternoon, doctors at University Medical Center and Lockhart’s family disclosed that she had been diagnosed with the extremely rare Creutzfeldt-Jakob disease. They said it is a “one in a million” diagnosis and the Speaker initially sought treatment for vertigo.
The degenerative disease progressed quickly.
Becky Lockhart, history-making Utah lawmaker, dies at 46
By ROBERT GEHRKE | The Salt Lake Tribune
My sincere condolences to the family and friends of the House Speaker Becky Lockhart. I am deeply saddened hear this.
with that said, with great respect, I must ask each and every one of you Politicians that are so deeply saddened to hear of this needless death of the Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am seriously going to ask you all this...I have been diplomatic for about 17 years and it has got no where. people are still dying. so, are you all stupid or what??? how many more need to die ??? how much is global trade of beef and other meat products that are not tested for the TSE prion disease, how much and how many bodies is this market worth? (I’m still a meat eater, don’t ask me why). NOT counting friendly fire i.e iatrogenic CJD TSE prion (who cares about second hand transmission$), nobody cares about any traceback anyone$$$). someone please tell me a number, how many more need to die, before this CJD TSE Prion mutates from one of the many TSEs in many different species right here in the USA, and really becomes nasty, say like the way CWD transmits in cervids (you all do know there is more than one strain of CWD in cervid)??? how many lobbyist does it take for you all to keep buying into this BSe Bullshit Encephalopathy BSe, science that is 30+ years old the USDA OIE Inc keep going by, ......really what the f... does it take to wake you folks up$$$ how many bodies??? how young do they have to go??? like the UK, down in the low teens? do you people not know what iatrogenic means? really...somebody please tell me, are we really going to keep going down this road??? I apologize for this rant, the cuss words, but these needless deaths are getting younger and younger from the infamous sporadic CJDs, the count is rising from year to year, with the none detected, misdiagnosed, keep going on as such, and I am getting old and gray. I watched my mother die from this damn disease on December 14, 1997. over the previous few months, at times, she jerked so bad it took 3 adults to hold her down to keep her from hurting herself, all the while screaming what’s wrong with me, why can’t I stop this. she did everything but spin her head 360 degrees on her shoulders. you never forget. YOU NEVER FORGET. then you listen to the same store bought junk science for the next 17 years via the USDA and OIE inc. I’m tired of listening to it. probable does not matter to anyone, but I said back in 2003, after that infamous day on December 23, 2003 when the USDA et al lost their BSE Gold care i.e. BSE FREE status. I said back then and was laughed at that the TSE Prion was linked to Alzheimer’s and other neurological disease, and I said that sporadic CJD was linked to mad cow disease some how. I have said that CWD in cervids is a great risk factor to humans, along with the atypical TSE prion disease. today, all has come to pass, all has come true, but nobody bothers to read the science. ...again, sorry about the cussing, but this really made me angry and I never been very diplomatic, but with this, and the recent case of the Navy Commander that was 41 years old, and all the past young victims of the TSE prion aka mad cow type disease in the USA, these cases of CJD TSE prion mad cow type disease cases in the USA are getting younger and younger, the names of these types disease are now varying from the sCJD subtypes, to the sporadic FFI, sporadic GSS, to the infamous VPSPr TSE prion disease. on my Mothers grave, you all better take heed...those fool hearted politicians that kept eating a hamburger for the camera’s to prove beef was safe, were just fools. it goes so much further than that. you people wanted that damn BSE MRR policy of the BSE GBR risk assessments after that fateful day, well, you got it. now, how long are you willing to keep passing the TSE prion mad cow type agent around.
I’m suppose to be retiring from this ongoing nightmare anyway....please stay with me, I urge you all to read the science, peer review, the confidential data from back in the BSE Inquiry days, the FOIA on feed and and TSE prion here in the USA, the truth is here, file it away, or not, all over my failed endeavor to try and warn and rid the word of the CJD TSE prion aka mad cow type disease. I have wasted 17 years daily. nobody would listen to me, I have no PhDs. I am only a layperson.
with great respect, and sincere urgency, I send you the following science, please read and try to understand this. that’s all I can say, and I have probably said too much...sorry I cussed...somebody please listen. I am not a Brad Pitt type star that can speak to Congress, there to busy trying to shut the government down (either side), both side have ignored this debacle, but for whatever it’s worth, I am going to give it a shot here...hey, the Australian Cattlemen Ass. Brad Bellinger read some of my statement’s in the Hansard’s Parliament, some maybe someone is listening.........
I kindly and respectfully submit the following ;
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission ;

