Wednesday, February 1, 2012

CJD and PLASMA / URINE PRODUCTS EMA Position Statements Alberto Ganan Jimenez, European Medicines Agency PDA TSE Safety Forum, 30 June 2011

Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety




PDA: A Global Association


CJD and PLASMA / URINE PRODUCTS


CJD and ATMPs


EMA Position Statements


Alberto Ganan Jimenez, European Medicines Agency


TSE Safety Forum, 30 June 2011








EMA guidance on CJD and medicinal products


EMA Position Statement on plasma/urine products 2011


- Human TSEs current status


- Plasma products: Recommendations


- Urine products: Recommendations


EMA Position Statement on ATMPs





EMA guidance on CJD and medicinal products





CHMP Position Statements:




CHMP Position Statement on CJD and plasma-derived and urine-derived

medicinal products (2011) (EMA/CHMP/BWP/303353/2010)




CAT/CHMP Position Statement on CJD and advanced therapy medicinal

products (2011) (EMA/CHMP/BWP/353632/2010)




Guidelines:




Investigation of manufacturing processes for plasma-derived medicinal

products with regards to vCJD risk (2004) (CPMP/BWP/5136/03)




Warning on transmissible agents in summary of product characteristics

(SmPC) and package leaflets for plasma-derived medicinal products (2003)

(CPMP/BPWP/BWP/561/03)




Workshops:




Report on Expert Workshop on CJD risk and urine-medicinal products (07-2007)





EMA Guidance on CJD / medicinal products




1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011




CHMP Position Statement

on plasma-derived

and urine-derived

medicinal products

Guid. on investigation

of manufacturing

processes for plasma

products with

regard to vCJD risk

Expert meetings at EMA

CJD related CHMP/CAT Position

Statement on ATMPs

Guid. on Warning

statements transmissible

agents SmPC / PL





Initial

Publication

(CPMP/201/98)

Rev. 1

(CPMP/BWP

/2879/02)

Rev. 2 Rev. 3

(CHMP/BWP/

303352/2010)

Initial

Publication

(CPMP/BWP/

353632/2010)

Initial

Publication

(CPMP/BWP/5136/03)

Initial

Publication

(CPMP/BPWP/BWP

561/03)

Under Revision





EMA Position Statement on plasma/urine products 2011




- Human TSEs current status




sCJD, gCJD, iCJD





Epidemiological evidence does not support transmission of s, g, iCJD by blood, blood components or plasma products




No case of sCJD, gCJD, iCJD has been causally linked to prior treatment with plasma products or blood transfusion




* It cannot formally excluded the possibility of blood transmission in a small number of cases based:



* -limitations in statistical power of epidemiological studies



* -limited experimental evidence of peripherical tissue infectivity in various subtypes of sCJD



* -potential diagnostic confusion



* Cases of sCJD with treatment of infertility have not been identified,



* -uncertainty about the validity of this observation



* -strength of evidence of exclusion transmission by urine products is less secure




vCJD



Number of cases:








image






UK France Ireland Italy USA Canada Saudi Arabia Japan Netherlands Portugal Spain Taiwan Total






Mar-11 175 25 4 2 3 2 1 1 3 2 5 1 224





Jun-04 146 6 1 1 1 1 156





Source NCJDRSU-University of Edinburgh














Still uncertainties on the number of cases of vCJD that will occur




UK figures for the quarterly incidence of deaths may indicate that vCJD incidence in the UK is in decline -> caution interpretation




All definitive and probable cases are Met/Met Codon 129 PrP gene




In 2009, one possible case vCJD Met/Val but could not be confirmed as autopsy was not performed









vCJD





Importance of estimation of vCJD prevalence with respect to any potential

secondary transmission while individuals are in the incubation phase



Estimated prevalence of the disease in different UK studies:



- 267 infections / million (95% CI [49-692]) (Hilton et al. 2004))



- 0-113 (95%; 1961-1995 birth cohort) (Clevlew et al. 2009)



- 109 infection / million (95% CI [3-608]) (De Marco et al. 2010)





Infectivity/ transmissibility via blood





Animal blood




Low levels of infectivity found in the blood of rodents infected with

TSE agents.




Half of infectivity is in cellular components, mainly buffy coat




Orally infected sheep or natural scrapie can be transmitted by blood

transfusion in the majority of cases collected half way through incubation period




Experiments on BSE infected sheep demonstrate that all blood components,

incl. plasma contain transmissible TSE agent and remain infectious

after leucoreduction






Human blood




Strong evidence that vCJD is transmissible through blood transfusion




Four instances of secondary transmission in blood transfusion from UK donors




- received non-leucodepleted transfusions from healthy donors that

developed vCJD 17-40 months later




- 3 recipients developed vCJD (6.5-8.5 years later)




- 1 heterozygous case died 5 yr. later by unrelated causes

and tested positive for PrPTSE in spleen




Infectivity in human blood of vCJD cases was not detected using the

methods capable of detecting in peripheral tissues (e.g. tonsil, spleen)





Human blood




Warning that some plasma derived products might contain

residual prion infectivity




Presumed case of asymptomatic vCJD infection identified in an elderly

haemophilic patient:




• heterozygous Met/Val.




