ORIGINAL ARTICLE
Lack of evidence of transfusion transmission of Creutzfeldt-Jakob disease in a US surveillance study
Kerri Dorsey, Shimian Zou, Lawrence B. Schonberger, Marian Sullivan, Debra Kessler, Edward Notari IV, Chyang T. Fang, and Roger Y. Dodd From the Jerome H. Holland Laboratory for the Biomedical Sciences, American Red Cross, and RTI International, Rockville, Maryland; the Division of Viral & Rickettsial Diseases, National Center for Zoonotic, Vector-Borne & Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; and the New York Blood Center, New York City, New York. Correspondence to Kerri Dorsey, MPH, Transmissible Diseases Department, Jerome H. Holland Laboratory for the Biomedical Sciences, American Red Cross, 15601 Crabbs Branch Way, Rockville, MD 20855; e-mail:
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000289/!x-usc:mailto:dorseyke@usa.redcross.org. Copyright © 2008 AABB
ABSTRACT
BACKGROUND: Since 2004, several reported transfusion transmissions of variant Creutzfeldt-Jakob disease (vCJD) in the United Kingdom have reawakened concerns about the possible risk of similar transmissions of nonvariant or classic forms of CJD.
STUDY DESIGN AND METHODS: Patients with a CJD diagnosis and a history of donating blood were reported to the study coordinator. Through review of blood distribution and hospital records, the recipients of blood components from these donors were identified. We then determined each recipient's vital status and, if deceased, the cause(s) of death identified by matching the recipient's personal identifiers with the Centers for Disease Control and Prevention's National Death Index database. We conducted such searches after recipients were enrolled in this study and annually thereafter for those who remained alive.
RESULTS: The study included a total of 36 blood donors who subsequently developed CJD and 436 recipients. Through 2006, 91 of these recipients were still alive, 329 were deceased, and 16 were lost to follow-up. After transfusion, these three groups had survived a total of 2096.0 person-years. A total of 144 recipients survived 5 years or longer after transfusion and 68 of them had received blood donated 60 or fewer months before the onset of CJD in the donor. We identified no recipient with CJD.
CONCLUSIONS: The current results of this large, ongoing lookback study show no evidence of transfusion transmission of CJD. They reinforce the conclusion that the risk, if any, of transfusion transmission of prion disease by CJD donors is significantly lower than the comparable risk of such transmission by vCJD donors.
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Received for publication September 22, 2008; revision received October 28, 2008; and accepted October 29, 2008.
DIGITAL OBJECT IDENTIFIER (DOI) 10.1111/j.1537-2995.2008.02056.x About DOI
http://www3.interscience.wiley.com/journal/121615994/abstractwhat did you expect $
FDA FAILED US
http://fdafailedus.blogspot.com/SCIENCE BUSHWHACKED
http://sciencebushwhacked.blogspot.com/Sunday, July 20, 2008 Red Cross told to fix blood collection or face charges 15 years after warnings issued, few changes made to ensure safety
http://vcjdblood.blogspot.com/2008/07/red-cross-told-to-fix-blood-collection.htmlyep, that's what they said about nvCJD, until now, and with the present surveillance all human TSE in the USA, they would not know it until it was way too late, espeically with the atypical TSE showing up, and the long incubation periods, they wont' know it, like the nvCJD and blood transmission, until it's way too late.
BY lumping all cjd's as sporadic, as one strain, of young and old here in the USA, with all the different TSEs in the bovine in North America i.e. c-BSE, h-BSE, and l-BSE, and then claiming them to be of a 'spontaneous' nature, we are still in cover-up mode for mad cow disease and any human TSE thereof in North America.
you first have to have a CJD surveillance system that is place in all states, of all age groups, with a written cjd questionnaire going out to all victims and their families asking REAL questions pertaining to route and source of agent. with proper transmission studies done on all phenotypes of human TSE. until then, this study means nothing.
explain then about GSS and blood ???
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.
Subject: PRION2007 ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007 Date: September 24, 2007 at 6:52 pm PST
P02.35 Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.
FC5.5.1 BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and PrPSc C-terminal Truncated Fragments
Zanusso, G1; Commoy, E2; Fasoli, E3; Fiorini, M3; Lescoutra, N4; Ruchoux, MM4; Casalone, C5; Caramelli, M5; Ferrari, S3; Lasmezas, C6; Deslys, J-P4; Monaco, S3 1University of Verona, of Neurological and Visual Sciences, Italy; 2CEA, IMETI/SEPIA, France; 3University of Verona, Neurological and Visual Sciences, Italy; 4IMETI/SEPIA, France; 5IZSPLVA, Italy; 6The Scripps Research Insitute, USA
The etiology of sporadic Creutzfeldt-Jakob disease (sCJD), the most frequent human prion disease, remains still unknown. The marked disease phenotype heterogeneity observed in sCJD is thought to be influenced by the type of proteinase K-resistant prion protein, or PrPSc (type 1 or type 2 according to the electrophoretic mobility of the unglycosylated backbone), and by the host polymorphic Methionine/Valine (M/V) codon 129 of the PRNP. By using a two-dimensional gel electrophoresis (2D-PAGE) and imunoblotting we previously showed that in sCJD, in addition to the PrPSc type, distinct PrPSc C-terminal truncated fragments (CTFs) correlated with different sCJD subtypes. Based on the combination of CTFs and PrPSc type, we distinguished three PrPSc patterns: (i) the first was observed in sCJD with PrPSc type 1 of all genotypes,;
(ii) the second was found in M/M-2 (cortical form); (iii) the third in amyloidogenic M/V- 2 and V/V-2 subtypes (Zanusso et al., JBC 2004) . Recently, we showed that sCJD subtype M/V-2 shared molecular and pathological features with an atypical form of BSE, named BASE, thus suggesting a potential link between the two conditions. This connection was further confirmed after 2D-PAGE analysis, which showed an identical PrPSc signature, including the biochemical pattern of CTFs. To pursue this issue, we obtained brain homogenates from Cynomolgus macaques intracerebrally inoculated with brain homogenates from BASE. Samples were separated by using a twodimensional electrophoresis (2D-PAGE) followed by immunoblotting. We here show that the PrPSc pattern obtained in infected primates is identical to BASE and sCJD MV-2 subtype. These data strongly support the link, or at least a common ancestry, between a sCJD subtype and BASE. This work was supported by Neuroprion (FOOD-CT-2004-506579)
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FC5.5.2 Transmission of Italian BSE and BASE Isolates in Cattle Results into a Typical BSE Phenotype and a Muscle Wasting Disease
Zanusso, G1; Lombardi, G2; Casalone, C3; D’Angelo, A4; Gelmetti, D2; Torcoli, G2; Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini, M1; Gelati, M1; Iulini, B3; Tagliavini, F5; Ferrari, S1; Monaco, S1; Caramelli, M3; Capucci, L2 1University of Verona, Neurological and Visual Sciences, Italy; 2IZSLER, Italy; 3IZSPLVA, Italy; 4University of Turin, Animal Pathology, Italy; 5Isituto Carlo Besta, Italy
The clinical phenotype of bovine spongiform encephalopathy has been extensively reported in early accounts of the disorder. Following the introduction of statutory active surveillance, almost all BSE cases have been diagnosed on a pathological/molecular basis, in a pre-symptomatic clinical stage. In recent years, the active surveillance system has uncovered atypical BSE cases, which are characterized by distinct conformers of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose clinicopathological phenotypes remain unknown. We recently reported two Italian atypical cases with a PrPSc type similar to BSE-L, pathologically characterized by PrP amyloid plaques. Experimental transmission to TgBov mice has recently disclosed that BASE is caused by a distinct prion strain which is extremely virulent. A major limitation of transmission studies to mice is the lack of reliable information on clinical phenotype of BASE in its natural host. In the present study, we experimentally infected Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE isolates by i.c. route. BASE infected cattle showed survival times significantly shorter than BSE, a finding more readily evident in Fresian/Holstein, and in keeping with previous observations in TgBov mice. Clinically, BSE-infected cattle developed a disease phenotype highly comparable with that described in field BSE cases and in experimentally challenged cattle. On the contrary, BASE-inoculated cattle developed an amyotrophic disorder accompanied by mental dullness. The molecular and neuropathological profiles, including PrP deposition pattern, closely matched those observed in the original cases. This study further confirms that BASE is caused by a distinct prion isolate and discloses a novel disease phenotype in cattle, closely resembling the phenotype previous reported in scrapie-inoculated cattle and in some subtypes of inherited and sporadic Creutzfeldt-Jakob disease. Oral Abstracts 14
