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Location: BACLIFF, Texas, United States

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS

Friday, March 01, 2013

Prion infectivity in the spleen of a PRNP heterozygous individual with subclinical variant Creutzfeldt–Jakob disease

Prion infectivity in the spleen of a PRNP heterozygous individual with subclinical variant Creutzfeldt–Jakob disease



Matthew T. Bishop1,*, Abigail B. Diack2,*, Diane L. Ritchie1, James W. Ironside1, Robert G. Will1,* and Jean C. Manson2,* + Author Affiliations




1 National Creutzfeldt–Jakob Disease Research and Surveillance Unit, University of Edinburgh, Bryan Matthews Building, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK 2 Neurobiology Division, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian, EH25 9RG, UK Correspondence to: Professor Jean Manson, Head of Neurobiology Division, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian, EH25 9RG, UK E-mail: jean.manson@roslin.ed.ac.uk Received August 13, 2012. Revision received January 10, 2013. Accepted January 14, 2013.



Summary



Blood transfusion has been identified as a source of human-to-human transmission of variant Creutzfeldt–Jakob disease. Three cases of variant Creutzfeldt–Jakob disease have been identified following red cell transfusions from donors who subsequently developed variant Creutzfeldt–Jakob disease and an asymptomatic red cell transfusion recipient, who did not die of variant Creutzfeldt–Jakob disease, has been identified with prion protein deposition in the spleen and a lymph node, but not the brain. This individual was heterozygous (MV) at codon 129 of the prion protein gene (PRNP), whereas all previous definite and probable cases of variant Creutzfeldt–Jakob disease have been methionine homozygotes (MM). A critical question for public health is whether the prion protein deposition reported in peripheral tissues from this MV individual correlates with infectivity. Additionally it is important to establish whether the PRNP codon 129 genotype has influenced the transmission characteristics of the infectious agent. Brain and spleen from the MV blood recipient were inoculated into murine strains that have consistently demonstrated transmission of the variant Creutzfeldt–Jakob disease agent. Mice were assessed for clinical and pathological signs of disease and transmission data were compared with other transmission studies in variant Creutzfeldt–Jakob disease, including those on the spleen and brain of the donor to the index case. Transmission of variant Creutzfeldt–Jakob disease was observed from the MV blood recipient spleen, but not from the brain, whereas there was transmission from both spleen and brain tissues from the red blood cell donor. Longer incubation times were observed for the blood donor spleen inoculum compared with the blood donor brain inoculum, suggesting lower titres of infectivity in the spleen. The distribution of vacuolar pathology and abnormal prion protein in infected mice were similar following inoculation with both donor and recipient spleen homogenates, providing initial evidence of similar transmission properties after propagation in PRNP codon 129 MV and MM individuals. These studies demonstrate that spleen tissue from a PRNP MV genotype individual can propagate the variant Creutzfeldt–Jakob disease agent and that the infectious agent can be present in the spleen without CNS involvement.




snip...




Discussion




This study provides definitive evidence that spleen tissue from an asymptomatic individual contains variant Creutzfeldt–Jakob disease infectivity and that the variant Creutzfeldt–Jakob disease agent retains infectivity following passage through an MV genotype host. The findings are of importance as there has been uncertainty as to whether prion protein immunostaining in peripheral tissues from non-clinical variant Creutzfeldt–Jakob disease necessarily correlated with infectivity (Hilton et al., 2004; Wadsworth et al., 2011). The demonstration of infectivity in such tissues underlines the potential for asymptomatic carriers of variant Creutzfeldt– Jakob disease infection to pose a risk of secondary transmission of infection through blood transfusion or contamination of surgical instruments. The incubation times recorded in this study would suggest moderate but significant levels of infectivity are present in the spleen of the MV genotype recipient, raising the possibility that other peripheral tissues and the blood of this individual are also infected, as indicated by immunohistochemistry in the initial report of this case (Peden et al., 2004). Furthermore the confirmation that there is prion infectivity in an individual with a PRNP codon 129 MV genotype indicates that this genetic subgroup, which accounts for 50% of the UK population, can act as carriers of variant Creutzfeldt–Jakob disease infection.




Our results also provide initial evidence that the variant Creutzfeldt–Jakob disease transmission properties in the MV blood recipient spleen tissue are similar to those of the MM blood donor. This is a critical issue for public health as there is a potential for these infectious agents to change characteristics, including virulence, after serial transmission or following passage in a different genetic background. The relative stability of the agent also makes it more likely that the clinical phenotype of variant Creutzfeldt–Jakob disease infection in an MV background may be similar to that of the well-recognized clinical phenotype in an MM background. While a first passage of an agent between species is not normally sufficient to confirm strain identity, the similarities identified at first passage in this study are striking. We are now undertaking a more extensive strain comparison by our standard serial-passage method using inocula derived from this primary transmission experiment (Ritchie et al., 2009). This will help establish whether the strain characteristics have indeed remained stable following passage through an MV host.




