----- Original Message -----
From: Terry S. Singeltary Sr.
To: TERRY SINGELTARY
Sent: Thursday, May 12, 2011 10:46 PM
Subject: Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans
SCIENTIFIC OPINION
Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans1
EFSA Panel on Biological Hazards (BIOHAZ)2, 3
European Food Safety Authority (EFSA), Parma, Italy
European Centre for Disease Prevention and Control (ECDC)4, 5
Stockholm, Sweden
ABSTRACT
The existing scientific evidence that links animal and human TSEs is reviewed and discussed. The challenges involved in identifying TSEs as zoonoses are described and the example of the process that led to the establishment of a link between Bovine Spongiform Encephalopathy (BSE) and variant Creutzfeldt-Jakob Disease (vCJD) is reviewed. The strain diversity of animal and human TSE agents and the factors influencing the capacity of TSE agents to cross the species transmission barrier are also discussed. The scientific opinion critically assesses the tools and methodologies currently available to study and evaluate the possible association of animal and human TSEs, focussing on epidemiological and laboratory methods. The available scientific evidence on Classical BSE, Atypical BSE (H-type and L-type), Classical scrapie, Atypical scrapie, Chronic Wasting Disease (CWD), Transmissible Mink Encephalopathy (TME) and human TSEs is reviewed. 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 three 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.
© European Food Safety Authority, 2011
KEY WORDS
Zoonosis, Transmissible Spongiform Encephalopathy, Bovine Spongiform Encephalopathy, Scrapie, Creutzfeldt-Jakob Disease
1 On request from the European Commission, Question No EFSA-Q-2009-00799, adopted on 9 December 2010.
2 Panel members: Olivier Andreoletti, Herbert Budka, Sava Buncic, John D Collins, John Griffin, Tine Hald, Arie Havelaar, James Hope, Günter Klein, James McLauchlin, Christine Müller-Graf, Christophe Nguyen-The, Birgit Noerrung, Luisa Peixe, Miguel Prieto Maradona, Antonia Ricci, John Sofos, John Threlfall, Ivar Vågsholm and Emmanuel Vanopdenbosch. Correspondence: biohaz@efsa.europa.eu
3 Acknowledgement: The Panel wishes to thank the members of the Working Group on Any possible epidemiological or molecular association between TSEs in animals and humans: Olivier Andreoletti, Vincent Béringue, Herbert Budka, JoaquÃn Castilla, Emmanuel Comoy, Martin Groschup, James Hope, Jean Manson, Giuseppe Ru, Glenn Telling, Juan Maria Torres, Emmanuel Vanopdenbosch and Robert Will for the preparatory work on this scientific opinion.
4 Advisory Forum (ECDC) members:
www.ecdc.europa.eu/en/aboutus/organisation/af/Pages/AboutUs_Organisation_AdvisoryForum.aspx
5 Acknowledgement: ECDC wishes to thank Daniel Palm and Johanna Takkinen for the support provided to this scientific opinion.
Association between TSEs in animals and humans
EFSA Journal 2011;9(1):1945 2
Association between TSEs in animals and humans
EFSA Journal 2011;9(1):1945 3
SUMMARY
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 two 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.
Association between TSEs in animals and humans
EFSA Journal 2011;9(1):1945 4
The opinion highlights that the active screening has allowed the identification of three 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.
SNIP...
6. The uncertainty on “the origin of sCJD”.
There is speculation that sCJD is due to exposure to Atypical BSE, or is linked to Classical scrapie, Atypical scrapie etc. This uncertainty is the subject of this risk assessment.
SNIP...
6. Synopsis
The primary objective of this document is to assess potential associations between animal and human TSEs. An assessment of the potential causal links between animal and human TSEs according to the Bradford Hill’s guidelines (Bradford Hill, 1965) is shown in Table 5 below. One conclusion is that only the BSE/vCJD link is established. It is important to stress that future scientific information might result in changes to the assessment of one or more of the other animal TSEs.
