re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010
Sent: Wednesday, July 28, 2010 11:42 AM
Subject: re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE
Greetings again Ms Williams et al at FOIA USDA,
Thank You again for your kind reply on this important information. However, I am concerned that you may not be aware of new transmission studies. You (USDA et al) state Ma'am ;
================================================
The SCA with Italy was mainly to confirm our respective country’s diagnostic tests would detect the various atypical BSE cases as seen in each country), in the meantime, the Italians have published their transmissibility and pathogenesis work on their BASE cases in the following article:
Lombardi G, Casalone C, A DA, Gelmetti D, Torcoli G, Barbieri I, Corona C, Fasoli E, Farinazzo A, Fiorini M, Gelati M, Iulini B, Tagliavini F, Ferrari S, Caramelli M, Monaco S, Capucci L, Zanusso G (2008) Intraspecies transmission of BASE induces clinical dullness and amyotrophic changes. PLoS Pathog 4:e1000075
The above mentioned paper concludes, “In all experimentally infected animals, no PrP**TSE was detected in peripheral tissues, including cervical and mesenteric lymph nodes, spleen, thymus, liver, lung, peripheral nerves and forelimb and limb muscles, either by standard Western blot analysis or following phosphotungstic acid precipitation.“
It is not necessary to change SRM removal due to any different tissue infectivity distribution between classical BSE and atypical BSE. At this time, there is no scientific evidence to suggest a need for expanding the list of tissues included in the Specified Risk Material (SRM) ban as a result of published studies on atypical BSE.
snip...
Moreover, in the paper by Buschmann A, Groschup MH (2005,) Highly bovine spongiform encephalopathy-sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle. J Infect Dis 192:934-942; the authors, when speaking about the classical BSE food-borne epidemic in Europe, concluded their “results provide further indication that the pathogenesis of BSE in cattle is fundamentally different from that in sheep and mice, due to an exclusive intraneuronal spread of infectivity from the gut to the central nervous system.”
end...
================================================
Again, in my opinion, the USDA is cherry picking the science they want to use, and in doing so, I believe they are putting human lives at risk.
I disagree for the following reasons. New studies indeed show that ;
July 10, 2010
Conclusions We report accumulation of L-type atypical BSE prions in peripheral nerve tissues sampled from intracerebrally challenged cattle. Our study demonstrated that almost all of the peripheral nerve tissues tested became PrPres positive in a time-dependent manner, whereas no PrPres was detectable in lymphoid tissues, even in cattle with fatal atypical BSE. Our results suggest the possibility that, like classical BSE prions, L-type BSE prions propagated in the central nervous system and were spread centrifugally by nerve pathways (11,12). In Italy, L-type BSE prions have been characterized in detail by using cattle challenged intracerebrally. However, PrPres was not detected in their peripheral tissues, including the peripheral nerves (13). The reason for the discrepancy in PrPres detection is unclear. In view of the similarities between the L-type and BSE/JP24 prion characteristics (9), this discrepancy may result from differences in the methods used for PrPres detection.
Please see ;
Volume 16, Number 7–July 2010
Dispatch
Accumulation of L-type Bovine Prions in Peripheral Nerve Tissues
Yoshifumi Iwamaru, Morikazu Imamura, Yuichi Matsuura, Kentaro Masujin, Yoshihisa Shimizu, Yujing Shu, Megumi Kurachi, Kazuo Kasai, Yuichi Murayama, Shigeo Fukuda, Sadao Onoe, Ken'ichi Hagiwara, Yoshio Yamakawa, Tetsutaro Sata, Shirou Mohri, Hiroyuki Okada, and Takashi Yokoyama Author affiliations: National Institute of Animal Health, Tsukuba, Ibaraki, Japan (Y. Iwamaru, M. Imamura, Y. Matsuura, K. Masujin, Y. Shimizu, Y. Shu, M. Kurachi, K. Kasai, Y. Murayama, S. Mohri, H. Okada, T. Yokoyama); Hokkaido Animal Research Center, Hokkaido, Japan (S. Fukuda, S. Onoe); and National Institute of Infectious Diseases, Tokyo, Japan (K. Hagiwara, Y. Yamakawa, T. Sata)
Suggested citation for this article
Abstract We recently reported the intraspecies transmission of L-type atypical bovine spongiform encephalopathy (BSE). To clarify the peripheral pathogenesis of L-type BSE, we studied prion distribution in nerve and lymphoid tissues obtained from experimentally challenged cattle. As with classical BSE prions, L-type BSE prions accumulated in central and peripheral nerve tissues.
Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative disorder of cattle characterized by accumulation of a protease-resistant form of a normal cellular prion protein (PrPres) in the central nervous system. The scientific literature in general has assumed that BSE in cattle is caused by a uniform strain (classical BSE). However, different neuropathologic and molecular phenotypes of BSE (atypical BSEs) have recently been reported from various countries (1). Recent data from Western blot analyses of field cases of atypical BSEs are characterized by a higher (H-type BSE) or lower (L-type BSE) molecular mass of the unglycosylated form of PrPres than is classical BSE (2). The origins of atypical BSEs remain obscure; unlike classical BSE, atypical BSE has been detected mainly in aged cattle and suggested a as possible sporadic form of BSE (3).
Several lines of evidence demonstrate that classical BSE and a variant form of Creutzfeldt-Jacob disease are most likely caused by the same agent (4,5). Transmission of classical BSE to humans has been proposed to result from ingestion of contaminated food. Whether atypical BSEs are transmissible to humans remains uncertain; however, human susceptibility to L-type BSEs is suggested by recent experimental transmission in primates (6) and mice transgenic for human prion protein (PrP) (7) by using the most effective route of intracerebral inoculations of prions. The L-type BSE prion is much more virulent in primates and in humanized mice than is the classical BSE prion, which suggests the possibility of zoonotic risk associated with the L-type BSE prion. These findings emphasize the critical importance of understanding tissue distribution of L-type BSE prions in cattle because, among the current administrative measures for BSE controls, the specified risk materials removal policy plays a crucial role in consumer protection.
In Japan, atypical BSE was detected in an aged Japanese Black cow (BSE/JP24) (8). We recently reported the successful transmission of BSE/JP24 prions to cattle and showed that the characteristics of these prions closely resemble those of L-type BSE prions found in Italy (9). In this study, we report the peripheral distribution of L-type BSE prions in experimentally challenged cattle.
The Study
snip...
Conclusions We report accumulation of L-type atypical BSE prions in peripheral nerve tissues sampled from intracerebrally challenged cattle. Our study demonstrated that almost all of the peripheral nerve tissues tested became PrPres positive in a time-dependent manner, whereas no PrPres was detectable in lymphoid tissues, even in cattle with fatal atypical BSE. Our results suggest the possibility that, like classical BSE prions, L-type BSE prions propagated in the central nervous system and were spread centrifugally by nerve pathways (11,12). In Italy, L-type BSE prions have been characterized in detail by using cattle challenged intracerebrally. However, PrPres was not detected in their peripheral tissues, including the peripheral nerves (13). The reason for the discrepancy in PrPres detection is unclear. In view of the similarities between the L-type and BSE/JP24 prion characteristics (9), this discrepancy may result from differences in the methods used for PrPres detection.
We detected infectivity in the nerve tissue samples (including samples from the obex, sciatic nerve, adrenal gland, brachial nerve plexus, and vagus nerve) obtained 10, 12, and 16 mpi. On the basis of the incubation time of 223 ± 25 (mean ± SD) days in mice injected with a 1,000-fold dilution of the obex homogenate, infectious titers in peripheral nerve tissues appeared to be 1,000 × lower than those estimated in the obex during endpoint titration of infectivity.
Our results demonstrate that L-type atypical BSE prions can be distributed in the peripheral nerve tissues of intracerebrally challenged cattle. These findings are useful for understanding L-type BSE pathogenesis and accurately assessing the risks associated with this disease. Investigations of prion distribution in cattle that have been orally challenged with L-type BSE prions are critical.
full text ;
http://www.cdc.gov/eid/content/16/7/pdfs/1151.pdf
http://www.cdc.gov/eid/content/16/7/1151.htm
*****URGENT NOTE HERE ABOUT OIE AND THEIR JUNK SCIENCE ABOUT ATYPICAL BSE*****
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.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
snip...
please see full text ;
Thursday, June 24, 2010
Accumulation of L-type Bovine Prions in Peripheral Nerve Tissues
Volume 16, Number 7–July 2010
http://bse-atypical.blogspot.com/2010/06/accumulation-of-l-type-bovine-prions-in.html
ALSO, please note, atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype ;
P26
TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS
Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA
Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C. The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.
III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)
http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf
BUT yet, USDA scientist even managed to change that science around too, by having the only cow known in the world to date that is familial BSE $ PLEASE NOTE, this so-called BSE with mutated bovine PrP gene (termed BSE-M) that was found in 2006 in the USA. a supposedly new strain of familial BSE ? takes me back to the infamous sporadic FFI, that's not familial ? they don't have a clue, in my opinion. but yet the USDA officials will blame it on anything and everything, but the most likely cause i.e. MAD COW FEED IN COMMERCE. instead, we have another new strain of mad cow disease, only this is in the USA, and it is just a spontaneous old cow disease i.e. 'familial h-BSEalabama'.
