Bovine spongiform encephalopathy associated insertion/deletion polymorphisms of the prion protein gene in the four beef cattle breeds from North China
Xiang-Yuan Zhu,a Fu-Ying Feng,a Su-Yuan Xue,b Ting Hou,a Hui-Rong Liua
aDepartment of Biochemistry and Molecular Biology, College of Life Sciences, Inner Mongolia Agricultural University, Hohhot, China.
bInner Mongolia Academy of Agricultural Sciences, Hohhot, China.
Corresponding author: Hui-Rong Liu (e-mail: lhz17@yahoo.com.cn).
Paper handled by associate editor J. Bell
Published on the web 19 September 2011.
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Genome, 10.1139/g11-043
Abstract
Two insertion/deletion (indel) polymorphisms of the prion protein gene (PRNP), a 23-bp indel in the putative promoter region and a 12-bp indel within intron I, are associated with the susceptibility to bovine spongiform encephalopathy (BSE) in cattle. In the present study, the polymorphism frequencies of the two indels in four main beef cattle breeds (Hereford, Simmental, Black Angus, and Mongolian) from North China were studied. The results showed that the frequencies of deletion genotypes and alleles of 23- and 12-bp indels were lower, whereas the frequencies of insertion genotypes and alleles of the two indels were higher in Mongolian cattle than in the other three cattle breeds. In Mongolian cattle, the 23-bp insertion / 12-bp insertion was the major haplotype, whereas in Hereford, Simmental, and Black Angus cattle, the 23-bp deletion / 12-bp deletion was the major haplotype. These results demonstrated that Mongolian cattle could be more resistant to BSE, compared with the other three cattle breeds, because of its relatively low frequencies of deletion genotypes and alleles of 23- and 12-bp indel polymorphisms. Thus, this race could be important for selective breeding to improve resistance against BSE in this area.
Keywords: prion protein gene, insertion/deletion polymorphism, bovine spongiform encephalopathy, cattle, North China
http://www.nrcresearchpress.com/doi/abs/10.1139/g11-043?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed
An autopsied case of V180I Creutzfeldt-Jakob disease presenting with panencephalopathic-type pathology and a characteristic prion protein type
Yasushi Iwasaki1,*, Keiko Mori1, Masumi Ito1, Masamitsu Nagaoka2, Toshiaki Ieda3, Tetsuyuki Kitamoto4, Mari Yoshida5, Yoshio Hashizume5Article first published online: 27 JAN 2011 DOI: 10.1111/j.1440-1789.2010.01192.x © 2011 Japanese Society of Neuropathology
Keywords: akinetic mutism state; Creutzfeldt-Jakob disease; panencephalopathic-type; prion protein type; V180I
A 73-year-old Japanese woman showed slowly progressive aphasia, apraxia and dementia. She had no family history of prion disease or dementia. One year later she showed parkinsonism and corticobasal degeneration was initially suspected. On MRI, the left temporal neocortex seemed swollen on T2-weighted images in the initial stage, and a later high-signal intensity region was observed in the cerebral cortex in diffusion-weighted images. The patient developed myoclonus and an akinetic mutism state 15 months and 22 months after onset, respectively. Consecutive electroencephalography revealed no periodic sharp-wave complexes. Prion protein (PrP) gene analysis revealed a valine to isoleucine point mutation at codon 180, and methionine homozygosity at codon 129. This patient's clinical symptoms and disease course were atypical for Creutzfeldt–Jakob disease (CJD), and a stable state with nasal tube-feeding lasted several years. She died of respiratory failure at the age of 81, 102 months after the onset. Autopsy revealed widespread spongiform degeneration with weak synaptic-type PrP deposition, confirming the diagnosis of genetic CJD. Neurons in the cerebral cortex were relatively preserved in number and hypertrophic astrocytosis was generally moderate for such long-term disease, but cerebral white matter showed diffuse severe myelin pallor with tissue rarefaction suggestive of panencephalopatic-type pathology. The cerebellar cortex was relatively well preserved with observation of mild spongiform change in the molecular layer, moderate neuron loss in the Purkinje neuron layer, and scattered small plaque-like PrP deposition. Western blot analysis of protease-resistant PrP showed a characteristic pattern without a diglycoform band. V180I CJD is an interesting form of genetic CJD with regards to the clinicopathologic, molecular and genetic findings.
http://onlinelibrary.wiley.com/doi/10.1111/j.1440-1789.2010.01192.x/abstract
Oral.34: Variably Protease-Sensitive Prionopathy: Transmissibility and PMCA Studies
Pierluigi Gambetti,1,† Wenquan Zou,1 Juan Maria Torres,2 Claudio Soto,3 Silvio Notari,2 Juan Carlos Espinosa2 and Xiangzhu Xiao1
1 Case Western Reserve University; Cleveland, OH USA; 2 Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria; Madrid, Spain; 3 Mitchell Center for Alzheimer Disease and Related Brain Disorders, University of Texas; Houston, TX USA†Presenting author; Email: pxg13@case.edu
Variably protease-sensitive prionopathy (VPSPr) is an atypical, apparently sporadic prion disease affects all three genotypes—VV, MV and MM—at codon 129 of the prion protein (PrP) gene. A distinctive and common feature of VPSPr three genotypes is the presence of abnormal PrP forming a ladder-like electrophoretic pattern with variable sensitivity to protease digestion according to the 129 genotype. These atypical features have raised the issue of VPSPr transmissibility to animals and its propensity of being replicated in vitro.
We now report the initial results of an extensive study on the capacity of the VPSPr-associated abnormal PrP to propagate by bioassay and by protein misfolding cyclic amplification (PMCA). Inoculation of brain homogenates from cases of VPSPr-129VV to transgenic (Tg) mice expressing human PrP-129V at 6X normal revealed no clinical phenotype during the normal life span of the inoculated mice. Peculiar PrP plaques with a distinctive topography were present in approximately 30% of the mice with minimal or no spongiform degeneration (SD). Abnormal PrP from several of the plaque-bearing mice displayed a ladder-like electrophoretic profile similar to that of VPSPr. In contrast, Tg mice inoculated with brain homogenate from sporadic CJD-129VV associated with scrapie PrP type 2 became symptomatic and died approximately 220 days post inoculation. They showed widespread SD with only occasional, differently distributed plaques and a typical 3-band or PrP27-30 electrophoretic profile of the protease resistant PrP. Sham- or not inoculated mice revealed no pathology and no ladder or PrP27-30 profiles. The ladder-like electrophoretic profile was also obtained from VPSPr-129VV under modified PMCA conditions. Second passage experiments are underway.
These results support the notion that VPSPr is a prion condition different from classical prion diseases and more like other conformational neurodegenerative diseases such as Alzheimer disease and tauopathies.
Note
Supported by NIH NS062787, AG-08012, AG-14359, CDC UR8/CCU515004 and the Britton Fund.
Bio.183: Association Between a Familial and a Newly-Identified Prion Disease
Xiangzhu Xiao,1 Jue Yuan,1 Ignazio Cali,1 Xiaochen Zhou,1 Jeanne Grosclaude,2 Hubert Laude,2 Robert B. Petersen,1 Pierluigi Gambetti1 and Wenquan Zou1,†
1Case Western Reserve University; Cleveland, OH USA; 2Virologie Immunologie Moléculaires; Jouy-en-Josas, France†Presenting author; Email: wenquan.zou@case.edu
Variably protease-sensitive prionopathy (VPSPr) is a newly-identified sporadic prion disease characterized not only by an atypical clinical phenotype and neuropathology, but also by the deposition in the brain of a peculiar prion (PrPSc). The molecular mechanism underlying the formation of the peculiar PrPSc remains unknown. A naturally-occurring pathogenic mutation, valine (V) to isoleucine (I), at PrP residue 180 is linked to familial Creutzfeldt-Jakob disease (fCJDV180I). Here we report that the prions formed in VPSPr and fCJDV180I exhibit striking similarities in glycosylation, enzymatic fragmentation, and immunoreactivity even though they are associated with either wild-type PrP (PrPWt) or mutated PrP, respectively. First, we demonstrate that lack of the proteinase K (PK)-resistant diglycosylated PrP species (PrPDigly) observed in both fCJDV180I and VPSPr results from loss of glycosylation at the first N-linked glycosylation site. Second, although lack of PrPDigly has also been reported in fCJD linked to the PrP Thr183Ala mutation (fCJDT183A, which abolishes the first glycosylation site) and an atypical CJD case, so far fCJDV180I is the only one that is of the peculiar PrPSc with the five-step ladder-like electrophoretic profile (LLEP), a pathognomonic molecular hallmark of VPSPr. Third, PrP with LLEP from the two diseases is preferentially detected by the anti-PrP antibody 1E4, but not by 3F4 although these PrP fragments contain both epitopes. Fourth, unlike fCJDT183A, both VPSPr and fCJDV180I show lack of PrPDigly only in PK-treated but not in untreated PrP. Finally, PrPDigly was detected in PrPWt and PrPV180I, but not in PrPT183A, in cell models. Our study suggests that fCJDV180I shares similar pathogenetic mechanism(s) with VPSPr and that cells and animals expressing human PrPV180I can be used as models for investigating the molecular mechanism underlying the formation of the peculiar PrPSc.
Supported by the National Institutes of Health (NIH) NS062787, NIH AG-08012, AG-14359, the CJD Foundation, Alliance BioSecure, the University Center on Aging and Health with the support of the McGregor Foundation and the President’s Discretionary Fund (CWRU) as well as CDC Contract UR8/CCU515004.
Bio.135: Characterization of the Agent Strain in Sporadic Creutzfeldt-Jakob Disease by Transmission to Wild-Type Mice
Diane L. Ritchie,1,† Aileen Boyle,2 Irene McConnell,2 Mark W. Head,1 James W. Ironside1 and Moira E. Bruce2
1National CJD Surveillance Unit; Edinburgh, UK; 2Neuropathogenesis Division, The Roslin Institute and Royal (Dick) School of Veterinary Studies, The Roslin Institute, Roslin Biocentre; Roslin, UK†Presenting author; Email: diane.ritchie@ed.ac.uk
Transmissible spongiform encephalopathy (TSE) strains are defined by their biological properties on transmission to wild-type (wt) mice, specifically by their characteristic incubation periods and patterns of vacuolar pathology ("lesion profiles") in the brain. While a single TSE strain has been identified in variant Creutzfeldt-Jakob disease (vCJD), the phenotypic heterogeneity observed in sporadic CJD (sCJD) implies the existence of multiple strains of agent. These distinct strains are proposed to be enciphered by the different conformers of abnormal prion protein (PrP), recognized as different protease resistant PrP (PrPres) types by western blotting (type 1 or type 2) and are thought to be substantially influenced by the prion protein gene (PRNP) codon 129 (M/V) polymorphism.
To test the relationship between disease phenotype and agent strain, we investigated the transmission characteristics of the TSE agents present in brain tissue from 27 sCJD cases (comprising all six possible combinations of PRNP codon 129 genotype and PrPres type) in panels of wt mice using the standard strain typing properties of incubation period and lesion profiles, plus a full analysis of PrP present in the mouse brain. The work was extended to include analysis of subsequent mouse-to-mouse passages.
The results demonstrated the existence of at least two strains of agent, one associated with the MM1/MV1 sCJD subgroup and the other associated with the MM2 subgroup. The lack of transmission in mice challenged with tissues from VV1, MV2 and VV2 sCJD subgroups provided evidence of at least one further sCJD strain. Overall, the PrPres type in sCJD was maintained on transmission, which is consistent with the proposition that PrPres type plays a role in enciphering strain-specific information.
This study highlights a complex relationship between disease phenotype, codon 129 PRNP genotype, PrPres type and agent strain in sCJD and confirms that multiple strains of agent are associated with sCJD, some of which successfully propagate in wt mice. The sCJD strains identified here, by their biological properties partially correlates with the current sub-classification system for sCJD, which is based on the clinical and pathological phenotype of the disease.
Bio.144: Analyses of PrPSc Aggregation State and Protease-Resistance in Human Prions
Daniela Saverioni,1,† Silvio Notari,2 Sabina Capellari1 and Piero Parchi1
1Department of Neurological Sciences, University of Bologna; Bologna, Italy; 2Department of Pathology, National Prion Disease Pathology Surveillance Center, Case Western Reserve University; Cleveland, OH USA†Presenting author; Email: daniela.saverioni@studio.unibo.it
Background. Given the complexity and costs of transmission studies, the analyses of PrPSc properties is increasingly used as surrogate marker for strain typing. Early studies showed that PrPSc extracted from distinct disease phenotypes, in both animals and humans, often differ in physicochemical properties, such as fragment size after protease treatment or glycoform ratio. More recently, studies mainly conducted with scrapie strains isolated in mice or hamster have also reported strain-specific PrPSc differences in the degree of protease resistance, aggregation state, or conformational stability.
Objectives. To establish across the phenotypic spectrum of human prion disease: (1) whether and to what extent distinct PrPSc isoforms differ in protease-resistance; (2) whether and to what extent this PrPSc property is related to the aggregation state of the protein and (3) the relative amount of PK-sensitive PrPSc.
Materials and Methods. Frontal cortex PrPSc from the whole spectrum of sCJD subtypes, vCJD and VPsPr (MM and MV codon 129 genotypes) was purified through sample dilution in Sarkosyl and sequential ultracentrifugation in sucrose cushion and pellet resuspensions by sonication. PrPSc aggregates of different size were isolated after ultracentrifugation in sucrose gradient and fraction (12) collection. Whole purified samples and selected fractions of the sucrose gradient preparation were digested using a wide range of PK activities. A curve or "profile" of PrPSc digestion and the corresponding ED50 (PK activity required to decrease PrPSc by 50%) were obtained for each human strain analyzed.
Results. Protease resistance varied significantly among the TSE groups analysed, being highest in vCJD and sCJDVV2 and lowest in sCJDVV1. Fractions 1–4 always contained a fully PK-sensitive form of PrPSc (PrP-sen). However, PrP-sen only accounted for less than 10% of total purified PrPSc in all subtypes analyzed. Overall, the more "sensitive" subtypes contained a larger proportion of "small" PrPSc aggregates 82 Prion Volume 5 Supplement
(fractions 1–6) with respect to the more "resistant" ones. Nevertheless, PK-resistant aggregates of equal size (fractions 6, 9 and 12) extracted from sCJDMM1 and VV2 maintained, at least in part, the different degree of resistance.
