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CJD case in Saint John prompts letter to patients Canada

Posted Aug 02 2012 3:41pm
CJD case in Saint John prompts letter to patients



Horizon Health Network officials want to reassure patients risk is 'nil' CBC News Posted: Aug 2, 2012 1:29 PM AT Last Updated: Aug 2, 2012 3:00 PM


Health care officials in Saint John are hoping to meet with nearly 150 surgical patients to reassure them they have not been exposed to Creutzfeldt-Jakob disease, despite a confirmed case at one of the city's hospitals in July.


The operating rooms at St. Joseph's Hospital were closed for disinfection for two days after a patient was diagnosed with CJD, a rare brain disease.


The hospital sent letters to patients who had surgeries prior to that patient's diagnosis, inviting them to a question-and-answer session on Aug. 7, said Dr. David Marr, medical director for the Saint John region.


But he contends their risk is "nil."


The disease can only be transferred on brain or neurological tissues and that couldn't have happened in this case, said Marr.


"There's been no evidence, given the type of surgery that this particular patient had, and has ever been shown in the literature to result in the transferring of the disease."


Still, Marr feels the letters and meeting is the right thing to do.


"We felt they deserved to know," he said. "We thought they should know up front and we felt by taking this head on we would be reassuring to them in the long-term because in fact we don't believe that there's any risk to patients here."


The Horizon Health Network did not issue a news release when the patient's diagnosis was confirmed and patients who were scheduled for surgery during the two days of disinfection were not given any explanation when their procedures were cancelled.


The infected patient's condition remains unclear.


CJD is not related to so-called mad cow disease, which is contracted by eating meat from an infected cow, said Marr.


CJD is a disease caused by protein-like particles called prions. These attack the brain, killing cells and creating gaps in tissue. The disease is always fatal. There are two types of CJD — classical and variant.








CANADA





TOO bad Canada’s policy on BSE aka mad cow type disease, and the reporting there from of completed cases, have ceased to exist on the CFIA site for the public to follow. you have to request a copy. CFIA ceased giving those copies out to me. ...


•Request a copy of a completed BSE investigation report for a case after January 2009






Sunday, May 27, 2012


CANADA PLANS TO IMPRISON ANYONE SPEAKING ABOUT MAD COW or ANY OTHER DISEASE OUTBREAK, CENSORSHIP IS A TERRIBLE THING






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







CENSORSHIP IS A TERRIBLE THING $$$


Canada has had a COVER-UP policy of mad cow disease since about the 17th case OR 18th case of mad cow disease. AFTER THAT, all FOIA request were ignored $$$


THIS proves there is indeed an epidemic of mad cow disease in North America, and it has been covered up for years and years, if not for decades, and it’s getting worse $$$


Thursday, February 10, 2011


TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31






Wednesday, August 11, 2010


REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA






Thursday, August 19, 2010


REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA






Friday, March 4, 2011


Alberta dairy cow found with mad cow disease







please remember a few things, sporadic cjd is not a single strain. sporadic CJD is multiple strains of CJD from unknown route and source of agent. 85%+ of all human TSE i.e. sporadic CJD, does NOT happen spontaneously, this is a myth, one never proven. to date, there has never been a documented spontaneous TSE in any natural field cases of TSE in any species. all iatrogenic CJD is, is a sporadic CJD, until the route and source of the iatrogenic event has been proven. atypical TSE is mounting and spreading. we must make all human TSE reportable in ALL AGE GROUPS. remember, per the CJD Foundation, in the age group of 55 years and older, CJD cases jump to one in nine thousand. atypical BSE here in the USA has been linked to some cases of sporadic CJD. ...




TSE prion disease in species in the USA are multiplying and spreading. CWD in deer and elk is spreading, and now with more than one strain documented. scrapie in sheep and goats, and atypical scrapie (Nor-98), has spread from coast to coast in 5 years, and BSE in cattle mutating to different strains now, with the USA documenting the c-BSE, atypical h-BSE, atypical h-g-BSE, and the atypical l-bse (BASE) type, all being documented in the USA now. the partial and voluntary mad cow feed ban was a joke, and the BSE mad cow surveillance was even worse. NOW, add all this up to this new strain of sporadic CJD in the USA in young and old, some of which with long duration. then think all this, all these TSE, all these prions being consumed one way or the other, ...then think iatrogenic in all hospital surgical wards, blood donors, tissue donors? one final thought, IS ALZHEIMER'S TRANSMISSIBLE? is Alzheimer's a TSE ?” see my report with a few update protocols on TSE prion safety...




