SaBTO Advisory Committee on the Safety of Blood, Tissues and Organs 2nd Public Meeting 27 October 2009

SaBTO

Advisory Committee on the Safety of Blood, Tissues and Organs

2nd Public Meeting

“Blood Donation – Selection, Deferral and Exclusion”

27 October 2009

Royal Horticultural Halls, London SW1P

At their inaugural meeting in January 2008, members of SaBTO decided that a public meeting should be held every year, focusing on a particular issue within the committee’s remit. The 2009 Public Meeting will focus on the issue of donor selection. Selection of donors is key to the delivery of a safe blood supply. Many prospective donors may be turned down for a variety of reasons, including age, sexual history and medical concerns. As a scientific advisory committee, SaBTO is concerned that exclusion or deferral of prospective blood donors is done for justifiable reasons and in the best interests of blood recipients.

The format of the afternoon will include an introduction to SaBTO and donor selection, and an open forum with the opportunity for the audience to comment and ask questions.

The committee hopes that the audience will reflect a wide range of stakeholders and interest groups. Should the event be oversubscribed, there will be a limit of one delegate per organisation. If you are interested in attending. please e-mail SaBTO@dh.gsi.gov.uk or telephone 020 7972 4750 by 13 October 2009 (this deadline has been extended). Please note that this event is free of charge for all delegates.

The Advisory Committee on the Safety of Blood, Tissues, and Organs (SaBTO) is a Non-Departmental Public Body, with an independent Chair and members selected by the Appointments Commission for their specific areas of expertise. SaBTO provides independent advice to the UK Government and the Devolved Administrations on the most appropriate ways to ensure the safety of blood, cells, tissues, and organs for transfusion/transplantation. SaBTO also provides advice on the microbiological safety of gametes and stem cells, and considers both risk assessment and risk management options for Ministers and UK Health Departments to consider.

Further detailed information about SaBTO and its remit can be found at


http://www.dh.gov.uk/ab/SaBTO/index.htm


http://www.dh.gov.uk/prod_consum_dh/groups/dh_digitalassets/@dh/@ab/documents/digitalasset/dh_104789.pdf


see other SaBTO meetings minutes here ;

2009 Download summary of seventh meeting, 14-15 July 2009 (PDF, 65K)

Download minutes of sixth meeting, 28 April 2009 (PDF, 104K)

Download summary of sixth meeting, 28 April 2009 (PDF, 64K)

Download minutes of fifth meeting, 20 January 2009 (PDF, 102K)

Download agenda for the fifth meeting, 20 January 2009 (PDF, 15K)

2008

snip...end


http://www.dh.gov.uk/ab/SaBTO/DH_089412



Tuesday, November 11, 2008 SaBTO Summary of 1st Public Meeting – variant CJD and blood Tuesday 21st October 2008, 2pm-4pm


http://vcjdblood.blogspot.com/2008/11/sabto-summary-of-1st-public-meeting.html



SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Minutes of the 99th meeting held on 14th December 2007

snip...

ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION 40.

The Chair explained that the purpose of the question and answer session was to give members of the public an opportunity to ask questions related to the work of SEAC. Mr Terry Singeltary (Texas, USA) had submitted a question prior to the meeting, asking: “With the Nor-98 now documented in five different states so far in the USA in 2007, and with the two atypical BSE H-base cases in Texas and Alabama, with both scrapie and chronic 14 © SEAC 2007 wasting disease (CWD) running rampant in the USA, is there any concern from SEAC with the rise of sporadic CJD in the USA from ''unknown phenotype'', and what concerns if any, in relations to blood donations, surgery, optical, and dental treatment, do you have with these unknown atypical phenotypes in both humans and animals in the USA? Does it concern SEAC, or is it of no concern to SEAC? Should it concern USA animal and human health officials?” 41.

A member considered that this question appeared to be primarily related to possible links between animal and human TSEs in the USA.