Discussion. Our results indicate that: (1) only a limited portion of PrPSc associated to the majority of human prion strains is fully protease sensitive; (2) the analyses of PrP-sen does not differentiate among human prion strains; (3) the PrPSc forms associated to distinct human prion strains show a significant heterogeneity in the degree of protease resistance, which is at least partially explained by their differing aggregation state.
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
something to ponder i read in an old book (thanks cele!) take these words with how ever many grains of salt you wish.
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The familial mutations, Gajdusek proposed, lowered the barrier to such accidental conversion. "Thus," he wrote in 1996, "with these mutations, this ordinarily rare event becomes a ... dominant inherited trait." But Weissmann's qualification still remained to be refuted: the mutations might simply allow easier entry to a lurking virus. ...page 202 Deadly Feast
===================================
something to think about for sure.
but i interpret this as (1st not the gold standard, just my opinion;-), as because of certain gene mutations, one or a family, would be more susceptible to the many different strains of TSE, and the many different proven routes and sources, (which will cause different symptoms, different incubation periods from onset of clinical symptoms to death, different parts of the brain infected, etc.). in other words, it's NOT the gene mutation that CAUSES the disease, but the fact that it makes you more SUSCEPTIBLE, to the TSEs from the surrounding environment, and PLUS accumulation, i think this plays a critical role. maybe there is a one dose scenario, but i think there is more of the 'accumulators' that go clinical, than the 'one dose'. and what is the threshold to sub-clinical to clinical ?
anyway, just pondering out loud here.
also, for anyone interested, there are some studies with links to follow here ;
http://sporadicffi.blogspot.com/
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html
Thursday, July 21, 2011
A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:
August 2011 - Volume 70 - Issue 8 - pp 698-702
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Wednesday, June 15, 2011
Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
kind regards,
terry
Friday, September 23, 2011
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
Researchers’ Discovery May Revolutionize Treatment of ALS
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
September 20, 2011 (Vancouver, BC) - A team of researchers from the University of British Columbia and the Vancouver Coastal Health Research Institute have found a key link between prions and the neurodegenerative disease ALS (Amyotrophic Lateral Sclerosis), also known as Lou Gehrig’s disease. The discovery is significant as it opens the door to novel approaches to the treatment of ALS.
A pivotal paper published by the team this week in the Proceedings of the National Academy of Sciences (PNAS), demonstrates that the SOD1 protein (superoxide dismutase 1), which has been shown to be implicated in the ALS disease process, exhibits prion-like properties. The researchers found that SOD1 participates in a process called template-directed misfolding. This term refers to the coercion of one protein by another protein to change shape and accumulate in large complexes in a fashion similar to the process underlying prion diseases.
These findings provide a molecular explanation for the progressive spread of ALS through the nervous system, and highlight the central role of the propagation of misfolded proteins in the pathogenesis of neurodegenerative diseases, including ALS, Alzheimer’s and Parkinson’s.
“Our work has identified a specific molecular target, which when manipulated halts the conversion of the SOD1 protein to a misfolded, disease-causing form,” says Dr. Neil Cashman, Scientific Director of PrioNet Canada, Canada Research Chair in Neurodegeneration and Protein Misfolding at UBC, and academic director of the Vancouver Coastal Health ALS Centre. “This discovery is a first-step toward the development of targeted treatments that may stop progression of ALS.”
ALS is a progressive neuromuscular disease in which nerve cells die, resulting in paralysis and death. Approximately 2,500 to 3,000 Canadians currently live with this fatal disease, for which there is no effective treatment yet.
“For many years, ALS has remained a complex puzzle and we have found a key piece to help guide the research community to solutions,” says Dr. Leslie Grad, a co-first author of the project and current Manager of Scientific Programs at PrioNet Canada. “PrioNet is further exploring this discovery through newly-funded research projects.”
The work was completed by Dr. Neil Cashman’s lab at the Brain Research Centre based at the University of British Columbia and the Vancouver Coastal Health Research Institute, in collaboration with researchers at the University of Alberta. The research was supported by PrioNet Canada and in part by Amorfix Life Sciences and the Canadian Institutes of Health Research.
PrioNet Canada, based in Vancouver, has achieved international attention for scientific discoveries and risk management strategies directed at controlling prion diseases, and is now directing capacity into therapeutic solutions for prion-like diseases of aging, such as Alzheimer’s, Parkinson’s and ALS.
About: One of Canada’s Networks of Centres of Excellence, PrioNet Canada (www.prionetcanada.ca) is developing strategies to help solve the food, health safety, and socioeconomic problems associated with prion diseases. The network brings together scientists, industry, and public sector partners through its multidisciplinary research projects, training programs, events, and commercialization activities. PrioNet is hosted by the University of British Columbia and the Vancouver Coastal Health Research Institute in Vancouver.
The University of British Columbia (UBC) is one of North America’s largest public research and teaching institutions, and one of only two Canadian institutions consistently ranked among the world’s 40 best universities. UBC is a place that inspires bold, new ways of thinking that have helped make it a national leader in areas as diverse as community service learning, sustainability and research commercialization. UBC offers more than 50,000 students a range of innovative programs and attracts $550 million per year in research funding from government, non-profit organizations and industry through 7,000 grants.
Vancouver Coastal Health Research Institute (VCHRI) (www.vchri.ca) is the research body of Vancouver Coastal Health Authority, which includes BC’s largest academic and teaching health sciences centres: VGH, UBC Hospital, and GF Strong Rehabilitation Centre. In academic partnership with the University of British Columbia, VCHRI brings innovation and discovery to patient care, advancing healthier lives in healthy communities across British Columbia, Canada, and beyond.
The Brain Research Centre comprises more than 200 investigators with multidisciplinary expertise in neuroscience research ranging from the test tube, to the bedside, to industrial spin-offs. The centre is a partnership of UBC and Vancouver Coastal Health Research Institute. For more information, visit www.brain.ubc.ca.
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Media information or to set up interviews: Gail Bergman, Gail Bergman PR Tel: (905) 886-1340 or (905) 886-3345 E-mail: info@gailbergmanpr.com
Backgrounder - ALS as a "prion-like" disease
Amyotrophic lateral sclerosis (ALS): Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig ’s disease in the United States and motor neurone disease (MND) in Europe, is a fatal neurodegenerative disease caused by deterioration of motor neurons in the brain and spinal cord. Individuals living with the disease experience progressive paralysis, as well as difficulty breathing or swallowing. At this time, no cure or effective treatment exists.
According to the ALS Society of Canada: • ALS is the most common cause of neurological death • Every day two or three Canadians die of ALS • Eighty per cent of people with ALS die within two to five years of diagnosis; ten per cent of those affected may live for 10 years or longer • Approximately 2,500 - 3,000 Canadians currently live with this fatal disease • The World Health Organization predicts that neurodegenerative diseases will surpass cancer as the second leading cause of death in Canada by 2040
Background: Recent research highlights links between the biological mechanisms of common neurological disorders, such as ALS, Alzheimer’s and Parkinson’s disease with prion disease. While each of these diseases manifests itself in a different way, the hallmark of each is a progressive accumulation of misfolded protein aggregates in the central nervous system.
Correctly-folded proteins adopt one particular structure in order to carry out their intended function. A protein’s failure to adopt this correct structure is what threatens the health of cells. Prions are “misfolded” proteins -- the infectious, aggregating agents in diseases such as Creutzfeldt-Jakob disease (CJD) in humans, chronic wasting disease (CWD) in deer and elk and bovine spongiform encephalopathy (BSE), also known as “mad cow” disease in cattle. In ALS, Alzheimer’s and Parkinson’s, the misfolded proteins are SOD1, amyloid-ß, and a-synuclein, respectively.
Key Finding: “Intermolecular transmission of SOD-1 misfolding in living cells” - Published in the Proceedings of the National Academy of Sciences (PNAS), September 2011 • The paper shows that superoxide dismutase 1 (SOD1) participates in template-directed misfolding, in other words, the coercion of one protein by another protein to change shape and aggregate such as prion diseases do. • The results will be significant to the ALS field because it connects prion mechanisms behind the biological progression of ALS, and provides a molecular explanation for the linear and temporal spread of ALS through the nervous system. • Furthermore, the research has identified a specific molecular target, which when manipulated, halts the conversion of SOD1 to a misfolded, disease-causing form. This is a first-step towards the development of targeted treatments that may stop ALS, which PrioNet is further exploiting through newly-funded research. • This research was supported by PrioNet Canada and in part by Amorfix Life Sciences and the Canadian Institutes of Health Research.
Other Research: Studies showing how “seed” misfolded protein induce aggregation of other protein, which provide evidence for prion-like spread: • Lary Walker’s group at Emory University in Atlanta, in collaboration with Matthias Jucker and others at the Universities of Tübingen in Germany and Basel in Switzerland, discovered that aggregates of amyloid-ß protein from the brain of people with Alzheimer’s disease could be transmitted to the brain of healthy mice. • Another study by Patrik Brundin’s group in Sweden demonstrated that healthy tissue surgically implanted into the brain of people with Parkinson’s disease acquired the aggregates of a-synuclein protein characteristic of the disease. • Eliezer Masliah of the University of California San Diego and others discovered that aggregates of a-synuclein can travel from cell to cell, forming the aggregates in human neurons that are characteristic of Parkinson’s disease and certain types of dementia. • Anne Bertolotti from the University of Cambridge discovered that neuronal cells spontaneously and efficiently take up misfolded mutant SOD1 from their environment. The internalized mutant SOD1 triggers a change in shape of the normally soluble mutant SOD1 protein, which causes its aggregation, and is then transferred to neighbouring cells in a prion-like fashion.
Last Updated: 9/20/2011 3:19:45 PM
posted: 9/20/2011
http://www.prionetcanada.ca/detail.aspx?menu=12&dt=293797&app=70&cat1=211&tp=12&lk=no
Intermolecular transmission of superoxide dismutase 1 misfolding in living cells
Leslie I. Grada,1, Will C. Guesta,1, Anat Yanaia, Edward Pokrishevskya, Megan A. O'Neilla, Ebrima Gibbsa, Valentyna Semenchenkob, Masoud Yousefia, David S. Wishartc, Steven S. Plotkind, and Neil R. Cashmana,2
+ Author Affiliations
aBrain Research Centre, University of British Columbia, Vancouver, BC, Canada V6T 2B5;
bNational Institute for Nanotechnology, Edmonton, AB, Canada T6G 2M9;
cDepartments of Biological Sciences and Computing Science, University of Alberta, Edmonton, AB, Canada, T6G 2E8; and
dDepartment of Physics and Astronomy, University of British Columbia, Vancouver, BC, Canada V6T 1Z1
Edited* by Don W. Cleveland, University of California at San Diego, La Jolla, CA, and approved July 25, 2011 (received for review February 23, 2011)
Abstract
Human wild-type superoxide dismutase-1 (wtSOD1) is known to coaggregate with mutant SOD1 in familial amyotrophic lateral sclerosis (FALS), in double transgenic models of FALS, and in cell culture systems, but the structural determinants of this process are unclear. Here we molecularly dissect the effects of intracellular and cell-free obligately misfolded SOD1 mutant proteins on natively structured wild-type SOD1. Expression of the enzymatically inactive, natural familial ALS SOD1 mutations G127X and G85R in human mesenchymal and neural cell lines induces misfolding of wild-type natively structured SOD1, as indicated by: acquisition of immunoreactivity with SOD1 misfolding-specific monoclonal antibodies; markedly enhanced protease sensitivity suggestive of structural loosening; and nonnative disulfide-linked oligomer and multimer formation. Expression of G127X and G85R in mouse cell lines did not induce misfolding of murine wtSOD1, and a species restriction element for human wtSOD1 conversion was mapped to a region of sequence divergence in loop II and ß-strand 3 of the SOD1 ß-barrel (residues 24–36), then further refined surprisingly to a single tryptophan residue at codon 32 (W32) in human SOD1. Time course experiments enabled by W32 restriction revealed that G127X and misfolded wtSOD1 can induce misfolding of cell-endogenous wtSOD1. Finally, aggregated recombinant G127X is capable of inducing misfolding and protease sensitivity of recombinant human wtSOD1 in a cell-free system containing reducing and chelating agents; cell-free wtSOD1 conversion was also restricted by W32. These observations demonstrate that misfolded SOD1 can induce misfolding of natively structured wtSOD1 in a physiological intracellular milieu, consistent with a direct protein–protein interaction.
http://www.pnas.org/content/early/2011/09/13/1102645108.abstract?sid=5736bfb2-5e66-48be-9fed-3516c6bec709%20
Supporting Information Grad et al. 10.1073/pnas.1102645108 SI Materials and Methods
http://www.pnas.org/content/suppl/2011/09/14/1102645108.DCSupplemental/pnas.201102645SI.pdf
Saturday, January 22, 2011
Alzheimer's, Prion, and Neurological disease, and the misdiagnosis there of, a review 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/alzheimers-prion-and-neurological.html
Tuesday, June 7, 2011
Protein aggregate spreading in neurodegenerative diseases: Problems and perspectives
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/protein-aggregate-spreading-in.html
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight
Date: 5 January 1993
Copies: Dr Metters
Dr Skinner
Dr Pickles
Dr Morris
Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC.
2. Briefly, the meeting agreed that:
i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;
ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and
iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion.
93/01.05/4.1tss
http://collections.europarchive.org/tna/20080102191246/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992
CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible.
What are the implications for public health?
3. . The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.
92/11.4/1-1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832
121/YdeStss
92/11.4/1.2
http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
http://betaamyloidcjd.blogspot.com/
Wednesday, April 27, 2011
GENERATION ALZHEIMER'S: THE DEFINING DISEASE OF THE BABY BOOMERS
http://betaamyloidcjd.blogspot.com/2011/04/generation-alzheimers-defining-disease.html
what are they going to do with all us baby boomers by 2050 where an estimated 13.5 million Americans will be stricken with Alzheimer's, up from 5 million plus ? what about the non paid caregivers of these Alzheimer's figures, where by 2050, these figures for caregivers will rise as well, to some 20 million, if we are all still here ? sadly, to add to all this misery, the price of poker is going up too. i apologize for my mood, but i am mad about all these cuts. they have cut funding for prion disease to ZERO DOLLARS!
