Wednesday, December 11, 2013

Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease

 
>>>They found infectivity in the red and white blood cells and plasma of a variant CJD patient and in the plasma of two of four sporadic CJD patients tested. These findings indicate the need to continue assessing the possible risk for CJD transmission via transfusion of blood products.<<<


>>>In tgBov inoculated with vCJD and tgHu inoculated with sCJD, the PrPres banding patterns observed by Western blot in animals challenged with brain homogenate and blood components were identical (Figure, panels C, D). These results support the contention that the TSE agent propagated in tgBov mice and tgHu were vCJD and sCJD agents, respectively.<<<







>>>They found infectivity in the red and white blood cells and plasma of a variant CJD patient and in the plasma of two of four sporadic CJD patients tested. These findings indicate the need to continue assessing the possible risk for CJD transmission via transfusion of blood products.<<<

 

3. Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease, Jean Yves Douet, et al. Creutzfeldt-Jakob disease (CJD) is a rare but fatal brain disease of humans. Over the past 60 years, this disease has developed in several hundred patients who had received tissue (mainly growth hormone or nervous tissue grafts) from infected cadaver donors. A variant form of CJD, primarily occurring in Europe, has been causally linked with bovine spongiform encephalopathy (commonly known as mad cow disease). Recent research, which used a relatively new type of highly sensitive laboratory mice, enabled researchers to measure infectivity in blood. They found infectivity in the red and white blood cells and plasma of a variant CJD patient and in the plasma of two of four sporadic CJD patients tested. These findings indicate the need to continue assessing the possible risk for CJD transmission via transfusion of blood products.

 

Contact: Press Relations INRA News Office – Jeremy Zuber +33 1 42 75 91 69 presse@inra.fr Olivier Andreoletti Joint Research Unit “Interactions Hosts-Pathogens” (INRA/ENVT) o.andreoletti@envt.fr

 

Notice: Art in Science: Selections from Emerging Infectious Diseases, a book just published by Oxford University Press, offers a visual tour of the factors involved in disease emergence: microbial adaptation and change; climate, weather, and ecosystems; economic development and land use; human demographics and behavior; technology, industry, travel, and commerce; poverty and conflict. This interdisciplinary effort engages the reader at a creative level, demonstrating how art relates to science and to us all. The book is available on Amazon.

 

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Volume 20, Number 1—January 2014


Dispatch


Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease


Jean Yves Douet, Saima Zafar, Armand Perret-Liaudet, Caroline Lacroux, Séverine Lugan, Naima Aron, Herve Cassard, Claudia Ponto, Fabien Corbière, Juan Maria Torres, Inga Zerr, and Olivier AndreolettiComments to Author 
Author affiliations: Ecole Nationale Vétérinaire Toulouse, France (J.Y. Douet, C. Lacroux, S. Lugan, N. Aron, H. Cassard, F. Corbière, O. Andréoletti); National Reference Center for Transmissible Spongiform Encephalopathy, Georg August University, Göttingen, Germany (S. Zafar, C. Ponto, I. Zerr); Hospices Civils de Lyon, France (A. Perret-Liaudet); BioRan, Bron, France (A. Perret-Liaudet); Centro de Investigación en Sanidad Animal, Madrid, Spain (J.M. Torres)
 

 

Abstract
 
We report the presence of infectivity in erythrocytes, leukocytes, and plasma of 1 person with variant Creutzfeldt-Jakob disease and in the plasma of 2 in 4 persons whose tests were positive for sporadic Creutzfeldt-Jakob disease. The measured infectivity levels were comparable to those reported in various animals with transmissible spongiform encephalopathies.
 
 
Among humans, Creutzfeldt-Jakob disease (CJD) is a low incidence disease (≈1 case per million per year) that occurs as either a sporadic (sCJD) or a familial/genetic (fCJD) form. Whereas familial disease forms are linked to a mutation in the prion protein gene (Prnp), no clear epidemiologic risk factors have been identified for sporadic disease forms. sCJD is not a uniform disorder in terms of clinical and neuropathological phenotype. sCJD cases are classified as type 1 or 2 according to the polymorphism at codon 129 of the protease-resistant prion protein (PrP) sequence (methionine/valine) and to the electromobility of the proteinase K–resistant core of the abnormal PrP (PrPres) (1). Type 1 and type 2 isoforms in sCJD are believed to correspond to different transmissible spongiform encephalopathy (TSE) agents
 
 
Despite their relative rarity, several hundred iatrogenically transmitted CJD cases were identified during the past 60 years (2). Some data supporting the presence of infectivity in the blood of sCJD-affected patients were reported following the intracerebral inoculation of blood fractions from affected patients into rodents. These observations remain ambiguous because other studies did not confirm them (3,4).
 
 
In 1996, a new form of CJD, named variant CJD (vCJD), was identified in humans. Variant CJD was demonstrated to be caused by the agent that causes bovine spongiform encephalopathy in cattle (5). In the United Kingdom, 4 vCJD transmissions (3 clinical cases and 1 asymptomatic infection) were probably caused by the transfusion of non–leuco-depleted erythrocyte concentrates prepared from donors who later had positive test results for vCJD (6). More recently, a presumed additional case of vCJD infection was reported in the United Kingdom in a hemophilic patient who had received fractionated plasma products, including some units linked to a donor who later was diagnosed with vCJD (7). Despite the epidemiologic evidence of bloodborne transmission in vCJD, bioassays performed on conventional rodent models failed to demonstrate the presence of infectivity in the blood (8). The lack of TSE transmission in conventional rodent models could be a consequence of a low infectivity level in blood from vCJD- and sCJD-affected patients (as described in sheep and rodent TSE models) (9) or of the existence of the species barrier phenomenon that limits the transmission of human prions to these animal models. The development during the last decade of transgenic mice models expressing PrP from others species that abrogate the species barrier now offers the potential to detect low level of infectivity (10).

 
In this study, we used 2 transgenic mouse models that displayed a high sensitivity to the vCJD or sCJD TSE agents to estimate the infectious titer in certain blood fractions from vCJD- and sCJD-affected patients. According to legislation of the United Kingdom, Germany, and France, the experimental protocol, including the use of human samples, was approved by UK National CJD Research & Surveillance Unit tissue bank: REC reference number 2000/4/157-German TSE reference center: Ref Nr 11/11/93, PHRC ref 2004-D50-353 for patient from France.