FC5.1.2 Interim Transmission Results in Cynomolgus Macaques Inoculated with BSE and
vCJD Blood Specimens
Lasmezas, C1; Lescoutra, N2; Comoy, E2; Holznagel, E3; Loewer, J3; Motzkus, D4; Hunsmann, G4; Ingrosso, L5; Bierke, P6; Pocchiari, M5; Ironside, J7; Will, R7; Deslys, JP2 1Scripps Florida, Infectology, USA; 2CEA, France; 3PEI, Germany; 4DPZ, Germany; 5Istituto Superiore di Sanita, Italy; 6SMI, Sweden; 7CJD Surveillance Unit, UK
BSE and vCJD transmitted to cynomolgus macaques reproduce many features of human vCJD, including clinical symptoms, neuropathological hallmarks of vCJD, PrPres electrophoretical pattern and, most importantly, the wide distribution of infectivity in peripheral organs. The latter characteristic distinguishes vCJD from sCJD in both humans and cynomolgus macaques, and prompted us to use this non-human primate model for further investigations of vCJD and its risk for human health. The occurrence of four vCJD infections in humans transfused with blood from patients who later developed vCJD has raised concern about blood transfusion safety in countries with vCJD. In this collaborative European study, we investigated the infectivity of blood components and whole blood administered by intracerebral (ic) and intravenous (iv) routes. Buffy-coat and whole blood was inoculated by ic and iv route, respectively, from two vCJD patients and from two clinical vCJD-inoculated macaques. Transfusions were also performed from whole blood and blood leucodepleted according to hospital practice standards from two clinical BSE inoculated macaques. Blood infectivity during the preclinical phase is being examined in orally infected macaques. Whole blood was collected and transfused from one such animal two years after oral challenge, whereas buffy-coat and plasma from two animals at 2 and 4.5 years post-challenge, respectively, have been inoculated by the ic route. This is an ongoing study in which recipient animals continue to be observed at various times post-inoculation. So far, we have had one positive transmission in one animal transfused 65 months earlier with 40 ml of whole blood from a vCJD macaque (the characteristics of the disease in this animal will be shown in a separate poster by E. Comoy). This positive transmission reproduces transfusion transmission of vCJD in humans, with an incubation of 5.5 years compatible with incubation periods observed in humans.
FC5.3 Assessing the Risk of vCJD Transmission by Dentistry; Distribution of Infectivity in Oral Tissues of VM Mice after Simulated Oral Feeding of BSE-301V
Sutton, JM1; Kirby, E1; Dickinson, J1; Dennis, M1; Cornwall, M1; Vassey, MJ1; Smith, A2; Marsh, PD3; Walker, JT1; Raven, NDH1 1Health Protection Agency, Centre for Emergency Preparedness and Response,, TSE Research group, UK; 2University of Glasgow, Dental School, UK; 3Health Protection Agency, Centre for Emergency Preparedness and Response,, UK
Background: Ongoing concerns about the prevalence of variant Creutzfeldt Jakob Disease (vCJD) in the UK population has heightened concerns about the risks of iatrogenic transmission of the disease. Although there have been no cases to date of transmission by surgery there have been 4 cases involving blood transfusion. This study aims to assess the potential of transmission of the disease by dental procedures. Whilst the risks are undoubtably low the very large numbers of procedures carried out annually have the potential to amplify the risks considerably and there is very little data in this area to form the basis for accurate risk assessments. Aim(s)/Objective(s): To assess the relative levels of infectivity in oral tissues from a murine model following exposure to BSE-301V through the small intestine. Methods. The study uses a BSE-301V, VM mouse model as a clinically relevant model for assessing iatrogenic vCJD transmission between humans. Infectious mouse brain homogenate was prepared and inoculated into a loop of the duodenum, to prevent direct contamination of the oral tissues. Mice were sacrificed at 3-weekly intervals and at appearance of clinical symptoms. A range of oral tissues, including dental pulp, gingival margin, salivary gland, saliva, lingual tonsil and trigeminal ganglia, together with brain and spleen tissues were removed, processed as homogenates and reinoculated intracranially (ic.) into indicator mice. Results: The primary challenge proved to be a very efficient route of infection with a 100% attack rate and a mean incubation to clinical disease of 157 ± 17 days (compared to 120 days for the same titre inoculum ic.). Infectivity was observed in all oral and control tissues with varying time-courses and titres estimated from incubation period. Discussion: The results throw new light on the potential routes of dissemination and spread of infectivity from the small intestine to the oral cavity and its implications for possible iatrogenic transmission of vCJD via dental, endoscopic or other forms of surgery. Conclusion: The data generated from the study provides support for ongoing risk assessments to look at the potential for vCJD transmission via dental procedures alongside other elements of studies looking at effectiveness of decontamination and re-use of dental instruments.
P02.15 Beyond the PrPres Type1/ Type2 dichotomy in Creutzfeldt-Jakob Disease
Cassard, H1; Uro-Coste, E2; Simon, S3; Bilheude, JM4; Perret-Liaudet, A5; Ironside, J6; Haik, S7; Basset-Leobon, C2; Lacroux, C1; Peoch’, K8; Stressenberger, N9; Langeveld, J10; Head, M11; Hauw, JJ12; Schecher, F1; Delisle, MB13; Andreoletti, O1 1Ecole Natinale Vétérinaire de Toulouse, France; 22Service d’Anatomie Pathologique and INSERM U466 R, France; 3DRM, CEA/Saclay, France; 4 Bio-Rad, R&D, France; 5 Hôpital Neurologique Service de Neurochimie, France; 6School of Molecular & Clinical Medicine (Pathology),, National Creutzfeldt-Jakob Disease Surveillance Un, UK; 7Pitié Salpetriere Universitary Hospital, France; 8Hôpital Lariboisière, Service de Biochimie et Biologie Moléculaire,, France; 9Hôpital Neurologique -Service de Neurochimie, France; 10CIDC-Lelystad, Netherlands; 11University of Edinburgh, Western General Hospital, UK; 12Pitié Salpetriere Universitary Hospital,, Laboratoire de Neuropathologie, France; 13Rangueil Universitary Hospital, Service d’Anatomie Pathologique, France
Creutzfeldt-Jakob disease (CJD) cases are currently classified according to established diagnostic criteria and by the genotype at codon 129 of the PRNP gene and the Western blotting of the proteinase K digested abnormal prion protein that distinguishes a type 1 and a type 2 profile. These biochemically distinct PrPres types have been proposed to represent distinct prion strains. However, since the cooccurence of type 1 and type 2 PrPres in the same patient is common, the rationale of this classification and strain concept as applied to CJD are currently under discussion. Five different brain areas from of 40 sporadic CJD and 11 iatrogenic CJD (both dura matter-, and growth hormone-associated) cases, originating from UK and France, were systematically investigated, using Western blotting typing, and by two others biochemical assays that depend on the behaviour of PrPSc in variable PK digestion conditions. As described previously, co-occurrence of type 1 and type 2 PrPres was found in 30% of the CJD patients examined. However, our novel PK concentration dependent assays identified a single uniform PrP type in cases where both type 1 and type 2 were present. Moreover, in sCJD four distinct biochemical PrPSc signatures were identified by the PK concentration dependent assays and these correlated to the current genotype/clinico-pathological sCJD groups. In iCJD the four similar biochemical signatures were observed, but were not correlated to particular PRNP 129 polymorphism or Western Blot PrPres patterns. Moreover notable differences were observed between PrPSc biochemical properties of French and UK GH-CJD cases, which could reflect, as already suspected, differences in the causative agents. Identification, in sCJD and iCJD, of four different PrPSc phenotypes irrespective of patients PRNP polymorphism at codon 129 and Western blot profile provides new insights into human prion disease aetiology and could reflects an unsuspected diversity of TSE agents in human disease. Further investigations are currently underway using animal transmission to correlate agent strain with our new discriminant biochemical assays.
see full text 143 pages ;
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdfh type has been documented in the texas and alabama cow.
l type was documented in canada.
all this confirmed.