This study has established that variant Creutzfeldt–Jakob disease infectivity can be replicated within a PRNP codon 129 MV genotype host and within a non-CNS tissue, in the absence of variant Creutzfeldt–Jakob disease pathology in the brain. This demonstrates the potential for asymptomatic carriage of variant Creutzfeldt–Jakob disease infection in the UK population, underlining the risk of a silent subclinical epidemic that could result from transfer of infection through blood transfusion or surgery (Garske and Ghani, 2010). It is imperative therefore that continued active surveillance and infection control measures for variant Creutzfeldt– Jakob disease are continued into the future.




Key words variant Creutzfeldt–Jakob disease infection subclinical blood transfusion prion




Abbreviations




HuMM transgenic mouse line expressing human prion protein with MM genotype at codon 129 PrPSc disease associated (‘scrapie’) form of the prion protein




© The Author (2013). Published by Oxford University Press on behalf of the Guarantors of Brain.




This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.












 
 
 

MARCH 2010




CJD SUPPORT NETWORK




In a fourth case an elderly lady died of un-related causes and was found to show evidence of accumulation of prions in her spleen and one lymph node.




A fifth, plasma related transmission has recently been identified in a patient with haemophilia who also died of other causes and was found to have evidence of abnormal prion protein accumulation in his spleen.











Saturday, January 20, 2007
 
 
 
 
Fourth case of transfusion-associated vCJD infection in the United Kingdom


Saturday, January 20, 2007
 
 
 
 
Fourth case of transfusion-associated vCJD infection in the United Kingdom


Subject: Fourth case of transfusion-associated vCJD infection in the United Kingdom
 
 
 
 
Date: January 18, 2007 at 8:32 am PST


Fourth case of transfusion-associated vCJD infection in the United Kingdom


Editorial team (eurosurveillance.weekly@hpa.org.uk), Eurosurveillance editorial office




A suspected case of variant Creutzfeldt-Jakob disease (vCJD) has recently been diagnosed in a patient in the United Kingdom (UK), who received a blood transfusion from a donor who later developed vCJD [1]. This is the fourth case of probable transfusion transmission of vCJD infection in the UK. Three of the four recipients developed symptoms of vCJD. The first symptomatic case of vCJD associated with blood transfusion was identified in December 2003. This individual developed vCJD six and a half years after transfusion of red cells donated by an individual who developed symptoms of vCJD three and a half years after donation.




A second case of vCJD 'infection' was identified a few months later in a person who had received red cells from a donor who developed symptoms of vCJD 18 months after donation. This patient (the second case) died from causes unrelated to vCJD five years after transfusion. Post-mortem investigations found abnormal prion protein in the spleen and a cervical lymph node., However, prion protein was not found in the brain, and no pathological features of vCJD were found.




A third case developed symptoms of vCJD six years after receiving a transfusion of red blood cells, and died two years and eight months later. The donor of the blood involved developed vCJD about 20 months after donating it.

 
 

These three cases have been published as case reports and in the findings of the ongoing collaborative study between the National Blood Services, the National CJD Surveillance Unit, and the Office for National Statistics. This study aims to collect evidence about transmission of CJD or vCJD via the blood supply [2,3,4,5].

 
 
 
The new, fourth case is in a patient who developed symptoms of vCJD eight and a half years after receiving a transfusion of red blood cells from a donor who developed vCJD about 17 months after this blood was donated [1]. The donor to this case also donated the vCJD-implicated blood transfused to the third case. As for all other reported clinical vCJD cases that have been tested for genotype, this patient is a methionine homozygote at codon 129 of the prion protein gene. The patient is currently alive.




All four cases had received transfusions of non-leucodepleted red blood cells between 1996 and 1999. Since October 1999, leucocytes have been removed from all blood used for transfusion in the UK. The effect of leucodepletion on the reduction of the risk of transmission of vCJD from an infective donation is uncertain.




This fourth case of vCJD infection associated with blood transfusion further increases the level of concern about the risk of vCJD transmission between humans by blood transfusion, although much remains unknown. This reinforces the importance of the existing precautions that have been introduced to reduce the risk of transmission of vCJD infection by blood and blood products [6]. No cases of vCJD have been associated with fractionated plasma products. The small group of living recipients of vCJD-implicated blood transfusion in the UK have been informed of their potential exposure to vCJD by blood transfusion, asked to take certain precautions to reduce the risk of onward person-to-person transmission of vCJD during health care, and offered specialist neurological evaluation and advice.