All Other Emerging and Zoonotic Infectious Diseases CDC's FY 2012 request of $52,658,000 for all other emerging and zoonotic infectious disease activities is a decrease of $13,607,000 below the FY 2010 level, which includes the elimination of Prion activities ($5,473,000), a reduction for other cross-cutting infectious disease activities, and administrative savings. These funds support a range of critical emerging and zoonotic infectious disease programs such Lyme Disease, Chronic Fatigue Syndrome, and Special Pathogens, as well as other activities described below.
http://www.cdc.gov/fmo/topic/Budget%20Information/appropriations_budget_form_pdf/FY2012_CDC_CJ_Final.pdf
Saturday, January 22, 2011
Alzheimer's, Prion, and Neurological disease, and the misdiagnosis there of, a review 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/alzheimers-prion-and-neurological.html
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE
http://betaamyloidcjd.blogspot.com/2010/09/alzheimers-autism-amyotrophic-lateral.html
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
Thursday, December 23, 2010
Alimentary prion infections: Touch-down in the intestine, Alzheimer, Parkinson disease and TSE mad cow diseases $ The Center for Consumer Freedom
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
http://betaamyloidcjd.blogspot.com/
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/there-is-no-safe-dose-of-prions.html
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
tss
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
September 20, 2011 (Vancouver, BC) - A team of researchers from the University of British Columbia and the Vancouver Coastal Health Research Institute have found a key link between prions and the neurodegenerative disease ALS (Amyotrophic Lateral Sclerosis), also known as Lou Gehrig’s disease. The discovery is significant as it opens the door to novel approaches to the treatment of ALS.
A pivotal paper published by the team this week in the Proceedings of the National Academy of Sciences (PNAS), demonstrates that the SOD1 protein (superoxide dismutase 1), which has been shown to be implicated in the ALS disease process, exhibits prion-like properties. The researchers found that SOD1 participates in a process called template-directed misfolding. This term refers to the coercion of one protein by another protein to change shape and accumulate in large complexes in a fashion similar to the process underlying prion diseases.
These findings provide a molecular explanation for the progressive spread of ALS through the nervous system, and highlight the central role of the propagation of misfolded proteins in the pathogenesis of neurodegenerative diseases, including ALS, Alzheimer’s and Parkinson’s.
“Our work has identified a specific molecular target, which when manipulated halts the conversion of the SOD1 protein to a misfolded, disease-causing form,” says Dr. Neil Cashman, Scientific Director of PrioNet Canada, Canada Research Chair in Neurodegeneration and Protein Misfolding at UBC, and academic director of the Vancouver Coastal Health ALS Centre. “This discovery is a first-step toward the development of targeted treatments that may stop progression of ALS.”
ALS is a progressive neuromuscular disease in which nerve cells die, resulting in paralysis and death. Approximately 2,500 to 3,000 Canadians currently live with this fatal disease, for which there is no effective treatment yet.
“For many years, ALS has remained a complex puzzle and we have found a key piece to help guide the research community to solutions,” says Dr. Leslie Grad, a co-first author of the project and current Manager of Scientific Programs at PrioNet Canada. “PrioNet is further exploring this discovery through newly-funded research projects.”
The work was completed by Dr. Neil Cashman’s lab at the Brain Research Centre based at the University of British Columbia and the Vancouver Coastal Health Research Institute, in collaboration with researchers at the University of Alberta. The research was supported by PrioNet Canada and in part by Amorfix Life Sciences and the Canadian Institutes of Health Research.
PrioNet Canada, based in Vancouver, has achieved international attention for scientific discoveries and risk management strategies directed at controlling prion diseases, and is now directing capacity into therapeutic solutions for prion-like diseases of aging, such as Alzheimer’s, Parkinson’s and ALS.
About: One of Canada’s Networks of Centres of Excellence, PrioNet Canada (www.prionetcanada.ca) is developing strategies to help solve the food, health safety, and socioeconomic problems associated with prion diseases. The network brings together scientists, industry, and public sector partners through its multidisciplinary research projects, training programs, events, and commercialization activities. PrioNet is hosted by the University of British Columbia and the Vancouver Coastal Health Research Institute in Vancouver.
The University of British Columbia (UBC) is one of North America’s largest public research and teaching institutions, and one of only two Canadian institutions consistently ranked among the world’s 40 best universities. UBC is a place that inspires bold, new ways of thinking that have helped make it a national leader in areas as diverse as community service learning, sustainability and research commercialization. UBC offers more than 50,000 students a range of innovative programs and attracts $550 million per year in research funding from government, non-profit organizations and industry through 7,000 grants.
Vancouver Coastal Health Research Institute (VCHRI) (www.vchri.ca) is the research body of Vancouver Coastal Health Authority, which includes BC’s largest academic and teaching health sciences centres: VGH, UBC Hospital, and GF Strong Rehabilitation Centre. In academic partnership with the University of British Columbia, VCHRI brings innovation and discovery to patient care, advancing healthier lives in healthy communities across British Columbia, Canada, and beyond.
The Brain Research Centre comprises more than 200 investigators with multidisciplinary expertise in neuroscience research ranging from the test tube, to the bedside, to industrial spin-offs. The centre is a partnership of UBC and Vancouver Coastal Health Research Institute. For more information, visit www.brain.ubc.ca.
- 30 -
Media information or to set up interviews: Gail Bergman, Gail Bergman PR Tel: (905) 886-1340 or (905) 886-3345 E-mail: info@gailbergmanpr.com
Backgrounder - ALS as a "prion-like" disease
Amyotrophic lateral sclerosis (ALS): Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig ’s disease in the United States and motor neurone disease (MND) in Europe, is a fatal neurodegenerative disease caused by deterioration of motor neurons in the brain and spinal cord. Individuals living with the disease experience progressive paralysis, as well as difficulty breathing or swallowing. At this time, no cure or effective treatment exists.
According to the ALS Society of Canada: • ALS is the most common cause of neurological death • Every day two or three Canadians die of ALS • Eighty per cent of people with ALS die within two to five years of diagnosis; ten per cent of those affected may live for 10 years or longer • Approximately 2,500 - 3,000 Canadians currently live with this fatal disease • The World Health Organization predicts that neurodegenerative diseases will surpass cancer as the second leading cause of death in Canada by 2040
Background: Recent research highlights links between the biological mechanisms of common neurological disorders, such as ALS, Alzheimer’s and Parkinson’s disease with prion disease. While each of these diseases manifests itself in a different way, the hallmark of each is a progressive accumulation of misfolded protein aggregates in the central nervous system.
Correctly-folded proteins adopt one particular structure in order to carry out their intended function. A protein’s failure to adopt this correct structure is what threatens the health of cells. Prions are “misfolded” proteins -- the infectious, aggregating agents in diseases such as Creutzfeldt-Jakob disease (CJD) in humans, chronic wasting disease (CWD) in deer and elk and bovine spongiform encephalopathy (BSE), also known as “mad cow” disease in cattle. In ALS, Alzheimer’s and Parkinson’s, the misfolded proteins are SOD1, amyloid-ß, and a-synuclein, respectively.
Key Finding: “Intermolecular transmission of SOD-1 misfolding in living cells” - Published in the Proceedings of the National Academy of Sciences (PNAS), September 2011 • The paper shows that superoxide dismutase 1 (SOD1) participates in template-directed misfolding, in other words, the coercion of one protein by another protein to change shape and aggregate such as prion diseases do. • The results will be significant to the ALS field because it connects prion mechanisms behind the biological progression of ALS, and provides a molecular explanation for the linear and temporal spread of ALS through the nervous system. • Furthermore, the research has identified a specific molecular target, which when manipulated, halts the conversion of SOD1 to a misfolded, disease-causing form. This is a first-step towards the development of targeted treatments that may stop ALS, which PrioNet is further exploiting through newly-funded research. • This research was supported by PrioNet Canada and in part by Amorfix Life Sciences and the Canadian Institutes of Health Research.
Other Research: Studies showing how “seed” misfolded protein induce aggregation of other protein, which provide evidence for prion-like spread: • Lary Walker’s group at Emory University in Atlanta, in collaboration with Matthias Jucker and others at the Universities of Tübingen in Germany and Basel in Switzerland, discovered that aggregates of amyloid-ß protein from the brain of people with Alzheimer’s disease could be transmitted to the brain of healthy mice. • Another study by Patrik Brundin’s group in Sweden demonstrated that healthy tissue surgically implanted into the brain of people with Parkinson’s disease acquired the aggregates of a-synuclein protein characteristic of the disease. • Eliezer Masliah of the University of California San Diego and others discovered that aggregates of a-synuclein can travel from cell to cell, forming the aggregates in human neurons that are characteristic of Parkinson’s disease and certain types of dementia. • Anne Bertolotti from the University of Cambridge discovered that neuronal cells spontaneously and efficiently take up misfolded mutant SOD1 from their environment. The internalized mutant SOD1 triggers a change in shape of the normally soluble mutant SOD1 protein, which causes its aggregation, and is then transferred to neighbouring cells in a prion-like fashion.
Last Updated: 9/20/2011 3:19:45 PM
posted: 9/20/2011
http://www.prionetcanada.ca/detail.aspx?menu=12&dt=293797&app=70&cat1=211&tp=12&lk=no
Intermolecular transmission of superoxide dismutase 1 misfolding in living cells
Leslie I. Grada,1, Will C. Guesta,1, Anat Yanaia, Edward Pokrishevskya, Megan A. O'Neilla, Ebrima Gibbsa, Valentyna Semenchenkob, Masoud Yousefia, David S. Wishartc, Steven S. Plotkind, and Neil R. Cashmana,2
+ Author Affiliations
aBrain Research Centre, University of British Columbia, Vancouver, BC, Canada V6T 2B5;
bNational Institute for Nanotechnology, Edmonton, AB, Canada T6G 2M9;
cDepartments of Biological Sciences and Computing Science, University of Alberta, Edmonton, AB, Canada, T6G 2E8; and
dDepartment of Physics and Astronomy, University of British Columbia, Vancouver, BC, Canada V6T 1Z1
Edited* by Don W. Cleveland, University of California at San Diego, La Jolla, CA, and approved July 25, 2011 (received for review February 23, 2011)
Abstract
Human wild-type superoxide dismutase-1 (wtSOD1) is known to coaggregate with mutant SOD1 in familial amyotrophic lateral sclerosis (FALS), in double transgenic models of FALS, and in cell culture systems, but the structural determinants of this process are unclear. Here we molecularly dissect the effects of intracellular and cell-free obligately misfolded SOD1 mutant proteins on natively structured wild-type SOD1. Expression of the enzymatically inactive, natural familial ALS SOD1 mutations G127X and G85R in human mesenchymal and neural cell lines induces misfolding of wild-type natively structured SOD1, as indicated by: acquisition of immunoreactivity with SOD1 misfolding-specific monoclonal antibodies; markedly enhanced protease sensitivity suggestive of structural loosening; and nonnative disulfide-linked oligomer and multimer formation. Expression of G127X and G85R in mouse cell lines did not induce misfolding of murine wtSOD1, and a species restriction element for human wtSOD1 conversion was mapped to a region of sequence divergence in loop II and ß-strand 3 of the SOD1 ß-barrel (residues 24–36), then further refined surprisingly to a single tryptophan residue at codon 32 (W32) in human SOD1. Time course experiments enabled by W32 restriction revealed that G127X and misfolded wtSOD1 can induce misfolding of cell-endogenous wtSOD1. Finally, aggregated recombinant G127X is capable of inducing misfolding and protease sensitivity of recombinant human wtSOD1 in a cell-free system containing reducing and chelating agents; cell-free wtSOD1 conversion was also restricted by W32. These observations demonstrate that misfolded SOD1 can induce misfolding of natively structured wtSOD1 in a physiological intracellular milieu, consistent with a direct protein–protein interaction.
http://www.pnas.org/content/early/2011/09/13/1102645108.abstract?sid=5736bfb2-5e66-48be-9fed-3516c6bec709%20
Supporting Information Grad et al. 10.1073/pnas.1102645108 SI Materials and Methods
http://www.pnas.org/content/suppl/2011/09/14/1102645108.DCSupplemental/pnas.201102645SI.pdf
Saturday, January 22, 2011
Alzheimer's, Prion, and Neurological disease, and the misdiagnosis there of, a review 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/alzheimers-prion-and-neurological.html
Tuesday, June 7, 2011
Protein aggregate spreading in neurodegenerative diseases: Problems and perspectives
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/protein-aggregate-spreading-in.html
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight
Date: 5 January 1993
Copies: Dr Metters
Dr Skinner
Dr Pickles
Dr Morris
Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC.
2. Briefly, the meeting agreed that:
i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;
ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and
iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion.
93/01.05/4.1tss
http://collections.europarchive.org/tna/20080102191246/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992
CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible.
What are the implications for public health?
3. . The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.
92/11.4/1-1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832
121/YdeStss
92/11.4/1.2
http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
http://betaamyloidcjd.blogspot.com/
Wednesday, April 27, 2011
GENERATION ALZHEIMER'S: THE DEFINING DISEASE OF THE BABY BOOMERS
http://betaamyloidcjd.blogspot.com/2011/04/generation-alzheimers-defining-disease.html
what are they going to do with all us baby boomers by 2050 where an estimated 13.5 million Americans will be stricken with Alzheimer's, up from 5 million plus ? what about the non paid caregivers of these Alzheimer's figures, where by 2050, these figures for caregivers will rise as well, to some 20 million, if we are all still here ? sadly, to add to all this misery, the price of poker is going up too. i apologize for my mood, but i am mad about all these cuts. they have cut funding for prion disease to ZERO DOLLARS!