J. Virol. doi:10.1128/JVI.02561-07 Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain Qingzhong Kong*, Mengjie Zheng, Cristina Casalone, Liuting Qing, Shenghai Huang, Bikram Chakraborty, Ping Wang, Fusong Chen, Ignazio Cali, Cristiano Corona, Francesca Martucci, Barbara Iulini, Pierluigi Acutis, Lan Wang, Jingjing Liang, Meiling Wang, Xinyi Li, Salvatore Monaco, Gianluigi Zanusso, Wen-Quan Zou, Maria Caramelli, and Pierluigi Gambetti* Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy; Department of Neurological and Visual Sciences, University of Verona, 37134 Verona, Italy
* To whom correspondence should be addressed. Email:
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000289/!x-usc:mailto:qxk2@case.edu.
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000289/!x-usc:mailto:pxg13@case.edu.
Abstract
Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed to have only one strain (BSE-C). BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob disease in humans. Two atypical BSE strains, BASE (or BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE by inoculating transgenic (Tg) mice expressing the human prion protein with brain homogenates from two BASE-affected cattle. Sixty percent of the inoculated Tg mice became infected after 20-22 months incubation, a transmission rate higher than those reported for BSE-C. A quarter of BASE-infected Tg mice, but none of the Tg mice infected with a sporadic human prion disease, showed presence of pathogenic prion protein isoforms in the spleen, indicating that the BASE prion is intrinsically lymphotropic. The pathological prion protein isoforms in BASE-infected humanized Tg mouse brains are different from those of the original cattle BASE or sporadic human prion disease. Minimal brain spongiosis and long incubation time are observed in the BASE-infected Tg mice. These results suggest that, in humans, BASE is a more virulent BSE strain and likely lymphotropic.
http://jvi.asm.org/cgi/content/abstract/JVI.02561-07v1?papetocpersonal communication that h type bse will transmit to humans ;
Wednesday, February 11, 2009 Atypical BSE North America Update February 2009
Greetings,
Considering that Mad Cow disease of all documented phenotypes, either the c-BSE, or the atypical h-BSE and or the l-BSE, ALL of which have been documented in North America, how many more, who knows, but they seem to be throwing all there marbles in the pot now by calling the h-type BSE 'familial'. what happens if we come up with another strain ? kinda like the sporadic FFI, that's not familial, what's that all about ? considering the many different strains of the typical scrapie 20+, and then the atypical Nor-98 Scrapie, which the USA has documented 6 cases the last i heard, and the thought of more than one strain of CWD in deer and elk, where will the next year, 4 years, 8 years, and beyond take us in the world of human and animal Transmissible Spongiform Encephalopathy and 'sound science' in the USA ? WILL the New Administration see the enfamous enhanced bse surveillance program of 2004 for what it was, a fraud, and have a 'redo' ? WE can hope i suppose. ...TSS
Both of the BSE cases ascertained in the US native-born cattle were atypical cases (H-type), which contributed to the initial ambiguity of the diagnosis. 174, 185 In Canada, there have been 2 atypical BSE cases in addition to the 14 cases of the classic UK strain of BSE2: one was the H-type, and the other was of the L-type.198
snip...end
source :
Enhanced Abstract Journal of the American Veterinary Medical Association January 1, 2009, Vol. 234, No. 1, Pages 59-72
Bovine spongiform encephalopathy
Jane L. Harman, DVM, PhD; Christopher J. Silva, PhD
http://avmajournals.avma.org/doi/ref/10.2460/javma.234.1.59Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
see full text ;
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.htmlSOURCE PERSONAL COMMUNICATION AND SEE ATTACHMENT;
0022-538X/08/$08.000 doi:10.1128/JVI.02561-07 Copyright © 2008, American Society for Microbiology. All Rights Reserved. Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain Qingzhong Kong,1* Mengjie Zheng,1 Cristina Casalone,2 Liuting Qing,1 Shenghai Huang,1† Bikram Chakraborty,1 Ping Wang,1 Fusong Chen,1 Ignazio Cali,1 Cristiano Corona,2 Francesca Martucci,2 Barbara Iulini,2 Pierluigi Acutis,2 Lan Wang,1 Jingjing Liang,1 Meiling Wang,1 Xinyi Li,1 Salvatore Monaco,3 Gianluigi Zanusso,3 Wen-Quan Zou,1 Maria Caramelli,2 and Pierluigi Gambetti1* Department of Pathology, Case Western Reserve University, Cleveland, Ohio 441061; CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy2; and Department of Neurological and Visual Sciences, University of Verona, 37134 Verona, Italy3 Received 30 November 2007/Accepted 16 January 2008
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4. Edward P. Notari IV, M.P.H Project Leader of the Transmissible Diseases Department at the Jerome H. Holland Laboratory, American Red Cross (attribution used with permission) reports that "the Jerome Holland Laboratory of the American Red Cross (ARC), in collaboration with the Centers for Disease Control and Prevention (CDC) and with support from blood centers across the country, has been conducting look-back investigations on blood donors who are diagnosed with classic CJD. The objective of the study is to assess whether classic CJD can be transmitted through blood transfusion. This study was originally started in 1995 by the American Red Cross and was transferred to the National Blood Data Resource Center, an independent subsidiary of the American Association of Blood Banks, in 1997. As of October 2003, study management returned to the American Red Cross. Our study looks at blood donors who subsequently developed classic CJD and requests information on the recipients from the entire span of the donor's history. If you are aware of a blood donor who received a positive CJD diagnosis and you are interested in the study, you can contact Ms. Kerri Dorsey, MPH of the CJD Look-back Study Group at
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000289/!x-usc:mailto:dorseyke@usa.redcross.org to report a donor case or to inquire further about the study. Thank you for your support."
http://www.cbbsweb.org/enf/2006/cjd_recalls.htmlOLD Schonberger et al stays ''asleep at the wheel' ;
Saturday, December 08, 2007 Transfusion Transmission of Human Prion Diseases Volume 22, Issue 1, Pages A1-A8, 1-96 (January 2008)
Transfusion Transmission of Human Prion Diseases
Shimian Zou, Chyang T. Fang, and Lawrence B. Schonberger
No transmission through transfusion has been reported for classic Creutzfeldt-Jakob disease (CJD). Moreover, a series of epidemiological surveillance, case-control, and look-back studies have provided no evidence of such transmission of CJD. Hence, the risk of such transfusion transmission of classic CJD remains theoretical. In contrast, based on data from the United Kingdom, the likelihood of transmission of the agent of the variant formof CJD (vCJD) through blood transfusion by donors who develop the disease within several years of donation is about 14% for recipients who survive longer than 5 years post transfusion. Leukodepletion may reduce the likelihoodof vCJD transmissions, although this procedure by itself removes less than half of the prion infectivity of blood. The potentially longer incubation periods of vCJD with infections in donors who are not methionine/methionine homozygous at codon 129 of the prion protein gene, the unknown number of such donors, and the unknown infectivity of their blood during the incubation period suggests caution in assuming that only known cases of vCJD represent a risk for the transfusion transmission of vCJD. Results from ongoing look-back investigations and other studies will enable continued monitoring and more precise estimations of the risks ofthe transfusion transmission of CJD and vCJD.