Tuesday, July 31, 2012


11 patients may have been exposed to fatal disease Creutzfeldt-Jakob Disease CJD Greenville Memorial Hospital










Wednesday, June 27, 2012


First US BSE Case Since 2006 Underscores Need for Vigilance


Neurology Today 21 June 2012






PO-028: Oral transmission of L-type bovine spongiform encephalopathy (L-BSE) in primate model Microcebus murinus


Nadine Mestre-Frances,1 Simon Nicot,2 Sylvie Rouland,1 Anne-Gaëlle Biacabe,2 Isabelle Quadrio,3 Armand Perret-Liaudet,3 Thierry Baron,2 Jean-Michel Verdier1 1IN SER M UM2; Montpellier, France; 2Anses; Lyon, France; 3Hopitaux Civils de Lyon; Lyon, France


An atypical form of bovine spongiform encephalopathy has been identified in cattle in Europe, North America and Japan and was designed as L-type BSE (L-BSE) due to the lower apparent molecular mass of the unglycosylated, protease-resistant prion protein (PrPres) detected by western blot compared with classical BSE. Experimental evidences from studies in transgenic mice expressing human PrP and in primate models suggest a higher risk of transmission to humans of the L-BSE form than for classical BSE agent. However, a major unresolved issue concerns the potential transmissibility of the L-BSE agent by oral route. To address this question, we infected mouse lemurs (Microcebus murinus), a non-human primate model, with L-BSE by intracerebral or oral route.


Four adult lemurs were intracerebrally (IC) inoculated with 5mg of L-BSE infected brain homogenate of an atypical French BSE case (02-2528). Four young and four adult animals were fed with 5 mg or 50 mg of infected brain. After sacrifice, the brain tissues were biochemically and immunocytochemically investigated for PrPres.


The 4 animals IC inoculated died at 19 and 22 months postinoculation (mpi). They developed blindness, tremor, abnormal posture, incoordinated movements, balance loss. Symptoms get worse according to the disease progression, until severe ataxia. Severe spongiosis was evidenced into the thalamus, the striatum, the mesencephalon, and the brainstem, whereas into the cortex the vacuolisation was weaker. Strong deposits of PrPres were detected into the thalamus, the striatum, and the hippocampus whereas in the cerebral cortex, PrPres was prominently accumulated in plaques.


The orally inoculated animals showed similar clinical symptoms occurring between 27 and 34 mpi. Disease was characterized by progressive prostration, loss of appetite and poor appearance of the fur. Only one adult animal showed disequilibrium. PrPres was strongly accumulated only in the striatum and thalamus and weakly into the cortex. No plaques were evidenced. Two animals that were orally challenged at the age of two years are still alive and healthy 34 months after inoculation. The western blot analysis showed uniform molecular profiles, irrespective of the route or dose of infection, and included notably a PrPres form with low apparent molecular mass (~19 kDa) similar to the PrPres in the original cattle brain. However, the PrPres profile in lemurs was characterized by a higher proportion of di- and mono-glycosylated species (up to 95% of the total signal) than in the bovine L-BSE inoculum (~80%). In addition, small amounts of PrPres were detected by western blotting in the spleen of three animals (one intra-cerebrally inoculated and two fed with 5 mg of cattle brain).


Here, we demonstrate that the L-BSE agent can be transmitted by oral route from cattle to young and adult mouse lemurs. In comparison to IC inoculated animals, orally challenged lemurs were characterized by longer survival periods as expected with this route of infection.








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...










see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;







chronic wasting disease cwd 2012 cdc report






Tuesday, July 17, 2012


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






Thursday, March 29, 2012


atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012


NIAA Annual Conference April 11-14, 2011San Antonio, Texas






Monday, November 30, 2009


USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE






***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.






*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.


119






*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.






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






12/10/76


AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE


Office Note CHAIRMAN: PROFESSOR PETER WILDY


snip...


A The Present Position with respect to Scrapie A] The Problem Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries. The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep. It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible. 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.


snip...


76/10.12/4.6





Tuesday, June 26, 2012


Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012


type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA





Wednesday, August 01, 2012


Behavioural and Psychiatric Features of the Human Prion Diseases: Experience in 368 Prospectively Studied Patients






Scottish TSE Network November Symposium Announcement Event: 12 November 2012


Chair: Prof Hugh Perry, University of Southampton, Southampton UK


Location: The Roslin Institute Building Auditorium


If you would like to book a place at this event, please let Gila Holliman know.