 
 

This article has been adapted from reference 1

 
 

References: Health Protection Agency.
 
 
 
 
 
Fourth case of variant CJD associated with blood transfusion (press release).
 
 
 
 
 
Press release, 18 January 2007.
 
 
 
 
 
 
 
 
 
 
 
 
Llewelyn CA, Hewitt PE, Knight RSG, Amar K, Cousens S, Mackenzie J, et al.
 
 
 
 
 
Possible transmission of variant CJD disease by blood transfusion. Lancet 2004; 363:417-21. Peden AH, Head MW, Ritchie DL, Bell JE, Ironside JW. Preclinical vCJD after blood transfusion in a PRNP codon 129 heterozygous patient. Lancet 2004 ; 364: 527-9. Wroe SJ, Pal S, Siddique D, Hyare H, Macfarlane R, et al Clinical presentation and pre-mortem diagnosis of blood transfusion-associated variant CJD. Lancet 2006;368:2061-67. Hewitt PE, Llewelyn CA, Mackenzie J, Will RG. Creutzfeldt-Jakob disease and blood transfusion: results of the UK Transfusion Medicine Epidemiology review study. Vox Sang. 2006;91(3):221-230. Department of Health [London]. Further precautions to protect blood supply. Press release 2004/0104, 16 March 2004.
 
 
 
 
 
 
 
 
 
 










HPA Press Statement



18 January 2007



4th case of variant CJD infection associated with blood transfusion



A new case of variant-Creutzfeldt-Jakob disease (vCJD ) associated with a blood transfusion has recently been diagnosed.



This latest patient has been diagnosed with vCJD about nine years after receiving a blood transfusion from a donor who later went on to develop vCJD. A transfusion from the same blood donor was also associated with one of the previously identified cases. The patient is still alive and is under specialist care.


This fourth case of vCJD infection associated with blood transfusion increases the concern about the risk of vCJD transmission between humans via blood transfusion. All four cases relate to the transfusion of blood components: no cases have been reported relating to treatment with plasma products.


The patient is one of a small number (less than 30) of living individuals who are known to have received a blood transfusion in the UK from a donor who later developed vCJD. All these individuals have previously been informed of their potential exposure to vCJD and asked to take certain precautions to reduce the chance of passing on vCJD to other people via healthcare procedures, such as surgery.


The Health Protection Agency has been in contact with doctors caring for the other patients who have been exposed to blood transfusions from donors who later developed vCJD. This is to ensure that they are informed of this new development and provide access to the latest information and specialist advice about their risk due to blood transfusion.


Professor Peter Borriello, Director of the HPA's Centre for Infections said, "This new case of vCJD infection increases our concern about the risk to the small group of people who had blood transfusions from donors who unknowingly at the time of donation must have had vCJD infection. However, this new case does not change our understanding of the risk for other people in any specific way. It does however reinforce the importance of the precautions that have already been taken to reduce the risk of transmission of vCJD infection by blood."


Dr Angela Robinson, Medical Director of NHS Blood and Transplant said, "Blood transfusions are often given to save or prolong the life of patients who are very ill and the benefit of receiving a transfusion when needed must always be balanced against any possible risk. Nonetheless, our primary concern is the safety of our patients through maintaining the quality of blood used for medical treatment. Since 1997, the NBS has introduced a range of precautionary measures against the risk of vCJD."


vCJD is a rare disease, and less than 2% of the vCJD cases reported to date in the UK have been associated with blood transfusion.


Notes to Editors:


To date, there have been 66 people identified in the UK who have received vCJD implicated blood transfusions. The transfusions received by these 66 individuals were donated by eighteen different donors who were diagnosed with vCJD after their blood donation. Of these 66 people, 40 have died of illnesses other than vCJD, including one patient who was found to have evidence of vCJD in parts of their body after their death. Including the new (4th) case, 3 of these people who have received vCJD implicated blood transfusions have developed symptoms of vCJD. There are 23 people who have received vCJD implicated blood transfusions who are alive and have not been diagnosed with vCJD.


The identification of cases of variant-CJD associated with blood transfusion has depended on the Transfusion Medicine Epidemiology Review, a collaborative study between the National Blood Services, the National CJD Surveillance Unit and the Office of National Statistics. For further information about this study see Hewitt et al Creutzfeldt-Jakob disease and blood transfusion: results of the UK Transfusion Epidemiology Review study. Vox Sanguinis 2006 91:221-230.