There is no evidence that sCJD is increasing in the USA and no evidence of any direct link between TSEs and CJD in the USA. Current evidence does not suggest that CWD is a significant risk to human health. There are unpublished data from a case of human TSE in the USA that are suggestive of an apparently novel form of prion disease with distinct molecular characteristics. However, it is unclear whether the case had been further characterised, if it could be linked to animal TSEs or if other similar cases had been found in the USA or elsewhere. In relation to the possible public health implications of atypical scrapie, H-type BSE and CWD, research was being conducted to investigate possible links and surveillance was in place to detect any changes in human TSEs. Although possible links between these diseases and human TSEs are of concern and require research, there is no evidence to suggest immediate public health action is warranted. The possible human health risks from classical scrapie had been discussed earlier in the meeting. Members noted that there are effective channels of discussion and collaboration on research between USA and European groups. Members agreed it is important to keep a watching brief on new developments on TSEs.

snip...



http://www.seac.gov.uk/minutes/99.pdf



http://seac992007.blogspot.com/2008/07/seac-draft-minutes-of-100th-meeting.html



http://seac992007.blogspot.com/




>>>There is no evidence that sCJD is increasing in the USA and no evidence of any direct link between TSEs and CJD in the USA.<<<

10 people killed by new CJD-like disease

Public release date: 9-Jul-2008 [ Print Article E-mail Article Close Window ]

Contact: Claire Bowles mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000076/!x-usc:mailto:claire.bowles@rbi.co.uk 44-207-611-1210 New Scientist

10 people killed by new CJD-like disease A NEW form of fatal dementia has been discovered in 16 Americans, 10 of whom have already died of the condition. It resembles Creutzfeldt-Jakob disease - with patients gradually losing their ability to think, speak and move - but has features that make it distinct from known forms of CJD.

No one yet knows how the disease originates, or under what conditions it might spread. Nor is it clear how many people have the condition. "I believe the disease has been around for many years, unnoticed," says Pierluigi Gambetti, director of the US National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland, Ohio. Cases may previously have been mistaken for other forms of dementia.

Since Gambetti's team wrote a paper describing an initial 11 cases referred to his centre between 2002 and 2006 (Annals of Neurology, vol 63, p 697), another five have come to light. "So it is possible that it could be just the tip of the iceberg," Gambetti says.

snip... see full text ;


http://www.eurekalert.org/pub_releases/2008-07/ns-tpk070908.php



Thursday, July 10, 2008

A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008


http://cjdmadcowbaseoct2007.blogspot.com/2008/07/novel-human-disease-with-abnormal-prion.html



Thursday, July 10, 2008

A New Prionopathy update July 10, 2008



http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html




Communicated by: Terry S. Singeltary Sr. <:flounder9@verizon.net>

[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]



http://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.html



http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963



There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.

He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm



http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf



2008

The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.



http://www.cjdfoundation.org/fact.html



Friday, October 23, 2009

Creutzfeldt-Jakob Disease Surveillance Texas Data for Reporting Years 2000-2008



http://cjdtexas.blogspot.com/2009/10/creutzfeldt-jakob-disease-surveillance.html



O.2.2

vCJD infection in an asymptomatic UK haemophilic patient

Alexander Peden1, Graham Fairfoul1, Suzanne Lowrie1, Linda McCardle1, Mark Head1, Seth Love2, Hester Ward1, Simon Cousens3, David Keeling4, Carolyn Millar5, FGH Hill6, James Ironside1 1University of Edinburgh, UK; 2Frenchay Hospital, Bristol, UK; 3London School of Hygiene and Tropical Medicine, UK; 4Churchill Hospital, Oxford, UK; 5Imperial College London, UK; 6Birmingham Children’s Hospital, Birmingham, UK