All Other Emerging and Zoonotic Infectious Diseases CDC's FY 2012 request of $52,658,000 for all other emerging and zoonotic infectious disease activities is a decrease of $13,607,000 below the FY 2010 level, which includes the elimination of Prion activities ($5,473,000), a reduction for other cross-cutting infectious disease activities, and administrative savings. These funds support a range of critical emerging and zoonotic infectious disease programs such Lyme Disease, Chronic Fatigue Syndrome, and Special Pathogens, as well as other activities described below.
http://www.cdc.gov/fmo/topic/Budget%20Information/appropriations_budget_form_pdf/FY2012_CDC_CJ_Final.pdf
Saturday, January 22, 2011
Alzheimer's, Prion, and Neurological disease, and the misdiagnosis there of, a review 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/alzheimers-prion-and-neurological.html
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE
http://betaamyloidcjd.blogspot.com/2010/09/alzheimers-autism-amyotrophic-lateral.html
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
Thursday, December 23, 2010
Alimentary prion infections: Touch-down in the intestine, Alzheimer, Parkinson disease and TSE mad cow diseases $ The Center for Consumer Freedom
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
http://betaamyloidcjd.blogspot.com/
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/there-is-no-safe-dose-of-prions.html
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
tss
Monday, September 19, 2011
We need to know the truth about vCJD numbers
We need to know the truth about vCJD numbers
It's estimated that one in 4,000 people are unknowingly infected. The government must authorise trials of a new blood test
Frank Dobson guardian.co.uk, Monday 19 September 2011 06.06 EDT
'The prions that cause vCJD can lie dormant for decades and people who are infected pose a risk to others if they are blood donors.' Photograph: Toby Melville/Reuters
The government's expert advisers assume that as many as 15,000 people in this country are infected with the prion infection agents that cause the lethal brain disease, variant Creutzfeldt-Jakob (vCJD), the human form of BSE or "mad cow disease". The experts don't know if this is the right figure. It could be a lot higher but ministers are refusing to fund trials of a new test to find out.
So far just 200 of our fellow citizens have developed the disease. But the prions that cause the disease can lie dormant for decades and people who are infected pose a risk to others if they are blood or organ donors, or if surgical instruments used on them are then reused on other patients.
The Medical Research Council Prion Unit at the UCL Institute of Neurology, led by Professor John Collinge, was set up at my behest to come up with ways to treat vCJD and, better still, prevent it. They were also asked to devise a test to identify vCJD in the general population. They recently announced a new blood test that does just that. This is a great breakthrough. It should enable our doctors and scientists, for the first time, to assess accurately the incidence of vCJD infection so policy decisions on how best to protect patients can be based on evidence, not guesswork.
As health secretary, the day I became aware in 1998 that it might be possible to transmit vCJD by blood and blood products, I got the experts together. Their advice was that infection through blood and blood products was likely but not certain and that the infection, if any, would probably be carried in the white blood cells. "What should we do?" I asked. The answer for the blood supply was leucodepletion (removing the white cells) at a cost of £100m. When I told Tony Blair that I'd authorised spending this £100m but hoped it would prove to be a waste of money, his response was "fuck me". The blood for a transfusion usually comes from just a few donors but blood products come from many more donors, so the chances of infection were much greater. I had to agree that we should end UK sourcing of blood products – easier said than done.
At the time these decisions had to be taken, there was no way of assessing how many people might be infected. Officials produced "computer projections", ranging from fewer than 200 vCJD fatalities to 3.5 million. These were no more than guesses. I authorised testing of tissue samples from tonsils and appendixes which eventually produced some data which was a little bit more reliable but not much. And so it has continued to this day. In their current risk assessment, the Department of Health assume that 15,000 people (one person in every 4,000) are infected but don't know.
So largely on the basis of the precautionary principle, no less than £540m has been invested since 1998 to try to protect the integrity of blood supplies and blood products. The current annual cost is over £40m plus £200m a year to supply synthetic clotting factor for the treatment of bleeding disorders.
With so many lives possibly at stake and so much money being spent, the new blood test offers the prospect of certainty for the first time. The researchers want the government to authorise trials of the new blood test so we will know how many people are likely to be infected with vCJD. Things may turn out to be better than expected or may be worse. But at least we will know and will be able to tailor the precautionary measures to the scale of the problem. That in turn may raise ethical problems about advising patients believed to be infected with vCJD until there is a treatment. Fortunately the work carried out by the Prion Unit has made such progress that doctors may soon be able to inhibit the development of vCJD, ultimately to cure it and, better still, prevent it – along with other degenerative diseases of the brain, possibly including Alzheimer's. Sadly, so far, the government have refused to authorise and fund the trials. They prefer to continue to remain in ignorance.
The health secretary Andrew Lansley has a lot on his plate at the moment, but he shouldn't let political problems divert him from his basic duty to promote the long-term interests of the nation's health. He should authorise and fund the trials of the new blood test and do it now.
http://www.guardian.co.uk/commentisfree/2011/sep/19/vcjd-blood-test-trials
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/there-is-no-safe-dose-of-prions.html
Wednesday, August 24, 2011
All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/all-clinically-relevant-blood.html
Friday, August 12, 2011
Creutzfeldt-Jakob disease (CJD) biannual update (2011/2), Incidents Panel, National Anonymous Tonsil Archive
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/creutzfeldt-jakob-disease-cjd-biannual.html
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
Monday, September 12, 2011
BSE PRION Agriculture Animal Feed Question House of Lords Thursday, 8 September 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/bse-prion-agriculture-animal-feed.html
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
TSS
It's estimated that one in 4,000 people are unknowingly infected. The government must authorise trials of a new blood test
Frank Dobson guardian.co.uk, Monday 19 September 2011 06.06 EDT
'The prions that cause vCJD can lie dormant for decades and people who are infected pose a risk to others if they are blood donors.' Photograph: Toby Melville/Reuters
The government's expert advisers assume that as many as 15,000 people in this country are infected with the prion infection agents that cause the lethal brain disease, variant Creutzfeldt-Jakob (vCJD), the human form of BSE or "mad cow disease". The experts don't know if this is the right figure. It could be a lot higher but ministers are refusing to fund trials of a new test to find out.
So far just 200 of our fellow citizens have developed the disease. But the prions that cause the disease can lie dormant for decades and people who are infected pose a risk to others if they are blood or organ donors, or if surgical instruments used on them are then reused on other patients.
The Medical Research Council Prion Unit at the UCL Institute of Neurology, led by Professor John Collinge, was set up at my behest to come up with ways to treat vCJD and, better still, prevent it. They were also asked to devise a test to identify vCJD in the general population. They recently announced a new blood test that does just that. This is a great breakthrough. It should enable our doctors and scientists, for the first time, to assess accurately the incidence of vCJD infection so policy decisions on how best to protect patients can be based on evidence, not guesswork.
As health secretary, the day I became aware in 1998 that it might be possible to transmit vCJD by blood and blood products, I got the experts together. Their advice was that infection through blood and blood products was likely but not certain and that the infection, if any, would probably be carried in the white blood cells. "What should we do?" I asked. The answer for the blood supply was leucodepletion (removing the white cells) at a cost of £100m. When I told Tony Blair that I'd authorised spending this £100m but hoped it would prove to be a waste of money, his response was "fuck me". The blood for a transfusion usually comes from just a few donors but blood products come from many more donors, so the chances of infection were much greater. I had to agree that we should end UK sourcing of blood products – easier said than done.
At the time these decisions had to be taken, there was no way of assessing how many people might be infected. Officials produced "computer projections", ranging from fewer than 200 vCJD fatalities to 3.5 million. These were no more than guesses. I authorised testing of tissue samples from tonsils and appendixes which eventually produced some data which was a little bit more reliable but not much. And so it has continued to this day. In their current risk assessment, the Department of Health assume that 15,000 people (one person in every 4,000) are infected but don't know.
So largely on the basis of the precautionary principle, no less than £540m has been invested since 1998 to try to protect the integrity of blood supplies and blood products. The current annual cost is over £40m plus £200m a year to supply synthetic clotting factor for the treatment of bleeding disorders.
With so many lives possibly at stake and so much money being spent, the new blood test offers the prospect of certainty for the first time. The researchers want the government to authorise trials of the new blood test so we will know how many people are likely to be infected with vCJD. Things may turn out to be better than expected or may be worse. But at least we will know and will be able to tailor the precautionary measures to the scale of the problem. That in turn may raise ethical problems about advising patients believed to be infected with vCJD until there is a treatment. Fortunately the work carried out by the Prion Unit has made such progress that doctors may soon be able to inhibit the development of vCJD, ultimately to cure it and, better still, prevent it – along with other degenerative diseases of the brain, possibly including Alzheimer's. Sadly, so far, the government have refused to authorise and fund the trials. They prefer to continue to remain in ignorance.
The health secretary Andrew Lansley has a lot on his plate at the moment, but he shouldn't let political problems divert him from his basic duty to promote the long-term interests of the nation's health. He should authorise and fund the trials of the new blood test and do it now.
http://www.guardian.co.uk/commentisfree/2011/sep/19/vcjd-blood-test-trials
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/there-is-no-safe-dose-of-prions.html
Wednesday, August 24, 2011
All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/all-clinically-relevant-blood.html
Friday, August 12, 2011
Creutzfeldt-Jakob disease (CJD) biannual update (2011/2), Incidents Panel, National Anonymous Tonsil Archive
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/creutzfeldt-jakob-disease-cjd-biannual.html
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
Monday, September 12, 2011
BSE PRION Agriculture Animal Feed Question House of Lords Thursday, 8 September 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/bse-prion-agriculture-animal-feed.html
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
TSS
Monday, September 12, 2011
BSE PRION Agriculture Animal Feed Question House of Lords Thursday, 8 September 2011
House of LordsThursday, 8 September 2011
Agriculture: Animal Feed Question 11.15 am Asked by Baroness Jenkin of Kennington
To ask Her Majesty's Government what is the scientific basis for continuing the ban on feeding animal by-products and catering waste to pigs and chickens.
The Parliamentary Under-Secretary of State, Department for Environment, Food and Rural Affairs (Lord Henley): My Lords, the basis for banning the feeding of animal by-products and catering waste to
8 Sep 2011 : Column 386
pigs and chickens is to prevent the spread of serious animal diseases for which these materials may be a vector. The European Commission is proposing to lift the ban on feeding certain processed animal proteins to pigs and chickens in the light of scientific advice that the ban is no longer justified. The Government are considering their position.
Baroness Jenkin of Kennington: I thank my noble friend for his reply. Can he confirm that if the EC relaxes the ban on non-ruminant ABP being fed to pigs and chickens; and if, following the consultations he refers to, the Government are satisfied by the scientific evidence that there are no public health risks, they will then lift the ban in the UK?
Lord Henley: My Lords, obviously we want to take the scientific evidence into account and consider it very carefully. We also want to take into account likely consumer reaction because we want to take consumers along with us. If that were the case, yes, we would be prepared to lift the ban.
Lord May of Oxford: My Lords, does the Minister agree that although there is remaining uncertainty as to exactly the origins of the rogue prion that caused BSE and how it hopped into cattle, the balance of opinion and evidence is that it came from the unnatural practice of feeding animal by-products to cattle? In the light of that, would it not be wise to continue the current precautionary legislation?
Lord Henley: My Lords, as a very eminent scientist, the noble Lord is right to draw the attention of the House to the scientific evidence. At this stage there is no question of lifting the ban on feeding to cattle. We are talking purely about non-ruminants, such as pigs and chickens, at this stage. Obviously we will look at the evidence and at what the Food Standards Agency has to say, and then make a decision.
Lord Grantchester: We must proceed only on a risk-based approach and, as the Minister said, the other element to be considered is the acceptance by consumers of food so produced. The supermarkets are the gateway to the consumer. Can the Minister tell the House the attitude of supermarkets to reducing food waste by this change of policy? What discussion has his department had with supermarkets and the Food and Drink Federation?
Lord Henley: My Lords, we will continue to discuss these matters with the supermarkets and others. Obviously, where it is appropriate, food waste can go to feed animals-already some food waste can do so, when it has been appropriately separated from meat and other such products. However, as I made clear earlier, any loosening of what is happening will depend on scientific evidence and consideration of these matters. I also think that it is important, as the noble Lord makes clear, that we take opinion along with us on this matter.
Baroness Miller of Chilthorne Domer: My Lords, would the Minister accept that traditionally fed pigs are very popular with the public in terms of the flavour of pork, and so on? They certainly were until the change in their food. Feeding pigs largely on soya
8 Sep 2011 : Column 387
has an unintended consequence, in that all the imports of soya are leading to the further destruction of the rainforests. We really must make clear that using our food waste as best we can to feed to pigs has important consequences much further away in the world.
Lord Henley: My noble friend is right to point to further consequences of feeding animals in this way, in terms of producing the amount of soya used. Again, I stress to her, we should not make any changes unless the scientific evidence assures us that that is right and proper.
Lord Whitty: My Lords, would the Minister accept that the Government and the European authorities are right to proceed with caution on this front? I speak both as the Minister who was allegedly in charge during the last stages of food and mouth and as a former consumer champion. The noble Lord, Lord May, has spoken about BSE and we still do not know how the foot and mouth virus entered the chain. While some relaxation may be possible, I advise extreme caution.
Lord Henley: My Lords, I am sure that the noble Lord was totally in charge, and not just allegedly. As he puts it, we will proceed only if the scientific evidence is right and proper.
Baroness O'Cathain: My Lords, it is very important we realise that the public perception is that the outbreak of foot and mouth disease in February 2001, which had such horrific consequences for the economy and everything else, was the result of feeding animals to animals. Although there is a suggestion-or at least the Minister has stated-that that will not happen with cattle, in the minds of the Great British public it does not matter whether it is cattle, pigs or poultry; they would still have this feeling. We must be awfully careful before relaxing the ban.
Lord Henley: My Lords, the ban in 2001 that my noble friend refers to was a ban on swill. We had already banned the use of processed animal protein as a result of the BSE problems. I reiterate what I have said in answer to every question: we will proceed with extreme caution and we will base any decisions, as will the European Commission, on the scientific evidence available to us.
http://www.publications.parliament.uk/pa/ld201011/ldhansrd/text/110908-0001.htm#11090855000822
ARCHIVE: BSE: Disease control & eradication - The feed ban
The aim of our BSE-related feed control policy is to ensure the continued decline and eventual eradication of BSE in the UK. Effective controls on livestock feed are the key to achieving this.
The rate of BSE cases in cattle being reported now is significantly lower than in 1988, when the disease was first made notifiable, and the number of new cases continues to decline yet further. The key factor behind this success has been the very high level of compliance with BSE-related feed controls throughout the feed manufacture, supply, and livestock industries. Industry quality assurance schemes have considerably enhanced the level of compliance.