 

 The Study

 

Previous studies reported a high sensitivity in transgenic mice overexpressing bovine PrP (tgBov) for the detection of the bovine spongiform encephalopathy agent. To demonstrate that tgBov also displays a high sensitivity to vCJD infection, we titrated to endpoint a vCJD isolate (10% brain homogenate) by intracerebral inoculation in this model (Tg110) (11). Considering the potential diversity of TSE agents that may cause sCJD, we decided to focus only on type 1 homozygous for methionine at codon 129 of the PRP gene (MM1) sCJD cases. An endpoint titration of a MM1 sCJD 10% brain homogenate was performed in a mouse model that express the methionine 129 variant of the human PrP gene (tgHu:Tg340) (12). This enabled confirmation of the capacity of the tgBov and tgHu models to detect the vCJD and sCJD MM1 agent, respectively, up to a 10−6 dilution of the reference brain homogenates (Table 1; 13). This value was within the range of the brain/blood relative infectivity reported in various TSE animal models (9,14).

 

Figure

 

Thumbnail of Abnormal prion protein (PrPres) detection by using Western blot (WB) and paraffin-embedded tissue (PET) blot in the brain of transgenic mice expressing the methionine 129 variant of the human prion protein (PrP) (tgHu) or bovine PrP (tgBov). A, B) PET blot PrPres distribution in coronal section (thalamus level) of tgHu mice inoculated with sporadic Creutzfeldt-Jakob disease (sCJD) MM1 isolates (10% brain homogenate): A) reference isolate used for the endpoint titration in Table 1; B Figure. [[caption]]

 

In the next step of our experiment, blood fractions (erythrocytes, plasma, and leukocytes) from 1 vCJD-confirmed patient were injected intracerebrally in tgBov mice. Similarly, plasma samples from 4 sCJD MM1 patients were inoculated with tgHu (Table 2). The blood fraction preparation was performed by using laboratory scale hematologic protocols (Technical Appendix Adobe PDF file [PDF - 31 KB - 3 pages]), not by following the procedure applied by blood banking services. This method implies that the leucodepletion that is applied to blood labile products in most countries to reduce the vCJD bloodborne transmission risk was not performed. Brain tissue samples from each of the 4 sCJD cases were also inoculated with tgHu. On the basis of the incubation period (Table 2) and PrPres distribution pattern in the brain as assessed by using paraffin-embedded tissue blot, the TSE agents in those isolates were indistinguishable from those in the MM1 sCJD case that was used for endpoint titration (Figure, panel A).

 

 No TSE clinical signs or PrPres accumulation were observed in the tgBov or tgHu mice inoculated with phosphate-buffered saline or brain and plasma from healthy human controls. The 3 blood fractions from the vCJD-affected patient caused a positive result but low attack rate among tgBov mice (Table 2). On the basis of these results, infectivity in erythrocytes and plasma was estimated to be 2.12 infectious dose (ID)/mL of inoculum. In leukocytes, the infectious titer was estimated to be 2.23 ID/mL of whole blood. According to these values and the hematocrit of the sample (Technical Appendix Adobe PDF file [PDF - 31 KB - 3 pages]), the global infectious titer whole blood in the tested patient would be ≈4.45 ID/mL. Such infectious level is approximately equivalent to 1.4 µg of the reference vCJD brain sample that was endpoint-titrated (Table 1).

 

In tgHu mice, positive transmission was observed among mice inoculated with 2 of 4 plasma samples (Table 2). The infectious titers in both positive plasma samples were estimated to be 2.12 and 3.7 ID/mL of plasma, which is equivalent to 0.3–0.5 µg of the reference sCJD MM1 brain sample that was endpoint titrated (Table 1). However, because of the limited number of mice inoculated (n = 24) and the overall sensitivity of the assay (upper CI limit 6.24 ID/mL), the absence of transmission in mice inoculated with the 2 other plasma samples cannot be interpreted conclusively

 

In tgBov inoculated with vCJD and tgHu inoculated with sCJD, the PrPres banding patterns observed by Western blot in animals challenged with brain homogenate and blood components were identical (Figure, panels C, D). These results support the contention that the TSE agent propagated in tgBov mice and tgHu were vCJD and sCJD agents, respectively.

 

Conclusions

 

The data reported here confirm the presence of infectivity in erythrocytes, leukocytes, and plasma from vCJD-affected patients and demonstrate unambiguously the presence of infectivity in the plasma of some, but not all, sCJD-affected patients. The infectivity levels that we measured in the tested vCJD and sCJD blood components were comparable to those reported in various TSE animal models. The number of cases included in our study was limited; a new experiment that would include a larger number of cases and different blood fractions from sCJD cases will be necessary to refine the data. However, these results represent a substantial input for assessing the risk for interindividual bloodborne transmission of sCJD and vCJD.

 

 Mr Douet is assistant lecturer in ophthalmology at the National Veterinary School of Toulouse and a PhD student in the TSE group in the UMR INRA ENVT 1225 unit. His primary research interests are the pathogenesis of the prion disease with special emphasis on the iatrogenic risk of transmission.

 

Acknowledgment

 

 The authors are greatly indebted to the National Creutzfeldt-Jakob Disease Surveillance Unit (UK-Edinburgh) for providing variant CJD brain samples.

 

This work was supported by a grant from the European Commission: Protecting the food chain from prions: shaping European priorities through basic and applied research (PRIORITY, N°222887; project no. FP7-KBBE-2007-2A) and by grants from the JPND program (DEMTEST: Biomarker based diagnosis of rapid progressive dementias-optimization of diagnostic protocols, 01ED1201A). The study in Germany was funded by the Robert Koch-Institute through funds of the Federal Ministry of Health (grant no. 1369-341).

 

 References

 

 

snip...

 

 


 


 

Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease

 

Technical Appendix

 

Biochemical Typing and PrP ORF Sequencing of Sporadic and Variant Creutzfeldt-Jakob Disease Genes Confirmation of the disease diagnosis, PrPres WB typing and PrnP gene sequencing in the patients were performed by the national CJD reference center of the country of origin of each patient. All patients were Methionine/Methionine at codon 129 and no other mutation was observed. sCJD cases were all originating from Germany. The vCJD case whose blood was tested by bioassay was originating from France. The vCJD case that was used in the endpoint titration experiment was provided by the UK CJD reference center in Edinburgh.