We describe a study of 17 UK patients with haemophilia considered to be at increased risk of vCJD through exposure to UK plasma products. 10 autopsy cases and 7 biopsy cases were analysed for disease- associated, protease-resistant prion protein (PrPres). The tissues available from each case were variable, ranging from a single biopsy sample to a wide range of autopsy tissues. A single specimen from the spleen of one autopsy case gave a strong positive result on repeated testing for PrPres by Western blot analysis. This tissue came from a 73 year-old male with no history of neurological disease, who was heterozygous (methionine/valine) at codon 129 in the prion protein gene. He had received over 9,000 units of Factor VIII concentrate prepared from plasma pools known to include donations from a vCJD-infected donor, and some 400,000 units not known to include donations from vCJD-infected donors. He had also received 14 units of red blood cells and had undergone several surgical and invasive endoscopic procedures. Estimates of the relative risks of exposure though diet, surgery, endoscopy, blood transfusion and receipt of UK plasma products suggest that by far the most likely route of infection was receipt of UK plasma products.

O.2.3

Detection of prion particles in body fluids of humans and animals

Detlev Riesner Institut fur Physikalische Biologie, Heinrich-Heine- Universitat Dusseldorf, Germany

A major structural difference between the cellular isoform of the prion protein PrPC and the pathogenic isoform PrPSc is the much higher state of molecular aggregation of PrPSc. PK-resistance as normally used for PrPSc-characterization is not reliably valid for all species, strains and sources of prions. The method of suface-FIDA (fluorescence-intensity distribution analysis) was developed avoiding PK-digestion and detecting specifically disease related PrP-aggregates (Birkmann et al 2007, J. Vet. Microbiol 123, 294-304). After partial purification PrP-aggregates are bound to a chip covered with the captureantibody SAF32, labeled with two types of antibodies against two different epitopes and carrying two different fluorescent dyes. A dual-color laser beam is scanning the chip surface, and the fluorescence signals are evaluated in respect to local coincidence, intensities and particle size. The method was applied to brain homogenate of sCJD-victims (post mortem), to CSF-samples of BSE-afflicted cattle (ante mortem) and blood plasma of scrapie sheep (ante mortem). Particles of PrP-aggregates could be detected in all samples, exhibiting a diameter range of 300 nm (optical resolution) to 1ƒÊm. PrP-aggregates were detected with 100% sensitivity in the sCJD-brain homogenate samples; studies on CSF are ongoing. PrP-aggregates were detected in CSF of BSE-cattle, but the number of samples was too little to evaluate the sensitivity. Only one antibody was available to detect scrapie-PrP-aggregates from blood plasma; the sensitivity of 60% will be improved in the ongoing experiments with a second antibody. PrP-aggregates can be used as seeds for fibril formation with recombinant PrP as template (Stohr et al., 2008, PNAS 105, 2409-14). This system will be used as amplification of the particle detection method.

O.2.4

Detection of prions in blood leucocytes

Linda A. Terry, Laurence Howells, Jeremy Hawthorn, Sally Everest, Sarah Jo Moore, Jane C. Edwards Veterinary Laboratories Agency, UK

Background: Infected human blood has been implicated in the iatrogenic transmission of vCJD in four reported cases. Experimental transmission studies have demonstrated that blood from scrapie and BSE infected sheep also contains infectivity. Rodent models of prion disease implicated both cellular and plasma fractions. However, direct detection of PrPsc from blood in the absence of in vitro amplification or bioassay has proved difficult. Methods for the direct detection of PrPsc in blood would be advantageous for the study of the pathogenesis of TSEs and as a basis for a blood test. Objectives: To develop a method for the direct detection of PrPsc in blood cells from scrapie and BSE infected sheep; to study the temporal distribution of PrPsc in blood and to determine the identity of the cells bearing prions in blood. Methods: Peripheral blood mononuclear cells (PBMC) were isolated from sheep naturally infected with scrapie or experimentally infected with BSE at the clinical stage of disease and from scrapie infected sheep from 3 months of age through to clinical end-point. PBMCs were tested for PrPsc content by a direct immunoassay based on the IDEXX CWD HerdChek kit. Different subsets of PBMCs were isolated by subset specific cell surface markers and magnetic bead separation and analysed for PrPsc content. Results: PrPSc was detected in 54% of sheep with clinical scrapie and 71% of sheep with clinical BSE. A longitudinal study of the temporal distribution of blood PBMC associated PrPsc showed that the detection rate increases during the course of disease and is more likely to be observed during the second half of the incubation period. Additionally detection is more likely in scrapie infected sheep if they carry the PRNP genotype of VRQ/VRQ. Cell separation studies showed that the PrPsc is associated with a specific cell subset implicating a subset of B lymphocytes. Discussion. This is the first report of the direct detection of PrPsc in cells isolated from sheep blood in the absence of in vitro amplification or bioassay. Since PrPsc can be detected from as early as 3 months of age in sheep naturally infected with scrapie, correlating with initial replication in the gut-associated lymphoid tissue, the assay could be the basis of a preclinical test. The identification of the cell subset carrying PrPsc progresses our understanding of the pathogenesis of the disease. However, it remains unclear whether this cell subset is responsible for the dissemination of prions or in clearance of circulating PrPsc. Funded by defra, UK and IDEXX.