''We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in “the approximately 10-year-old cow” carrying the E221K mutation.''
WHAT a hoot. They have now taken the same strain of mad cow disease (h-BSE), that Kong et al in 2009 showed was transmissible to humans via human TG mice, and termed it another new mad cow disease, termed ‘‘U.S. BSE Alabama’’ as being another spontaneous happening from nothing. I swear, this just get's better and better. what about IBNC BSE, no cases yet in the USA ? and just what is IBNC BSE ? (more on that later).
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
Wednesday, March 31, 2010
Atypical BSE in Cattle / position: Post Doctoral Fellow
http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html
Wednesday, February 24, 2010
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th
ICID International Scientific Exchange Brochure -
http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html
Tuesday, July 27, 2010
Spontaneous generation of mammalian prions
http://madcowspontaneousnot.blogspot.com/2010/07/spontaneous-generation-of-mammalian.html
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse
http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html
Thank You Ms Williams, I hope you can understand my disgust. ...
Kind Regards,
Terry S. Singeltary SR.
P.O. Box 42
Bacliff, Texas USA
----- Original Message -----
From: Williams, Monica
To: flounder9@verizon.net
Sent: Wednesday, July 28, 2010 9:26 AM
Subject: Freedom of Information Act
Mr. Terry Singeltary, Sr:
This is a follow up to your Freedom of Information Act (FOIA) request with regard to our response to you on June 18, 2010, concerning the results of Project Number: 3625-32000-086-05, Study of Atypical BSE, and whether it is necessary to change SRM removal due to any different tissue infectivity distribution. Your request was assigned FOIA No. 10-93.
In speaking with our National Animal Disease Center (NADC), we are providing the following clarification responsive to your request:
The Italians submitted the manuscript which is still in review at the journal and we do not have an idea when the manuscript will be accepted or published. Our hope is later this calendar year. Also, the manuscript in review does not contain information relating to transmission or tissue distribution. The Italians have already published their work on the topic. Our animal studies at the National Animal Disease Center (NADC) only started in February and will take many years to complete. We have no way of predicting the time of onset of disease and it could be several years, if ever, before the cattle become diseased.
The SCA with Italy was mainly to confirm our respective country’s diagnostic tests would detect the various atypical BSE cases as seen in each country), in the meantime, the Italians have published their transmissibility and pathogenesis work on their BASE cases in the following article:
Lombardi G, Casalone C, A DA, Gelmetti D, Torcoli G, Barbieri I, Corona C, Fasoli E, Farinazzo A, Fiorini M, Gelati M, Iulini B, Tagliavini F, Ferrari S, Caramelli M, Monaco S, Capucci L, Zanusso G (2008) Intraspecies transmission of BASE induces clinical dullness and amyotrophic changes. PLoS Pathog 4:e1000075
The above mentioned paper concludes, “In all experimentally infected animals, no PrP**TSE was detected in peripheral tissues, including cervical and mesenteric lymph nodes, spleen, thymus, liver, lung, peripheral nerves and forelimb and limb muscles, either by standard Western blot analysis or following phosphotungstic acid precipitation.“
It is not necessary to change SRM removal due to any different tissue infectivity distribution between classical BSE and atypical BSE. At this time, there is no scientific evidence to suggest a need for expanding the list of tissues included in the Specified Risk Material (SRM) ban as a result of published studies on atypical BSE.
Moreover, in the paper by Buschmann A, Groschup MH (2005,) Highly bovine spongiform encephalopathy-sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle. J Infect Dis 192:934-942; the authors, when speaking about the classical BSE food-borne epidemic in Europe, concluded their “results provide further indication that the pathogenesis of BSE in cattle is fundamentally different from that in sheep and mice, due to an exclusive intraneuronal spread of infectivity from the gut to the central nervous system.”
We hope this information is helpful.
Sincerely,
Monica Williams
FOIA Office, REE, USDA
5601 Sunnyside Avenue
Room 1-2248, Mail Stop 5128
Beltsville, MD 20705-5128
monica.williams@ars.usda.gov
Telephone: 301-504-1640
----- Original Message -----
From: Terry S. Singeltary Sr.
To: BSE-L@LISTS.AEGEE.ORG
Sent: Friday, June 18, 2010 11:48 AM
Subject: Re: [BSE-L] Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE
Greetings Ms Williams, ARS, USDA, ET AL,
Thank you for your kind reply and correction of the information in your data base on the Project Number 3625-32000-086-05, Study of Atypical BSE, and whether it is necessary to change SRM removal due to any different tissue infectivity distribution. Your request was logged in and assigned FOIA No. 10-93.