 

Blood Collection and Fractionation

 

sCJD blood samples were collected by using S-Monovette® Coagulation Sodium Citrate 1 in 3 mL tubes according to manufacturer instruction (SARSTEDT AG & Co. · www.sarstedt.com) . Tubes were centrifuged for 20 minutes at 2000 rpm, plasma was then collected and cell-free fraction underwent another centrifugation step at 13000 rpm for 10 minutes. Supernatant was collected and stored frozen. The hematocrit values corresponding to the different samples were: sCJD case 1: 37.6%, sCJD case 2: 39.7%, sCJD case 3: 43%, sCJD case 4: 43.7%.

 

vCJD blood sample on EDTA and fractionated by a 10 minutes 3000 g centrifugation at 12°C . Plasma was collected and directly frozen stored. The buffy coat was collected and washed twice in NaCl 0.9% (2 min, RT) before being pelleted at 3000 g 10 min and frozen.

 

The sample was submitted to standard biochemical analyze and the blood formula was red cells 5.21 1012/L, hemoglobin 149 g/L, hematocrit: 48%, total white cells 17.1 109/L, lymphocytes: 27.1%, monocytes 9.3%, neutrophils: 60%, eosinophil: 1.8%, Basophils: 1.8%, Platelets:356 109/L.

 

Page 2 of 3

 

Brain and Blood Samples Handling and Bioassay

 

Blood was collected during the diagnostic procedures when patients were evaluated for CJD diagnosis at notifying hospital. The time between blood sampling and patients’ decease are reported in Technical Appendix Table 1.

 

For sCJD patients, blood was processed at the CSF reference laboratory of the National TSE Reference Center at the Department of Neurology Göttingen, Germany. Autopsy was performed by the Department of Pathology of the notifying hospital and reference material was sent to the Department of Neuropathology, Göttingen, Germany. Blood and brain samples were stored in separate department and handled by different staff in the Gottingen University hospital.

 

The vCJD blood sample was collected and fractionated in the Bron Hospital (France). In this hospital the department handling CSF and blood samples and the pathology department (post mortem sampling) are distinct. The vCJD reference brain sample was obtained from the UK CJD reference laboratory in Edinburgh.

 

All the samples were dispatched to the laboratory that performed the bioassays (UMR INRA ENVT 1225) in separated sealed containers. Samples were kept untouched and prepared only a few hours before their inoculation in mice.

 

The sCJD endpoint titration in tgHu mice was performed 1 year before the reception of sCJD plasma samples.

 

Plasma and Brain samples from the four sCJD affected patients were prepared and inoculated separately; Brain from the affected patients (text Table 2) were inoculated after the first positive transmission occurred in mice inoculated with sCJD plasma.

 

Similarly the vCJD endpoint titration experiment and the inoculation of the vCJD blood samples in tg Bov were performed at different dates (9 months interval).

 

Negative control (phosphate-buffered saline and healthy blood samples) were inoculated during the same inoculation session than the inoculation of the blood fractions from the vCJD and sCJD patients. Healthy brain controls (human and bovine) were inoculated during the same session than the endpoint titration of sCJD and vCJD brain material. Page 3 of 3

 
 


 

 

Monday, December 02, 2013

 

A parliamentary inquiry has been launched today into the safety of blood, tissue and organ screening following fears that vCJD – the human form of ‘mad cow’ disease – may be being spread by medical procedures

 


 

 

Friday, November 29, 2013

 

Identification of Misfolded Proteins in Body Fluids for the Diagnosis of Prion Diseases

 

International Journal of Cell Biology

 


 
 

Oral.05: Contaminated blood products induce a highly atypical prion disease devoid of PrPres in primates

 

Emmanuel Corney,1 Nina Jaffre,1 Jacqueline Mikol,1 Valerie Durand,1 Christelle Jas-Duval,1,2 Sophie Luccantoni-Freire,1 Evelyne Correia,1 Nathalie Lescoutra-Etcheqaray,3 Nathalie Streichenberqer,4 Stephane Haik,5 Chryslain Sumian,3 Paul Brown1 and Jean-Philippe Deslys1

 

1Commissariat a l'Energie Atomique; Institute of Emerging Diseases and Innovative Therapies (iMETI); Division of Prions and Related Diseases (SEPIA); Fontenay-aux- Roses, France; 2EFS·Nord de France; Lille, France; 3MacoPharm; Tourcoing, France; 4Hospices Civils de Lyon; Prion Unit; Neurobiology Department; Bron, France; 5Inserm; U 975·CNRS; UMR 7225 - Universite Pierre et Marie Curie; Paris, France

 

Background, Concerns about the blood-borne risk of prion infection have been confirmed by the occurrence in the UK of four transfusion-related infections of vCJD and an apparently silent infection in an hemophiliac patient. Asymptomatic incubation periods in prion diseases can extend over decades in humans. We present here unexpected results of experiments evaluating blood transmission risk in a non-human primate model.

 

Material and Methods, Cynomolgus macaques were inoculated with brain or blood specimens from vCJD infected humans or monkeys. Neuropathological and biochemical findings were obtained using current methods used for human patients.

 

Results, Thirteen out of 23 primates exposed to various human or macaque blood products exhibited a previously undescribed myelopathic syndrome, devoid of the classical features of prion disease, notably abnormal prion protein (PrPres) deposition, whereas the 14 corresponding brain-inoculated donor animals and 1 transfused animal exhibited the classical vCJD pattern. In passage experiments, plasma transfusion induced the same atypical phenotype after two years (again, with no detectable PrPres), whereas the intracerebral inoculation of spinal cord led to a typical prion disease with cerebral spongiosis and PrPres accumulation in the brain of the primate recipient. Interestingly, passage experiments in transgenic mice were largely unsuccessful.

 

In another experiment designed to test the efficacy of antiprion filters, three recipients of filtered red blood cells suspended in plasma are still healthy 4.5 y after transfusion whereas the recipients of unfiltered inocula died after 2.5 y with the atypical neurological profile.

 

Conclusion. We describe a new fatal neurological myelopathic syndrome in monkeys exposed to various vCJD/BSE-infected blood components.

 

 

Secondary transmission in primates confirms

 

(I) the transmissibility of this myelopathy, and

 

(2) its prion origin which could not be diagnosed as such in the first recipients.