O.2.6

Human urine and PrP

Silvio Notari1*, Liuting Qing1*, Ayuna Dagdanova1*, Sergei Ilchenko1, Mark E. Obrenovich1, Wen-Quan Zou1, Maurizio Pocchiari2, Pierluigi Gambetti1, Qingzhong Kong1, Shu G. Chen1 1Case Western Reserve University, USA; 2Istituto Superiore di Sanità, Italy

Background: The presence and the characteristics of prion protein (PrP) in human urine under normal conditions are controversial. Similarly, there are no definite data on the presence of infectivity in urine in the course of naturally occurring human prion diseases. Objectives: 1) To definitely determine the presence and characteristics of PrPC in normal urine. 2) To evaluate the prion infectivity in human urine in sporadic Creutzfeldt-Jakob disease (sCJD), we have carried out a set of bioassays in humanized transgenic mouse with urine samples collected from sCJD subjects. Methods: 1) Advanced mass spectrometry and experimental treatments have been used to demonstrate the presence, primary structure and posttranslational modifications of purified urinary PrPC (uPrP). 2) Bioassays were performed by intracerebral inoculation of 100 times concentrated and dialyzed urine, collected from three sCJD-MM1 cases to humanized transgenic mice and from appropriate controls. Results: We found that human urine contains significant amount of PrP (approximately 10 ng/ml) that is truncated with the major N-terminus at residue 112 as the PrPC fragment identified as C1, and it carries an anchor, which is soluble because likely lacks the phosholipid component. None of the humanized transgenic mice inoculated with sCJD concentrated urine had evidence of prion disease during a period of over 700 days (their normal life expectancy) leading to the conclusion that prion infectivity in sCJD urine, if present, must be less than 6 infectious units/100ml. Discussion: The issues raised in the discussion will include: 1) The origin of the truncated uPrP; 2) How the present data compare with the experimental studies published to date that indicate presence of infectivity; 3) The practical implications of our findings. *

These authors contributed equally

O.4.6

All separated components, prepared from BSE-infected sheep blood, are infectious upon transfusion

Sandra McCutcheon1, Anthony Richard Alejo Blanco1, Christopher de Wolf1, Boon Chin Tan1, Nora Hunter1, Valerie Hornsey2, Christopher Prowse2, Marc Turner2, Martin H Groschup3, Dietmar Becher4, Fiona Houston5, Jean C Manson1 1The Roslin Institute and R (D) SVS, University of Edinburgh, UK; 2Scottish National Blood Transfusion Service, UK; 3FLIFederal Research Institute for Animal Health, Germany; 4Micromun, Germany; 5University of Glasgow, UK

Background: The possibility that vCJD may be transmitted by blood transfusion is serious public health issue, of which 4 probable (3 clinical) cases have been attributed. Recently a case of asymptomatic vCJD infection was identified in a haemophiliac; following treatment with clotting factors from UK plasma pools. Sheep orally infected with BSE provide a suitable model, to assess vCJD infection in humans & risk reduction methods, as the distribution of PrPSc & infectivity in lymphoid tissues resembles that of vCJD patients.