Published by Elsevier Inc.
snip...
Until recently, in the United States, the BSE monitoring and control efforts have not been justified or assessed based on preserving blood safety but rather on maintaining the safety of food and protecting trade. ...
http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B75B5-4R94X2C-7-1&_cdi=12973&_user=10&_orig=browse&_coverDate=01%2F31%2F2008&_sk=999779998&view=c&wchp=dGLbVlz-zSkzS&md5=6e0852421bd3e02af92fd1d9da0d14bb&ie=/sdarticle.pdfhttp://vcjdblood.blogspot.com/2007/12/transfusion-transmission-of-human-prion.htmlOLDER CJD ''LOOKBACK''
Additionally, a look back study involving 180 recipients of donations linked to CJD donors has yet to identify a transfusion-associated case of the disease. This study, conducted by the Red Cross, the New York Blood Center and the CDC involves 281 donations between 1959 and 1996 including blood from 10 confirmed and 4 probable cases of CJD.
http://www.nhlbi.nih.gov/meetings/workshops/cjd_min.txtAppendix 1: Knowledge about the risk of transmission by blood transfusion of Creutzfeldt–Jakob disease in 1995 and 1999
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There was limited scientific knowledge about the risk of transmission of classic Creutzfeldt–Jakob disease (CJD) by blood transfusion in 1995. Animal studies suggested that intracerebral inoculation of guinea pigs and hamsters with blood from human donors with CJD could produce disease, although no blood-to-blood transmission had been demonstrated at this time.35,36 In humans, transmission of the condition from cadaveric human growth hormone provided a model for acquisition of the condition via a peripheral route. Iatrogenic transmission had also been documented with human gonadotropin hormone, the reuse of neurosurgical equipment and stereotactic electroencephalogram electrodes, and from dura mater transplants. All of these involved transfer of material that had been in contact with the central nervous system of an individual with classic CJD to a previously unaffected individual.37 There was, however, no epidemiological evidence to support transmission of the condition via blood transfusion. One case report documented the development of classic CJD in an individual who had received a liver transplant. It was hypothesized that either the liver or a potentially infected albumin transfusion may have caused the development of the disease. However, the rapidity of onset of the condition following transplant made the causative association unlikely given the normally long latency period of CJD.38 Other case reports of CJD developing after blood transfusion also had important limitations such as the existence of CJD in the donor not having been documented.39 No controlled cohort studies to examine the question of blood transmission of CJD had been carried out by 1995. Three case–control studies had been carried out to identify the rates of blood transfusion in individuals with CJD and in controls. None of these studies demonstrated higher rates of transfusion among patients with CJD.40,41,42 CJD had also been shown not to have a higher incidence in those who received blood frequently, although this question had not been studied formally in 1995.43 Overall, most researchers who studied CJD considered the risk of transmission of the condition by blood transfusion to be theoretical.44
Between 1995 and 1999, further evidence accumulated that suggested that classic CJD was not transmitted through transfusion of blood products. In addition to 3 previous case–control studies, the results of which were available in 1995, 2 further large case–control studies did not show a higher rate of blood transfusion among individuals with CJD compared with controls.45,46 However, no long-term cohort studies were carried out to examine the question. Furthermore, several of the case–control studies had important methodological limitations related to the choice of control population, which could have biased their results. Look-back studies following recipients who had received blood products from individuals later diagnosed with CJD did not demonstrate development of the condition among the recipients.47,48 In addition, studies of hemophiliacs, a population exposed to large amounts of blood products, found that they were not predisposed to acquiring the condition.49
There was considerably less evidence regarding the question of whether variant CJD (vCJD) could be transmitted by blood. In 1999, there was no substantive epidemiological evidence, and the results of animal studies examining the question were not expected for another 2 years. Scientists considered the risk of transmission of the condition to be theoretical, although higher than for CJD. The primary reason for the increased risk was the higher concentration of the prion protein in the brains of individuals with vCJD, suggesting a higher "infectious" load, in addition to the presence of the prion protein in lymphoid tissue, which is intimately linked to blood. Furthermore, vCJD was believed to have crossed species barriers, presumably having been transmitted by the oral route. This demonstrated the potential for peripheral transmission of the condition. The fact that vCJD had only recently been described and had a potentially long latency period also suggested to scientists and decision-makers that a precautionary approach should be taken.50
http://www.cmaj.ca/cgi/content/full/165/1/59/DC1/1VA study dodges nvCJD blood issue U.S. Department of Veterans Affairs 18 Apr 99 press release Comment (webmaster): This is a dangerous and highly irresponsible bit of political science from the VA. What is the point, in a disease with an incubation period of 40 years or more, of looking at 1994-95 recipients of CJD blood from a single uncharacterized single donor, using the death certificate method? Note the main press release from the VA even fails to state the date of donation. Even Prusiner's group, which rarely comments on public policy issues, felt obliged to point out deficiencies in the study. This study is like looking at people exposed to chicken pox 4 days after exposure and saying it is not transmissible when the incubation period is 7-21 days. The VA should butt out of prion research if it can't do better than this. If you aren't part of the solution, you're part of the problem.
The hidden agenda here is a very real concern about nvCJD blood donors from military personel stationed in Britain during the height of the mad cow epidemic. nvCJD blood is a completely issue from sporadic CJD in that it was food-borne and thus strongly infected the lympho-reticular system (white blood cells).
Why did the VA study fail to look at tonsils of GIs stationed in Britain who died of other causes to see if they were incubating disease? Are they afraid of what they might find? Is the VA planning to pooh-pooh nvCJD blood risks the way it did Gulf War Syndrome and post-traumatic stress disorder to short-change service personnel? It looks like they are headed that way, to rationalize continued use of blood donated by high risk vets carrying a very different form of the disease and save money on blood recalls and notifications. Not to mention cover up a failure to take decisive steps earlier to reduce risk from overseas donors. America's veterans deserve better.
Meanwhile, Paul Brown of NIH is scheduled to give a talk at the National Blood Safety Council ln May 6 In Vancouver, BC entitled, "New experimental data from a TSE-infected mouse model: why CJD is not transmitted by blood products despite evidence that at least occasional blood donations may contain the infectious agent." No conference web site is available. Dr Penny Chan tel 416-256-2675 or fax 416-256-3944 is listed as conference staff.
SAN FRANCISCO -- Classic or sporadic Creutzfeldt-Jackob Disease (CJD) does not appear to be transmitted through contaminated blood transfusions or blood products, according to new research from the U.S. Department of Affairs (VA). Researchers examined more than 8,000 inpatient episodes and 500 death certificates of veterans who received blood products prepared from plasma of donors subsequently found to have died from CJD.
The researchers report that their data showed none of the patients died from, or had medical conditions consistent with CJD -- a rare and fatal degenerative disorder for which no treatment exists. The VA study is one of the largest to date to look at the potential risk of contracting this infectious disease from CJD-contaminated blood or plasma derivatives. The findings will be presented at the Ninth Annual Scientific Meeting of the Society for Healthcare Epidemiology of America (SHEA), in San Francisco, April 18-20.
...The major focus of VA research at the SHEA meeting will be the CJD paper presented by lead author, Abid Rahman, Ph.D., Epidemiologist, VA AIDS Service, Office of Public Health. This study came about as a result of VA's look-back notification program of patients who potentially received CJD-contaminated blood products. According to medical experts, there is no evidentiary basis showing the illness can be transmitted through blood components. In fact, the Centers for Disease Control and Prevention has described the risk as "small, immeasurable and theoretical."