 

This myelopathy might be compared in some respects to certain forms of human lower motor neuron disease, including neuromyelitis optica, the flail arm syndrome of amyotrophic lateral sclerosis (ALS), and the recently described FOSMN (facial onset sensory and motor neuronopathy) syndrome.

 

 


 

 


 

 

Friday, August 16, 2013

 

Creutzfeldt-Jakob disease (CJD) biannual update August 2013 U.K. and Contaminated blood products induce a highly atypical prion disease devoid of PrPres in primates

 


 

 

 

Sunday, August 11, 2013

 

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

 

Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010

 


 

 
Friday, January 07, 2011

 

Transmission of sporadic Creutzfeldt-Jakob disease by blood transfusion: risk factor or possible biases

 


 

Singeltary submission to FDA 2001



Singeltary submission to FDA 2003


 
Owens, Julie

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

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


 
FSIS, USDA, REPLY TO SINGELTARY


 

4th CASE VCJD VIA BLOOD TRANSFUSION

 


 


 





Other US BSE risks: the imported products picture

 

24 Jul 00

 

Trade Statistics: UK to US Compiled by Terry S.Singeltary Sr of Bacliff, Texas

 

[Opinion (webmaster): The US has focused for years on tracing, containing, and eradicating live animal imports from the UK or other countries with acknowledged BSE like Belgium, including some 499 cattle and the Vermont sheep. This strategy does not acknowledge imports of rendered bovine products from England during the BSE period nor secondary products such as surgical catgut, which is to say surgical cowgut, or dairy cattle embryos, vaccines for veterinarian and human medicines. What has become of these? Mr. Singeltary, who lost his mother to CJD of unexplained origin a few years back and went on to became a well-known TSE activist, has tracked down voluminous pertinent import data through correspondence with UK officials and searches of government web sites. Imports of such products are frequently cited by Europeans in rating BSE risks in the US and in shutting out US exports.

 

Many people's eyes glaze over when reviewing reams of sometimes older trade statistics. There is no proof that any of the imported products was contaminated with BSE nor if so, any evidence that any BSE product lead to infection in US livestock, surgical patients, or what not. Nonetheless, the data obtained by Mr. Singeltary establish that an appalling variety and tonnage of products that were imported by the US from the UK and othr BSE-affected countries during the peak of the BSE epidemic years.]

 

10 January 1990 COMMERCIAL IN CONFIDENCE

 

NOT FOR PUBLICATION

 

COMMITTEE ON SAFETY OF MEDICINES WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY

 

SURGICAL CATGUT SUTURES

 


 

 The documents below were provided by Terry S. Singeltary Sr on 8 May 2000. They are optically character read (scanned into computer) and so may contain typos and unreadable parts.

 

TIP740203/l 0424 CONFIDENTIAL

 


 

 
RIP MOM 12/14/97 CONFIRMED HEIDENHAIN VARIANT CREUTZFELDT JAKOD DISEAE

 

TSS

Monday, December 02, 2013

A parliamentary inquiry has been launched today into the safety of blood, tissue and organ screening following fears that vCJD – the human form of ‘mad cow’ disease – may be being spread by medical procedures

 
 
Sent: Monday, December 02, 2013 9:00 PM
 
 
 
Subject: A parliamentary inquiry has been launched today into the safety of blood, tissue and organ screening following fears that vCJD – the human form of ‘mad cow’ disease – may be being spread by medical procedures
 

Greetings Honorable Members of the U.K. Parliament, House of Commons, et al,
 
 
I tried to comment, but the comment page was not working electronically, so I kindly wish to submit the following please.
 
 
IN REPLY TO ;
 
 
03 December 2013
A parliamentary inquiry has been launched today into the safety of blood, tissue and organ screening following fears that vCJD – the human form of ‘mad cow’ disease – may be being spread by medical procedures.
At a hearing in Parliament last Wednesday, the Science and Technology Committee was told that vCJD continued to pose a “significant” risk to UK public health and that more than one in every 2000 people could be silent carriers of the disease. vCJD can have an incubation period of over 30 years.
Leading scientific experts told the Committee that the infectious agent responsible for vCJD—a type of abnormal protein called a prion—could be present in the UK blood supply and that blood and organ donation could therefore represent a major source of future vCJD infections.
Following this session, the Science and Technology Committee has agreed to hold an inquiry into blood, tissue and organ screening. Chair of the Committee Andrew Miller MP stated:
“Variant Creutzfeldt-Jakob Disease is a terrible condition and we were extremely concerned to hear evidence that this incurable disease still poses a significant risk to public health.
Although the risk of developing the disease as a result of eating contaminated beef was long ago eliminated, it is possible that the infection could still be unwittingly spread through medical procedures. We were told that this may happen through failure to properly clean medical instruments, or, even more worryingly, through widespread contamination of the blood and organ supply.
We want to explore whether the Government is taking this threat as seriously as it should be. Our new inquiry will investigate these issues in more detail and consider ways in which the UK can protect its vital supply of donated blood, tissues and organs.”
The new inquiry follows on from a one-off evidence session that took place on Wednesday 27 November.

Terms of Reference

The Committee is seeking written submissions on the following matters:
  1. Are UK policies governing who can donate blood and blood products, tissues and organs sufficiently evidence-based? Is NHS Blood and Transplant overly restrictive about who can donate, or should greater precautions be taken to further reduce risk?
  2. Is the Government and its scientific advisory structure sufficiently responsive to the threat posed by emerging diseases being transmitted through blood and blood products, tissues and organs?
  3. Has the threat of ongoing transmission of vCJD through the blood and blood product supply been adequately mitigated?
  4. What are the strengths and weaknesses of NHS Blood and Transplant’s strategy, “Taking Organ Transplantation to 2020”? What further changes could be made to safely increase the supply of blood and blood products, tissues and organs?
  5. What lessons could be learnt from the screening and donation practices of other countries?