Table 5: Assessment of Putative Links Between Animal and Human TSEs according to the criteria of the Bradford Hill guidelines.
TABLE 5 OMITTED, please see full text url link below for table 5...TSS
+: some scientific evidence is available for a positive interpretation
+/-: debatable or conflicting evidence is available
(a): Classical BSE has not been identified in sheep, but two cases of BSE in goat have been reported in France and UK
(b): there are multiple strains of the Classical scrapie agent
(c): a single study has reported transmission of a natural sheep Classical scrapie isolate to primates
SNIP...
CONCLUSIONS
• At present, the only TSE agent demonstrated to be zoonotic is the Classical BSE agent.
• In general, 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.
• Except for Classical BSE, there is limited epidemiological information on the prevalence and distribution of individual ruminant TSE agents.
• These uncertainties indicate that even a rough comparison of the present epidemiological patterns of human TSEs and animal TSEs other than Classical BSE is unlikely to be informative. Thus, it is an imperative to continue to carry out systematic surveillance of human TSEs, and to continue and improve the surveillance of animal TSEs.
• The active screening has allowed the identification of three new forms of animal TSEs (L-type Atypical BSE, H-type Atypical BSE, Atypical scrapie). However, the information obtained has major limitations due to the unknown sensitivity of the monitoring system for these TSEs.
• There is no epidemiological evidence provided 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 zoonotic potential (H-type Atypical BSE and CWD agents) or no published studies are available (Classical and Atypical scrapie agents).
• 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.
• 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.
• 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.
• Human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To which extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. The Classical BSE agent, as known zoonotic agent, might be used as a benchmark to evaluate the zoonotic potential of other animal TSE agents.
• The ability to create TSE agents by in vitro conversion assays with a novel or unprecedented host range (such as those that can infect rabbits) indicate that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species.
• The qualitative correlation between in vivo data and in vitro results suggests that in vitro conversion assays may be developed as a tool for quantifying the transmission barriers between diverse species and for different TSE agents. However, there is at the moment no means by which to calibrate and transpose the ease of heterologous conversion in vitro into the likelihood of transmission between species in vivo.
http://www.efsa.europa.eu/de/efsajournal/doc/1945.pdf
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from the OPINION above ;
6. The uncertainty on “the origin of sCJD”.
There is speculation that sCJD is due to exposure to Atypical BSE, or is linked to Classical scrapie, Atypical scrapie etc. This uncertainty is the subject of this risk assessment.
snip...
• 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 zoonotic potential (H-type Atypical BSE and CWD agents) or no published studies are available (Classical and Atypical scrapie agents).
• 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.
• 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.
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let's look at some data shall we ;
Is Prion interspecies transmission barrier tissue-dependent?
Hubert Laude1 Laetitia Herzog1 Emilie Jaumain1 Fabienne Reine1 Annick Le Dur1 Jean-Luc Vilotte2 Vincent Beringue1
1. INRA, UR892, Virologie Immunologie Moléculaires, Jouy en Josas, France;
2. INRA, UMR1313, Génétique Animale et Biologie Intégrative, Jouy en Josas, France
The conformational selection model posits that prion interspecies transmission is essentially constrained by the degree of steric compatibility between the incoming PrPSc and the spectrum of conformations the exposed host PrP primary structure can adopt in the PrPSc state. However the question arises of whether the portfolio of PrPSc conformations allowed by PrPC might differ to a certain extent among brain and extraneural tissues due to different cellular environment or PrPC isoform variation. Of particular concern is the lymphoid tissue in which a number of prion strains can replicate at fairly high levels.