Notwithstanding the theoretical risk, in 1995 VA voluntarily elected to notify all patients of the exposure to potentially contaminated blood products, when it was discovered that patients might have received blood components from donors who died of the disease. "Our patients had the right to know of the potential problem [of blood contamination], even if the risk was minimal," said Dr. Rahman.
"The next thing to do was to develop a means of tracking and clinically managing these patients, and determining if there was any indication of CJD in this group." Rahman and colleagues examined the morbidity and mortality records of 1,568 patients at 62 VA medical centers, who were administered potentially CJD-infected blood derivatives or plasma products. The patient group examined was 98.6% male, 86% white, with nearly 77% over the age of 60.
The researchers reviewed 8,614 inpatient episodes of care (including 862 episodes of care since the administration of the contaminated products) and 543 death certificates of patients who may have been infected. They found the primary diagnoses for inpatient stays was circulatory system diseases (29%), followed by 15% for digestive system diseases and 11.3% for neoplasms. None of the 862 episodes were consistent with conditions associated with CJD. The death certificate review produced similar results. The immediate causes of death indicated that neoplasms and circulatory system disease were the major causes of death at 30% and 28.2%, respectively. Respiratory, infectious and nervous system diseases, along with mental disorders, accounted for the rest.
"The study has significant public heath care implications," said Rahman. "Based on what the data show, thus far, there is only a small theoretical risk of transmitting CJD from contaminated blood products." Noting the disease's long incubation period, Rahman said VA continues to monitor the clinical history of these veterans.
Creutzfeldt-Jackob Disease is rare degenerative disease of the brain and central nervous system characterized by a rapidly progressive dementia. Other symptoms may include cognitive impairment and muscle spasms. It belongs to the class of diseases known as transmissible spongiform encephalopathies. It is the human equivalent of bovine spongiform encephalopathy, more popularly known as "Mad Cow" disease. The illness reportedly affects one in a million people in the U.S. annually.
1994 CJD donor studied Mon, 19 Apr 1999 ProMed
No one seems to have caught the deadly, brain-destroying Creutzfeldt-Jakob disease (CJD) from infected blood -- at least not yet, researchers said Sunday. A study of 1,500 patients who were given blood from an infected donor has found that none show any sign of CJD, said Abid Rahman and colleagues at the U.S. Department of Veterans Affairs (VA). This does not mean the patients were not infected but researchers were hopeful following the study, Rahman told a meeting in Washington, DC of the Federation of American Scientists Experimental Biology (FASEB).
In 1994 the American Red Cross said a blood donor had later died of CJD, which is always fatal and which has no cure. Blood products from the patient had been given to more than 1,500 people at VA medical centers. (The number is so large because blood from many donors is often pooled before being distributed.) No one knew in 1994, if CJD could be passed on in the blood, although CJD is known to be infectious through brain matter.
Rahman's team looked at medical records for every time one of the patients went to the hospital, and got death certificates from 543 of them. None seemed to have any symptoms of the disease, which can only be ultimately diagnosed by examination of the brain after death.
"Thus far, CJD does not appear to have been transmitted from the blood products manufactured from the plasma of the CJD patient," Rahman told the meeting. "However, caution must be exercised because of the long incubation period of transmissible CJD."
It can take decades for CJD to start showing symptoms. It is a rare disease, affecting about one in a million people for no apparent reason. It can also be spread through infected brain matter -- for instance, if an infected person has a brain operation and the instruments are re-used or if infected brain matter is used in a tissue transplant.
There are also signs that it (new variant CJD, nvCJD) can spread to people who eat beef from cattle infected with mad cow disease, also known as bovine spongiform encephalopathy (BSE). BSE swept British herds in the 1980s and doctors believe that about 30 people who died of a new form of CJD (nvCJD) contracted it by eating infected beef.
"Mad cow' study checks blood of vets April 19, 1999 San Francisco Examiner Tue, Apr 20, 1999 Ulysses Torassa
Disease not linked to transfusions: A new study of more than 1,500 veterans who received blood products from people who later died from the human equivalent of "mad cow" disease has found no evidence that any of them came down with the rare ailment. The study, presented Sunday at a conference of epidemiologists in San Francisco, coincides with other inquiries that have yet to find a documented case of Creutzfeldt-Jakob disease, which is transmitted by blood or blood products. However, the disease has been linked to transplants of infected tissues, including corneas and brain material. An outbreak of the disease in Great Britain has been linked to eating beef of infected cows. In Creutzfeldt-Jakob disease, as well as mad cow disease in animals, spongelike holes form in the brain, leading to dementia and death. Strange, misshapen proteins called prions are believed to be responsible. They can be infectious, but scientists believe they can also arise spontaneously from genetic mutations. Researchers at UC-San Francisco, where prions were discovered, cautioned against drawing firm conclusions from the study. For one thing, proving a negative - that the disease is not passed through blood - requires a very high standard, said Fred E. Cohen, a UCSF scientist researching prions.
The study by researchers at the Department of Veterans Affairs looked at death certificates from patients known to have gotten blood products from people who later came down with the disease. But death certificates are notoriously inaccurate, Cohen said, especially when it comes to diagnosing rare diseases like Creutzfeldt-Jakob, which occurs in one person in a million each year in the United States.
Furthermore, Cohen said past research in animals has shown that prions probably are carried in white blood cells at an early stage of infection. "One just needs to be extremely careful if the conclusion is the blood supply is safe," Cohen said.
The study's author, Abid Rahman, an epidemiologist with the Department of Veterans Affairs Office of Public Health, agreed that the results don't prove that the disease cannot be transmitted via blood. However, he said it appears there is only a "small, theoretical risk" of getting it that way. "It at least gives us some evidentiary basis for no transmission through blood so far," Rahman said.
The FDA banned blood products from people with Creutzfeldt-Jakob disease in 1995. However, the disease can have a very long incubation period, so it may be many years before it is discovered that someone who gave blood had the disease. More recently, the FDA has considered a proposal to ban blood donations from people who have spent time in Britain at the height of the mad cow disease outbreak. A decision has yet to be made, however it is estimated such a ban could cut the blood supply by 10 percent.
http://www.mad-cow.org/apr99_mid_news.htmlBlood: infectivity of buffy coat in new variant CJD Transfusion, Vol. 40, No. 6, 754-755, June 2000 Letters to the Editor Muttuswamy Sivakumaran, MSc, FRCP, MRCPath, PhD
"I read with interest the timely article of Brown and coworkers, recently published in TRANSFUSION.1 Their experimental work has produced several important findings that are relevant to current blood transfusion practice in several countries. First, the observation is reassuring that components prepared from the plasma of mice infected with a mouse-adapted strain of human transmissible spongiform encephalopathy are associated with very low infectivity. However, their other finding, that plasma infectivity is not eliminated by WBC reduction filtration, is obviously a worrying one and may imply that additional measures may be required to reduce the "theoretical risk" of transmission of variant CJD (vCJD) through the use of FFP. Their study also confirms that most of the infectivity in blood is associated with buffy coat. This finding has been, in my opinion, erroneously interpreted by Brown et al. as evidence that WBCs are the major source of infectivity in blood. I would like to point out that buffy coat and WBCs are not synonymous, and it is well known that buffy coat preparations contain large numbers of platelets.
Unfortunately, because of either a flaw in the method of Brown et al. or their omission of a vital piece of information (i.e., platelet contents of the buffy coat preparations used in the study), the validity of their conclusion that WBCs are the major source of infectivity in vCJD is questionable. An experiment carried out to ascertain the composition of buffy coat preparations made by the method described in their report (centrifugation at 2280 x g for 4 minutes at ambient temperature, which is followed by complete removal of supernatant plasma) using six normal mouse blood samples (Harlan Sera-Lab, Belton, UK) reveals that the average platelet content of the buffy coat preparations is at least 30 times greater than that of WBCs (the average platelet:WBC ratio of normal mouse blood samples was 76:1). This confirms my assertion that unmanipulated buffy coat preparations contain large numbers of platelets.