Submitting written evidence

The personal information you supply will be processed in accordance with the provisions of the Data Protection Act 1998 for the purposes of attributing the evidence you submit and contacting you as necessary in connection with its processing. The Clerk of the House of Commons is the data controller for the purposes of the Act. We may also ask you to comment on the process of submitting evidence via the web portal so that we can look to make improvements. If you have any queries or concerns about the collection and use of this information or do not wish your details to be used for the purpose of collecting feedback, please email the Committee  providing your full name, address, and if relevant your organisation.
The Committee invites written submissions on these issues by noon on Wednesday 15 January 2014.
Each submission should:
  • be no more than 3,000 words in length
  • be in Word format with as little use of logos as possible
  • have numbered paragraphs
  • include a declaration of interests.
If you need to send a paper copy please send it to:
The Clerk
Science and Technology Committee
House of Commons
14 Tothill Street
London
SW1H 9NB

Please note that:
  • Material already published elsewhere should not form the basis of a submission, but may be referred to within a proposed memorandum, in which case a hard copy of the published work should be included.
  • Memoranda submitted must be kept confidential until published by the Committee, unless publication by the person or organisation submitting it is specifically authorised.
  • Once submitted, evidence is the property of the Committee. The Committee normally, though not always, chooses to make public the written evidence it receives, by publishing it on the internet (where it will be searchable), by printing it or by making it available through the Parliamentary Archives. If there is any information you believe to be sensitive you should highlight it and explain what harm you believe would result from its disclosure. The Committee will take this into account in deciding whether to publish or further disclose the evidence.
  • Select Committees are unable to investigate individual cases.

Further information

Image: iStockphoto

http://www.parliament.uk/business/committees/committees-a-z/commons-select/science-and-technology-committee/inquiries/parliament-2010/blood-tissue-and-organ-screening/

Written submissions to the inquiry should be submitted online:
http://www.parliament.uk/business/committees/committees-a-z/commons-select/science-and-technology-committee/inquiries/parliament-2010/blood-tissue-and-organ-screening/commons-written-submission-form/


??? DID NOT WORK FOR ME ???

House of Commons
Science and Technology CommitteeOral evidence: variant Creutzfeldt-Jakob Disease (vCJD), HC
 
846
 
Wednesday 27 November 2013
 
Ordered by the House of Commons to be published on 27 November 2013.
 
Written evidence from witnesses:
 
– Professor James Ironside
 
– Dr Roland Salmon
 
– Professor John Collinge
 
Watch the meeting
 
Members present: Andrew Miller (Chair); Jim Dowd; Mr David Heath; Stephen Metcalfe;
Pamela Nash; Sarah Newton; Graham Stringer; David Tredinnick
 
Questions 1-46
 
 

Witnesses

Wednesday 27 November 2013, Thatcher Room, Portcullis House
At 9.05 am
  • Dr Roland Salmon, Joint Chair, Advisory Committee on Dangerous Pathogens TSE Sub Group
  • Professor James Ironside, Professor of Clinical Neuropathology, National CJD Research and Surveillance Unit, University of Edinburgh
  • Professor John Collinge, Professor of Neurology at the UCL Institute of Neurology and Director of the MRC Prion Unit
The Committee will hear evidence from scientific experts on the potential prevalence of vCJD in the population, modes of ongoing transmission and current UK surveillance, control and prevention strategies.
Andrew Miller MP, Chair of the Science and Technology Committee, said:
“More than twenty years on from the BSE crisis, studies have suggested that thousands of people may still carry the infectious agent thought to cause variant Creutzfeldt-Jakob Disease—the human form of “mad cow disease”.
“Although these people may never go on to develop symptoms of vCJD, important questions remain to be asked about the potential risk posed by this terrible condition and what the Government should be doing to reduce the spread of infection.”

Further information

Image: Parliamentary copyright

27 Nov 2013 - variant Creutzfeldt-Jakob Disease (vCJD) - oral evidence | PDF version (PDF309 KB) Opens in a new window Published 02 Dec 2013 Evidence given by Professor James Ironside, Professor of Clinical Neuropathology, National CJD Research and Surveillance Unit, University of Edinburgh, Dr Roland Salmon, Joint Chair, Advisory Committee on Dangerous Pathogens TSE Sub Group, and Professor John Collinge, Professor of Neurology, UCL Institute of Neurology and Director of the MRC Prion Unit.

 
 
 
NHS failed to sterilise surgical instruments contaminated with 'mad cow' disease

Regular sterilisation procedure wasn't suitable for the task, says leading specialist Steve Connor Author Biography Science Editor Wednesday 27 November 2013

The NHS has failed to use an effective method of sterilising surgical instruments contaminated with the human form of “mad cow” disease because it did not fit in with its established washing procedures, a leading specialist in variant Creutzfeldt-Jakob disease (vCJD) claimed yesterday.

The result is that hundreds of people have had their lives blighted by surgery performed with instruments possibly contaminated the prion protein responsible for vCJD said Professor John Collinge, director of the Medical Research Council’s Prion Unit at University College London.

Professor Collinge led one of a number of research groups that came up with novel ways of destroying the lethal prion protein, which sticks to the stainless steel of surgical instruments like superglue and can survive the high temperatures of hospital autoclaves.

However, in evidence to the House of Commons science and technology committee, Professor Collinge said that he was astonished and disappointed that the Department of Health and the NHS failed to adopt any of the suggestions for decontaminating surgical instruments.

“The solution we developed was a combination of enzymes and detergents, if you like a sort of bespoke biological washing powder which very effectively prion-decontaminated metal surfaces,” Professor Collinge said.

It was one of several decontamination procedures developed by a number of research groups sponsored by the health department over a decade ago to find ways of making surgical instruments safe, he said.

“Neither this nor the other products that were available – I think there were three – have ever been taken up by the NHS. They simply haven’t been used. These issues have been bounced around various committees to my and other peoples’ great frustration,” Professor Collinge said.

“It’s perhaps not surprising given that the NHS is notoriously resistant to change and to introducing new methodologies,” he said.

“Absolutely nothing has happened despite all this research and all this effort. Currently several hundred people have been notified that they have been exposed to [potentially contaminated] surgical instruments,” he told the committee.

“We’re blighting these peoples’ lives and all this has been avoidable for some years by applying this research. I find it quite extraordinary that the system just does not work,” he said.

“They’ve had to be notified that they’ve had a significant exposure to prions because they are expected to take precautions. They are not allowed to be blood donors and if they go on to have surgery they have to notify the surgeons that they are high risk individuals.

“Needless to say this has a major effect on their lives and needless to say it makes me very angry because all of this was avoidable,” he added.

DuPont, an American chemicals company, worked out a way of manufacturing Professor Collinge’s product as a 50C pre-soak for surgical instruments, but because this would involve changing the standard procedures for how medical devices were sterilised, NHS hospitals refused to adopt it, Professor Collinge claimed.