Experiments show that doses of infected tissue as low as 1 mg can infect a calf so there is a need for everyone involved in the feed chain to maintain the very high level of compliance seen to date.
Feed controls
In the UK, the original feed ban was introduced in 1988 to prevent ruminant protein being fed to ruminants. In addition, it has been illegal to feed ruminants with all forms of mammalian protein (with specific exceptions) since November 1994 and to feed any farmed livestock, including fish and horses, with mammalian meat and bone meal (mammalian MBM) since 04 April 1996.
EU-wide Feed Controls
Regulation (EC) No.999/2001 introduced EU controls to combat the spread of BSE. The measures included a ban on the feeding of processed animal proteins to animals which are kept, fattened or bred for the production of food. Some of these measures have been amended in line with the European Commission’s TSE Roadmap and further amendments are possible in the future. The Regulation is administered by the Transmissible Spongiform Encephalopathies Regulations.
Feed controls - At a glance
snip...see full text ;
http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bse/controls-eradication/feed-ban.htm
ARCHIVE: BSE: Disease control & eradication - the feed ban - born after the July 1988 ban (BAB) cases
[back toThe feed ban]
The July 1988 ban on feeding ruminant proteins to ruminants (e.g. cattle, sheep, goats and deer) in Great Britain, significantly reduced the risk of BSE infection. There was a marked decrease in the number of confirmed BSE cases born after the July 1988 ban (BAB cases) although the long incubation period delayed the impact on BSE cases by approximately five years. Investigations of the initial BAB cases indicated that the most likely source of infection in these cases was the continued use of feed manufactured before the 1988 ban.
Reasons for BAB cases
By autumn 1994 the decline in the epidemic was occurring more slowly in the north and east of England in which the proportion of pigs relative to cattle was highest. At that time pig and poultry feed could legitimately contain ruminant meat and bone meal (MBM) and there was an increased risk of cross contamination of cattle feed with MBM in these areas. Samples of cattle feed taken in August 1994 were found to contain ruminant MBM, demonstrating that such cross-contamination could occur. A 1994 case-control study looked at possible causes of BSE in BAB animals concluding that a food borne source of infection was the most likely explanation.
The continued presence of BSE infectivity in MBM suggested failings in the Specified Risk Material (formerly Specified Bovine Offals (SBO)) controls. The most likely source of this problem came from the practice of splitting bovine skulls. Brain was disposed as SBO and the skull was rendered to MBM, but brain tissue sometimes remained in the skull, allowing infectivity to enter MBM. Other SBO may have been inadequately separated from non-SBO material, providing another potential route of infection. Subsequent research has shown that some of the rendering systems in use until December 1994 had little effect on BSE.
Prevention of Cross Contamination
In August 1995, the controls on the handling of SBO were strengthened further to protect animal health. They required that the whole skull (except the tongue) be disposed of as SBO and that rendering plants use dedicated lines for processing SBO. In April 1996 the use of mammalian MBM was banned in all feed for livestock, fish and equine animals. This was not as a result of fears of BSE in non-ruminant species but to remove any possible risk of cross-contamination of cattle rations with MBM in feed intended for other species. A Voluntary Feed Recall Scheme, in June 1996, offered free collection and disposal of residual stocks of feed. From 1 August 1996 it became an offence (except in very tightly defined and controlled circumstances) to hold mammalian MBM on farms or in feed mills and premises where livestock feed is used, produced, prepared or stored.
BSE: Disease Control & Eradication - The Feed Ban - Born After the Reinforced Ban (BARB) Cases
1 August 1996 is regarded as the date the reinforced feed ban became effective. BSE cases born after July 1996 are referred to as born after the reinforced ban (BARB) cases.
Incidence
Details for cases in animals born after the reinforced feed ban of August 1996, that have been confirmed in Great Britain and in Northern Ireland, are available on the Veterinary Laboratories Agency website (PDF 300 KB).
Reasons for BARB Cases
Animal Health carries out a detailed epidemiological investigation into all BARB cases in Great Britain. One possible reason for BARB cases is the contamination of cattle feed ingredients with mammalian MBM handled, stored and transported outside the UK, prior to the 2001 EU-wide ban feeding of processed animal protein (PAP) to all farmed animals. Newer Member States may not have implemented full BSE controls until after January 2001.There is also evidence from epidemiological investigations into BARB cases that some cases result from the persistence of infection in feed stores.
In 2004, Professor William Hill FRS of the University of Edinburgh carried out an independent review of BARB cases in the UK. Professor Hill concluded that the UK controls in place to eliminate BSE in cattle were soundly based and confirmed that the elimination of food-borne sources was key to the eradication of BSE. He recommended that risk-based controls and monitoring should be maintained on animals and feed.
The report is available (PDF 177 KB) and the Defra response is available here (PDF 55KB).
Spontaneous occurrence (14-16) The evidence from the absence of BSE in many countries and the surveillance schemes abroad indicates that most BARBs cases cannot have arisen spontaneously, although the possibility cannot be excluded that a very few of them did so. The possibility of a very low frequency of spontaneous occurrence of BSE may be monitored from the output of surveillance in cattle populations elsewhere.
snip...
Genetic variation in susceptibility (17-21) a) Previous statistical and molecular genetic studies indicate there is little genetic variation of cattle associated with susceptibility to BSE. b) Preliminary information from the GB analysis and detailed information from the NI analyses of DNA sequence data on BARBs cases and controls as yet show no clear associations, with no genotype exclusively associated with BARBs cases whether acquired by infection or arising spontaneously.
snip...
Feed borne infection (31-34) a) Recent unpublished experiments at the VLA have shown that feeding exceptionally low doses (0.001g) of infected neural tissue can cause BSE. b) The working hypothesis of Defra that the major cause of BSE in BARBs cases has been through the ingestion of contaminated feed, most likely by young animals, is strongly supported. Thus control of the disease requires, as it has always required, completely eliminating the agent from the cattle feed chain. c) Understanding causes of variation in infectivity are important in terms of understanding the disease, but do not particularly impinge on the control of BSE, where risks have to be avoided. R: Defra continues to operate on the basis that BSE transmission via feed is the major route involved in BARB cases.
snip...
General conclusions Elimination of feed borne sources seems to be now, as before, the key to elimination of BSE. The incidence of the disease can be greatly reduced but not readily eliminated in any country by adequate imposition of controls, particularly on animal feed. As the level of incidence falls both in the UK and internationally, the risks of contamination through cattle feed, pet food, or indeed through any other source, fall whether or not controls in the UK and abroad are further tightened. With the current expertise in Defra and the VLA, GB is well placed to keep on top of and promote developments. R: It is essential that appropriate, risk based, controls and monitoring should be maintained on animals and feed until no cases of BSE are found, and controls tightened up where feasible, both in the UK and elsewhere that the UK can influence. In view of the very long incubation period of BSE in some animals, long-continued vigilance is necessary. It is not evident, however, that specific new measures are needed. Basically it is necessary to ‘keep taking the medicine’. Nevertheless, in view of new discoveries on the nature of the disease and the possibilities of new or changed TSEs arising, relevant research capacity in GB should be maintained.
snip...
http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bse/documents/hillreport.pdf
see full text ;
http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bse/controls-eradication/feedban-bornafterban.htm
BSE SUMMARY OF PASSIVE SURVEILLANCE REPORTS IN GREAT BRITAIN
http://vla.defra.gov.uk/science/docs/sci_tse_stats_gboverview.pdf
GENERAL STATISTICS ON BSE CASES IN GREAT BRITAIN
http://vla.defra.gov.uk/science/docs/sci_tse_stats_gen.pdf
TSE EXOTIC SPECIES
http://vla.defra.gov.uk/science/docs/sci_tse_stats_exotic.pdf
Envt.11: Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation
Justin Greenlee,† Robert Kunkle and Jodi Smith
National Animal Disease Center, ARS, USDA; Ames, IA USA †Presenting author; Email: justin.greenlee@ars.usda.gov
Transmissible spongiform encephalopathies (TSEs, prion diseases) are chronic neurodegenerative diseases that occur in humans, cattle, sheep, goats, cervids and a number of laboratory animal models. There is no evidence of the natural occurrence of any form of TSE in the pig, but pigs have been shown to be susceptible to Bovine Spongiform Encephalopathy (BSE) infection by multiple-route parenteral challenge. However, pigs orally exposed at eight weeks of age to large amounts of brain from cattle clinically affected with BSE did not support infection after seven years of observation. In the US, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine, mink and poultry still occurs. Although unlikely, the potential for swine to have access to TSE-contaminated feedstuffs exists. The potential for swine to serve as a host for the agent of chronic wasting disease (CWD) is unknown. The purpose of this study was to perform intracerebral inoculation of the CWD agent to determine the potential of swine as a host for the CWD agent and their clinical susceptibility. This study utilized 26 swine randomly divided into controls (n = 6) and intracranial inoculates (n = 20). CWD inoculum was a pooled 10% (w/v) homogenate derived from three white-tailed deer clinically ill with CWD from three different sources (elk, white-tailed deer, mule deer) and was given by a single intracranial injection of 0.75 ml. Necropsies were done on ten animals at six months post inoculation (PI), at approximately the time the pigs were expected to reach market weight. Additional pigs have been necropsied due to intercurrent disease (primarily lameness) over the course of the study (29–64 months). Samples collected at necropsy were examined for spongiform change after routine staining (hematoxylin and eosin) and for immunoreactivity to prion protein (PrPSc) by immunohistochemistry. Further, brain samples from at least two regions were tested by western blot. No results suggestive of spongiform encephalopathy were obtained from animals necropsied at six months PI, but positive results after an incubation period of only six months would be uncharacteristic. A single animal was positive for CWD by IHC and WB at 64 months PI. Two inoculated pigs and one control pig remain alive, so it is not possible to determine the attack rate of CWD in swine at this time. However, lack of positive results in pigs necropsied at 29–56 months PI and the long incubation of the single positive case suggest that swine are unlikely to be affected by CWD if inoculated by a natural route.
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;
1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,
The neuropathology of experimental bovine spongiform encephalopathy in the pig
Ryder SJ, Hawkins SA, Dawson M, Wells GA.
Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.
In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.
PMID: 10684682 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract
IN CONFIENCE
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought igs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. ...see full text ;
http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf
IN CONFIDENCE
So it is plausible pigs could be preclinically affected with BSE but since so few are allowed to reach adulthood this has not been recognised through clinical disease. ...
http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf
BSE TO PIGS NEWS RELEASE
http://web.archive.org/web/20030822162313/www.bseinquiry.gov.uk/files/yb/1990/09/24001001.pdf
CONFIDENTIAL
BSE: PRESS PRESENTATION
http://web.archive.org/web/20030822160958/www.bseinquiry.gov.uk/files/yb/1990/09/20003001.pdf
http://web.archive.org/web/20040623191707/www.bseinquiry.gov.uk/files/yb/1990/09/24013001.pdf
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf
INDUSTRY RESPONSE TYPICAL
http://web.archive.org/web/20030822055917/www.bseinquiry.gov.uk/files/yb/1990/09/25007001.pdf
DEFENSIVE BRIEFING
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf
CONFIDENTIAL
pigs & pharmaceuticals
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf
COMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUP
There are only two products using porcine brain and these use corticotrophin BP, made from porcine pituitary, source from outside the UK.............
http://web.archive.org/web/20040622220349/www.bseinquiry.gov.uk/files/yb/1990/10/31003001.pdf
It was not until . . . August 1990, that the result from the pig persuaded both SEAC and us to change our view and to take out of pig rations any residual infectivity that might have arisen from the SBOs.
http://web.archive.org/web/20071014143511/http://www.bseinquiry.gov.uk/files/tr/tab69.pdf
4.303 The minutes of the meeting record that:
It was very difficult to draw conclusions from one experimental result for what may happen in the field. However it would be prudent to exclude specified bovine offals from the pig diet. Although any relationship between BSE and the finding of a spongiform encephalopathy in cats had yet to be demonstrated, the fact that this had occurred suggested that a cautious view should be taken of those species which might be susceptible. The 'specified offals' of bovines should therefore be excluded from the feed of all species. 17
http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf
4.308 SEAC issued formal advice on 20 September 1990, following its meeting on the previous day. The advice stated:
Since this result shows that pigs can get spongiform encephalopathy, even though there is no evidence that they have done so in the field, we believe that pigs should no longer be fed with protein derived from bovine tissues which might contain the BSE agent, ie, those 'specified' bovine offals that are already excluded from human consumption. It would make sense to extend this prohibition to feed for all species, including household pets, as other species have now developed spongiform encephalopathies. We are aware that many animal feed compounders and pet food manufacturers are already applying such a ban on a voluntary basis. 22
http://web.archive.org/web/20060625223925/http://www.bseinquiry.gov.uk/files/yb/1990/09/20002001.pdf
4.309 In a statement to the Inquiry, Dr Tyrrell said:
It was the rapid increase in the BSE epidemic, the occurrence of more cases of FSE and the results of the pig transmission experiment which led SEAC to give the advice we did on the extension of the SBO ban. Before then (September 1990), we were not asked to advise on the extension of the SBO ban. It was important to consider humans before other animals. It should be remembered that prior to the test results of the pig transmission experiment, pigs and poultry were not known to be susceptible to TSEs. Breeding pigs, in particular, were thought to have received a very high exposure to the same type of contaminated MBM as cattle but without any evidence of the occurrence of TSE. The issue of symptom-less hosts was considered very carefully because it could apply to all domestic and farmed animal species. 23
http://web.archive.org/web/20040225164252/http://www.bseinquiry.gov.uk/files/ws/s011b.pdf
SE1805 Transmissibility of BSE to domestic fowl by injection with brain homogenate.
1 challenged bird died overnight (42 months p.i.) following a period of ataxia histopathological examination pending.
2 further challenged birds are also showing neurological signs of ataxia and tremor (43 months p.i.). All affected birds are cock birds. The remaining 4 challenged hens are clinically normal (43 months p.i.).
2 control birds were culled due to intercurrent disease (40 and 43 months p.i.) .. No significant lesions were observed in one and histopathological examination is pending on the other.
The remaining 6 control birds are clinically normal.
SEI806 Transmissibility of ESE to domestic fowl by oral exposure to brain homogenate.