Objectives: To determine qualitative and quantitative data on the changes in infectivity in blood and its clinically relevant components with time, to assess the effect of leucodepletion of such products and the potential for secondary transmission by blood transfusion.

Methods: We orally infected sheep with bovine BSE brain homogenate and collected two full-sized donations of whole blood, before the onset of clinical signs. The following components were transfused into naive recipients: whole blood, buffy coat and leucoreduced and non leucoreduced plasma, platelets and red cells. A sub sample of all components was inoculated into TgShpXI mice for determination of infectivity titers. A unit of whole blood from selected primary recipients was transfused into secondary recipients. We are creating a blood archive throughout this study.

Results: 33% of the infected donors have been confirmed as having BSE. We have 4 transmissions of BSE-infectivity following the transfusion of whole blood, buffy coat and plasma. Short incubation times were recorded in these recipients (468, 513, 567 and 594 days) & were similar to those seen in their respective donors (534, 628, 614 and 614 days). The donor of buffy coat also donated both leucodepleted and non leucodepleted blood components to other recipients.

Discussion: Our study will provide invaluable data on the safety of blood products, in relation to TSE infection, used in human medicine (DoH 007/0162)

O.8.1

Variant CJD and plasma products

Robert G. Will National CJD Surveillance Unit, Edinburgh, UK

Evidence from the Transfusion Medicine Epidemiology Review (TMER) project indicates that variant CJD is transmissible through transfusion of labile blood components. The question as to whether plasma products sourced from vCJD contaminated plasma pools has been addressed by a number of risk assessments, with conflicting conclusions. Recently a case of possible vCJD infection in an individual with haemophilia has been described and analysis has suggested that infection may have been related to prior treatment with vCJD implicated Factor VIII. The details of this case will be described together with an analysis of plasma product exposures in UK clinical cases of vCJD.

O.8.2

Blood safety: from screening tests to prion removal

Marc Turner Scottish National Blood Transfusion Service and Department of Haematology, Royal Infirmary, Edinburgh, UK

Although the number of clinical cases of variant CJD continues to fall, concern remains within UK and Western European Blood Services in relation to the risk of transmission of variant CJD due to the estimated prevalence of sub-clinical infection in the general population and the clinical cases of transmission of variant CJD prions by blood components and plasma products. The UK Advisory Committee on the Safety of Blood, Tissues and Organs (SaBTO) has considered a number of further precautionary measures including reducing exposure to blood transfusion, importation of blood components, implementation of prion assays and prion reduction for red cell concentrates. The latter two technologies are currently under independent evaluation and it is expected that contingent on the outcome of these an initial decision on whether or not to recommend implementation of these technologies will be made by SaBTO in Autumn 2009.

O.9.3

Updated risk assessment of variant Creutzfeldt-Jakob disease (vCJD) risks for recipients of plasma-derived blood clotting products in the U.S.

Hong Yang, Richard Forshee, Mark Walderhaug, Steven Anderson US Food and Drug Administration, USA

Background: A recent announcement by UK health authorities of a case of vCJD infection in a >70 year old person with hemophilia has prompted the US Food & Drug Administration (FDA) to re-evaluate vCJD risks in the U.S. via plasma-derived Factor VIII (pdFVIII) and to update its 2006 risk assessment. As of May 2009, confirmed vCJD deaths have occurred in persons who are homozygous methionine (MM) at codon 129 of the PRP gene. Several reports in the last few years have indicated signs of vCJD infection in persons of methionine-valine (MV) and homozygous valine (VV) genotypes. FDA updated risk assessment by assuming all genotypes are susceptible to vCJD and modeling the incubation periods for all three genotypes.

Objectives: To evaluate the vCJD risk for pdFVIII recipients with severe hemophilia and vonWillebrand diseases.