The issue of a possible tissue-dependence of prion interspecies transmission efficacy was examined in three different transgenic mouse models, all exhibiting a strong transmission barrier based on the absence of clear neurological signs and of PrPres in the brains of most inoculated animals. These models consisted in ovine PrP mice (VRQ allele; tg338 line) exposed to either elk CWD or hamster Sc237 prions sources, and in human PrP mice (Met129 allele; tg650 line) inoculated with cattle BSE. Mice inoculated intracerebrally were euthanized at regular intervals after exposure over the entire lifespan and analyzed for the presence of PrPres in brain and spleen tissues. As a common finding, ~75% to 100% of the inoculated mice scored positive for the presence of PrPres in the spleen from ~1 year post-infection onwards, while a minority (~5 %) accumulated PrPres in their brain even at very end of life. When PrPres negative brain and PrPres positive spleen tissues from the same mouse were further transmitted to ad hoc mice, disease was only observed with spleen tissue. Upon serial passaging of Sc237 prions to tg338 mice, a “mutant” strain exhibiting a 19kDa signature emerged in the brain but not the spleen. While the brain-derived agent failed to reinfect hamster PrP tg7mice, the spleen-passaged one did.
These data therefore demonstrate that prion transmission to a foreign host can exhibit a marked tissuedependence, with a much greater permissiveness of the lymphoid over the nervous tissue. This phenomenon did not seem to imply a preexisting lymphotropism of the infecting prion, since Sc237 agent is considered poorly lymphotropic compared to CWD agent.
Our data call for closer examination of extraneural PrPres in humanized or primate models when assessing any zoonotic potential of animal prions. Thus, as shown here, human species barrier to BSE prions may be much lower than previously anticipated according to brain PrPres detection-based studies.
2011 Pre-congress Workshop: TSEs in animals and their environment 13
http://www.prion2011.ca/files/2011TSEBookletV6Final.pdf
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE.
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
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
snip...
please see all seven threats listed in the USA, and more...FULL TEXT ;
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed. ***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al.
JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor:
In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
FREE FULL TEXT
http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
Views ; Reviews
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
Ermias D. Belay, MD,
Ryan A. Maddox, MPH,
Pierluigi Gambetti, MD and
Lawrence B. Schonberger, MD
+ Author Affiliations
From the Division of Viral and Rickettsial Diseases (Drs. Belay and Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA; and National Prion Disease Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600 Clifton Road, Mailstop A-39, Atlanta, GA 30333.
Abstract
Transmissible spongiform encephalopathies (TSEs) attracted increased attention in the mid-1980s because of the emergence among UK cattle of bovine spongiform encephalopathy (BSE), which has been shown to be transmitted to humans, causing a variant form of Creutzfeldt-Jakob disease (vCJD). The BSE outbreak has been reported in 19 European countries, Israel, and Japan, and human cases have so far been identified in four European countries, and more recently in a Canadian resident and a US resident who each lived in Britain during the BSE outbreak. To monitor the occurrence of emerging forms of CJD, such as vCJD, in the United States, the Centers for Disease Control and Prevention has been conducting surveillance for human TSEs through several mechanisms, including the establishment of the National Prion Disease Pathology Surveillance Center. Physicians are encouraged to maintain a high index of suspicion for vCJD and use the free services of the pathology center to assess the neuropathology of clinically diagnosed and suspected cases of CJD or other TSEs.
Received May 7, 2002.
Accepted August 28, 2002.
http://www.neurology.org/content/60/2/176.abstract
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
Published March 26, 2003
http://www.neurology.org/content/60/2/176.abstract/reply#neurology_el_535
Reply to Singletary
Ryan A. Maddox, MPH Ermias D. Belay, MD, Lawrence B. Schonberger, MD Centers for Disease Control and Prevention Atlanta GA
Mr. Singletary raises several issues related to current Creutzfeldt- Jakob disease (CJD) surveillance activities. Although CJD is not a notifiable disease in most states, its unique characteristics, particularly its invariably fatal outcome within usually a year of onset, make routine mortality surveillance a useful surrogate for ongoing CJD
Mr. Singletary raises several issues related to current Creutzfeldt- Jakob disease (CJD) surveillance activities. Although CJD is not a notifiable disease in most states, its unique characteristics, particularly its invariably fatal outcome within usually a year of onset, make routine mortality surveillance a useful surrogate for ongoing CJD surveillance.[1] In addition, because CJD is least accurately diagnosed early in the course of illness, notifiable-disease surveillance could be less accurate than, if not duplicative of, current mortality surveillance.[1] However, in states where making CJD officially notifiable would meaningfully facilitate the collection of data to monitor for variant CJD (vCJD) or other emerging prion diseases, CDC encourages the designation of CJD as a notifiable disease.[1] Moreover, CDC encourages physicians to report any diagnosed or suspected CJD cases that may be of special public health importance (e.g., vCJD, iatrogenic CJD, unusual CJD clusters).