1 challenged cock bird was necropsied (41 months p.i.) following a period of ataxia, tremor, limb abduction and other neurological signs. Histopathological examination failed to reveal any signi ficant lesions of the central or peripheral nervous systems.
94/01.19/7.1
1 other challenged cock bird is also showing ataxia (43 months p.i.). The remaining 2 challenged cocks and 5 hens are clinically normal (43 months p.i.).
Further examinations are in progress to determine the cause of morbidity in these studies (SE1805 and SE1806).
For controls see SE1805. ...
snip...full text ;
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/01/19007001.pdf
SEE FULL TEXT ;
http://madporcinedisease.blogspot.com/
TRANSLATION
F437/91
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY -
* The Red-Neck Ostrich 'THE AUTOPSY' & TSEs
THE AUTOPSY
Date: Mon, 11 Jun 2001 16:24:51 -0700
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs 'THE AUTOPSY'
http://collections.europarchive.org/tna/20080102120315/http://www.bseinquiry.gov.uk/files/sc/Seac10/tab06.pdf
1 The carrion birds are animals whose diet regularly or occasionally includes the consumption of carcasses, including possibly TSE infected ruminant carcasses.
http://ec.europa.eu/food/fs/sc/ssc/out295_en.pdf
It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20040523230128/www.bseinquiry.gov.uk/files/ws/s145d.pdf
it is clear that the designing scientists must have also shared Mr Bradleyâs surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20030526212610/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background: In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims: The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods: Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results: In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions: Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
Tuesday, October 27, 2009
Petition to Declare Poultry Litter as a Food Additive and to Ban Its Use as Cattle Feed August 12, 2009 UNITED STATES
DEPARTMENT OF HEALTH AND HUMAN SERVICES FOOD AND DRUG ADMINISTRATION
http://madcowfeed.blogspot.com/2009/10/petition-to-declare-poultry-litter-as.html
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr." To: fdadockets@oc.fda.gov
http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html
Wednesday, July 6, 2011
Mad cow disease: EU must maintain strict controls, says Parliament
snip...
but the ban on feeding animal protein to non-ruminants, such as pigs, could gradually be lifted if further safeguards are put in place, they add.
snip...
http://efsaopinionbseanimalprotein.blogspot.com/2011/07/mad-cow-disease-eu-must-maintain-strict.html
WHAT HAPPENS WHEN YOU RENDER UNTO FEED, AND FEED EVERY LIVESTOCK SPECIES, GAME SPEICIES, ALL STRAINS OF TSE THERE FROM, AND THEN FEED THERE FROM, TO HUMANS AND ANIMALS ???
WE WILL KNOW IN DUE TIME, BECAUSE THIS IS AN ONGOING LONG TERM STUDY FOR THE NORTH AMERICAN CONSUMER $$$
BE WARNED, YOU HAVE, AND CONTINUE TO BE EXPOSED $$$
LET'S LOOK AT A FEW SPECIES THAT HAVE BEEN FED BANNED SUSPECT MAD COW FEED IN THE USA OVER THE DECADES ;
a) EVSRC Custom dairy feed, Recall # V-130-6; b) Performance Chick Starter, Recall # V-131-6; c) Performance Quail Grower, Recall # V-132-6; d) Performance Pheasant Finisher, Recall # V-133-6. a) CO-OP 32% Sinking Catfish, Recall # V-100-6; b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6; c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6; e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6; f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6; g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6; h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6; i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6; j) CO-OP LAYING CRUMBLES, Recall # V-109-6; k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6; l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6; m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
NOW, LET'S LOOK AT A FEW 100S OF TONS OF THESE BANNED SUSPECT MAD COW FEED IN COMMERCE IN THE USA ;
BANNED SUSPECT MAD COW FEED IN COMMERCE 2006-2007, SOME 10 YEARS AFTER THE INFAMOUS PARTIAL AND VOLUNTARY MAD COW FEED BAN or August 4, 1997, that was nothing more than ink on paper, so really, there was no BSE triple fire wall at all, and this was improving ???
*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS
THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
see Alabama banned suspect mad cow feed in commerce ;
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE
Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
snip...
To minimise the risk of farmers' claims for compensation from feed compounders.
To minimise the potential damage to compound feed markets through adverse publicity.
To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.
snip...
THE FUTURE
4..........
MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.
5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.
6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...
SEE full text ;
http://collections.europarchive.org/tna/20080102153800/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf
RE - "BSE-L in North America may have existed for decades" YA THINK ???
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html
Thursday, July 21, 2011
A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:
August 2011 - Volume 70 - Issue 8 - pp 698-702
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Wednesday, June 15, 2011
Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html
sporadic CJD accounts for over 85% plus of all human TSE prion disease.
sporadic CJD, of unknown phenotype is rising in Canada and the USA.
animal TSE are rising and spreading in the USA.
we do not know if human TSE from atypical BSE, or from CWD infected deer and elk, or from scrapie infected sheep and goats, would look like nvCJD or sporadic CJD, or this UNKNOWN PHENOTYPE that is rising in North America.
we do know now however, that some of the sporadic CJD cases have now been linked to the atypical BSE cases, which is of no surprise to me.
so in my opinion, and as i have stated before, the continued belief in the UKBSEnvCJD only theory, will only continue to help spread this disease around the globe, via multiple proven routes and sources. ...
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
The conclusions state that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Active screening has allowed the identification of 3 new forms of animal TSEs (H-type atypical BSE, L-type atypical BSE, and atypical scrapie), but the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs. There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential. Transmission experiments to human PrP transgenic mice or primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential and indicate that that of the L-type atypical BSE agent appears similar or even higher than that of the classical BSE agent. A single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
Commentary ---------- Following to a request from the European Commission, the Panel on Biological Hazards (BIOHAZ) and the European Centre for Disease Prevention and Control (ECDC) were asked to deliver a scientific opinion on any possible epidemiological or molecular association between transmissible spongiform encephalopathies (TSEs) in animals and humans. The opinion reviews and discusses the existing scientific evidence that links animal and human TSEs currently known.
The opinion first considers the definition of zoonoses and the principles for the identification of zoonotic diseases, which can be based on evidence gathered from both epidemiological and laboratory studies. The opinion describes the challenges involved in identifying TSEs as zoonoses, due to the specific characteristics of TSE infections/diseases, such as the nature of TSE agents, the occurrence of animal and human TSEs, and the type of monitoring applied, the long incubation period of TSEs etc. The example of the process that led to establishing a link between bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) is reviewed. The epidemiological and laboratory criteria that can be used to investigate such a link are described in detail, since those criteria might be useful for the identification of links between other animal and human TSEs.
The opinion discusses the strain diversity of the TSE agents described in sheep, goats, cattle, cervids, and humans, based on the current knowledge, which highlights that multiple TSE agents exist in each species. The factors influencing the capacity of TSE agents to cross the species transmission barrier are then considered in detail, including the variability in host and donor PrP gene and protein, the TSE strain type involved and its interaction with the host PrP, and the route of infection.
The opinion critically assesses the tools and methodologies currently available to study and evaluate the possible association between animal and human TSEs. The use of epidemiology is discussed for TSEs in both animals and humans, and the possibility to compare the 2 sources of information is presented as a possible method to study the possible links.
Both in vivo and in vitro laboratory methods are considered and discussed, including neuropathology, transmission experiments involving different animal models (wild type and transgenic mice, primates and other species), biochemical methods, cell-free conversion assays, protein misfolding cyclic amplification (PMCA), and cell culture assays. Characteristics, advantages, and disadvantages of the different methods are reviewed, including the opportunity to collate data from different types of experiments for the study of potential associations between animal and human TSEs.
The opinion then reviews the scientific evidence currently available for the different animal and human TSEs, including classical BSE, atypical BSE (H-type and L-type), classical scrapie, atypical scrapie, chronic wasting disease (CWD), transmissible mink encephalopathy (TME), and human TSEs. In particular, the following aspects are systematically discussed for each TSE agent: epidemiology, pathogenesis, and in vivo and in vitro transmission experiments.
The opinion concludes that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. With regard to human TSEs, detected cases of sporadic CJD are randomly distributed in time and geographical location. These observations have been interpreted as a supportive argument that sporadic CJD is not environmentally acquired. However, the epidemiological evidence in relation to sporadic CJD cannot be regarded as definitive, and the possibility that a small proportion of cases are zoonotic cannot be excluded.
It also concludes that a series of uncertainties in relation to the epidemiological patterns of animal and human TSEs indicate that even a rough comparison of the present epidemiological patterns of human and animal TSEs other than classical BSE is unlikely to be informative. Because of these uncertainties, it is an imperative to continue to carry out systematic surveillance of human TSE diseases, and to continue and improve the surveillance of animal TSE diseases.
The opinion highlights that the active screening has allowed the identification of 3 new forms of animal TSEs (L-type atypical BSE, H-type atypical BSE, and atypical scrapie), but that the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs.
There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential.
Transmission experiments to human PrP transgenic mice suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE and classical BSE in sheep agents) might have zoonotic potential, whereas for other agents there is no evidence provided of a zoonotic potential (H-type atypical BSE and CWD), or no published studies are available (classical and atypical scrapie). In addition, transmission experiments to primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential. In particular, primates are highly permissive to L-type atypical BSE, even by the oral route.
The opinion emphasizes that laboratory transmission experiments indicate that the L-type atypical BSE agent has a significant zoonotic potential, which appears similar or even higher than that of the classical BSE agent. While transmission data for evaluating the zoonotic potential of classical scrapie in primates and human PrP transgenic mice are extremely limited or not yet available, a single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
The opinion concludes that human PrP transgenic mice and primates are currently the most relevant models for investigating the human transmission barrier, but the extent to which such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. It is unpredictable whether a TSE agent will transmit to a new host, and if the transmission principally occurs, what the transmission rate will be.
Based on the results obtained with in vitro conversion assays, the opinion concludes that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species. Results also suggest that these assays may be developed as a tool for quantifying the transmission barriers between species for different TSE agent strains; however, there is no means at the moment to transpose in vitro results into the likelihood of in vivo interspecies transmission.
-- Communicated by: Terry S Singeltary Sr
[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals.
It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]
******
http://www.promedmail.org/pls/apex/f?p=2400:1202:888892554804923::NO::F2400_P1202_CHECK_DISPLAY,F2400_P1202_PUB_MAIL_ID:X,88784
Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed
http://whqlibdoc.who.int/publications/2003/9241545887.pdf
http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101
Wednesday, August 24, 2011
All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/all-clinically-relevant-blood.html
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/there-is-no-safe-dose-of-prions.html
sporadic CJD slowly, and steadily, on the rise ;
U.K. CJD Statistics
--------------------------------------------------------------------------------
CJD Figures These figures show the number of suspect cases referred to the NCJDRSU in Edinburgh, and the number of deaths of definite and probable cases in the UK, from 1 January 1990 up to 5th September 2011
see steady increase in sporadic CJD cases ;
http://www.cjd.ed.ac.uk/figures.htm
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
SEE CANADA CJD STATS, UNKNOWN PHENOTYPE CJD ON THE RISE IN CANADA ALSO ;
Tuesday, June 14, 2011
Clinical research in CJD at a U.S. clinical prion research center: CJD Quinacrine Study results and improved diagnosis of prion disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/clinical-research-in-cjd-at-us-clinical.html
Tuesday, April 26, 2011
sporadic CJD RISING Text and figures of the latest annual report of the NCJDRSU covering the period 1990-2009 (published 11th March 2011)
http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html
Tuesday, March 29, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY EXPOSURE SPREADING VIA HOSPITALS AND SURGICAL PROCEDURES AROUND THE GLOBE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/transmissible-spongiform-encephalopathy.html
snip...SEE FULL TEXT WITH VIDEOS ;
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
(see video here) ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
(see video here)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
TSS
layperson
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
Agriculture: Animal Feed Question 11.15 am Asked by Baroness Jenkin of Kennington
To ask Her Majesty's Government what is the scientific basis for continuing the ban on feeding animal by-products and catering waste to pigs and chickens.
The Parliamentary Under-Secretary of State, Department for Environment, Food and Rural Affairs (Lord Henley): My Lords, the basis for banning the feeding of animal by-products and catering waste to
8 Sep 2011 : Column 386
pigs and chickens is to prevent the spread of serious animal diseases for which these materials may be a vector. The European Commission is proposing to lift the ban on feeding certain processed animal proteins to pigs and chickens in the light of scientific advice that the ban is no longer justified. The Government are considering their position.
Baroness Jenkin of Kennington: I thank my noble friend for his reply. Can he confirm that if the EC relaxes the ban on non-ruminant ABP being fed to pigs and chickens; and if, following the consultations he refers to, the Government are satisfied by the scientific evidence that there are no public health risks, they will then lift the ban in the UK?
Lord Henley: My Lords, obviously we want to take the scientific evidence into account and consider it very carefully. We also want to take into account likely consumer reaction because we want to take consumers along with us. If that were the case, yes, we would be prepared to lift the ban.
Lord May of Oxford: My Lords, does the Minister agree that although there is remaining uncertainty as to exactly the origins of the rogue prion that caused BSE and how it hopped into cattle, the balance of opinion and evidence is that it came from the unnatural practice of feeding animal by-products to cattle? In the light of that, would it not be wise to continue the current precautionary legislation?
Lord Henley: My Lords, as a very eminent scientist, the noble Lord is right to draw the attention of the House to the scientific evidence. At this stage there is no question of lifting the ban on feeding to cattle. We are talking purely about non-ruminants, such as pigs and chickens, at this stage. Obviously we will look at the evidence and at what the Food Standards Agency has to say, and then make a decision.
Lord Grantchester: We must proceed only on a risk-based approach and, as the Minister said, the other element to be considered is the acceptance by consumers of food so produced. The supermarkets are the gateway to the consumer. Can the Minister tell the House the attitude of supermarkets to reducing food waste by this change of policy? What discussion has his department had with supermarkets and the Food and Drink Federation?
Lord Henley: My Lords, we will continue to discuss these matters with the supermarkets and others. Obviously, where it is appropriate, food waste can go to feed animals-already some food waste can do so, when it has been appropriately separated from meat and other such products. However, as I made clear earlier, any loosening of what is happening will depend on scientific evidence and consideration of these matters. I also think that it is important, as the noble Lord makes clear, that we take opinion along with us on this matter.