Methods: The model assumed equal susceptibility of three genotypes, a median incubation period of 12 years for the MM and 32 years for MV and VV genotypes, and vCJD infectivity was present in the blood of infected donors during the last 50% to 90% of incubation period. Model used statistical distributions for inputs including susceptibility to the disease, donation rates, frequency and duration of travel to the UK, France and other countries in Europe since 1980, the effectiveness of donor deferral policies and infectivity clearance during manufacturing processes.

Results: For severe hemophilia patients at the highest risk (prophylaxis, with inhibitor, with immune tolerance) the model estimated annual mean exposure to be ~7 x 10-8 iv ID50 or ~1 in 270,000 with the lower prevalence (4 per million) assumption, and ~1 x 10-4 iv ID50 or ~1 in 12,000 with the higher prevalence (1 per 4,225) assumption. Donor deferral policies reduce the risk by >92%.

Discussion: Due to limited data and knowledge of vCJD, the model estimates are uncertain. However, it suggests the risk is small, and donor deferral and manufacturing processes greatly reduce the risk.

P.10.7

Serial passage of sCJD in humanised transgenic mice indicates two major transmission strains associated with PrPSc of either type 1 or 2

Matthew Bishop, Robert Will, Enrico Cancellotti, Jean Manson University of Edinburgh, UK

Background: Questions remain about the aetiology of sporadic CJD and whether phenotypic variation is solely controlled by factors such as codon 129 genotype and biochemistry of PrPC. Variation in infective strain has not been clearly demonstrated in sCJD.

Objectives: By serial passage of sCJD in transgenic mice expressing human prion protein with MM, MV, and VV codon 129 genotypes we aimed to understand strain transmission characteristics for the three most commonly observed phenotypes of sCJD.

Methods: We performed intracerebral inoculation of humanised transgenic mice with brain homogenates derived from similar mice previously inoculated with frontal cortex from sCJD patients of subgroups MM1, MV2, and VV2. These mice were assessed for clinical TSE signs, for TSE vacuolation, and deposition of PrPSc.

Results: sCJD(MM1) passage via all mice showed transmission profiles similar to primary inoculation. sCJD(MV2) passage via HuMM and HuVV mice showed a transmission profile similar to primary inoculation. Passage via a HuMV mouse showed transmission properties similar to not only the primary inoculum but also sCJD(MM1). sCJD(VV2) passage via HuMV and HuVV mice showed transmission profiles similar to the primary inoculation. Passage via a HuMM mouse showed transmission properties similar to not only the sCJD(VV2) primary inoculum but also sCJD(MM1). Cluster analysis of the lesion profile data showed that three clusters seen after primary inoculation were reduced to two following second passage, identified by the biochemical type of PrPSc (1 or 2) found in the host mice.

Discussion: Serial passage of sCJD subgroups MM1, MV2, and VV2 shows that PrPSc type and mouse codon 129 genotype determine the secondary transmission profile, independently of the originating inoculum strain. There are associations between type 1 PrPSc and C129-Met, and type 2 PrPSc and C129-Val. This should allow us to investigate further the relationship between PrPSc, genotype, infection, and pathology.

P.5.1

Detection of cellular prion protein (PrPc) in plasma from healthy cynomolgus monkeys (Macaca fascicularis) and changes observed after BSE infection

Barbara Yutzy, Edgar Holznagel, Johannes Löwer Paul-Ehrlich-Institut, Germany

Background: Orally BSE-dosed cynomolgus monkeys represent a valuable model to examine the kinetic of blood infectivity and to assess the risk of blood-borne transmission of variant Creutzfeldt-Jacob disease (vCJD).

Methods: Blood samples were collected monthly from BSE-infected (n = 18) and non-infected female cynomolgus monkeys (n = 8) over a period of up to 9 years. PrPc concentrations were retrospectively analyzed in plasma samples by a dot blot assay and by a sandwich ELISA using a highly sensitive dissociation- enhanced lanthanide fluoro-immunoassay (DELFIA) for detection. Different blood preparation protocols were evaluated to obtain plasma.