• had received large quantities of intermediate purity UK-sourced factor VIII




• at least one batch included some units manufactured from a plasma

from a donor that later developed CJD




Risk assessment suggest that the most likely route of infection was the

reception of plasma products




These findings highlight the importance of national databases of blood

donors and the maintenance of an effective traceability donor/receptor system




donor <-> receptor





EMA Position Statement on plasma/urine products 2011





- Plasma products: Recommendations






Donor selection





Donor selection criteria should be implemented to minimise

the risk of developing CJD





sCJD, gCJD, iCJD





Donor selection criteria:





deferral of donors who might be at higher risk of developing CJD

(family history of TSE, corneal or dura mater graft receptors,

treated patients with medicines derived from human pituitary glands)





Donor exclusion criteria






vCJD





Country based donor selection criteria based on the identification

of high risk donors





UK





- donor exclusion who have spent long periods in UK





- recommended 1 year or more cumulative UK residence

between 1980-1996





- member States (MS) may define stricter limits but will accept

plasma products from other MS that at least 1 yr time limit is applied




France and other BSE-exposed MS





-not recommended exclusion of donors that spent cumulative periods

in these countries





• Additional further deferral criteria may be recommended

by MS






weighing the odds




safety impact vs donation volumes





Batch recall of plasma products




sCJD, gCJD, iCJD




Precautionary recalls for batches when post donation reports of CJD

or risk factors donors is NOT recommended




- not justified based on current epidemiological evidence




- risk of shortages of plasma products




vCJD




Maintenance of recommendation of batch recall where a donor to

a plasma pool subsequently develops vCJD.





vCJD




Maintenance of recommendation of batch recall where a donor to

a plasma pool subsequently develops vCJD




It applies for plasma products used as such or as excipients




The risk of infectivity transmission of albumin is particularly low




In case of albumin used as excipient or during manufacture

product recall should be considered




However, a case-by-case risk analysis taking into account the prion reduction

data and amount of albumin use could justify not needing a recall.




Plasma products used in manufacture of other medicinal products:

case–by-case consideration depending on nature, amount,

point of use in the manufacturing process.





Leucoreduction





Not appropriate to recommend the introduction of

leucoreduction steps at this moment in plasma for fractionation




• At the moment, the benefit of leucoreduction to improve safety of

plasma not demonstrated.





• UK implemented in 1999 in transfusion.





SCMPMD opinion is that:




Transfusion: might be a precautionary step




Fractionation: no compelling scientific evidence to introduce to

reduce vCJD transmission




Studies in infected hamsters showed only 42-72% reduction of

infectivity





No effective complete removal in blood of BSE sheeps






Affinity filters





The efficacy for introduction of affinity media / filter is still

under investigation.





Animal studies showed clearance capabilities of filter, resin matrix.





Oct 09 SaBTO stated that:





there was sufficient evidence of infectivity reduction by affinity

ligand filters





recommended use in children born since 1-Jan-1996

subject to satisfactory completion PRISM clinical trial





Data on prion binding capacity of an affinity ligand chromatography

step in a plasma product has been published. Further evaluation is

considered needed prior to conclusions can be drawn on possible

efficacy.






Manufacturing processes






Recommendation of estimation the potential

to reduce infectivity of manuf. processes





Stepwise approach based on:





Available relevant published data





Product specific investigational studies

on key steps





using biochemical assays is sufficient if

correlation with infectivity data has been

established







Warning Statements on CJD and plasma products






Standard texts for Warning Statements (WS) on transmissible agents

in the Summary of Product Characteristics (SmPC) and

Package leaflet (PL) for blood products.




In 2003, it was not recommended to include a specific reference to CJD

as this would give impression of increased concern about potential

transmissibility by plasma products.




In 2011, this recommendation is reconfirmed




CJD risk is already covered in the general texts:





image






“Standard measures to prevent infections resulting from the use of medicinal products prepared from human blood or plasma include selection of donors, screening of individual donations and plasma pools for specific markers of infection and the inclusion of effective manufacturing steps for the inactivation removal of viruses. Despite this, when medicinal products prepared from human blood or plasma are administered, the possibility of transmitting infective agents CANNOT BE TOTALLY EXCLUDED. This also applies to unknown or emerging viruses and other pathogens.







Overview







EMA Position Statement on plasma/urine products 2011







- Urine products: Recommendations







TSE Urine: Current status







Presence of PrP in human urine has been reported. No evidence

that infectivity is present.






Low levels of TSE infectivity detected in urine in animal models

by several groups (incl. scrapie-infected rodents, deer with CWD).