I believe that there is more risk to the world from Transmissible Spongiform Encephalopathy TSE prion aka mad cow type disease now, coming from the United States and all of North America, than there is risk coming to the USA and North America, from other Countries. I am NOT saying I dont think there is any risk for the BSE type TSE prion coming from other Countries, I am just saying that in 2015, why is the APHIS/USDA/FSIS/FDA still ignoring these present mad cow risk factors in North America like they are not here?

North America has more strains of TSE prion disease, in more species (excluding zoo animals in the early BSE days, and excluding the Feline TSE and or Canine TSE, because they dont look, and yes, there has been documented evidence and scientific studies, and DEFRA Hound study, that shows the canine spongiform encephalopathy is very possible, if it has not already happened, just not documented), then any other Country in the world. Mink TME, Deer Elk cervid CWD (multiple strains), cBSE cattle, atypical L-type BSE cattle, atypical H-type BSE cattle, atyical HG type BSE cow (the only cow documented in the world to date with this strain), typical sheep goat Scrapie (multiple strains), and the atypical Nor-98 Scrapie, which has been linked to sporadic CJD, Nor-98 atypical Scrapie has spread from coast to coast. sporadic CJD on the rise, with different strains mounting, victims becoming younger, with the latest nvCJD human mad cow case being documented in Texas again, this case, NOT LINKED TO EUROPEAN TRAVEL CDC.

typical BSE can propagate as nvCJD and or sporadic CJD (Collinge et al), and sporadic CJD has now been linked to atypical BSE, Scrapie and atypical Scrapie, and scientist are very concerned with CWD TSE prion in the Cervid populations. in my opinion, the BSE MRR policy, which overtook the BSE GBR risk assessments for each country, and then made BSE confirmed countries legal to trade mad cow disease, which was all brought forth AFTER that fateful day December 23, 2003, when the USA lost its gold card i.e. BSE FREE status, thats the day it all started. once the BSE MRR policy was shoved down every countries throat by USDA inc and the OIE, then the legal trading of Scrapie was validated to be a legal trading commodity, also shoved through by the USDA inc and the OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion disease typical and atypical strains, and the BSE TSE Prion aka mad cow type disease was thus made a legal trading commodity, like it or not. its all about money now folks, trade, to hell with human health with a slow incubating disease, that is 100% fatal once clinical, and forget the fact of exposure, sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion disease, the pass it forward mode of the TSE PRION aka mad cow type disease. its all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the infamous VPSPr. ...problem solved $$$

the USDA/APHIS/FSIS/FDA triple mad cow BSE firewall, well, that was nothing but ink on paper.

for this very reason I believe the BSE MRR policy is a total failure, and that this policy should be immediately withdrawn, and set back in place the BSE GBR Risk Assessments, with the BSE GBR risk assessments set up to monitor all TSE PRION disease in all species of animals, and that the BSE GBR risk assessments be made stronger than before.

lets start with the recent notice that beef from Ireland will be coming to America.

Ireland confirmed around 1655 cases of mad cow disease. with the highest year confirming about 333 cases in 2002, with numbers of BSE confirmed cases dropping from that point on, to a documentation of 1 confirmed case in 2013, to date. a drastic decrease in the feeding of cows to cows i.e. the ruminant mad cow feed ban, and the enforcement of that ban, has drastically reduced the number of BSE cases in Europe, minus a few BABs or BARBs. a far cry from the USDA FDA triple BSE firewall, which was nothing more than ink on paper, where in 2007, in one week recall alone, some 10 MILLION POUNDS OF BANNED POTENTIAL MAD COW FEED WENT OUT INTO COMMERCE IN THE USA. this is 10 years post feed ban. in my honest opinion, due to the blatant cover up of BSE TSE prion aka mad cow disease in the USA, we still have no clue as to the true number of cases of BSE mad cow disease in the USA or North America as a whole. ...just saying.