Because of the uncertainty of the composition of the buffy coat preparations used in the experiments of Brown et al., any attempt to draw conclusions as to the relative infectivities of WBCs and platelets in vCJD would be misleading. It would be reasonable to surmise that, although buffy coat has the highest infectivity concentration of any blood component, the relative contributions from WBCs and platelets remain unknown. Experiments using "purer" preparations of WBCs and platelets would be needed to resolve the above issue.
Needless to say, the question of whether WBCs or platelets account for the infectivity of buffy coat is of great importance, as the answer would have direct relevance for the strategies formulated to reduce the "theoretical" risk of transfusion-associated transmission of vCJD. For example, if platelets are found to be the "culprit," the removal of WBCs (WBC reduction) will have very little impact indeed! "
1. Brown P, Cerven?kov? L, McShane LM, et al. Further studies of blood infectivity in an experimental model of transmissible spongiform encephalopathy, with an explanation of why blood components do not transmit Creutzfeldt-Jakob disease in humans. Transfusion 1999;39:1169-78.[Abstract/Full Text]
The above letter was sent to Dr. Brown and Ms. Cerven?kov?, who offer the following reply: "We thank Dr. Sivakumaran for this perceptive reading of our article about blood infectivity in an experimental model of transmissible spongiform encephalopathy (TSE). He is correct in thinking that the evidence presented in the article does not provide any basis for distinguishing infectivity in buffy coat as belonging to either of its components, WBCs or platelets.1 Wherever we have referred to WBCs, the proper term should have been buffy coat. We were probably subconsciously anticipating data we knew existed from as yet unpublished studies in hamsters, which indicate that washed platelets have a substantially lower concentration of infectivity than buffy coat and thus imply that most of the buffy coat infectivity is associated with WBCs.2
It is of course possible that the hamster model (like our own mouse model) will not be applicable to the situation in humans with TSE. A recent study of the normal precursor of the pathogenic amyloid protein ("prion protein," or PrP) in human blood components has shown that by far the highest concentration is associated with platelets, not WBCs.3 However, the tissue distribution of the precursor in normal animals may not reflect the distribution of PrP or infectivity in diseased animals: muscle, for example, contains high levels of the precursor in normal animals, but, in diseased animals, it contains neither the converted pathogenic form of PrP nor any detectable infectivity.4-6
The question of which component of buffy coat contains more infectivity therefore remains open, but it should be settled by experiments currently in progress to assay the infectivity in purified WBCs and platelets from the blood of primates inoculated with several different strains of human TSE, including new variant CJD. "
1. Brown P, Cerven?kov? L, McShane LM, et al. Further studies of blood infectivity in an experimental model of transmissible spongiform encephalopathy, with an explanation of why blood components do not transmit Creutzfeldt-Jakob disease in humans. Transfusion 1999;39:1169-78.[Abstract/Full Text]
2. Rohwer RG. Titer, distribution, and transmissibility of blood-born TSE infectivity. Presented at Cambridge Healthtech Institute 6th Annual Meeting, "Blood Product Safety: TSE, Perception versus Reality," McLean, Virginia, February 13-15, 2000.
3. MacGregor I, Hope J, Barnard G, et al. Application of a time-resolved fluoroimmunoassay for the analysis of normal prion protein in human blood and its components. Vox Sang 1999;77:88-96.
4. Bendheim PE, Brown HR, Rudelli RD, et al. Nearly ubiquitous tissue distribution of the scapie agent precursor protein. Neurology 1992;42:149-56.
5. Hadlow WJ, Kennedy RC, Race RE. Natural infection of Suffolk sheep with scrapie virus. J Infect Dis 1982;146:657-64.
6. Brown P, Gibbs CJ Jr, Rodgers-Johnson P, et al. Human spongiform encephalopathy: the National Institutes of Health series of 300 cases of experimentally transmitted disease. Ann Neurol 1994;35:513-29.
http://www.mad-cow.org/00/jun00_news.html#bbb4TH October 2004
SUBMISSION TO THE TRANSMISSABLE SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE MEETING
INTRODUCTION
-----------------independent campaign and support group in the UK for haemophiliacs infected with HIV and hepatitis viruses through blood products, and more recently exposed to v CJD as a result of their treatment. My husband, is a haemophiliac infected with HIV, hepatitis B and C, and exposed to the blood of donor(s) who have since died from v CJD, on at least 12 occasions in 1996 and 1997. We are currently waiting to discover whether my husband has had further exposures, following a recent “look-back” study commissioned by the government. My brother-in-law also a haemophiliac died of AIDS in 1986.
In 2000, our group was sent two “leaked” documents. One was a letter from a British plasma company BPL (dated 1997), and the second, was a letter from the NHS Executive (1998). The content of both, was that haemophiliacs had been exposed to the blood of donors that had died from v CJD, that products if not used should be withdrawn, but “don’t tell haemophiliacs”, as “it would blight their lives forever”. Naturally, after living with the past government cover-up over blood contamination, and the day to day problems of HIV, and hepatitis C, and being promised more openness with regard to any future blood borne viruses, prion diseases, we were furious to learn that once again our government was keeping information from us, which may in turn have put our families and other patients at risk. We went to the press in October/November 2000, and as a result the British government (Department of Health), were shamed into contacting all haematologists to advise them in turn to contact all haemophilia patients, (January 2001 notification), giving haemophiliacs the opportunity of knowing if they had received the implicated batch numbers.
The Westminster government in conjunction with the Scottish parliament have recently commissioned a vCJD blood risk assessment carried out by Det Norske Veritas Consulting, to identify those groups/individuals that have surpassed the “at-risk” threshold for public health purposes. This was as a result of the first death from vCJD related to a blood transfusion. A second probable case of v CJD related to blood transfusion was later identified, where a person was found to be incubating vCJD at post-mortem, but died from unrelated causes. As a result of information we have received from the Health Protection Agency (HPA) (and other sources), we have a number of concerns with regard to v CJD and blood which we wish to raise at the meeting.
ISSUES OF CONCERN
1.We are aware that since 1998 plasma has been imported from the USA for fractionation to manufacture plasma products, as we can no longer use our own plasma because of the risk of v CJD. I have some concerns about this as I am aware that over the years citizens from European countries with cases of BSE/v CJD have sold their blood in the U.S. and been accepted as donors. Even if this practice has now stopped, if vCJD is transmittable via blood products, is there not a risk that vCJD could already have been in the blood supply and that American recipients may be incubating v CJD?
For example, my friend’s son who has lived in the UK for the first 20 years of his life, (the UK has cases of BSE/v CJD), went to study in the U.S. in 1999. I discovered to my horror that he had seen a notice on campus for plasma donors, and had proceeded to sell his blood on several occasions. He wrote telling me that he had been economical with the truth as he had smoked dope on the way to donate, and was afraid he would be barred from donating. (This is one of the reasons why we have a volunteer donor system in the UK). Dr J Garrott Allen, (former Professor Of Surgery, Stanford University, USA), pointed out in a letter to Dr William Maycock, Head of Blood Transfusion Service, England, as far back as 1975, that paying donors tempted them to lie about their circumstances and compromised safety.
I checked with the CJD Surveillance Unit, Edinburgh, and they informed me that if a UK citizen dies from v CJD, they ask the family if they have donated blood in the UK, but they don’t ask if they have donated in any other country. They give some details to the U.S. authorities but not the name of the person for reasons of confidentiality. If my friend’s son were to be incubating v CJD when he donated in the U.S, and then died of the prion disease, how would recipients of his blood products be traced in the U.S.? How many citizens from European countries with BSE/v CJD have donated blood in the U.S. since 1980?