Epidemiological evidence (>25 yrs) of use of urine products does not

suggest a risk form sCJD.






No epidemiological evidence of CJD/vCJD transmission by urine

products








Urine: Recommendations







Urine to be collected from countries where there is TSE surveillance

system, unless otherwise justified.






Use of exclusion criteria in donor selection is encouraged.

Feasible to apply donor selection in small well-defined donor

population






• Hormones: already in place by some manufacturers






• Urokinase: more difficult to apply






Same exclusion criteria for CJD/vCJD as for plasma donors

Manufacturers should follow up the donor criteria at defined intervals







Manufacturers are required to estimate the

potential reduction capacity of their manufacturing

processes






Same general stepwise approach as for plasma

-Extrapolation of results on investigational studies

of certain steps of plasma products is not justified






-Investigational studies should address prion:






- potential accumulation in chromatographic columns






- batch-to-batch contamination due to carry over






-If reduction capacity is limited, manufacturers should

consider including additional steps






Record keeping for traceability encouraged

when possible to trace back to donor






Overview






EMA Position Statement on ATMPs






Position Statement on CJD / ATMPs






• ATMPs: gene therapy, cell therapy and tissue engineering

medicinal products





Gene therapy

medicinal

products




Cell based medicinal

products from

autologous donors





- No specific considerations,

- Risk assessment for potential TSE

contamination with components of

human origin used as excipients raw

materials






Position Statement on CJD / ATMPs






Cell based medicinal

products from

allogeic donors






- Case-by-risk assessment





- Normally there isn’t any TSE infectivity

reduction step in the manufacturing process







- TSE Safety of the products mainly

dependent on donor selection:







- Exclusion criteria for human tissues and cells Dir:

2006/17







- Where blood cells are used -> exclusion criteria on

donor selection and TSE in Directive 2004/33/EC apply







- Additional requirements may be implemented at the

level of MS taking into account scientific evidence and

impact on donated tissues/cells.






Acknowledgements







J. Blümel (Chair Blood/Urine) – PEI, DE






S. Ruiz (Chair ATMPs) – AEMPS, ES






K. Kluge – Bfarm, DE






J. Ironside - National CJD Surveillance Unit, UK






V. Irwin – IMB, IE






S. Janssen – RIVM, NL






M. Pocchiari – ISS, IT






M. Martin – AFSSAPs, FR






P. Minor – NIBSC, UK





G. Silvester – EMA, EU





A. Thomas – MHRA, UK





J.-H. Trouvin (Chair of EMA BWP) - AFSSAPS, FR






R. Will - National CJD Surveillance Unit, UK







snip...end...tss





Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety








PDA: A Global Association






CJD and PLASMA / URINE PRODUCTS






CJD and ATMPs







EMA Position Statements







Alberto Ganan Jimenez, European Medicines Agency







TSE Safety Forum, 30 June 2011














Greetings again Sporadic CJD victims and families around the globe.








here, we see the writing on the wall. the what if’s, again ???






now this report does mention sporadic CJD. but nothing about new science showing links between atypical BSE and atypical Scrapie with sporadic CJD, and the fact that atypical BSE much more virulent, and that it has a 50% shorter incubation period than typical BSE, and the link to sporadic CJD ??? this should be very disturbing to all. ...







To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.












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...















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...


















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 ;





















Thursday, January 26, 2012






The Risk of Prion Zoonoses






Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

















Thursday, January 26, 2012






Facilitated Cross-Species Transmission of Prions in Extraneural Tissue







Science 27 January 2012:




Vol. 335 no. 6067 pp. 472-475





DOI: 10.1126/science.1215659














FC5.1.1





Transmission Results in Squirrel Monkeys Inoculated with Human sCJD, vCJD, and GSS Blood Specimens: the Baxter Study






Brown, P1; Gibson, S2; Williams, L3; Ironside, J4; Will, R4; Kreil, T5; Abee, C3 1Fondation Alliance BioSecure, France; 2University of South Alabama, USA; 3University of Texas MD Anderson Cancer Center, USA; 4Western General Hospital, UK; 5Baxter BioSience, Austria






Background: Rodent and sheep models of Transmissible Spongiform Encephalopathy (TSE) have documented blood infectivity in both the pre-clinical and clinical phases of disease. Results in a (presumably more appropriate) non-human primate model have not been reported.






Objective: To determine if blood components (red cells, white cells, platelets, and plasma) from various forms of human TSE are infectious.






Methods: Blood components were inoculated intra-cerebrally (0.1 ml) and intravenously (0.5 ml) into squirrel monkeys from 2 patients with sporadic Creutzfeldt- Jakob disease (sCJD) and 3 patients with variant Creutzfeldt-Jakob disease (vCJD). Additional monkeys were inoculated with buffy coat or plasma samples from chimpanzees infected with either sCJD or Gerstmann-Sträussler-Scheinker disease (GSS). Animals were monitored for a period of 5 years, and all dying or sacrificed animals had post-mortem neuropathological examinations and Western blots to determine the presence or absence of the misfolded prion protein (PrPTSE).