Number of reported cases of bovine spongiform encephalopathy (BSE) in farmed cattle worldwide* (excluding the United Kingdom)


snip...please see attached pdf file, with references of breaches in the USA triple BSE mad cow firewalls, and recent science on the TSE prion disease. ...TSS



Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission

View Attachment:
Sunday, January 11, 2015
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission
Sporadic Creutzfeldt–Jakob Disease in a Navy Commander: Case Report and Review of the Literature
LT Xin Wei , MC USN
Carlson Lawall , MD
CAPT Patricia Pepper , MC USN
Naval Medical Center San Diego, 34800 Bob Wilson Drive, San Diego, CA 92134.
Sporadic Creutzfeldt–Jakob disease is a rare disorder that typically presents as rapidly progressive dementia. We present a case of a highly functioning 41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease, to include the diagnostic challenges, rapid clinical deterioration, and limited treatment options.
1. Geschwind MD, Shu H, Haman A, Sejvar JJ, Miller BL: Rapidly progressive dementia. Ann Neurol 2008; 64(1): 97–108. 2. Rosenbloom MH, Atri A: The evaluation of rapidly progressive dementia. Neurologist 2011; 17(2): 67–74. 3. Coulthart MB, Jansen GH, Olsen E, et al: Diagnostic accuracy of cerebrospinal fluid protein markers for sporadic Creutzfeldt-Jakob disease in Canada: a 6-year prospective study. BMC Neurol 2011; 11: 133. 4. Skillback T, Rosén C, Asztely F, Mattsson N, Blennow K, Zetterberg H: Diagnostic performance of cerebrospinal fluid total tau and phosphorylated tau in Creutzfeldt-Jakob disease: results from the Swedish Mortality Registry. JAMA Neurol 2014; 71(4): 476–83. 5. Orru CD, Bongianni M, Tonoli G, et al: A test for Creutzfeldt–Jakob disease using nasal brushings. N Engl J Med 2014; 371: 519–29. 6. Moda F, Gambetti P, Notari S, et al: Prions in the urine of patients with variant Creutzfeldt–Jakob disease. N Engl J Med 2014; 371: 530–9. 7. Rabinovici GD, Wang PN, Levin J, et al: First symptom in sporadic Creutzfeldt-Jakob disease. Neurology 2006; 66: 286–7. 8. Holman RC, Khan AS, Belay ED, Schonberger LB: Creutzfeldt-Jakob disease in the United States, 1979–1994: using national mortality data to assess the possible occurrence of variant cases. Emerg Infect Dis 1996; 2: 333–7. 9. Brown P, Cathala F, Castaigne P, Gajdusek DC: Creutzfeldt-Jakob disease: clinical analysis of a consecutive series of 230 neuropathologically verified cases. Ann Neurol 1986; 20: 597–602. 10. WHO: Variant Creutzfeldt-Jakob Disease. Available at; accessed August 11, 2014. 11. Beghi E, Gandolfo C, Ferrarese C, et al: Bovine spongiform encephalopathy and Creutzfeldt-Jakob disease: facts and uncertainties underlying the causal link between animal and human diseases. Neurol Sci 2004; 25(3): 122–9. 12. Hammersmith KM, Cohen EJ, Rapuano CJ, Laibson PR: Creutzfeldt-Jakob disease following corneal transplantation. Cornea 2004; 23(4): 406–8. 13. Thomas JG, Chenoweth CE, Sullivan SE: Iatrogenic Creutzfeldt-Jakob disease via surgical instruments. J Clin Neurosci 2013; 20(9): 1207–12. 14. Zaman SM, Hill FG, Palmer B, et al: The risk of variant Creutzfeldt-Jakob disease among UK patients with bleeding disorders, known to have received potentially contaminated plasma products. Haemophilia 2011; 17(6): 931–7. 15. Shiga Y, Miyazawa K, Sato S, et al: Diffusion-weighted MRI abnormalities as an early diagnostic marker for Creutzfeldt-Jakob disease. Neurology 2004; I63: 443–9. 16. CDC: CDC's Diagnostic Criteria for Creutzfeldt-Jakob Disease (CJD), 2010. Available at; accessed September 1, 2013. 17. Vitali P, Maccagnano E, Caverzasi E, et al: Diffusion-weighted MRI hyperdensity patterns differentiate CJD from other rapid dementias. Neurology 2011; 76(20): 1711–9. 18. USCF: CJD Treatments and Trials. Available at; accessed November 5, 2013. 19. Geschwind MD, Kuo AL, Wong KS, et al: Quinacrine treatment trial for sporadic Creutzfeldt-Jakob disease. Neurology 2013; 81(23): 2015–23. 20. Haik S, Marcon G, Mallet A, et al: Doxycycline in Creutzfeldt-Jakob disease: a phase 2, randomised, double-blind, placebo-controlled trial. Lancet Neurol 2014; 13(2): 150–8.
we now know that some sporadic CJD has been linked to atypical BSE, atypical scrapie, and recent to typical scrapie again, and the CWD in cervids is a very real risk factor.
this is another unusually young victim for the sporadic CJD. I have argued for 17 years that the diagnostic criteria to differentiate between the nvCJD and the sporadic CJD is far from perfect. I kindly submit the following ;
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, 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 ***
UPDATE* NOVEMBER 16, 2014 vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