“What we had developed was seen to be inconvenient…The NHS didn’t buy a single unit of the product so was it surprising that the manufacturer just walked away?” he said.

“It was extraordinary [that] it was discussed in I don’t know how many committees and subcommittees when patients are being put in this position and having their lives blighted. It’s disgraceful,” he told the committee.

About 200 hospital patients have been told that they have been exposed to the vCJD prion through instruments that were used on other patients who subsequently died of the brain disease. Three out of the 177 people in the UK who have died of vCJD received contaminated blood, and the rest are assumed to have been infected by meat or meat products contaminated with bovine spongiform encephalopathy (BSE).

A spokesman for the Department of Health said that Professor Collinge’s research group has received £18m for various research projects and that DuPont’s prion inactivation product has been reviewed twice by Public Health England’s Rapid Review Panel, which established “gaps” in DuPont’s application.

Roland Salmon, the joint chairman of the government’s advisory sub-committee on dangerous pathogens, defended the Department of Health’s stance on introducing new ways of sterilising surgical instruments.

“I don’t think it’s fair on the department [of health] to say that nothing was done…they did institute a number of improvements,” Dr Salmon said.

“It’s perfectly true they haven’t introduced specific products…the barrier had been I’ve told with having a product composed in such a way that it can be introduced into what is an industrialised process in a cycle,” he said.

How vCJD can be contracted

Almost all of the 177 cases of vCJD – the human form of “mad cow” disease – have been contracted through eating contaminated meat or meat products before the introduction of controls to limit the spread of bovine spongiform encephalopathy (BSE) from cattle to people.

Three of these deaths, however, are believed to have resulted from blood donors infected with vCJD, but showing no clinical symptoms. There is one further case of a person who died of something else but who was shown at post-mortem to be infected following a blood transfusion.

There are fears of secondary infections from asymptomatic carriers in the population. Latest estimates suggest that up to one in 2,000 people in Britain could be carriers of vCJD.

Because the prion protein responsible for vCJD is found in a wide range of tissues, such as spleen, tonsils and appendix, the fear is that asymptomatic carriers may spread the infection to others through contaminated surgical instruments and blood donations.


http://www.independent.co.uk/news/science/nhs-failed-to-sterilise-surgical-instruments-contaminated-with-mad-cow-disease-8967763.html
 
 
 
I kindly submit the following ;
 
 
 
Greetings again,



AS usual, the media and the medical community missing the bigger picture. this incident also risk the medical iatrogenic transmission of ALL TSE PRION DISEASE, not just the UKBSEnvCJD only myth.

IN fact, there has never been an iatrogenic CJD event with nvCJD, except the 5 documented iatrogenic events with blood and nvCJD.

all other medical, surgical transmission was all with sporadic CJD, which is all iatrogenic CJD is, is sporadic CJD, until the the iatrogenic event is documented, proven, and then placed in the academic domain.

sadly, in my honest opinion, this will just be another BSE human TSE mad cow whitewash, like the BSE Inquiry, and the UKBSEnvCJD _only_ theory/myth was.

I kept up with the BSE Inquiry _daily_, even made a submission in 1998 to the BSE Inquiry about Nutritional Supplements and SRMs, and I see this having no chance of being any different $$$ 
I pray that I am wrong. I am waiting for that day in the USA and North America mad cow bse cjd inquiry, but that day will never come$$$

I apologize if I sound angry, I suppose I still am. ...

with kindest regards, terry



kind regards,
terry
 
 
 
Wednesday, November 27, 2013

NHS failed to sterilise surgical instruments contaminated with 'mad cow' disease


http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/nhs-failed-to-sterilise-surgical.html
 
 
 
see my history of the BSE Inquiry whitewash at bottom...for anyone still interested...tss
 
 


IATROGENIC


all iatrogenic cjd is, is sporadic CJD, until route and source of the iatrogenic event that took place, is detected, documented, placed in the academic domain as fact, and recorded, which happens very seldom due to a lot of factors, besides the incubation period, and that be mainly industry. kind of like asbestos and tobacco and the industry there from, they knew in the early 1900’s that they both were killing, and they both had long incubation, and somebody chose not to do anything about if for decades and decades. kind of like what we have here with the TSE prion disease. $$$

> In 12 of 15 hospitals with neurosurgical incidents, a decision was made to notify patients of their potential exposure.

SO, X number of patients, from 3 hospitals, where

''exposure to potentially CJD-contaminated instruments ''

took place on these patients, the final decision NOT to tell those folks about the potential exposure to the CJD TSE prion

insane, thus, the TSE prion agent continues to spread. ...please see further comments here ;


 
Saturday, November 16, 2013

Management of neurosurgical instruments and patients exposed to creutzfeldt-jakob disease 2013 December

Infect Control Hosp Epidemiol.


http://creutzfeldt-jakob-disease.blogspot.com/2013/11/management-of-neurosurgical-instruments.html


 
Thursday, November 14, 2013

Prion diseases in humans: Oral and dental implications


http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/prion-diseases-in-humans-oral-and.html


Saturday, November 2, 2013

Recommendation of the Swiss Expert Committee for Biosafety on the classification of activities using prion genes and prion protein January 2013


http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/recommendation-of-swiss-expert.html
 

Friday, November 29, 2013

Identification of Misfolded Proteins in Body Fluids for the Diagnosis of Prion Diseases

International Journal of Cell Biology


http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/identification-of-misfolded-proteins-in.html
 
 
 
CJD Mark Tami: To ask the Secretary of State for Health (1) what steps his Department has put in place to monitor the number of people who carry the abnormal prion protein which causes variant Creutzfeldt-Jakob disease; [174628]

(2) when he plans that screening of the abnormal prion protein which causes variant Creutzfeldt-Jakob disease will be introduced; [174631]

(3) what assessment he has made of the number of people who carry the abnormal prion protein which causes variant Creutzfeldt-Jakob disease. [174633]

12 Nov 2013 : Column 615W

Jane Ellison: The presence of abnormal prion protein is currently taken as a marker for asymptomatic carriage of variant Creutzfeldt-Jakob disease or for symptomatic infection. A recent study to assess carriage by looking at stored appendix tissue samples, first published in the Health Protection Report in August 2012, found abnormal prion protein in 16 appendices out of 32,441 samples. This suggests a prevalence of about 1 in 2,000.

There is no monitoring of people who may carry the abnormal prion protein; all appendix prevalence studies are anonymised.