As noted in our article, strong evidence is lacking for a causal link between chronic wasting disease (CWD) of deer and elk and human disease,[2] but only limited data seeking such evidence exist. Overall, the previously published case-control studies that have evaluated environmental sources of infection for sporadic CJD have not consistently identified strong evidence for a common risk factor.[3] However, the power of a case-control study to detect a rare cause of CJD is limited, particularly given the relatively small number of subjects generally involved and its long incubation period, which may last for decades. Because only a very small proportion of the US population has been exposed to CWD, a targeted surveillance and investigation of unusual cases or case clusters of prion diseases among persons at increased risk of exposure to CWD is a more efficient approach to detecting the possible transmission of CWD to humans. In collaboration with appropriate local and state health departments and the National Prion Disease Pathology Surveillance Center, CDC is facilitating or conducting such surveillance and case- investigations, including related laboratory studies to characterize CJD and CWD prions.
Mr. Singletary also expresses concern over a recent publication by Asante and colleagues indicating the possibility that some sporadic CJD cases may be attributable to bovine spongiform encephalopathy (BSE).[4] The authors reported that transgenic mice expressing human prion protein homozygous for methionine at codon 129, when inoculated with BSE prions, developed a molecular phenotype consistent with a subtype of sporadic CJD. Although the authors implied that BSE might cause a sporadic CJD-like illness among persons homozygous for methionine, the results of their research with mice do not necessarily directly apply to the transmission of BSE to humans. If BSE causes a sporadic CJD-like illness in humans, an increase in sporadic CJD cases would be expected to first occur in the United Kingdom, where the vast majority of vCJD cases have been reported. In the United Kingdom during 1997 through 2002, however, the overall average annual mortality rate for sporadic CJD was not elevated; it was about 1 case per million population per year. In addition, during this most recent 6-year period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of UK sporadic CJD deaths.[3, 5] Furthermore, surveillance in the UK has shown no increase in the proportion of sporadic CJD cases that are homozygous for methionine (Will RG, National CJD Surveillance Unit, United Kingdom, 2003; personal communication).
References
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Diagnosis and reporting of Creutzfeldt-Jakob disease. JAMA 2001;285:733-734.
2. Belay ED, Maddox RA, Gambetti P, Schonberger LB. Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States. Neurology 2003;60:176-181.
3. Belay ED. Transmissible spongiform encephalopathies in humans. Annu Rev Microbiol 1999;53:283-314.
4. Asante EA, Linehan JM, Desbruslais M, et al. BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J 2002;21:6358-6366.
5. The UK Creutzfeldt-Jakob Disease Surveillance Unit. CJD statistics.
Available at: http://www.cjd.ed.ac.uk/figures.htm.
Accessed February 18, 2003.
http://www.neurology.org/content/60/2/176.abstract/reply#neurology_el_582
THE PATHOLOGICAL PROTEIN
BY Philip Yam
Yam Philip Yam News Editor Scientific American www.sciam.com
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
CHAPTER 14
Laying Odds
Are prion diseases more prevalent than we thought?
Researchers and government officials badly underestimated the threat that mad cow disease posed when it first appeared in Britain. They didn't think bovine spongiform encephalopathy was a zoonosis-an animal disease that can sicken people. The 1996 news that BSE could infect humans with a new form of Creutzfeldt-Jakob disease stunned the world. It also got some biomedical researchers wondering whether sporadic CJD may really be a manifestation of a zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD is?