'Blood Transfusion' means transfusion with labile blood components (e.g. red cells, platelets, fresh frozen plasma). This latest case (and the previous three referred to) relate to transfusion of blood components and not treatment with plasma products (i.e. products that are manufactured from plasma). To date, no case of vCJD has been associated with treatment with plasma-products (e.g. clotting factors used to treat individuals with bleeding disorders such as haemophilia).


This fourth case has been classified by the National CJD Surveillance Unit ( www.cjd.ed.ac.uk ) as a 'probable' case of vCJD. Of the 158 vCJD cases that have died (data to 5 Jan 2007), all 112 that have undergone post-mortem (46 have not) have been 'confirmed' by neuropathological examination (examination of brain tissue).


The first clinical case of vCJD associated with transfusion was identified in December 2003. A case of vCJD 'infection' associated with transfusion was identified a few months later. The patient had no symptoms but evidence of infection (abnormal prion proteins) was identified in a post mortem investigation. The individual died from causes unrelated to vCJD.


Following the first case of vCJD associated with a blood transfusion in 2003, the Department of Health asked all recipients of blood transfusions not to donate blood as a precautionary measure to protect the blood supply from vCJD.


Patients who are informed that they are considered to be 'at risk' of vCJD for public health purposes are asked to take the following precautions to reduce the chance of passing on vCJD to other people: Not to donate blood, tissues or organs and To inform their healthcare providers of their 'at-risk' status so that special procedures may be arranged for certain instruments used in their healthcare (NB. Their GPs are also asked to do this.)


A range of measures have been put in place by the Department of Health to minimise the possible risk of vCJD being passed through blood:


Since 1997 all cases of vCJD that are reported to the National CJD Surveillance Unit and diagnosed as having 'probable' vCJD, result in a searc h of the UK Blood Services blood donor records. If the patient has donated blood, any unused parts of that blood are immediately removed from stock. The fate of all used components of blood from the donor is traced, and surviving recipients informed of their risk. In July 1998, the Department of Health announced that plasma for the manufacture of blood products, such as clotting factors, would be obtained from non-UK sources. Since October 1999, white blood cells (which may carry the greatest risk of transmitting vCJD) have been removed from all blood used for transfusion. In August 2002 the Department of Health announced that fresh frozen plasma for treating babies and young children born after 1 January 1996 would be obtained from the USA, extended to all children under 16 years of age (Summer 2005). In December 2002, the Department of Health completed its purchase of the largest remaining independent US plasma collector, Life Resources Incorporated. This secures long-term supplies of non-UK blood plasma for the benefit of NHS patients. Since April 2004, blood donations have not been accepted from people who have themselves received a blood transfusion in the UK since 1980. This has been extended to include apheresis donors and donors who are unsure if they had previously had a blood transfusion (August 2004). Since late 2005, blood donations have not been accepted from donors whose blood was transfused to patients who later developed vCJD. The UK Blood Services continue to promote the appropriate use of blood and tissues and alternatives throughout the NHS.


The likelihood of a person who may be infected with vCJD going onto develop symptoms of the disease is uncertain, and may depend on individual susceptibility. It is possible that infected individuals may never develop symptoms.


For further information contact the HPA press office on 0208 327 7098/7097/6055


Specialist care for vCJD is available from The NHS National Prion Clinic, based at The Hospital for Neurology and Neurosurgery, Queen Square, London http://www.nationalprionclinic.org/


The National CJD Surveillance Unit is based at the Western General Hospital Edinburgh: www.cjd.ed.ac.uk


For further information about vCJD go to:













 
 
 
 



Thursday, February 14, 2013



Unique Properties of the Classical Bovine Spongiform Encephalopathy Strain and Its Emergence From H-Type Bovine Spongiform Encephalopathy Substantiated by VM Transmission Studies




please see ;




>>> Fourth, PrPSc was consistently detected in the spleen, similar to mice infected with BSE-C.