Results: No transmissions occurred in any of the animals inoculated with blood components from patients with sporadic or variant CJD. All donor chimpanzees (sCJD and GSS) became symptomatic within 6 weeks of their pre-clinical phase plasmapheresis, several months earlier than the expected onset of illness. One monkey inoculated with purified leukocytes from a pre-clinical GSS chimpanzee developed disease after 36 months.






Conclusion: No infectivity was found in small volumes of blood components from 4 patients with sporadic CJD and 3 patients with variant CJD. ***However, a single transmission from a chimpanzee-passaged strain of GSS shows that infectivity may be present in leukocytes, and the shock of general anaesthesia and plasmspheresis appears to have triggered the onset of illness in pre-clinical donor chimpanzees.









Saturday, September 5, 2009






TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS







snip...
















Wednesday, June 29, 2011






TSEAC Meeting August 1, 2011 donor deferral Saudi Arabia vCJD risk blood and blood products











P.9.21 Molecular characterization of BSE in Canada





Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada





Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.





Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.






Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis. Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.






Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *** It also suggests a similar cause or source for atypical BSE in these countries.












Saturday, July 23, 2011






CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE











Saturday, November 6, 2010





TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU






Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation














Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>






Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)











October 2009 O.11.3 Infectivity in skeletal muscle of BASE-infected cattle







Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1, Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3, Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5, Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS Torino, Italy; 5University of Verona, Italy



Background: BASE is an atypical form of bovine spongiform encephalopathy caused by a prion strain distinct from that of BSE. Upon experimental transmission to cattle, BASE induces a previously unrecognized disease phenotype marked by mental dullness and progressive atrophy of hind limb musculature. Whether affected muscles contain infectivity is unknown. This is a critical issue since the BASE strain is readily transmissible to a variety of hosts including primates, suggesting that humans may be susceptible.





Objectives: To investigate the distribution of infectivity in peripheral tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and i.p. with 10% homogenates of a variety of tissues including brain, spleen, cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from cattle intracerebrally infected with BASE. No PrPres was detectable in the peripheral tissues used for inoculation either by immunohistochemistry or Western blot.






Results: Mice inoculated with BASE-brain homogenates showed clinical signs of disease with incubation and survival times of 175±15 and 207±12 days. Five out of seven mice challenged with skeletal muscle developed a similar neurological disorder, with incubation and survival times of 380±11 and 410±12 days. At present (700 days after inoculation) mice challenged with the other peripheral tissues are still healthy. The neuropathological phenotype and PrPres type of the affected mice inoculated either with brain or muscle were indistinguishable and matched those of Tgbov XV mice infected with natural BASE.






Discussion: Our data indicate that the skeletal muscle of cattle experimentally infected with BASE contains significant amount of infectivity, at variance with BSE-affected cattle, raising the issue of intraspecies transmission and the potential risk for humans. Experiments are in progress to assess the presence of infectivity in skeletal muscles of natural BASE.



















18.173 page 189





Experimental Challenge of Cattle with H-type and L-type Atypical BSE






A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada






Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.






Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE. Results and






Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types.






Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.



















Saturday, November 19, 2011






Novel Prion Protein in BSE-affected Cattle, Switzerland













Saturday, December 3, 2011






Isolation of Prion with BSE Properties from Farmed Goat Volume 17, Number 12—December 2011


















Saturday, June 25, 2011





Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque




"BSE-L in North America may have existed for decades"













Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.





snip...






The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...















14th ICID International Scientific Exchange Brochure -





Final Abstract Number: ISE.114





Session: International Scientific Exchange






Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009






T. Singeltary






Bacliff, TX, USA






Background:






An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.







Methods:






12 years independent research of available data






Results:






I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.






Conclusion:





I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.













see where sporadic CJD cases went from 28 cases in 1990, to a high in 2008 of 88 cases of sporadic CJD, then 2009 dropped back a bit to 78 cases, and then in 2010 the sporadic CJD cases were back up to 84 cases. with a small rise in GSS and Familial cases of human TSE as well, through that time period ???

CJD Figures

These figures show the number of suspect cases referred to the NCJDRSU in Edinburgh, and the number of deaths of definite and probable cases in the UK, from 1 January 1990 up to 4th January 2012
see here ;
SO, we have atypical BSE and atypical Scrapie cases rising, we have sporadic CJD now linked to atypical BSE cases and atypical scrapie cases, and this report does not mention that $$$
BSe, and politics as usual $$$

2011 Monday, September 26, 2011







Tuesday, November 08, 2011




Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008




Vol. 37, No. 3-4, 2011 Original Paper Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.












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






























full text with source references ;












CANADA CJD UPDATE 2011





CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011






3. Final classification of 49 cases from 2009, 2010, 2011 is pending.






snip...