I am also aware of a French film crew, filming a documentary in 1999 on blood safety around the world, who stepped off a plane and headed for the nearest plasma centre on the U.S./Mexican border to sell their blood, and were accepted as plasma donors. (France has cases of BSE/v CJD).
It is pointless the UK importing plasma from the U.S. from 1998 onwards because of concerns over vCJD in this country, if the U.S. authorities allowed UK and other European donors from countries with BSE/v CJD to donate in America. UK donors that donated plasma in the U.S. in for example 1999/2000 could be incubating vCJD but be asymptomatic.
2. Recently a new rule came into being in the UK. This rule said that any person receiving a blood transfusion/blood products after 1980 can no longer give blood themselves because of the possibility of v CJD risk to others. Can you advise me, does the U.S. have this same exclusion rule for any person from the U.S. who has received a blood transfusion/blood products whilst a visitor to the UK, eg, if a person took ill/had an accident here whilst on holiday, or came to the UK for medical treatment requiring blood or blood transfusions. I am aware of the recent v CJD blood products notification to the American haemophilia community but I would have thought this might also apply to other U.S. citizens.
3. If U.S. haemophiliacs are identified as having implicated U.K.blood products, will the U.S. adopt the same safety measures with haemophiliacs in relation to v CJD as the authorities have in the UK?
4. If new cases such as U.S. haemophiliacs are identified as being “high-risk” in relation to vCJD for public health purposes, what measures will be taken with regard to surgical instruments used on high-risk groups? I note the following in the advice from the HPA:-
“Any risk of transmitting v CJD on such surgical instruments (that have come into contact with those “at –risk” of v CJD) will decrease each time they are used and decontaminated. After going through approximately ten cycles of use and standard decontamination, the instruments are unlikely to pose a significant risk of infection to others.”
5. If new cases such as U.S. haemophiliacs are identified as being “high-risk” in relation to v CJD for public health purposes, what advice will be given in relation to sexual transmission, given that in the UK, those identified as “at –risk” for public health purposes will no longer be allowed to donate sperm? What advice will be given to those who wish to conceive but who are identified as being in a “high-risk” category in relation to v CJD for public health purposes? As the haemophilia community learnt to their detriment in the early days of HIV and hepatitis C, no evidence of sexual or mother to child transmission at a particular time does not necessarily mean there is no risk.
6. If any U.S. haemophiliacs are identified as being exposed to v CJD from UK products, will there be guidelines for them on how to deal with a blood spillage in the community as well as for professionals in hospital? My husband recently had a burst vein in his foot, resulting in blood spillage. There were no guidelines in the community for our insurance company to follow, so as a precaution after speaking to the local HPA, men in full bio-hazard suits were dispensed to our home to remove our blood-stained carpet for disposal. Ironically if my husband bleeds onto his shirt there are no guidelines for me as the carer of a haemophiliac in the community!
I would be grateful if you could attempt to answer my questions, although I am not a U.S. citizen, many of our haemophilia community rely on plasma products made from plasma sourced in the U.S. I also have close connections to the U.S. haemophilia community. I have enclosed a copy of our letter to my husband’s consultant in the UK with regard to our concerns over v CJD and blood, to read at your leisure, as it may help you to understand some of the issues the haemophilia community are dealing with here at this present time. Unfortunately it may only be a matter of time before U.S. haemophiliacs or other U.S. citizens may find themselves in a “high-risk” group in relation to v CJD, and you may need to tighten or introduce new guidelines. Thank-you for your time.
Yours sincerely
------------------------------- (Haemophilia Action UK)
http://www.fda.gov/ohrms/dockets/AC/04/slides/2004-4075OP1_08.htmIs the virulence of BSE prions enhanced when passaged from human to human, as opposed to the original bovine to human situation?
Can vCJD infection of heterozygous individuals establish a permanent subclinical carrier state?
WHAT about atypical BSE (either h or l or the new IBNC BSE) ???
IN terms of transmission, considering too that the atypical BSE is more virulent to humans, and considering that both the h type BSE and the l type BSE have both been found in North America, as with the typical c BSE, considering as well, that all donors in North America have been exposed in one way or the other, what saftey factors have been put into place to assure the public that blood is safe from these new and emerging TSE's (not to mention the CWD's, and Scrapie's i.e. typical and atypicals) ???
SINCE the new TSE have emerged, some more virulant than the old TSEs, and the risk thereof superceeds that of the old UKBSEnvCJD only theory, are all victims and families of victims of the sporadic CJD's being questioned about their blood donations, and if not why not, considering the new emergence of these atypical TSEs, in both human and animals in North America, and the fact they are MORE VIRULENT ???
WHAT EVER HAPPENED TO THE RESULTS OF THE ''CJD LOOK BACK STUDY'' ??? would it not seem more important now than ever ???
----- Original Message -----
From: Terry S. Singeltary Sr.
To:
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000289/!x-usc:mailto:FREAS@CBER.FDA.GOVCc:
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000289/!x-usc:mailto:william.freas@fda.hhs.gov ;
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000289/!x-usc:mailto:rosanna.harvey@fda.hhs.govSent: 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.htmi 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-headlineshowever, 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
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http://www.fda.gov/bbs/topics/enforce/2006/ENF00975.htmlUSA 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
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http://www.fda.gov/bbs/topics/enforce/2006/ENF00969.htmlPRODUCT 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
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http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.htmlMon 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.htmlPRODUCT 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; Recovered Plasma, Recall # B-1423-6 CODE a) Unit 03E42218; b) Unit 03E38153 RECALLING FIRM/MANUFACTURER American Red Cross Blood Services, Atlanta, GA, by telephone, e-mail or letter on February 20 or 21, 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 GA and Switzerland
______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1374-6; b) Recovered Plasma, Recall # B-1375-6 CODE a) and b) unit 2453906 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by fax on October 31 and November 5, 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 and Austria
______________________________ PRODUCT Source Plasma. Recall # B-1295-6 CODE Units: NG0046551, NG0045950 RECALLING FIRM/MANUFACTURER DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax on December 20, 2002, Firm initiated recall is complete. REASON Blood products, collected from a donor who did not answer the questions on the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire appropriately, were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION KY
______________________________ PRODUCT Source Plasma. Recall # B-1296-6 CODE Unit: NG 0044520 RECALLING FIRM/MANUFACTURER DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax on December 12, 2002. Firm initiated recall is complete. REASON Blood product, collected from a donor who did not answer the questions on the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire, was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION KY
______________________________ PRODUCT Source Plasma. Recall # B-1297-6 CODE Units: NG0042874, NG0043139, NG0043312, NG0043618, NG0043797, NG0044020, NG0044209, NG0044507, NG0044718, NG0044977, NG0045161, NG0045412, NG0045555 RECALLING FIRM/MANUFACTURER DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax on December 20, 2002. 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 13 units DISTRIBUTION KY
______________________________ PRODUCT Source Plasma, Recall # B-1298-6 CODE Units: NG 0046823, NG 0046671, NG 0045205, NG 0044635, NG 0043095, NG 0042525, NG 0042341 RECALLING FIRM/MANUFACTURER DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax on December 20, 2002. Firm initiated recall is complete. REASON Blood products, collected from a donor who answered questions on the variant Creutzfeldt-Jacob disease (vCJD) questionnaire inappropriately, were distributed. VOLUME OF PRODUCT IN COMMERCE 7 units DISTRIBUTION KY
______________________________ PRODUCT Recovered Plasma, Recall # B-1299-6 CODE Unit: 4357117 RECALLING FIRM/MANUFACTURER Department of the Navy, Naval Medical Center, San Diego, CA, by fax and letter on September 25, 2003. Firm initiated recall is complete. REASON Blood product, collected from a donor considered to be at risk of exposure to Creutzfeldt-Jacob Disease (CJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION Germany
END OF ENFORCEMENT REPORT FOR July 12, 2006