No routine screening can yet take place as there are no suitable validated screening tests for abnormal prion protein available. The Department, together with the United Kingdom Blood Services, continues to monitor, scientific research and development in this area.


http://www.publications.parliament.uk/pa/cm201314/cmhansrd/cm131112/text/131112w0004.htm#13111283000003


Monday, October 14, 2013

Researchers estimate one in 2,000 people in the UK carry variant CJD proteins


http://creutzfeldt-jakob-disease.blogspot.com/2013/10/researchers-estimate-one-in-2000-people.html


Tuesday, October 29, 2013

VARIANT CJD PRESENTS DIFFERENTLY IN OLDER PATIENTS


http://creutzfeldt-jakob-disease.blogspot.com/2013/10/variant-cjd-presents-differently-in.html


Wednesday, October 09, 2013

*** WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY, £41,078,281 in compensation REVISED


http://creutzfeldt-jakob-disease.blogspot.com/2013/10/why-ukbsenvcjd-only-theory-is-so.html

 
Thursday, October 10, 2013

CJD REPORT 1994 increased risk for consumption of veal and venison and lamb


http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-report-1994-increased-risk-for.html


Friday, August 16, 2013

*** Creutzfeldt-Jakob disease (CJD) biannual update August 2013 U.K. and Contaminated blood products induce a highly atypical prion disease devoid of PrPres in primates


http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-biannual.html


WHAT about the sporadic CJD TSE proteins ?

WE now know that some cases of sporadic CJD are linked to atypical BSE and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all it’s sub-types $$$

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***


http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html


Sunday, October 13, 2013

CJD TSE Prion Disease Cases in Texas by Year, 2003-2012


http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-tse-prion-disease-cases-in-texas-by.html


Monday, September 02, 2013

Lessons from the response to the threat of transfusion-transmitted vCJD in Ireland


http://vcjdtransfusion.blogspot.com/2013/09/lessons-from-response-to-threat-of.html
 
 

Saturday, November 2, 2013

Recommendation of the Swiss Expert Committee for Biosafety on the classification of activities using prion genes and prion protein January 2013


http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/recommendation-of-swiss-expert.html


Saturday, November 2, 2013

APHIS Finalizes Bovine Import Regulations in Line with International Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type disease around the Globe


http://madcowusda.blogspot.com/2013/11/aphis-finalizes-bovine-import.html


I AGREE WITH MR. BULLARD, it’s all about trade and money, BSE TSE PRION aka mad cow type disease and sound science there from, was thrown out the window by the USDA et al that fateful day in December 23, 2003, when the USDA lost it’s ‘gold card’ of supposedly being BSE FREE, (that was and still is a sad joke though), that’s when mad cow junk science was adopted by the USDA...

see why below...kind regards, terry


Monday, November 4, 2013

*** R-CALF Bullard new BSE rule represents the abrogation of USDA’s responsibility to protect U.S. consumers and the U.S. cattle herd from the introduction of foreign animal disease


http://madcowusda.blogspot.com/2013/11/r-calf-bullard-new-bse-rule-represents.html


*** Saturday, November 2, 2013 ***

Exploring the risks of a putative transmission of BSE to new species
 


Wednesday, September 25, 2013

Presence of subclinical infection in gene-targeted human prion protein transgenic mice exposed to atypical BSE


http://bse-atypical.blogspot.com/2013/09/presence-of-subclinical-infection-in.html
 


I ask Professor Kong ; Thursday, December 04, 2008 3:37 PM

Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment ''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....'' Professor Kong reply ;

.....snip

''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''

Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA END...TSS

Thursday, December 04, 2008 2:37 PM

"we have found that H-BSE can infect humans."

personal communication with Professor Kong. ...TSS

BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.

Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.


http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf


please see below from PRION2013 ;


*** This study imply the possibility that the novel BSE prions with high virulence in cattle will be emerged during intraspecies transmission.


AD.56: The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice

Kentaro Masujin, Naoko Tabeta, Ritsuko Miwa, Kohtaro Miyazawa, Hiroyuki Okada, Shirou Mohri and Takashi Yokoyama National Institute of Animal Health; Tsukuba, Japan

H-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE, and has been detected in several European countries, and North America. Transmission studies of H-type BSE led to the emergence of the classical BSE (C-BSE) phenotypes during passages in inbred wild type and bovinized PrP-overexpressing transgenic mice. In this study, we conducted serial passages of Canadian H-type BSE isolate in bovinized PrP-overexpressing transgenic mice (TgBoPrP). H-type BSE isolate was transmitted to TgBoPrP with incubation periods of 320 ± 12.2 d at primary passage. The incubation period of 2nd and 3rd passage were constant (~= 220 d), no clear differences were observed in their biological and biochemical properties. However, at the forth passage, 2 different BSE phenotypes were confirmed; one is shorter survival times (109 ± 4 d) and the other is longer survival times. TgBoPrP mice with longer incubation period showed the H-type phenotype of PrPsc profile and pathology. However, those of shorter incubation period were different phenotypes from previously existed BSE prions (C-BSE, L-type BSE, and H-type BSE).

*** This study imply the possibility that the novel BSE prions with high virulence in cattle will be emerged during intraspecies transmission.


http://www.prion2013.ca/tiny_uploads/forms/Scientific-Program.pdf


please see ;

Thursday, August 15, 2013

The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice


http://bse-atypical.blogspot.com/2013/08/the-emergence-of-novel-bse-prions-by.html


Sunday, September 1, 2013

*** Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy

We previously described the biochemical similarities between PrPres derived from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations suggest a link between these two uncommon prion phenotypes in a primate model (it is to note that such a link has not been observed in other models less relevant from the human situation as hamsters or transgenic mice overexpressing ovine PrP [28]). We speculate that a group of related animal prion strains (L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion diseases in humans with a type 2 PrPres molecular signature (and more specifically type 2B for vCJD)

snip...

Together with previous experiments performed in ovinized and bovinized transgenic mice and hamsters [8,9] indicating similarities between TME and L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME outbreaks in North America and Europe during the mid-1900s.


http://transmissiblespongiformencephalopathy.blogspot.com/2013/09/evaluation-of-zoonotic-potential-of.html
 


Monday, October 10, 2011

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

snip...