Baroness Miller of Chilthorne Domer: My Lords, would the Minister accept that traditionally fed pigs are very popular with the public in terms of the flavour of pork, and so on? They certainly were until the change in their food. Feeding pigs largely on soya
8 Sep 2011 : Column 387
has an unintended consequence, in that all the imports of soya are leading to the further destruction of the rainforests. We really must make clear that using our food waste as best we can to feed to pigs has important consequences much further away in the world.
Lord Henley: My noble friend is right to point to further consequences of feeding animals in this way, in terms of producing the amount of soya used. Again, I stress to her, we should not make any changes unless the scientific evidence assures us that that is right and proper.
Lord Whitty: My Lords, would the Minister accept that the Government and the European authorities are right to proceed with caution on this front? I speak both as the Minister who was allegedly in charge during the last stages of food and mouth and as a former consumer champion. The noble Lord, Lord May, has spoken about BSE and we still do not know how the foot and mouth virus entered the chain. While some relaxation may be possible, I advise extreme caution.
Lord Henley: My Lords, I am sure that the noble Lord was totally in charge, and not just allegedly. As he puts it, we will proceed only if the scientific evidence is right and proper.
Baroness O'Cathain: My Lords, it is very important we realise that the public perception is that the outbreak of foot and mouth disease in February 2001, which had such horrific consequences for the economy and everything else, was the result of feeding animals to animals. Although there is a suggestion-or at least the Minister has stated-that that will not happen with cattle, in the minds of the Great British public it does not matter whether it is cattle, pigs or poultry; they would still have this feeling. We must be awfully careful before relaxing the ban.
Lord Henley: My Lords, the ban in 2001 that my noble friend refers to was a ban on swill. We had already banned the use of processed animal protein as a result of the BSE problems. I reiterate what I have said in answer to every question: we will proceed with extreme caution and we will base any decisions, as will the European Commission, on the scientific evidence available to us.
http://www.publications.parliament.uk/pa/ld201011/ldhansrd/text/110908-0001.htm#11090855000822
ARCHIVE: BSE: Disease control & eradication - The feed ban
The aim of our BSE-related feed control policy is to ensure the continued decline and eventual eradication of BSE in the UK. Effective controls on livestock feed are the key to achieving this.
The rate of BSE cases in cattle being reported now is significantly lower than in 1988, when the disease was first made notifiable, and the number of new cases continues to decline yet further. The key factor behind this success has been the very high level of compliance with BSE-related feed controls throughout the feed manufacture, supply, and livestock industries. Industry quality assurance schemes have considerably enhanced the level of compliance.
Experiments show that doses of infected tissue as low as 1 mg can infect a calf so there is a need for everyone involved in the feed chain to maintain the very high level of compliance seen to date.
Feed controls
In the UK, the original feed ban was introduced in 1988 to prevent ruminant protein being fed to ruminants. In addition, it has been illegal to feed ruminants with all forms of mammalian protein (with specific exceptions) since November 1994 and to feed any farmed livestock, including fish and horses, with mammalian meat and bone meal (mammalian MBM) since 04 April 1996.
EU-wide Feed Controls
Regulation (EC) No.999/2001 introduced EU controls to combat the spread of BSE. The measures included a ban on the feeding of processed animal proteins to animals which are kept, fattened or bred for the production of food. Some of these measures have been amended in line with the European Commission’s TSE Roadmap and further amendments are possible in the future. The Regulation is administered by the Transmissible Spongiform Encephalopathies Regulations.
Feed controls - At a glance
snip...see full text ;
http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bse/controls-eradication/feed-ban.htm
ARCHIVE: BSE: Disease control & eradication - the feed ban - born after the July 1988 ban (BAB) cases
[back toThe feed ban]
The July 1988 ban on feeding ruminant proteins to ruminants (e.g. cattle, sheep, goats and deer) in Great Britain, significantly reduced the risk of BSE infection. There was a marked decrease in the number of confirmed BSE cases born after the July 1988 ban (BAB cases) although the long incubation period delayed the impact on BSE cases by approximately five years. Investigations of the initial BAB cases indicated that the most likely source of infection in these cases was the continued use of feed manufactured before the 1988 ban.
Reasons for BAB cases
By autumn 1994 the decline in the epidemic was occurring more slowly in the north and east of England in which the proportion of pigs relative to cattle was highest. At that time pig and poultry feed could legitimately contain ruminant meat and bone meal (MBM) and there was an increased risk of cross contamination of cattle feed with MBM in these areas. Samples of cattle feed taken in August 1994 were found to contain ruminant MBM, demonstrating that such cross-contamination could occur. A 1994 case-control study looked at possible causes of BSE in BAB animals concluding that a food borne source of infection was the most likely explanation.
The continued presence of BSE infectivity in MBM suggested failings in the Specified Risk Material (formerly Specified Bovine Offals (SBO)) controls. The most likely source of this problem came from the practice of splitting bovine skulls. Brain was disposed as SBO and the skull was rendered to MBM, but brain tissue sometimes remained in the skull, allowing infectivity to enter MBM. Other SBO may have been inadequately separated from non-SBO material, providing another potential route of infection. Subsequent research has shown that some of the rendering systems in use until December 1994 had little effect on BSE.
Prevention of Cross Contamination
In August 1995, the controls on the handling of SBO were strengthened further to protect animal health. They required that the whole skull (except the tongue) be disposed of as SBO and that rendering plants use dedicated lines for processing SBO. In April 1996 the use of mammalian MBM was banned in all feed for livestock, fish and equine animals. This was not as a result of fears of BSE in non-ruminant species but to remove any possible risk of cross-contamination of cattle rations with MBM in feed intended for other species. A Voluntary Feed Recall Scheme, in June 1996, offered free collection and disposal of residual stocks of feed. From 1 August 1996 it became an offence (except in very tightly defined and controlled circumstances) to hold mammalian MBM on farms or in feed mills and premises where livestock feed is used, produced, prepared or stored.
BSE: Disease Control & Eradication - The Feed Ban - Born After the Reinforced Ban (BARB) Cases
1 August 1996 is regarded as the date the reinforced feed ban became effective. BSE cases born after July 1996 are referred to as born after the reinforced ban (BARB) cases.
Incidence
Details for cases in animals born after the reinforced feed ban of August 1996, that have been confirmed in Great Britain and in Northern Ireland, are available on the Veterinary Laboratories Agency website (PDF 300 KB).
Reasons for BARB Cases
Animal Health carries out a detailed epidemiological investigation into all BARB cases in Great Britain. One possible reason for BARB cases is the contamination of cattle feed ingredients with mammalian MBM handled, stored and transported outside the UK, prior to the 2001 EU-wide ban feeding of processed animal protein (PAP) to all farmed animals. Newer Member States may not have implemented full BSE controls until after January 2001.There is also evidence from epidemiological investigations into BARB cases that some cases result from the persistence of infection in feed stores.
In 2004, Professor William Hill FRS of the University of Edinburgh carried out an independent review of BARB cases in the UK. Professor Hill concluded that the UK controls in place to eliminate BSE in cattle were soundly based and confirmed that the elimination of food-borne sources was key to the eradication of BSE. He recommended that risk-based controls and monitoring should be maintained on animals and feed.
The report is available (PDF 177 KB) and the Defra response is available here (PDF 55KB).
Spontaneous occurrence (14-16) The evidence from the absence of BSE in many countries and the surveillance schemes abroad indicates that most BARBs cases cannot have arisen spontaneously, although the possibility cannot be excluded that a very few of them did so. The possibility of a very low frequency of spontaneous occurrence of BSE may be monitored from the output of surveillance in cattle populations elsewhere.
snip...
Genetic variation in susceptibility (17-21) a) Previous statistical and molecular genetic studies indicate there is little genetic variation of cattle associated with susceptibility to BSE. b) Preliminary information from the GB analysis and detailed information from the NI analyses of DNA sequence data on BARBs cases and controls as yet show no clear associations, with no genotype exclusively associated with BARBs cases whether acquired by infection or arising spontaneously.
snip...
Feed borne infection (31-34) a) Recent unpublished experiments at the VLA have shown that feeding exceptionally low doses (0.001g) of infected neural tissue can cause BSE. b) The working hypothesis of Defra that the major cause of BSE in BARBs cases has been through the ingestion of contaminated feed, most likely by young animals, is strongly supported. Thus control of the disease requires, as it has always required, completely eliminating the agent from the cattle feed chain. c) Understanding causes of variation in infectivity are important in terms of understanding the disease, but do not particularly impinge on the control of BSE, where risks have to be avoided. R: Defra continues to operate on the basis that BSE transmission via feed is the major route involved in BARB cases.
snip...
General conclusions Elimination of feed borne sources seems to be now, as before, the key to elimination of BSE. The incidence of the disease can be greatly reduced but not readily eliminated in any country by adequate imposition of controls, particularly on animal feed. As the level of incidence falls both in the UK and internationally, the risks of contamination through cattle feed, pet food, or indeed through any other source, fall whether or not controls in the UK and abroad are further tightened. With the current expertise in Defra and the VLA, GB is well placed to keep on top of and promote developments. R: It is essential that appropriate, risk based, controls and monitoring should be maintained on animals and feed until no cases of BSE are found, and controls tightened up where feasible, both in the UK and elsewhere that the UK can influence. In view of the very long incubation period of BSE in some animals, long-continued vigilance is necessary. It is not evident, however, that specific new measures are needed. Basically it is necessary to ‘keep taking the medicine’. Nevertheless, in view of new discoveries on the nature of the disease and the possibilities of new or changed TSEs arising, relevant research capacity in GB should be maintained.
snip...
http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bse/documents/hillreport.pdf
see full text ;
http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bse/controls-eradication/feedban-bornafterban.htm
BSE SUMMARY OF PASSIVE SURVEILLANCE REPORTS IN GREAT BRITAIN
http://vla.defra.gov.uk/science/docs/sci_tse_stats_gboverview.pdf
GENERAL STATISTICS ON BSE CASES IN GREAT BRITAIN
http://vla.defra.gov.uk/science/docs/sci_tse_stats_gen.pdf
TSE EXOTIC SPECIES
http://vla.defra.gov.uk/science/docs/sci_tse_stats_exotic.pdf
Envt.11: Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation
Justin Greenlee,† Robert Kunkle and Jodi Smith
National Animal Disease Center, ARS, USDA; Ames, IA USA †Presenting author; Email: justin.greenlee@ars.usda.gov
Transmissible spongiform encephalopathies (TSEs, prion diseases) are chronic neurodegenerative diseases that occur in humans, cattle, sheep, goats, cervids and a number of laboratory animal models. There is no evidence of the natural occurrence of any form of TSE in the pig, but pigs have been shown to be susceptible to Bovine Spongiform Encephalopathy (BSE) infection by multiple-route parenteral challenge. However, pigs orally exposed at eight weeks of age to large amounts of brain from cattle clinically affected with BSE did not support infection after seven years of observation. In the US, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine, mink and poultry still occurs. Although unlikely, the potential for swine to have access to TSE-contaminated feedstuffs exists. The potential for swine to serve as a host for the agent of chronic wasting disease (CWD) is unknown. The purpose of this study was to perform intracerebral inoculation of the CWD agent to determine the potential of swine as a host for the CWD agent and their clinical susceptibility. This study utilized 26 swine randomly divided into controls (n = 6) and intracranial inoculates (n = 20). CWD inoculum was a pooled 10% (w/v) homogenate derived from three white-tailed deer clinically ill with CWD from three different sources (elk, white-tailed deer, mule deer) and was given by a single intracranial injection of 0.75 ml. Necropsies were done on ten animals at six months post inoculation (PI), at approximately the time the pigs were expected to reach market weight. Additional pigs have been necropsied due to intercurrent disease (primarily lameness) over the course of the study (29–64 months). Samples collected at necropsy were examined for spongiform change after routine staining (hematoxylin and eosin) and for immunoreactivity to prion protein (PrPSc) by immunohistochemistry. Further, brain samples from at least two regions were tested by western blot. No results suggestive of spongiform encephalopathy were obtained from animals necropsied at six months PI, but positive results after an incubation period of only six months would be uncharacteristic. A single animal was positive for CWD by IHC and WB at 64 months PI. Two inoculated pigs and one control pig remain alive, so it is not possible to determine the attack rate of CWD in swine at this time. However, lack of positive results in pigs necropsied at 29–56 months PI and the long incubation of the single positive case suggest that swine are unlikely to be affected by CWD if inoculated by a natural route.
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;
1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,
The neuropathology of experimental bovine spongiform encephalopathy in the pig
Ryder SJ, Hawkins SA, Dawson M, Wells GA.
Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.
In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.