Thursday, February 14, 2013





Unique Properties of the Classical Bovine Spongiform Encephalopathy Strain and Its Emergence From H-Type Bovine Spongiform Encephalopathy Substantiated by VM Transmission Studies












see latest nvCJD USA blood recalls;










Thursday, February 14, 2013


The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease









Thursday, February 21, 2013


National Prion Disease Pathology Surveillance Center Cases Examined January 16, 2013









16 YEAR OLD SPORADIC FFI ?





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









Sunday, February 10, 2013


Creutzfeldt-Jakob disease (CJD) biannual update (February 2013) Infection report/CJD









Thursday, January 17, 2013


TSE guidance, surgical, dental, blood risk factors, Part 4 Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings (updated January 2013)









Tuesday, July 31, 2012


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









Thursday, August 02, 2012


CJD case in Saint John prompts letter to patients Canada CJD case in Saint John prompts letter to patients









Friday, February 10, 2012


Creutzfeldt-Jakob disease (CJD) biannual update (2012/1) potential iatrogenic (healthcare-acquired) exposure to CJD, and on the National Anonymous Tonsil Archive









Monday, November 26, 2012


Aerosol Transmission of Chronic Wasting Disease in White-tailed Deer









Thursday, December 29, 2011


Aerosols An underestimated vehicle for transmission of prion diseases?





please see more on Aerosols and TSE prion disease here ;









Saturday, February 12, 2011


Another Pathologists dies from CJD, another potential occupational death ?


another happenstance of bad luck, a spontaneous event from nothing, or friendly fire ???









Tuesday, December 14, 2010


Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J,


UPDATE DECEMBER 2010









Tuesday, September 14, 2010


Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)









Thursday, September 02, 2010


NEUROSURGERY AND CREUTZFELDT-JAKOB DISEASE Health Law, Ethics, and Human Rights The Disclosure Dilemma









Thursday, August 12, 2010


USA Blood products, collected from a donor who was at risk for vCJD, were distributed July-August 2010









Sunday, August 01, 2010


Blood product, collected from a donors possibly at increased risk for vCJD only, was distributed USA JULY 2010












Thursday, July 08, 2010


Nosocomial transmission of sporadic Creutzfeldt–Jakob disease: results from a risk-based assessment of surgical interventions Public release date: 8-Jul-2010









Thursday, July 08, 2010


GLOBAL CLUSTERS OF CREUTZFELDT JAKOB DISEASE - A REVIEW 2010









Wednesday, June 02, 2010


CJD Annex H UPDATE AFTER DEATH PRECAUTIONS Published: 2 June 2003 Updated: May 2010









Tuesday, May 11, 2010


Current risk of iatrogenic Creutzfeld–Jakob disease in the UK: efficacy of available cleaning chemistries and reusability of neurosurgical instruments









Tuesday, May 04, 2010


Review of the Human Pituitary Trust Account and CJD Issue 20 January 2010









Tuesday, March 16, 2010


Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 REVISED FEB. 2010









Monday, August 17, 2009


Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex J,K, AND D Published: 2009









Monday, July 20, 2009


Pre-surgical risk assessment for variant Creutzfeldt-Jakob disease (vCJD) risk in neurosurgery and eye surgery units









Friday, July 17, 2009


Revision to pre-surgical assessment of risk for vCJD in neurosurgery and eye surgery units Volume 3 No 28; 17 July 2009









Sunday, May 10, 2009


Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)









Thursday, January 29, 2009


Medical Procedures and Risk for Sporadic Creutzfeldt-Jakob Disease, Japan, 1999-2008 (WARNING TO Neurosurgeons and Ophthalmologists) Volume 15, Number 2-February 2009 Research









Wednesday, August 20, 2008


Tonometer disinfection practice in the United Kingdom: A national survey









Tuesday, August 12, 2008


Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)









Monday, December 31, 2007


Risk Assessment of Transmission of Sporadic Creutzfeldt-Jakob Disease in Endodontic Practice in Absence of Adequate Prion Inactivation








Subject: CJD: update for dental staff


Date: November 12, 2006 at 3:25 pm PST


1: Dent Update. 2006 Oct;33(8):454-6, 458-60.


CJD: update for dental staff.









Saturday, January 16, 2010


Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al


Evidence For CJD/TSE Transmission Via Endoscopes


From Terry S. Singletary, Sr flounder@wt.net 1-24-3










Thursday, October 25, 2012


Current limitations about the cleaning of luminal endoscopes and TSE prion risk factors there from


Article in Press









2011 TO 2012 UPDATE






Saturday, December 3, 2011


Candidate Cell Substrates, Vaccine Production, and Transmissible Spongiform Encephalopathies


Volume 17, Number 12—December 2011









Sunday, June 26, 2011


Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque









Monday, February 7, 2011


FDA’s Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???












Sunday, August 21, 2011


The British disease, or a disease gone global, The TSE Prion Disease (SEE VIDEO)










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











Wednesday, April 25, 2012


USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 – 2012










Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis

















full text with source references ;









Tuesday, July 29, 2008



Heidenhain Variant Creutzfeldt Jakob Disease Case Report



FINAL AUTOPSY DIAGNOSIS



I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.



SKROLL down a bit for Mom's autopsy of hvCJD. ...












TSS

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