USA 2011









USA






National Prion Disease Pathology Surveillance Center






Cases Examined1






(November 1, 2010)





Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD






1996 & earlier 51 33 28 5 0 0





1997 114 68 59 9 0 0





1998 87 51 43 7 1 0





1999 121 73 65 8 0 0





2000 146 103 89 14 0 0





2001 209 119 109 10 0 0





2002 248 149 125 22 2 0





2003 274 176 137 39 0 0





2004 325 186 164 21 0 13





2005 344 194 157 36 1 0





2006 383 197 166 29 0 24





2007 377 214 187 27 0 0






2008 394 231 205 25 0 0






2009 425 258 215 43 0 0






2010 333 213 158 33 0 0






TOTAL 38315 22656 1907 328 4 3






1 Listed based on the year of death or, if not available, on year of referral;





2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;






3 Disease acquired in the United Kingdom;






4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;






5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;






6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.















Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date. sporadic CJD is on a steady rise, and has been since 1996.






I also urge you to again notice these disturbing factors in lines 5 and 6 ;






5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;






6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.








========end=====tss=====2011






Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)






(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)










THE steady rise of sporadic CJD cases in Canada AND USA, with many unusual cases of ''PENDING CLASSIFICATIONS" which have been pending now FOR 3 YEARS. HOW long can this cover-up continue $$$









The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.












SEE FULL TEXT AND MORE HERE ;









Saturday, March 5, 2011






MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA













Tuesday, November 08, 2011






Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance?






A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011






Original Paper






Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.
















Tuesday, January 31, 2012






MM2-thalamic Creutzfeldt-Jakob disease: neuropathological, biochemical and transmission studies identify a distinctive prion strain












Monday, January 30, 2012




The First Report of a Patient with Probable Variant Creutzfeldt-Jakob Disease in Turkey





Dement Geriatr Cogn Dis Extra. 2011 Jan-Dec; 1(1): 429–432. Published online 2011 December 24. doi: 10.1159/000332024 PMCID: PMC3265806












Thursday, December 08, 2011





A case of Iatrogenic Creutzfeldt Jakob Disease (iCJD) in a patient who had received a German-manufactured human dura mater graft 23 years ago






Monday, December 12, 2011



Second iatrogenic CJD case confirmed Korea


http://creutzfeldt-jakob-disease.blogspot.com/2011/12/second-iatrogenic-cjd-case-confirmed.html







Saturday, December 18, 2010





First probable human case of mad cow disease in Taiwan was listed posthumously 2010/12/18 21:14:28












Thursday, November 25, 2010





Probable variant Creutzfeldt-Jakob disease in Asia: A case report from Taiwan and review of two prior cases












Tuesday, January 5, 2010





JOINT STATEMENT FROM USTR, USDA ON TAIWAN'S ACTIONS TO UNJUSTIFIABLY RESTRICT U.S. BEEF IMPORTS IN VIOLATION OF OUR BILATERAL AGREEMENT Release No. 0002.10 Contact: USTR, Nefeterius McPherson (202) 395-3230 USDA, Caleb Weaver (202) 720-4623












Tuesday, December 29, 2009





Taiwan to resume USA beef ban over mad cow disease threat














Friday, January 20, 2012





South Korea Lifts Canadian Beef Ban














Saturday, December 18, 2010





OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011












The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III.




Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.














Saturday, January 21, 2012






Quick facts about mad cow disease (all the facts, to date)










CWD TSE PRION UPDATE JANUARY 26, 2012







Tuesday, January 24, 2012





CWD found in two free-ranging deer from Macon County Missouri













Tuesday, December 20, 2011





CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

















Monday, January 16, 2012





9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD














Wednesday, January 04, 2012





CWD NEBRASKA NGPC 26 DEER CARCASSES TESTED POSITIVE BUFFALO, CUSTER AND HOLT COUNTIES DURING NOVEMBER HUNT















Saturday, December 31, 2011





Depopulation Plan Being Developed for Captive Deer Facility in Macon County after second CWD positive confirmation















Wednesday, December 21, 2011






CWD UTAH San Juan deer hunting unit















Monday, November 14, 2011






WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wyoming-creutzfeldt-jakob-disease-cwd.html

Wednesday, November 16, 2011













Sunday, January 22, 2012





Chronic Wasting Disease CWD cervids interspecies transmission














Thursday, December 29, 2011










Aerosols An underestimated vehicle for transmission of prion diseases?











PRION www.landesbioscience.com please see more on Aerosols and TSE prion disease here ;. ...
