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http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.htmlCJD WATCH MESSAGE BOARD TSS
FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY Fri Jul 7, 2006 09:37 70.110.83.160
FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY
PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1379-6; b) Platelets, Recall # B-1380-6; c) Fresh Frozen Plasma, Recall # 1381-6; d) Recovered Plasma, Recall # B-1382-6 CODE a) Unit numbers: 2343106, 2377779, and 2403533; b) and c) Unit numbers: 2377779; d) Unit numbers: 2343106 and 2403533 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on June 12, 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 7 units DISTRIBUTION TX and Austria ______________________________
PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1467-6; b) Recovered Plasma, Recall # B-1468-6 CODE a) and b) Unit numbers: 2329380 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on May 8, 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 and Switzerland
______________________________
PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1479-6; b) Cryoprecipitated AHF, Recall # B-1480-6; c) Recovered Plasma, Recall # B-1481-6 CODE a), b), and c) Unit numbers: 2383280 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on July 23 and 29, 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 3 units DISTRIBUTION TX and Switzerland
______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1482-6; b) Fresh Frozen Plasma, Recall # B-1483-6 CODE a) and b) Unit number: 2501452 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on October 5, 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 and NY
______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1484-6; b) Plasma Cryoprecipitated Reduced, Recall # B-1485-6; c) Recovered Plasma, Recall # B-1486-6 CODE a) and c) Unit number: 2554077; b) Unit number: 2415708 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on August 13, 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 3 units DISTRIBUTION TX and Austria
_____________________________________
END OF ENFORCEMENT REPORT FOR July 5, 2006
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http://www.fda.gov/bbs/topics/enforce/2006/ENF00959.htmlGreetings again Dr. Freas et al at FDA,
WITH new atypical TSE in the bovine, in the sheep, goat, and humans, and the fact that the new BASE TSE in cattle being very very similar to sporadic CJD, rather than the nvCJD, the fact that now science showing the TSE agent of the atypical cattle in Japan showing infectivity other than CNS tissue, the fact that the latest Texas mad cow and the recent Alabama mad cow both being of the atypical strain, it would seem prudent to include all human TSE in the blood ban, in my opinion. with sporadic CJD, you have many strains and or phenotypes, some of which are 'UNKNOWN', so we do not know how this will transmit, what tissues are infectious and or if blood transmits. that's the bottom line, however it has been reported that the BASE is more virulent to humans. With this, and the fact that sporadic CJD has tripled in the past few years or so, i see it as being prudent to take serious and immediate action ;
PERSPECTIVE
On the Question of Sporadic or Atypical Bovine Spongiform Encephalopathy and Creutzfeldt-Jakob Disease
Paul Brown,* Lisa M. McShane,? Gianluigi Zanusso,? and Linda Detwiler§
snip...
ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear with me)
THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted blood from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.
These are the facts as i have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
snip... see full text 48 pages, 1st page starts on page 13. ...TSS
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8Saturday, December 08, 2007
Transfusion Transmission of Human Prion Diseases
http://vcjdblood.blogspot.com/2006/12/vcjd-case-study-highlights-blood.htmlInfectivity of bovine materials used in medicinal products and the importance of inoculation route
3.221 The risk from infectivity present in medicinal products was considered by the Southwood Working Party. They noted that 'the greatest risk . . . would be from the parenteral injection of material derived from bovine brain or lymphoid tissue'.538 (As described previously, it was generally accepted that the oral route was considerably less efficient than the parenteral route.539)
3.222 In reality, different routes exist within the parenteral category - intracerebral, intraperitoneal, intramuscular, intravenous, intraspinal and subcutaneous. Experiments in 1978 looking at several of these routes found the efficiency between them to vary. Intracerebral and intraspinal were generally the most efficient, followed by intravenous, intraperitoneal and then subcutaneous.540 The fact that certain medicinal products could be injected directly into the body (most commonly intramuscularly) meant that in theory they would pose a greater risk than beef products in food.
3.223 Various cattle tissues were of relevance to medicinal products, including insulin, heparin, surgical catgut sutures and serum. The consideration given to these materials prior to March 1996 is addressed in vol. 7: Medicines and Cosmetics.
533 SEAC 22/5 534 Wells, G. (1998) Preliminary Observations on the Pathogenesis of Experimental Bovine Spongiform Encephalopathy (BSE): An Update, Veterinary Record, 142, 103 535 Wells, G., Hawkins, S., Green, P., Spencer, Y., Dexter, I. and Dawson, D. (1999) Limited Detection of Sternal Bone Marrow Infectivity in the Clinical Phase of Experimental Bovine Spongiform Encephalopathy (BSE), Veterinary Record, 144, 292-4 536 Scott, M.R., Will, R., Ironside, J., Nguyen, H.-O., Tremblay, P., DeArmond, S.J. and Prusiner, S.B. (1999) Compelling Transgenetic Evidence for Transmission of Bovine Spongiform Encephalopathy Prions to Humans, Proceedings of the National Academy of Sciences of the USA, 96, 15137-42 537 Scott, M.R., Safar, J., Telling, G., Nguyen, H.-O., Groth, D., Torchia, M., Kochler, R., Tremblay, P., Walther, D., Cohen, F., DeArmond, S. and Prusiner, S. (1997) Identification of a Prion Protein Epitope Modulating Transmission of Bovine Spongiform Encephalopathy Prions to Transgenic Mice, Proceedings of the National Academy of Sciences of the United States of America, 94, 14279-84 538 IBD1 tab 2 para. 5.3.3 539 Kimberlin, R. and Walker, C. (1989) Pathogenesis of Scrapie in Mice after Intragastric Infection, Virus Research, 12, 213-20; Diringer, H., Beekes, M. and Oberdieck, U. (1994) The Nature of the Scrapie Agent: The Virus Theory, Annals of The New York Academy of Science, 724, 246-58; Prusiner, S., Cochran, S. and Alpers, S. (1985) Transmission of Scrapie in Hamsters, Journal of Infectious Diseases, 152, 971-8 540 Kimberlin, R.H. and Walker, C.A. (1978) Pathogenesis of Mouse Scrapie: Effect of Route of Inoculation on Infectivity Titres and Dose-Response Curves, Journal of Comparative Pathology, 88, 39-47
http://www.bseinquiry.gov.uk/pdf/volume2/chapter3.pdfFrom: TSS (216-119-138-163.ipset18.wt.net) Subject: RE--CJD&CHILDREN-- could the 'v' in vCJD simply mean vaccineCJD? Date: September 10, 2000 at 8:47 am PST
######### Bovine Spongiform Encephalopathy #########
http://www.whale.to/v/singeltary7.html10 people killed by new CJD-like disease
Public release date: 9-Jul-2008
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...end
http://www.eurekalert.org/pub_releases/2008-07/ns-tpk070908.phpThursday, 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.htmlThursday, July 10, 2008 A New Prionopathy update July 10, 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.htmlWednesday, February 04, 2009
Creutzfeldt-Jacob disease presenting as severe depression: a case report
http://creutzfeldt-jakob-disease.blogspot.com/2009/02/creutzfeldt-jacob-disease-presenting-as.htmlA case-control study of sporadic Creutzfeldt-Jakob disease in Switzerland: analysis of potential risk factors with regard to an increased CJD incidence in the years 2001-2004
http://creutzfeldt-jakob-disease.blogspot.com/2009/02/case-control-study-of-sporadic.htmlSunday, August 10, 2008
A New Prionopathy OR more of the same old BSe and sporadic CJD
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.htmlSunday, March 16, 2008
MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE
http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.htmlHUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008
snip...
Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
snip...
http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.htmlElsevier Editorial System(tm) for The Lancet Infectious Diseases Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007.
snip...see full text 31 pages ;
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdfTSS
Labels: BLOOD PLASMA, BLOOD PRODUCTS, FDA, PRIONS, SPORADIC CJD