Revisiting Sporadic CJD
It's not hard to get Terry Singeltary going. "I have my conspiracy theories," admitted the 49-year-old Texan.1 Singeltary is probably the nation's most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union's Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous
www.mad-cow.org/
Web site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that prions represent more of a threat than people realize, and that the government has responded poorly to the dangers because it is more concerned about protecting the beef industry than people's health.
Singeltary has similar inclinations. ...
snip...
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/
http://books.google.com/books?id=ePbrQNFrHtoC&pg=PA223&lpg=PA223&dq=the+pathological+protein+laying+odds+It%E2%80%99s+not+hard+to+get+Terry+Singeltary+going&source=bl&ots=um0PFAZSZD&sig=JWaGR7M7-1WeAr2qAXq8D6J_jak&hl=en&ei=MhtjS8jMJM2ztgeFoa2iBg&sa=X&oi=book_result&ct=result&resnum=1&ved=0CAcQ6AEwAA#v=onepage&q=&f=false
http://www.springerlink.com/content/r2k2622661473336/fulltext.pdf?page=1
http://www.thepathologicalprotein.com/
http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.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
Human Prion Diseases in the United States
Article Metrics Related Content Comments: 1 .
Abstract Introduction Methods Results Discussion Acknowledgments Author Contributions References
Robert C. Holman1*, Ermias D. Belay1, Krista Y. Christensen1, Ryan A. Maddox1, Arialdi M. Minino2, Arianne M. Folkema1, Dana L. Haberling1, Teresa A. Hammett1, Kenneth D. Kochanek2, James J. Sejvar1, Lawrence B. Schonberger1
1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-borne and Enteric Diseases, Centers for Disease Control and Prevention (CDC), U.S. Department of Health and Human Services (USDHHS), Atlanta, Georgia, United States of America, 2 Division of Vital Statistics, National Center for Health Statistics, Centers for Disease Control and Prevention (CDC), U.S. Department of Health and Human Services (USDHHS), Hyattsville, Maryland, United States of America
Abstract
Background
Prion diseases are a family of rare, progressive, neurodegenerative disorders that affect humans and animals. The most common form of human prion disease, Creutzfeldt-Jakob disease (CJD), occurs worldwide. Variant CJD (vCJD), a recently emerged human prion disease, is a zoonotic foodborne disorder that occurs almost exclusively in countries with outbreaks of bovine spongiform encephalopathy.
This study describes the occurrence and epidemiology of CJD and vCJD in the United States.
Methodology/Principal Findings
Analysis of CJD and vCJD deaths using death certificates of US residents for 1979–2006, and those identified through other surveillance mechanisms during 1996–2008. Since CJD is invariably fatal and illness duration is usually less than one year, the CJD incidence is estimated as the death rate. During 1979 through 2006, an estimated 6,917 deaths with CJD as a cause of death were reported in the United States, an annual average of approximately 247 deaths (range 172–304 deaths). The average annual age-adjusted incidence for CJD was 0.97 per 1,000,000 persons. Most (61.8%) of the CJD deaths occurred among persons =65 years of age for an average annual incidence of 4.8 per 1,000,000 persons in this population. Most deaths were among whites (94.6%); the age-adjusted incidence for whites was 2.7 times higher than that for blacks (1.04 and 0.40, respectively). Three patients who died since 2004 were reported with vCJD; epidemiologic evidence indicated that their infection was acquired outside of the United States.
Conclusion/Significance
Surveillance continues to show an annual CJD incidence rate of about 1 case per 1,000,000 persons and marked differences in CJD rates by age and race in the United States. Ongoing surveillance remains important for monitoring the stability of the CJD incidence rates, and detecting occurrences of vCJD and possibly other novel prion diseases in the United States.
Citation: Holman RC, Belay ED, Christensen KY, Maddox RA, Minino AM, et al. (2010) Human Prion Diseases in the United States. PLoS ONE 5(1): e8521. doi:10.1371/journal.pone.0008521
Editor: Mick F. Tuite, University of Kent, United Kingdom
Received: July 21, 2009; Accepted: October 30, 2009; Published: January 1, 2010
Holman et al. This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.