Objective: To detect changes in the levels of soluble plasmaderived PrPc. Results: Different blood preparation protocols had a significant effect on the measured plasma PrPc concentrations. In non-infected macaques, concentrations of soluble, plasmaderived PrPc were at least 10-fold lower compared to plasma concentrations in healthy humans. Levels of plasma PrPc increased 6 – 12 months after experimental BSE infection, remained high during the asymptomatic phase, and dropped towards the clinical phase. Soluble, plasma-derived PrPc molecules were PK-sensitive in BSE-infected macaques.

Discussion: There is a species-specific difference in the PrPc concentrations between human and macaque. At least a part of the plasma-derived PrPc fraction originates from blood cells. Andfinally, BSE infection caused an increase in plasma PrPc levels during the asymptomatic phase of infection. Blood transfusion studies have been initiated to examine whether these PK-sensitive PrP molecules carry infectivity.



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



Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009



http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html



2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006



http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html



Tuesday, August 11, 2009

Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants



http://creutzfeldt-jakob-disease.blogspot.com/2009/08/characteristics-of-established-and.html



Saturday, June 13, 2009

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009



http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html




Friday, October 23, 2009

Creutzfeldt-Jakob Disease Surveillance Texas Data for Reporting Years 2000-2008



http://cjdtexas.blogspot.com/2009/10/creutzfeldt-jakob-disease-surveillance.html




Sunday, May 17, 2009

WHO WILL WATCH THE CHILDREN ? SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE



http://downercattle.blogspot.com/2009/05/who-will-watch-children.html



http://downercattle.blogspot.com/




Sunday, September 6, 2009

MAD COW USA 1997 SECRET VIDEO


http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html



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


http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html



DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN see video


http://maddeer.org/video/embedded/prusinerclip.html



Saturday, August 22, 2009

FREE Kim Min-sun, she is correct about mad cow fears from USDA BEEF


http://usdavskorea.blogspot.com/2009/08/free-kim-min-sun-she-is-correct-about.html



Office of Inspector General Semiannual Report to Congress FY 2007 - 2nd Half

Two Texas Companies Sentenced and Fined for Misbranding Meat Products In April 2007, two closely held and related Texas companies pled guilty in Federal court and were sentenced to 12 months of probation and ordered to pay $10,250 in fines for misbranding meat products. One of the companies sold adulterated meat products to a retail store in New Mexico. Additionally, portions of the invoices failed to properly and consistently identify the meat products as being from cattle more than 30 months old at time of slaughter. This information is required to be disclosed because of bovine spongiform encephalopathy (BSE, or "mad cow disease") concerns. No adulterated meat reached consumers.


http://www.usda.gov/oig/webdocs/sarc071212.pdf



Saturday, August 29, 2009

FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009


http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html



Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009


http://madcowfeed.blogspot.com/2009/09/foia-request-on-feed-recall-product.html



THIS recall is not confusing ;

10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

___________________________________

PRODUCT

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

CODE

Cattle feed delivered between 01/12/2007 and 01/26/2007

RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.

REASON

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

42,090 lbs.

DISTRIBUTION

WI

___________________________________

PRODUCT

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

CODE

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

REASON

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

9,997,976 lbs.

DISTRIBUTION

ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html


NEW URL


http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm



Thursday, March 19, 2009

MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL


http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html



Sunday, October 18, 2009

Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009


http://madcowfeed.blogspot.com/2009/10/wisconsin-firm-recalls-beef-tongues.html



Thursday, October 15, 2009

Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009


http://madcowfeed.blogspot.com/2009/10/nebraska-firm-recalls-beef-tongues-that.html



Tuesday, July 14, 2009

U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST

WHERE did we go wrong $$$


http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html



Sunday, December 28, 2008

MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy


http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html



Wednesday, August 20, 2008

Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ? August 20, 2008


http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html



Monday, May 11, 2009

Rare BSE mutation raises concerns over risks to public health


http://bse-atypical.blogspot.com/2009/05/rare-bse-mutation-raises-concerns-over.html





Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518