Wednesday, January 18, 2012






BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE






February 1, 2012




















Thursday, January 26, 2012






The Risk of Prion Zoonoses





Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167







Thursday, January 26, 2012





Facilitated Cross-Species Transmission of Prions in Extraneural Tissue




Science 27 January 2012:






Vol. 335 no. 6067 pp. 472-475
DOI: 10.1126/science.1215659











Sunday, January 29, 2012















Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Dr. Detwiler














Dr. Detwiler published Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Forum\Presentations TSE\ Page 33 and 34 of 44 ;













































Wednesday, February 1, 2012









Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Update on CJD and VCJD Transmission RG Will

http://www.pda.org/
http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/prion-disease-risks-in-21st-century.html
FDA NVCJD BLOOD LATEST RECALLS

PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-0576-7; b) Red Blood Cells, Recall # B-0577-7; c) Fresh Frozen Plasma, Recall # B-0578-7; d) Recovered Plasma, Recall # B-0579-7 CODE a) Units: 4588939, 4685381,4800041, 4892978, 4882799, 4883439, 4956157; b) Unit: 4662465; c) Units: 4800041, 4883439; d) Units: 4588939, 4662465, 4685381, 4800041, 4892978, 4882799, 4956157 RECALLING FIRM/MANUFACTURER Recalling Firm: Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma City, OK, by fax on March 11, 2005. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 17 units DISTRIBUTION OK, MS, MI, CA, and Switzerland ______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-0580-7; b) Recovered Plasma, Recall # B-0581-7 CODE a) and b) Unit: 5346932 RECALLING FIRM/MANUFACTURER Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma City, OK, by fax on October 27, 2005. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION OK and Switzerland

______________________________ PRODUCT a) Red Blood Cells Leukocytes, Recall # B-0582-7; b) Recovered Plasma, Recall # B-0583-7 CODE a) and b) Unit: 5208304 RECALLING FIRM/MANUFACTURER Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma City, OK, by fax on April 20, 2006. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased riskfor variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION OK and Switzerland

______________________________ PRODUCT Source Plasma, Recall # B-0585-7 CODE Units: 02JWIB9722, 02JWIC0263, 02JWIC0607, 02JWIC4253, 02JWIC4904, 02JWIC5216, 02JWID2018, 02JWID2958, 02JWID3310, 02JWID8505, 02JWID8842, 02JWID9390, 02JWID9844, 02JWIE0468, 02JWIE0836, 02JWIE1435, 02JWIE1812, 02JWIE2609, 02JWIE3289, 02JWIE3887, 02JWIE4309, 02JWIE4818, 02JWIE5277, 02JWIE5825, 03JWIA0857, 03JWIA1249, 03JWIA1850, 03JWIA2192, 03JWIA2825, 03JWIA3180, 03JWIA3724, 03JWIA4092, 03JWIA4691, 03JWIA5042, 03JWIA5586, 02JWIC1157, 02JWIC1458, 02JWIC2095, 02JWIC2551, 02JWIC3031, 02JWIC3491, 02JWIC3975, 02JWIC6689, 02JWIC7051, 02JWIC7609, 02JWIC7898, 02JWIC8547, 02JWIC8906, 02JWIC9494, 02JWIC9793, 02JWID0630, 02JWID1144, 02JWID1592, 02JWID3884, 02JWID4247, 02JWID4827, 02JWID5189, 02JWID5713, 02JWID6578, 02JWID6926, 02JWID7624, 02JWID7970 RECALLING FIRM/MANUFACTURER BioLife Plasma Services L.P., Janesville, WI, by fax on April 7, 2003. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 62 units DISTRIBUTION MI and Austria

______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-0586-7; b) Recovered Plasma, Recall # B-0587-7 CODE a) and b) Unit: 4499508 RECALLING FIRM/MANUFACTURER Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma City, OK, by fax on February 27, 2006. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION OK and Switzerland

______________________________

PRODUCT a) Red Blood Cells, Leukocytes Reduced, Recall # B-0644-7; b) Recovered Plasma, Recall # B-0645-7 CODE a) and b) Units: 5219381, 4759725 RECALLING FIRM/MANUFACTURER Oklahoma Blood Institute, Sylvan N. Goldman Center, Oklahoma City, OK, by facsimile on December 3, 2005 or by electronic notification on December 4, 2005. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 4 units DISTRIBUTION OK, VA, and Switzerland

______________________________

END OF ENFORCEMENT REPORT FOR JANUARY 17, 2007

###

http://www.fda.gov/bbs/topics/enforce/2007/ENF00987.html


----- Original Message ----- From: Terry S. Singeltary Sr. To: FREAS@CBER.FDA.GOV Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov Sent: Wednesday, November 29, 2006 1:24 PM Subject: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION]

November 29, 2006

Greetings FDA, DHH, Dr. Freas, and Dr. Harvey et al,

a kind and warm Holiday Greetings to you all.