Friday, January 10, 2014
Greetings again Friends, Neighbors, and Colleagues,
I would kindly like to follow up on ‘vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???’ ran across an old paper from 1984, that some might find interest in, and I will update the link with this old science paper from 1984, a 2010 paper from Japan, and some information on scrapie transmission. The paper from Japan first, then the 1984 paper, and then the scrapie transmission studies.
***The occurrence of contact cases raises the possibility that transmission in families may be effected by an unusually virulent strain of the agent.
From: Terry S. Singeltary Sr.
Sent: Saturday, November 15, 2014 9:29 PM
To: Terry S. Singeltary Sr.
snip...old link take a while to load...
my link...
vpspr-sgss-sffi-tse-iatrogenic TSE Prion, what if ???
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
Sunday, April 06, 2014
*** SPORADIC CJD and the potential for zoonotic transmission there from, either directly or indirectly via friendly fire iatrogenic mode, evidence to date ***
Sunday, June 29, 2014
*** Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014
Thursday, January 15, 2015
*** 41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE Prion: Case Report
Tuesday, December 30, 2014
TSEAC USA Reason For Recalls Blood products, collected from a donors considered to be at increased risk for Creutzfeldt-Jakob Disease (CJD), were distributed END OF YEAR REPORT 2014
Tuesday, February 8, 201 2002ish DeepThroat
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 is a big fat sponge...the agent continues to eat the brain 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 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 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 a buzzard to the 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.)
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 ***
Thursday, February 24, 2011
The risk of variant Creutzfeldt-Jakob disease among UK patients with bleeding disorders, known to have received potentially contaminated plasma products
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
*** Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2.
These data suggest that more than one BSEderived prion strain might infect humans;
***it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.
These studies further strengthen the evidence that vCJD is caused by a BSE-like prion strain.
Also, remarkably, the key neuropathological hallmark of vCJD, the presence of abundant florid PrP plaques, can be recapitulated on BSE or vCJD transmission to these mice.
***However, the most surprising aspect of the studies was the finding that an alternate pattern of disease can be induced in 129MM Tg35 mice from primary transmission of BSE, with a molecular phenotype indistinguishable from that of a subtype of sporadic CJD. This finding has important potential implications as it raises the possibility that some humans infected with BSE prions may develop a clinical disease indistinguishable from classical CJD associated with type 2 PrPSc. This is, in our experience, the commonest molecular sub-type of sporadic CJD. In this regard, it is of interest that the reported incidence of sporadic CJD has risen in the UK since the 1970s (Cousens et al., 1997)...
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A"
To: "''"
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, ***yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.
Emmanuel Asante
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: (until 9/12/02) New e-mail: (active from now)
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
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
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.
Sunday, January 11, 2015
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission
Tuesday, December 23, 2014
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.
Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other species
there is in fact evidence that the potential for cwd transmission to humans can NOT be ruled out.
I thought your readers and hunters and those that consume the venison, should have all the scientific facts, personally, I don’t care what you eat, but if it effects me and my family down the road, it should then concern everyone, and the potential of iatrogenic transmission of the TSE prion is real i.e. ‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there deer antler velvet and TSE prions and nutritional supplements there from, all a potential risk factor that should not be ignored or silenced. ...
the prion gods at the cdc state that there is ;
''no strong evidence''
but let's see exactly what the authors of this cwd to human at the cdc state ;
now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS (
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
Sent: Sunday, September 29, 2002 10:15 AM
To:;; ebb8@CDC.GOV
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
full text ;
***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
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).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and venison and lamb**************
October 1994
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and venison and lamb**************
Sunday, December 28, 2014
*** 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.
cwd exposure, and iatrogenic CJD, what if ???
*** our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions. ***
snip...see full text ;
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.
PLEASE REMEMBER, all iatrogenic CJD is, is sporadic CJD, until the route, source, time of the iatrogenic event is documented, and then put into the public domain, which very seldom happens do to it’s long incubation period, and the lack of trace back efforts. ...terry
Sunday, July 06, 2014
Dietary Risk Factors for Sporadic Creutzfeldt-Jakob Disease: A Confirmatory Case-Control Study
Conclusions—The a priori hypotheses were supported.
*Consumption of various meat products may be one method of transmission of the infectious agent for sCJD.
Tuesday, November 04, 2014
*** Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011
Thursday, March 20, 2014
Tuesday, July 01, 2014
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets? ***
Friday, January 16, 2015
*** Indiana SENATE BILL No. 442 Miller Pete Hunting wildlife Removes exotic mammals from the animals that may be propagated or offered for hunting at a shooting preserve Makes it a Class C misdemeanor
Scrapie Sheep and Goats is a risk factor for sporadic CJD
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
was this a case of Bioterrorism ???
Because he was so well traveled as a Special Forces soldier, his family said he may have eaten contaminated beef in England, where more than 125 persons have contracted the disease after eating beef from cows that were fed products rendered from scrapie-infected sheep. Scrapie is a form of a brain disorder found in sheep.
The soldier also told his family that in 2001 he ate a sheep's brain while stationed in Oman. However, while the disease is linked to cattle that have eaten sheep-byproducts, there has been no evidence of direct transfer from sheep to humans, according to the CJD Foundation.
Friday, August 22, 2008
Creutzfeldt Jakob Disease and Veterans and how they are treated at death UPDATED AUGUST 28, 2008
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise 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 acrapie problem urgent if the sheep industry is not to suffer grievously.
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
28 Mar 01
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.
*** Sunday, January 11, 2015 ***
*** Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission ***
Tuesday, December 23, 2014
Sunday, December 28, 2014
*** Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE PRION aka BSE MAD COW TYPE DISEASE December 2014 ***
*** Alzheimer’s disease and the potential for the Iatrogenic spread, friendly fire, pass it forward mode of transmission, medical, surgical, dental, blood, tissue ***
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014
Singeltary comment ;
Parkinson's Disease and Alpha Synuclein: Is Parkinson's Disease a Prion-Like Disorder?
Recent evidence now suggests the possibility that α-synuclein is a prion-like protein and that PD is a prion-like disease.
Researchers' Discovery May Revolutionize Treatment of ALS Sep 20, 2011
Dr. Neil CashmanPrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
September 20, 2011 - Vancouver, BC: A team of researchers from the University of British Columbia and the Vancouver Coastal Health Research Institute have found a key link between prions and the neurodegenerative disease ALS (Amyotrophic Lateral Sclerosis), also known as Lou Gehrig's disease.
Wednesday, January 5, 2011
David W. Colby1,* and Stanley B. Prusiner1,2
Patients suffering from Parkinson's disease who received fetal grafts of substantia nigral cells later showed aberrantly folded a-synuclein in Lewy bodies within the transplanted grafts, arguing that a-synuclein acted like a prion (Kordower et al. 2008; Li et al. 2008; Olanow and Prusiner 2009). Taken together, these findings argue that prion-like, self-propagating states feature in many different, if not all, neurodegenerative diseases.
Transmission of multiple system atrophy prions to transgenic mice
Joel C. Wattsa,b, Kurt Gilesa,b, Abby Oehlerc, Lefkos Middletond, David T. Dextere, Steve M. Gentlemane, Stephen J. DeArmonda,c, and Stanley B. Prusinera,b,1 Author Affiliations