Funding: The authors have no support or funding to report.
Competing interests: The authors have declared that no competing interests exist.
* E-mail: rholman@cdc.gov
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0008521&annotationId=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd;jsessionid=6325F7DEEF9F972F91B273E1E90A1087.ambra02
re-Human Prion Diseases in the United States
Original Article
Human Prion Diseases in the United States
re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
I kindly disagree with your synopsis for the following reasons ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
Greetings,
WITH more and more atypical Transmissible Spongiform Encephalopathy cases showing up in more and more species here in North America, and the enormous monumental amount of banned mad cow protein in commerce since the infamous partial and voluntary mad cow feed ban inked on paper, with tons and tons crossing back and forth between the USA, Canada, and Mexico, it just does not surprise me of all these "PENDING CLASSIFICATIONS" of human TSE in Canada, and the USA. UK c-BSE transmitted to humans became nvCJD. WE now have atypical strains of BSE in cattle. Mission Texas experiments long ago showed that transmitted USA sheep scrapie to USA bovine, produced a TSE much different than the UK typical c-BSE. SO why would human TSE in the USA look like UK human TSE ? The corruption is mind boggling. The UK saw a suspicious TSE in humans, and science linked it to cattle. North America is awash with human and animal TSE, CJD is rising in young and old, with the same pathology and same symptoms, and none of it is related to the other. isn't that nice. who, what, bestowed such miracles upon North America $
Archive Number 20100405.1091 Published Date 05-APR-2010
Subject PRO/AH/EDR> Prion disease update 1010 (04)
snip...
[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.
The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101
CANADA CJD UPDATE 2011
CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011
3. Final classification of 49 cases from 2009, 2010, 2011 is pending.
snip...
http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0111-eng.pdf
USA 2011
USA
National Prion Disease Pathology Surveillance Center
Cases Examined1
(November 1, 2010)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 87 51 43 7 1 0
1999 121 73 65 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 13
2005 344 194 157 36 1 0
2006 383 197 166 29 0 24
2007 377 214 187 27 0 0
2008 394 231 205 25 0 0
2009 425 258 215 43 0 0
2010 333 213 158 33 0 0
TOTAL 38315 22656 1907 328 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date. sporadic CJD is on a steady rise, and has been since 1996.
I also urge you to again notice these disturbing factors in lines 5 and 6 ;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
========end=====tss=====2011
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html
please see full text here ;
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
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
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
http://cjdusa.blogspot.com/
http://transmissiblespongiformencephalopathy.blogspot.com/
Sunday, May 01, 2011
STUDY OF ATYPICAL BSE 2010 Annual Report May 2011
http://bse-atypical.blogspot.com/2011/05/study-of-atypical-bse-2010-annual.html
Thursday, April 28, 2011
Chronic Wasting Disease Testing and Prevalence Wisconsin April 2011
http://chronic-wasting-disease.blogspot.com/2011/04/chronic-wasting-disease-testing-and.html
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.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://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
Mother to Offspring Transmission of Chronic Wasting Disease
Candace K. Mathiason; Amy Nalls; Kelly Anderson; Jeanette Hayes-Klug; Jenny G. Powers; Nicholas J. Haley; Edward A. Hoover Colorado State University, Fort Collins, CO, USA
We have developed a new cervid model in small Asian muntjac deer (Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by 4 months post infection. Ten fawns were born to these CWD-infected doe— 4 of the fawns were viable, 5 were non-viable, and 1 was a first trimester fetus harvested from a CWD-infected doe euthanized at end-stage disease. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn by IHC as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yielded positive results on another fawn at 10 days of age. In addition, sPMCA assays have demonstrated amplifiable prions in fetal placental or spleen tissue of 3 non-viable fawns and mammary tissue of the dams. Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.