i kindly wish to submit the following to the TSE advisory committee for the meeting December 15, 2006, about the assessment for potential exposure to vCJD in human plasma-derived antihemophilic factor (FVIII) products manufactured from U.S. plasma donors and related communication material ;

http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-20251.htm


i see the media picked up on this as a 'low risk', from what the gov. agency perceived to be to them;
http://www.newsday.com/news/health/ats-ap_health14nov27,0,7955259.story?coll=ny-leadhealthnews-headlines


however, i seem to disagree. from my primitive ciphering, i see it another way. this is a huge catastrophic risk. 3 in 160 is 1.9%. so call that 2% which is 1 in 50 or twenty per thousand or 20,000 per million. also, what about the mixed genotypes/mixed susceptibility? what about the silent carriers that donated tainted blood? what about the sporadic CJDs of UNKNOWN strain or phenotype? this risk assessment is just more BSe to me. just another in a long line of industry fed crap. i pray that my assessment is the one that is wrong. but it is THEY who roll the dice with your life. it is THEY who refuse to regulate an industry that has run amok. just from a recall aspect of potentially tainted blood, and these are just recent recalls ;

PRODUCT Source Plasma, Recall # B-0054-7 CODE Units: 03MMNC5465, 03MMNC6361, 03MMNC6801, 03MMNC7510, 03MMNC7891, 03MMNC8252, 03MMNC8801, 03MMNC9144, 03MMND1122, 03MMND1478, 03MMND1969, 03MMND2350, 03MMND2825, 03MMND3211, 03MMND3708, 03MMND4072, 03MMND4588, 03MMND4831, 03MMND5320, 03MMND5719, 03MMND6268, 03MMND6683, 03MMND7228, 03MMND7656, 03MMND8211, 03MMND8652, 03MMND9195, 03MMND9618, 03MMNE0628, 03MMNE0884, 03MMNE1597, 03MMNE1979, 03MMNE2644, 03MMNE3064, 03MMNE3707, 03MMNE4122, 03MMNE4750, 03MMNE5080, 03MMNE5876, 03MMNE6218, 03MMNE7189, 03MMNE7587, 03MMNE8027, 03MMNE8645, 03MMNE9029, 03MMNE9641, 03MMNE9979, 03MMNF0491, 03MMNF0685, 03MMNF0937, 03MMNF1260, 04MMNA0351, 04MMNA0707, 04MMNA1241, 04MMNA1650, 04MMNA2291, 04MMNA2646, 04MMNA3340, 04MMNA3719, 04MMNA4312, 04MMNA4683, 04MMNA5298, 04MMNA5750, 04MMNA6407, 04MMNA6816, 04MMNA7482, 04MMNA7915, 04MMNA8632, 04MMNA9076, 04MMNA9723, 04MMNB0063, 04MMNB0696, 04MMNB1100, 04MMNB1845, 04MMNB2285, 04MMNB3035, 04MMNB3485, 04MMNB4213, 04MMNB4672, 04MMNB5841, 04MMNB6652, 04MMNB7162, 04MMNB7930, 04MMNB8453, 04MMNB9239, 04MMNB9747, 04MMNC0456, 04MMNC0931, 04MMNC1578 RECALLING FIRM/MANUFACTURER BioLife Plasma Services, L.P., Mankato, MN, by facsimile on June 4, 2004. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 89 units DISTRIBUTION CA and Austria

END OF ENFORCEMENT REPORT FOR October 25, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00975.html


USA FDA MAD COW BLOOD HUMANS RECALL (these are dime a dozen)

RECALLS AND FIELD CORRECTIONS: BIOLOGICS -- CLASS II ______________________________ PRODUCT Source Plasma, Recall # B-1708-6 CODE Units: MI180733, MI180927, MI181625, MI181780, MI182337, MI182519, MI183140, MI183311, MI183955, MI185006, MI185278, MI185822, MI186081, MI186855, MI187183, MI187903, MI188273, MI188695, MI189257, MI189553, MI190136, MI190473, MI191073, MI191395, MI191972, MI192303, MI193473, MI194343, 04MINA0377, 04MINA0801, 05MINA7147, 05MINA7451, 05MINA8094, 05MINA8504, 05MINA9548, 05MINA9883, 05MINB0489, 05MINB0875, 05MINB1469, 05MINB1874, 05MINB3116, 05MINB7192, 05MINB7529, 05MINB8246, 05MINB8612, 05MINB9236, 05MINB9366, 05MINB9475, 05MINB9641, 05MINC0031, 05MINC0237, 05MINC0336, 05MINC0894, 05MINC0964, 05MINC1138, 05MINC1619, 05MINC1750, 05MINC1907, 05MINC1977, 05MINC2375, 05MINC2774, 05MINC3113, 05MINC3484, 05MINC4277, 05MINC4623, 05MINC5623, 05MINC5914, 05MINC7545, 05MINC7870, 05MINC8355, 05MINC8689, 05MINC9437, 05MINC9775, 05MIND0067, 05MIND0393, 05MIND0892, 05MIND0951, 05MIND1836, 05MIND2183 and 05MIND2962 RECALLING FIRM/MANUFACTURER BioLife Plasma Services L.P., Muncie, IN, by facsimile on November 22, 2005. Firm initiated recall is complete. REASON Blood products, collected from unsuitable donors based on risk factors for Creutzfeldt-Jakob Disease (CJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 80 units DISTRIBUTION CA, NC, and MD