PMID: 10684682 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract
IN CONFIENCE
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought igs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. ...see full text ;
http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf
IN CONFIDENCE
So it is plausible pigs could be preclinically affected with BSE but since so few are allowed to reach adulthood this has not been recognised through clinical disease. ...
http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf
BSE TO PIGS NEWS RELEASE
http://web.archive.org/web/20030822162313/www.bseinquiry.gov.uk/files/yb/1990/09/24001001.pdf
CONFIDENTIAL
BSE: PRESS PRESENTATION
http://web.archive.org/web/20030822160958/www.bseinquiry.gov.uk/files/yb/1990/09/20003001.pdf
http://web.archive.org/web/20040623191707/www.bseinquiry.gov.uk/files/yb/1990/09/24013001.pdf
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf
INDUSTRY RESPONSE TYPICAL
http://web.archive.org/web/20030822055917/www.bseinquiry.gov.uk/files/yb/1990/09/25007001.pdf
DEFENSIVE BRIEFING
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf
CONFIDENTIAL
pigs & pharmaceuticals
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf
COMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUP
There are only two products using porcine brain and these use corticotrophin BP, made from porcine pituitary, source from outside the UK.............
http://web.archive.org/web/20040622220349/www.bseinquiry.gov.uk/files/yb/1990/10/31003001.pdf
It was not until . . . August 1990, that the result from the pig persuaded both SEAC and us to change our view and to take out of pig rations any residual infectivity that might have arisen from the SBOs.
http://web.archive.org/web/20071014143511/http://www.bseinquiry.gov.uk/files/tr/tab69.pdf
4.303 The minutes of the meeting record that:
It was very difficult to draw conclusions from one experimental result for what may happen in the field. However it would be prudent to exclude specified bovine offals from the pig diet. Although any relationship between BSE and the finding of a spongiform encephalopathy in cats had yet to be demonstrated, the fact that this had occurred suggested that a cautious view should be taken of those species which might be susceptible. The 'specified offals' of bovines should therefore be excluded from the feed of all species. 17
http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf
4.308 SEAC issued formal advice on 20 September 1990, following its meeting on the previous day. The advice stated:
Since this result shows that pigs can get spongiform encephalopathy, even though there is no evidence that they have done so in the field, we believe that pigs should no longer be fed with protein derived from bovine tissues which might contain the BSE agent, ie, those 'specified' bovine offals that are already excluded from human consumption. It would make sense to extend this prohibition to feed for all species, including household pets, as other species have now developed spongiform encephalopathies. We are aware that many animal feed compounders and pet food manufacturers are already applying such a ban on a voluntary basis. 22
http://web.archive.org/web/20060625223925/http://www.bseinquiry.gov.uk/files/yb/1990/09/20002001.pdf
4.309 In a statement to the Inquiry, Dr Tyrrell said:
It was the rapid increase in the BSE epidemic, the occurrence of more cases of FSE and the results of the pig transmission experiment which led SEAC to give the advice we did on the extension of the SBO ban. Before then (September 1990), we were not asked to advise on the extension of the SBO ban. It was important to consider humans before other animals. It should be remembered that prior to the test results of the pig transmission experiment, pigs and poultry were not known to be susceptible to TSEs. Breeding pigs, in particular, were thought to have received a very high exposure to the same type of contaminated MBM as cattle but without any evidence of the occurrence of TSE. The issue of symptom-less hosts was considered very carefully because it could apply to all domestic and farmed animal species. 23
http://web.archive.org/web/20040225164252/http://www.bseinquiry.gov.uk/files/ws/s011b.pdf
SE1805 Transmissibility of BSE to domestic fowl by injection with brain homogenate.
1 challenged bird died overnight (42 months p.i.) following a period of ataxia histopathological examination pending.
2 further challenged birds are also showing neurological signs of ataxia and tremor (43 months p.i.). All affected birds are cock birds. The remaining 4 challenged hens are clinically normal (43 months p.i.).
2 control birds were culled due to intercurrent disease (40 and 43 months p.i.) .. No significant lesions were observed in one and histopathological examination is pending on the other.
The remaining 6 control birds are clinically normal.
SEI806 Transmissibility of ESE to domestic fowl by oral exposure to brain homogenate.
1 challenged cock bird was necropsied (41 months p.i.) following a period of ataxia, tremor, limb abduction and other neurological signs. Histopathological examination failed to reveal any signi ficant lesions of the central or peripheral nervous systems.
94/01.19/7.1
1 other challenged cock bird is also showing ataxia (43 months p.i.). The remaining 2 challenged cocks and 5 hens are clinically normal (43 months p.i.).
Further examinations are in progress to determine the cause of morbidity in these studies (SE1805 and SE1806).
For controls see SE1805. ...
snip...full text ;
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/01/19007001.pdf
SEE FULL TEXT ;
http://madporcinedisease.blogspot.com/
TRANSLATION
F437/91
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY -
* The Red-Neck Ostrich 'THE AUTOPSY' & TSEs
THE AUTOPSY
Date: Mon, 11 Jun 2001 16:24:51 -0700
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs 'THE AUTOPSY'
http://collections.europarchive.org/tna/20080102120315/http://www.bseinquiry.gov.uk/files/sc/Seac10/tab06.pdf
1 The carrion birds are animals whose diet regularly or occasionally includes the consumption of carcasses, including possibly TSE infected ruminant carcasses.
http://ec.europa.eu/food/fs/sc/ssc/out295_en.pdf
It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20040523230128/www.bseinquiry.gov.uk/files/ws/s145d.pdf
it is clear that the designing scientists must have also shared Mr Bradleyâs surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20030526212610/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background: In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims: The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods: Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results: In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions: Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
Tuesday, October 27, 2009
Petition to Declare Poultry Litter as a Food Additive and to Ban Its Use as Cattle Feed August 12, 2009 UNITED STATES
DEPARTMENT OF HEALTH AND HUMAN SERVICES FOOD AND DRUG ADMINISTRATION
http://madcowfeed.blogspot.com/2009/10/petition-to-declare-poultry-litter-as.html
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr." To: fdadockets@oc.fda.gov
http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html
Wednesday, July 6, 2011
Mad cow disease: EU must maintain strict controls, says Parliament
snip...
but the ban on feeding animal protein to non-ruminants, such as pigs, could gradually be lifted if further safeguards are put in place, they add.
snip...
http://efsaopinionbseanimalprotein.blogspot.com/2011/07/mad-cow-disease-eu-must-maintain-strict.html
WHAT HAPPENS WHEN YOU RENDER UNTO FEED, AND FEED EVERY LIVESTOCK SPECIES, GAME SPEICIES, ALL STRAINS OF TSE THERE FROM, AND THEN FEED THERE FROM, TO HUMANS AND ANIMALS ???
WE WILL KNOW IN DUE TIME, BECAUSE THIS IS AN ONGOING LONG TERM STUDY FOR THE NORTH AMERICAN CONSUMER $$$
BE WARNED, YOU HAVE, AND CONTINUE TO BE EXPOSED $$$
LET'S LOOK AT A FEW SPECIES THAT HAVE BEEN FED BANNED SUSPECT MAD COW FEED IN THE USA OVER THE DECADES ;
a) EVSRC Custom dairy feed, Recall # V-130-6; b) Performance Chick Starter, Recall # V-131-6; c) Performance Quail Grower, Recall # V-132-6; d) Performance Pheasant Finisher, Recall # V-133-6. a) CO-OP 32% Sinking Catfish, Recall # V-100-6; b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6; c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6; e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6; f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6; g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6; h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6; i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6; j) CO-OP LAYING CRUMBLES, Recall # V-109-6; k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6; l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6; m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
NOW, LET'S LOOK AT A FEW 100S OF TONS OF THESE BANNED SUSPECT MAD COW FEED IN COMMERCE IN THE USA ;
BANNED SUSPECT MAD COW FEED IN COMMERCE 2006-2007, SOME 10 YEARS AFTER THE INFAMOUS PARTIAL AND VOLUNTARY MAD COW FEED BAN or August 4, 1997, that was nothing more than ink on paper, so really, there was no BSE triple fire wall at all, and this was improving ???
*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS
THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
see Alabama banned suspect mad cow feed in commerce ;
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE
Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
snip...
To minimise the risk of farmers' claims for compensation from feed compounders.
To minimise the potential damage to compound feed markets through adverse publicity.
To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.
snip...
THE FUTURE
4..........
MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.
5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.
6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...
SEE full text ;
http://collections.europarchive.org/tna/20080102153800/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf
RE - "BSE-L in North America may have existed for decades" YA THINK ???
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html
Thursday, July 21, 2011
A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:
August 2011 - Volume 70 - Issue 8 - pp 698-702
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Wednesday, June 15, 2011
Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html
sporadic CJD accounts for over 85% plus of all human TSE prion disease.
sporadic CJD, of unknown phenotype is rising in Canada and the USA.
animal TSE are rising and spreading in the USA.
we do not know if human TSE from atypical BSE, or from CWD infected deer and elk, or from scrapie infected sheep and goats, would look like nvCJD or sporadic CJD, or this UNKNOWN PHENOTYPE that is rising in North America.
we do know now however, that some of the sporadic CJD cases have now been linked to the atypical BSE cases, which is of no surprise to me.
so in my opinion, and as i have stated before, the continued belief in the UKBSEnvCJD only theory, will only continue to help spread this disease around the globe, via multiple proven routes and sources. ...
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
The conclusions state that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Active screening has allowed the identification of 3 new forms of animal TSEs (H-type atypical BSE, L-type atypical BSE, and atypical scrapie), but the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs. There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential. Transmission experiments to human PrP transgenic mice or primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential and indicate that that of the L-type atypical BSE agent appears similar or even higher than that of the classical BSE agent. A single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
Commentary ---------- Following to a request from the European Commission, the Panel on Biological Hazards (BIOHAZ) and the European Centre for Disease Prevention and Control (ECDC) were asked to deliver a scientific opinion on any possible epidemiological or molecular association between transmissible spongiform encephalopathies (TSEs) in animals and humans. The opinion reviews and discusses the existing scientific evidence that links animal and human TSEs currently known.
The opinion first considers the definition of zoonoses and the principles for the identification of zoonotic diseases, which can be based on evidence gathered from both epidemiological and laboratory studies. The opinion describes the challenges involved in identifying TSEs as zoonoses, due to the specific characteristics of TSE infections/diseases, such as the nature of TSE agents, the occurrence of animal and human TSEs, and the type of monitoring applied, the long incubation period of TSEs etc. The example of the process that led to establishing a link between bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) is reviewed. The epidemiological and laboratory criteria that can be used to investigate such a link are described in detail, since those criteria might be useful for the identification of links between other animal and human TSEs.
The opinion discusses the strain diversity of the TSE agents described in sheep, goats, cattle, cervids, and humans, based on the current knowledge, which highlights that multiple TSE agents exist in each species. The factors influencing the capacity of TSE agents to cross the species transmission barrier are then considered in detail, including the variability in host and donor PrP gene and protein, the TSE strain type involved and its interaction with the host PrP, and the route of infection.
The opinion critically assesses the tools and methodologies currently available to study and evaluate the possible association between animal and human TSEs. The use of epidemiology is discussed for TSEs in both animals and humans, and the possibility to compare the 2 sources of information is presented as a possible method to study the possible links.
Both in vivo and in vitro laboratory methods are considered and discussed, including neuropathology, transmission experiments involving different animal models (wild type and transgenic mice, primates and other species), biochemical methods, cell-free conversion assays, protein misfolding cyclic amplification (PMCA), and cell culture assays. Characteristics, advantages, and disadvantages of the different methods are reviewed, including the opportunity to collate data from different types of experiments for the study of potential associations between animal and human TSEs.
The opinion then reviews the scientific evidence currently available for the different animal and human TSEs, including classical BSE, atypical BSE (H-type and L-type), classical scrapie, atypical scrapie, chronic wasting disease (CWD), transmissible mink encephalopathy (TME), and human TSEs. In particular, the following aspects are systematically discussed for each TSE agent: epidemiology, pathogenesis, and in vivo and in vitro transmission experiments.
The opinion concludes that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. With regard to human TSEs, detected cases of sporadic CJD are randomly distributed in time and geographical location. These observations have been interpreted as a supportive argument that sporadic CJD is not environmentally acquired. However, the epidemiological evidence in relation to sporadic CJD cannot be regarded as definitive, and the possibility that a small proportion of cases are zoonotic cannot be excluded.
It also concludes that a series of uncertainties in relation to the epidemiological patterns of animal and human TSEs indicate that even a rough comparison of the present epidemiological patterns of human and animal TSEs other than classical BSE is unlikely to be informative. Because of these uncertainties, it is an imperative to continue to carry out systematic surveillance of human TSE diseases, and to continue and improve the surveillance of animal TSE diseases.
The opinion highlights that the active screening has allowed the identification of 3 new forms of animal TSEs (L-type atypical BSE, H-type atypical BSE, and atypical scrapie), but that the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs.
There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential.
Transmission experiments to human PrP transgenic mice suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE and classical BSE in sheep agents) might have zoonotic potential, whereas for other agents there is no evidence provided of a zoonotic potential (H-type atypical BSE and CWD), or no published studies are available (classical and atypical scrapie). In addition, transmission experiments to primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential. In particular, primates are highly permissive to L-type atypical BSE, even by the oral route.
The opinion emphasizes that laboratory transmission experiments indicate that the L-type atypical BSE agent has a significant zoonotic potential, which appears similar or even higher than that of the classical BSE agent. While transmission data for evaluating the zoonotic potential of classical scrapie in primates and human PrP transgenic mice are extremely limited or not yet available, a single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
The opinion concludes that human PrP transgenic mice and primates are currently the most relevant models for investigating the human transmission barrier, but the extent to which such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. It is unpredictable whether a TSE agent will transmit to a new host, and if the transmission principally occurs, what the transmission rate will be.
Based on the results obtained with in vitro conversion assays, the opinion concludes that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species. Results also suggest that these assays may be developed as a tool for quantifying the transmission barriers between species for different TSE agent strains; however, there is no means at the moment to transpose in vitro results into the likelihood of in vivo interspecies transmission.
-- Communicated by: Terry S Singeltary Sr
[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals.
It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]
******
http://www.promedmail.org/pls/apex/f?p=2400:1202:888892554804923::NO::F2400_P1202_CHECK_DISPLAY,F2400_P1202_PUB_MAIL_ID:X,88784
Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed
http://whqlibdoc.who.int/publications/2003/9241545887.pdf
http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101
Wednesday, August 24, 2011
All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/all-clinically-relevant-blood.html
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/there-is-no-safe-dose-of-prions.html
sporadic CJD slowly, and steadily, on the rise ;
U.K. CJD Statistics
--------------------------------------------------------------------------------
CJD Figures These figures show the number of suspect cases referred to the NCJDRSU in Edinburgh, and the number of deaths of definite and probable cases in the UK, from 1 January 1990 up to 5th September 2011
see steady increase in sporadic CJD cases ;
http://www.cjd.ed.ac.uk/figures.htm
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
SEE CANADA CJD STATS, UNKNOWN PHENOTYPE CJD ON THE RISE IN CANADA ALSO ;
Tuesday, June 14, 2011
Clinical research in CJD at a U.S. clinical prion research center: CJD Quinacrine Study results and improved diagnosis of prion disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/clinical-research-in-cjd-at-us-clinical.html
Tuesday, April 26, 2011
sporadic CJD RISING Text and figures of the latest annual report of the NCJDRSU covering the period 1990-2009 (published 11th March 2011)
http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html
Tuesday, March 29, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY EXPOSURE SPREADING VIA HOSPITALS AND SURGICAL PROCEDURES AROUND THE GLOBE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/transmissible-spongiform-encephalopathy.html
snip...SEE FULL TEXT WITH VIDEOS ;
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
(see video here) ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
(see video here)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
TSS
layperson
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
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