2011 Pre-congress Workshop: TSEs in animals and their environment 9
http://www.prion2011.ca/files/2011TSEBookletV6Final.pdf
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
ENVT.11
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation
Justin Greenlee, Robert Kunkle, Jodi Smith
http://www.prion2011.ca/files/2011TSEBookletV6Final.pdf
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
RISK.21
Thirty-Year Review of Prion Disease Surveillance in the United States
Robert C. Holman, Ryan A. Maddox, Arianne M. Folkema, Arialdi M. Minino, Teresa A. Hammett, Kenneth D. Kochanek, James J. Sejvar, Ermias D. Belay, Lawrence B. Schonberger
http://www.prion2011.ca/files/2011TSEBookletV6Final.pdf
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
Manuscript
Draft Manuscript Number:
Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory
Article Type: Personal View
Corresponding Author: Mr. Terry S. Singeltary,
Corresponding Author's Institution: na
First Author: Terry S Singeltary, none
Order of Authors: Terry S Singeltary, none; Terry S. Singeltary
Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2007.
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
Monday, August 9, 2010
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?
http://prionunitusaupdate2008.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html
***+++***
Thursday, July 10, 2008
A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008 Friday, June 20, 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/novel-human-disease-with-abnormal-prion.html
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report
http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html
IBNC
"All of the 15 cattle tested showed that the brains had abnormally accumulated prion protein."
Saturday, February 28, 2009
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009
SEAC 102/2
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
Saturday, January 29, 2011
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Jpn. J. Infect. Dis., 64 (1), 81-84, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
TSE
http://transmissiblespongiformencephalopathy.blogspot.com/
suppressed peer review of Harvard study October 31, 2002
http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf
Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 INTRODUCTION The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website: http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp).
Comments on technical aspects of the risk assessment were then submitted to FSIS. Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.
This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:
http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 a nd how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Wednesday, March 9, 2011
27 U.S. Senators want to force feed Japan Highly Potential North America Mad Cow Beef TSE PRION CJD
March 8, 2011
President Barack Obama The White House
1600 Pennsylvania Avenue, W Washington, DC 20500
Dear President Obama:
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/27-us-senators-want-to-force-feed-japan.html
http://madcowtesting.blogspot.com/
NOW FOR RISK FACTORS FOR CWD TRANSMISSION TO CATTLE ;
----- Original Message -----
From: David Colby
To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter.
Warm Regards, David Colby
--
David Colby, PhDAssistant ProfessorDepartment of Chemical EngineeringUniversity of Delaware
PLEASE SEE FULL TEXT ;
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
re-ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.
http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194089
" although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.
http://cshperspectives.cshlp.org/letters/submit
please see full text of my submission here ;
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://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
Thursday, April 28, 2011
Chronic Wasting Disease Testing and Prevalence Wisconsin April 2011
http://chronic-wasting-disease.blogspot.com/2011/04/chronic-wasting-disease-testing-and.html
Sunday, March 27, 2011
SCRAPIE USA UPDATE FEBRUARY 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/scrapie-usa-update-february-2011.html
Wednesday, February 16, 2011
IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5–May 2011
http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html
Saturday, December 01, 2007
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model
Volume 13, Number 12–December 2007
Research
http://transmissible-mink-encephalopathy.blogspot.com/2007/12/phenotypic-similarity-of-transmissible.html
TRANSMISSIBLE MINK ENCEPHALOPATHY
http://transmissible-mink-encephalopathy.blogspot.com/
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
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
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
Friday, April 15, 2011
PRION TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PROJECTS, RESEARCH FUNDING, BSE VOLUNTARY TESTING UPDATE IN NORTH AMERICA 2011
http://prionunitusaupdate2008.blogspot.com/2011/04/prion-transmissible-spongiform.html
Einstein once said, 'The definition of insanity is doing the same thing over and over again and expecting different results.' re-transmission studies on TSE's...TSS
Showing posts with label Transmissible Spongiform Encephalopathy. Show all posts
Showing posts with label Transmissible Spongiform Encephalopathy. Show all posts
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