______________________________

PRODUCT a) Red Blood Cells, Leukocytes Reduced, Recall # B-1714-6; b) Fresh Frozen Plasma, Recall # B-1715-6; c) Platelets, Recall # B-1716-6 CODE a), b), and c) Unit: 2443732 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by letters dated November 11, 2003 and December 18, 2003. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION TX and WI

END OF ENFORCEMENT REPORT FOR SEPTEMBER 13, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00969.html


PRODUCT Fresh Frozen Plasma, Recall # B-1751-6 CODE Unit: 4936623 RECALLING FIRM/MANUFACTURER Gulf Coast Regional Blood Center, Houston, TX, by facsimile dated September 16, 2005. Firm initiated recall is complete. REASON Blood product, which was collected from an unsuitable donor based on risk factors for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION TX

END OF ENFORCEMENT REPORT FOR SEPTEMBER 6, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html


Mon Aug 7, 2006 10:24 71.248.132.189

PRODUCT a) Red Blood Cells, Recall # B-1587-6; b) Cryoprecipitated AHF, Recall # B-1588-6; c) Recovered Plasma, Recal # B-1589-6 CODE a), b) and c) Unit: 2016719 RECALLING FIRM/MANUFACTURER Walter Shepeard Community Blood Center, Inc., Augusta, GA, by facsimile on March 13, 2003. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION GA and Germany

______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1590-6; b) Fresh Frozen Plasma, Recall # B-1591-6 CODE a) and b) Unit: 2443595 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on June 30, 2004. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION TX

______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1592-6; b) Fresh Frozen Plasma, Recall # B-1593-6 CODE a) and b) Unit: 2545596 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on December 14, 2004 and January 3, 2005. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION TX

______________________________

http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1550-6; b) Fresh Frozen Plasma, Recall # B-1551-6 CODE a) and b) Unit 2395371 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by fax on August 20, 2003. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION TX ______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1552-6; b) Platelets, Recall # B-1553-6; c) Fresh Frozen Plasma, Recall # B-1554-6 CODE a), b) and c) Unit 2438702 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by fax on May 29, 2003. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION TX

______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1555-6; b) Fresh Frozen Plasma, Recall # B-1556-6 CODE a) and b) Unit 2454970 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by fax on July 23 and December 11. 2003. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION TX

______________________________ PRODUCT a) Red Blood Cells, Recall # B-1494-6 b) Cryoprecipitated AHF, Recall # B-1495-6 CODE a) and b) Unit 5013100 RECALLING FIRM/MANUFACTURER Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on May 17, 2005. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION GA

______________________________ PRODUCT Source Plasma, Recall # B-1450-6 CODE Unit numbers ST0824313 and ST0824764 RECALLING FIRM/MANUFACTURER Stillwater Plasma Center LLC, Stillwater, OK, by fax on November 21, 2003. Firm initiated recall is complete. REASON Blood products, which were collected from a donor whose suitability pertaining to risk factors for Creutzfeldt-Jakob Disease (vCJD) was not adequately determined, were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION UK

______________________________ PRODUCT Plasma Frozen, Recall # B-1422-6;

SNIP...END

----- Original Message ----- From: Terry S. Singeltary Sr. To: FREAS@CBER.FDA.GOV Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov Sent: Friday, December 01, 2006 2:59 PM Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION PART III]

Lancet Neurology DOI:10.1016/S1474-4422(06)70413-6

Predicting susceptibility and incubation time of human-to-human transmission of vCJD
snip... see full text here ;
http://vcjdtransfusion.blogspot.com/2007/01/fourth-case-of-transfusion-associated.html


Thursday, January 26, 2012


Prionemia and Leukocyte-Platelet-Associated Infectivity in Sheep Transmissible Spongiform Encephalopathy Models

http://vcjdtransfusion.blogspot.com/2012/01/prionemia-and-leukocyte-platelet.html



Wednesday, August 24, 2011

All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD










Wednesday, August 24, 2011




There Is No Safe Dose of Prions





http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/there-is-no-safe-dose-of-prions.html










Tuesday, September 14, 2010





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





http://tseac.blogspot.com/2010/09/transmissible-spongiform_14.html









Monday, February 7, 2011






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






http://tseac.blogspot.com/2011/02/fdas-currently-recommended-policies-to.html








Friday, March 25, 2011






Detection of Prion Protein in Urine-Derived Injectable Fertility Products by a Targeted Proteomic Approach















Sunday, December 18, 2011






A blood test for variant Creutzfeldt‐Jakob disease: briefing note for patients, carers and health professionals















http://vcjdtransfusion.blogspot.com/






http://vcjd.blogspot.com/















































TSS


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