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

snip...


http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1



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 ;


http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html



Thursday, August 12, 2010

Seven main threats for the future linked to prions

First threat

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

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

Second threat

snip...


http://www.neuroprion.org/en/np-neuroprion.html

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/variably-protease-sensitive-prionopathy.html

http://prionopathy.blogspot.com/2010/11/variably-protease-sensitive-prionopathy.html
 
 


Friday, October 25, 2013

UK FSA TSE BSE Board meeting agenda: 5 November 2013


http://transmissiblespongiformencephalopathy.blogspot.com/2013/10/uk-fsa-tse-bse-board-meeting-agenda-5.html
 



Wednesday, November 13, 2013

CJD House of Commons Tuesday 12 November 2013


http://creutzfeldt-jakob-disease.blogspot.com/2013/11/cjd-house-of-commons-tuesday-12.html
 
 

*** 1998 MY SUBMISSION TO THE BSE INQUIRY ENGLAND ***

Sender: "Patricia Cantos"

To: "Terry S Singeltary Sr. (E-mail)"

Subject: Your submission to the Inquiry

Date: Fri, 3 Jul 1998 10:10:05 +0100

3 July 1998 Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.net Ref: E2979

Dear Mr Singeltary,

Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died.

As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments. Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD. I would refer you to the transcripts of evidence we have already heard which are found on our internet site at
http://www.bse.org.uk. Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on 0171 261 8332 should you have any queries.

Yours sincerely Patricia Cantos Families Team Leader Attachments TSS

==============

My neighbors Mom also died from CJD. She had been taking a nutritional supplement which contained the following; vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. As I said, this woman taking these nutritional supplements, died from CJD. The particular batch of pills that was located, in which she was taking, was tested. From what I have heard, they came up negative, for the prion protein. But, in the same breath, they said their testing, may not have been strong enough to pick up the infectivity. Plus, she had been taking these type pills for years, so, could it have come from another batch?


http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406

IPLEX, mad by standard process;

vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach.

also;

i will only list animal ingredients of the following Nutritional Supplements by only ONE company; Standard Process Co.

IPLEX; bovine EYE PMG Extract, veal bone PMG Extract, bovine liver powder, vaccuum dried porcine stomach, vacuum dried bovine adrenal, vacuum dried bovine kidney, bovine adrenal, vacuum dried BOVINE BRAIN, bone meal, vacuum dried veal bone.

A-FBetafood R vacuum dried bovine prostate, bovine liver powder, vacuum dried bovine kidney, bovine orchic glandular extract, bovine liver fat extract.

Arginex R bovine liver powder.

Adrenal, Desiccated TM Vacuum dried bovine adrenal.

Albaplex R bovine liver PMG Extract, vacuum dried bovine adrenal, bovine kidney PMF Extract, bovine thymus Cytosol Extract, bovine liver powder, bone meal, vacuum dried bovine kidney, veal bone meal.

Allerplex TM bovine lung PMF Extract, bovine adrenal PMF Extract, bovine liver fat extract (yakriton), bone meal, vacuum dried bovine kidney, vacuum dried veal bone.

Immuplex R Bovine liver PMG Extract, bovine liver powder, veal bone PMF Extract, bovine spleen PMF Extract, vacuum dried bovine and ovine spleen, bovine thymus PMF Extract, bovine thymus Cytosol Extract.

Vasculin R Bovine Heart PMG Extract, veal bone PMF Extract, bovine liver powder, vacuum dried porcine duodenum, bovine adrenal Cytosol Extract, vacuum dried bovine and ovine spleen.

Zypan R bovine pancreas Cytosol Extract, vacuum dried bovine and ovine spleen.

last i heard, they were getting sued;

Suit Filed Over Mad Cow Disclaimer

By Jason Hoppin The Recorder March 23, 2001

snip...see full text ;


http://creutzfeldt-jakob-disease.blogspot.com/2010/02/import-alert-17-04-bse-cjd-high-risk.html
 
 
snip...see full text ;
 
 
Sunday, November 10, 2013

LARGE CJD TSE PRION POTENTIAL CASE STUDY AMONG HUMANS WHO TAKE DEER ANTLER VELVET WILL BE ONGOING FOR YEARS IF NOT DECADES, but who's cares $


 http://creutzfeldt-jakob-disease.blogspot.com/2013/11/large-cjd-tse-prion-potential-case.html
 
 
Wednesday, March 20, 2013

GAO-13-244, Mar 18, 2013 Dietary Supplements FDA May Have Opportunities to Expand Its Use of Reported Health Problems to Oversee Product

From: Terry S. Singeltary Sr.

Sent: Tuesday, March 19, 2013 2:46 PM

To:
gomezj@gao.gov Cc: siggerudk@gao.gov ; youngc1@gao.gov ; oighotline@gao.gov http://transmissiblespongiformencephalopathy.blogspot.com/2013/03/gao-13-244-mar-18-2013-dietary.html
 
 
Tuesday, September 24, 2013

NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow TSE prion Contamination Suit Cethrin(R)

Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1 of 15


http://creutzfeldt-jakob-disease.blogspot.com/2013/09/nordion-us-inc-and-bioaxone-biosciences.html
 
 
Sunday, June 9, 2013

TSEAC March 14, 2013: Transmissible Spongiform Encephalopathies Advisory Committee Meeting Webcast


http://tseac.blogspot.com/2013/06/tseac-march-14-2013-transmissible.html
 
 
BSE INQUIRY WHITEWASH
 
BSE INQUIRY DFAs
 
 
 
Sunday, May 18, 2008


BSE Inquiry DRAFT FACTUAL ACCOUNT DFA


BSE Inquiry DRAFT FACTUAL ACCOUNTS DFA's


 
Sunday, May 18, 2008


BSE, CJD, and Baby foods (the great debate 1999 to 2005)

 
 

Sunday, May 18, 2008
 
MAD COW DISEASE BSE CJD CHILDREN VACCINES
 
 

LAYPERSON
 
 
MOM DOD DECEMBER 14, 1997 CONFIRMED HEIDENHAIN VARIANT CREUTZFELDT JAKOB DISEASE hvCJD...just made a promise to mom, never forget, never let them forget. ...TSS
 



 
Sent: Tuesday, December 03, 2013 4:49 AM
Subject: Written submission to House of Commons Science and Technology Committee inquiry

 

Parliament UK
Thank you for your written submission to the House of Commons Science and Technology Committee inquiry on Blood, tissue and organ screening.
We will be in touch if we have any further questions.