Cost: £125.


Title: Is Alzheimer’s Disease a transmissible disease?


Speakers:


Session 1:


Prof Bob Will, National CJD Surveillance Unit, Edinburgh UK


Prof James Ironside, National CJD Surveillance Unit, Edinburgh UK


Prof Lary Walker, Emory School of Medicine, Atlanta USA


Session 2:


Prof Mathias Jucker, Hertie Institute for Clinical Brain Research, Stuttgart Germany


Prof William Van Nostrand, Stony Brook University, Stony Brook USA


Dr Claudio Soto, University of Texas Medical School, Houston USA


Session 3:


Dr Fabrizio Tagliavini, Instituto Neurologico Carlo Besta, Milan Italy


Prof Pedro Piccardo, Food and Drug Administration, Washington DC USA


Dr Bruce Chesebro, National Institutes of Health, Missoula USA










From: Terry S. Singeltary Sr. Sent: Wednesday, May 16, 2012 3:29 PM To: BSE-L@LISTS.AEGEE.ORG


Subject: [BSE-L] Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?


Proposal ID: 29403


Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?


Background


Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both disease, and it’s variants, in many cases are merely names of the people that first discovered them. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer than the TSE prion disease. Symptoms are very similar, and pathology is very similar. I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. today, there is enough documented science (some confidential), that shows that indeed Alzheimer’s is transmissible. The risk factor for friendly fire, and or the pass-it-forward mode i.e. Iatrogenic transmission is a real threat, and one that needs to be addressed immediately.


Methods


Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.


Results


The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease. TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. the TSE prion agent also survives Simulated Wastewater Treatment Processes. IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. you can bury it and it will not go away. TSE prion agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.


Conclusions


There should be a Global Congressional Science round table event (one of scientist and doctors et al only, NO CORPORATE, POLITICIANS ALLOWED) set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics let science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already. what’s the use of science progressing human life to the century mark, if your brain does not work?






combined cannot exceed 350 Words


shortened to proper word count ;


Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?


Background


Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.


Methods


Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.


Results


I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.


Conclusions


There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.


end...tss


Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?


source references


Ann N Y Acad Sci. 1982;396:131-43.


Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).


Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.


Abstract


Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.






BSE101/1 0136


IN CONFIDENCE


CMO


From: Dr J S Metters DCMO


4 November 1992


TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES







CJD1/9 0185


Ref: 1M51A


IN STRICT CONFIDENCE


From: Dr. A Wight Date: 5 January 1993


Copies:


Dr Metters


Dr Skinner


Dr Pickles


Dr Morris


Mr Murray


TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES







Wednesday, January 5, 2011


ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions


David W. Colby1,* and Stanley B. Prusiner1,2












Tuesday, October 4, 2011


Molecular Psychiatry


advance online publication 4 October 2011; doi: 10.1038/mp.2011.120


De novo induction of amyloid-ß deposition in vivo


Our results suggest that some of the typical brain abnormalities associated with AD can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding. These findings may have broad implications for understanding the molecular mechanisms responsible for the initiation of AD, and may contribute to the development of new strategies for disease prevention and intervention. Keywords: amyloid; prion; protein misfolding; disease transmission






see more here ;












Wednesday, September 21, 2011


PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)











snip...end



Thank You for accepting my submission


# 29403, Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? and the opportunity to present it, at the Alzheimer’s Association International Conference 2012 (AAIC), as a poster presentation. However, with great sadness, I must regretfully decline the invitation due to a medical reasons, and traveling to Canada, of which is not possible. ...


Thank You,


With Kindest Regards,


I am sincerely,


Terry S. Singeltary Sr.


P.O. Box 42


Bacliff, Texas USA 77518


flounder9@verizon.net


From:


Sent: Saturday, April 07, 2012 8:20 PM


To: Terry S. Singeltary Sr.


Subject: RE: re-submission


Dear Terry,


Yes, your proposal was accepted as a poster presentation. Please decline the invitation if appropriate.


Best Regards,


______________________________________


Alzheimer’s Association – National Office 225 North Michigan Avenue – Floor 17 Chicago, Illinois 60601


=============snip...end...source reference...# 29403==========








Wednesday, May 16, 2012


Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?


Proposal ID: 29403








TSS



==============JUNE 2012 UPDATE TSE USA=====================




Tuesday, July 31, 2012


11 patients may have been exposed to fatal disease Creutzfeldt-Jakob Disease CJD Greenville Memorial Hospital






layperson


Terry S. Singeltary SR. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
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