Prions are proteins that adopt alternative conformations, which become self-propagating. Increasing evidence argues that prions feature in the synucleinopathies that include Parkinson’s disease, Lewy body dementia, and multiple system atrophy (MSA).
Our results provide compelling evidence that α-synuclein aggregates formed in the brains of MSA patients are transmissible and, as such, are prions.
The MSA prion represents a unique human pathogen that is lethal upon transmission to Tg mice and as such, is reminiscent of the prion causing kuru, which was transmitted to chimpanzees nearly 5 decades ago.
Tuesday, September 16, 2014
*** mad cow scaremongers December 20, 2003 article and a 2014 review
Among Singeltary's worries now, he said, are widespread violations of an August 1997 ban on feeding animal products to U.S. cattle. The FDA reported in January that hundreds of feed manufacturers were not complying with regulations designed to keep BSE out of this country.
(That same month, a Purina Mills feedlot near San Antonio told the FDA that a "very low level" of cow parts had been found in cattle feed. The company voluntarily removed 1,222 animals who had been fed the prohibited materials.)
He obtained copies of FDA letters to various feed mills that had been found in violation of the regulations and immediately sent them by e-mail to hundreds of people around the world.
Singeltary might not be so zealous in getting the word out if he weren't convinced that someone is covering up the truth.
"They used to say BSE would never transmit to humans," he said, "and it has. They lied about the feed ban being in place.
"I've lost faith in the whole process. I've discovered too many things."
Tuesday, March 16, 2010
Proof Committee Hansard
RRA&T 2 Senate Friday, 5 February 2010
[9.03 am]
BELLINGER, Mr Brad, Chairman, Australian Beef Association CARTER, Mr John Edward, Director, Australian Beef Association CHAIR—Welcome. Would you like to make an opening statement? Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14 December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so: You should be worried. Please let me explain. I’ve kept up with the mad cow saga for 12 years today, on December 14th 1997, some four months post voluntary and partial mad cow feed ban in the USA, I lost my mother to the Heinemann variant Creutzfeldt-Jakob disease (CJD). I know this is just another phenotype of the infamous sporadic CJDs. Here in the USA, when USA sheep scrapie was transmitted to USA bovine, the agent was not UK BSE—it was a different strain. So why then would human TSE from USA cattle look like UK CJD from UK BSE? It would not. So this accentuates that the science is inconclusive still on this devastating disease. He goes on to state:
snip...see full text 110 pages ;
for those interested, please see much more here ;
This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:
Owens, Julie From: Terry S. Singeltary Sr. []
Sent: Monday, July 24, 2006 1:09 PM To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98 8/3/2006
Greetings FSIS, I would kindly like to comment on the following ;
Nature | Editorial
Needless conflict Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b Published online 16 May 2012
Tuesday, December 2, 2014
UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion aka Mad Cow Disease
USA, NORTH AMERICA, MBM (or any potential TSE prion disease) EXPORTS TO THE WORLD (?) [protected by the BSE MRR policy] $$$
*** Qualitative Analysis of BSE Risk Factors in the United States
February 13, 2000 at 3:37 pm PST (BSE red book)
Tuesday, July 14, 2009 U.S.
*** Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book
Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population CWD TSE PRION disease in cervids
The Scottish Parliament’s Rural Affairs, Climate Change and Environment Committee has been looking into deer management, as you can see from the following press release,
***and your email has been forwarded to the committee for information:
Sunday, July 21, 2013
Welsh Government and Food Standards Agency Wales Joint Public Consultation on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations 2013
*** Singeltary Submission WG18417
*** 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.
Friday, December 5, 2014
The OIE recommends strengthening animal disease surveillance worldwide
‘’the silence was deafening’’ ...tss
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis *video*
Saturday, December 13, 2014
*** Terry S. Singeltary Sr. Publications TSE prion disease Peer Review ***
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Thank you,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

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