Ms Williams ARS USDA et al stated ;
>>>In searching for records responsive to your request, we discovered that our Agricultural Research Information System (ARIS) database contained incorrect information. The ARIS database incorrectly linked the same progress report to Project Numbers 3625-32000-086-05S and 3625-32000-086-04S, which resulted in inaccurate information being reported for the Study of Atypical BSE. This discrepancy was reported to the managing office and has been resolved. To view the progress report, click or copy and paste the URL into your browser window:
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490&showpars=true&fy=2009
<<<> 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
http://www.ushrl.saa.ars.usda.gov/research/projects/projects.htm?accn_no=408490
my FOIA, two questions still have not been answered. There have been 5 years gone by now
>>> Start Date: Sep 15, 2004 End Date: Sep 14, 2009
<<<> 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
THE STUDY objective specifically said ;
>>> 1a.Objectives (from AD-416) The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species. <<<
>>> 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
http://www.ushrl.saa.ars.usda.gov/research/projects/projects.htm?accn_no=408490
Ms Williams et al at ARS USDA, please tell me via FOIA or not, what the results of the tissue distribution and transmissibility of atypical BSE isolates and comparisons were as stated ;
>>> 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
The study plainly stated that during the 5 years study in question, that Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species would be done ;
>>> Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal. <<<
http://foiamadsheepmadrivervalley.blogspot.com/2010/02/final-report-of-testing-of-belgian.html
http://foiamadsheepmadrivervalley.blogspot.com/
Thank You, Kindly
still waiting
FOIA request answers Project Number 3625-32000-086-05, Study of Atypical BSE, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY UPDATE
June 16, 2010 J Clin Invest. doi:10.1172/JCI42051. Copyright © 2010, The American Society for Clinical Investigation.
Research Article A molecular switch controls interspecies prion disease transmission in mice
Christina J. Sigurdson1,2,3, K. Peter R. Nilsson3, Simone Hornemann4, Giuseppe Manco3, Natalia Fernández-Borges5, Petra Schwarz3, Joaquín Castilla5,6, Kurt Wüthrich4,7 and Adriano Aguzzi3 1Department of Pathology and Department of Medicine, University of California, San Diego, La Jolla, California, USA. 2Department of Pathology, Immunology, and Microbiology, University of California, Davis, Davis, California, USA. 3UniversitätsSpital Zürich, Institute of Neuropathology, Zürich, Switzerland. 4Institut für Molekularbiologie und Biophysik, ETH Zürich, Zürich, Switzerland. 5CIC BioGUNE, Parque tecnológico de Bizkaia, Bizkaia, Spain. 6Ikerbasque, Basque Foundation for Science, Bizkaia, Spain. 7Department of Molecular Biology and Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California, USA. Address correspondence to: Adriano Aguzzi, UniversitätsSpital Zürich, Institute of Neuropathology, Department of Pathology, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland. Phone: 41.44.255.2107; Fax: 41.44.255.4402; E-mail: adriano.aguzzi@usz.ch. Or to: Christina Sigurdson, Department of Pathology, University of California, San Diego, 9500 Gilman Dr., La Jolla, California 92093, USA. Phone: 858.534.0978; Fax: 858.246.0523; E-mail: csigurdson@ucsd.edu. Published June 14, 2010 Received for publication December 15, 2009, and accepted in revised form April 28, 2010.
Transmissible spongiform encephalopathies are lethal neurodegenerative disorders that present with aggregated forms of the cellular prion protein (PrPC), which are known as PrPSc. Prions from different species vary considerably in their transmissibility to xenogeneic hosts. The variable transmission barriers depend on sequence differences between incoming PrPSc and host PrPC and additionally, on strain-dependent conformational properties of PrPSc. The ß2-a2 loop region within PrPC varies substantially between species, with its structure being influenced by the residue types in the 2 amino acid sequence positions 170 (most commonly S or N) and 174 (N or T). In this study, we inoculated prions from 5 different species into transgenic mice expressing either disordered-loop or rigid-loop PrPC variants. Similar ß2-a2 loop structures correlated with efficient transmission, whereas dissimilar loops correlated with strong transmission barriers. We then classified literature data on cross-species transmission according to the 170S/N polymorphism. Transmission barriers were generally low between species with the same amino acid residue in position 170 and high between those with different residues. These findings point to a triggering role of the local ß2-a2 loop structure for prion transmissibility between different species.
snip...
These observations suggest striking differences in the ß-sheet alignment of PrPSc aggregates between prion-infected 170S and 170N animals and may provide a plausible starting point for clarifying the structural basis of prion species barriers that are highly relevant to public health, including the potential transmissibility of bovine and cervid prions to humans. snip... As a possible exception to these observations, cattle may be susceptible to CWD from white-tailed deer (86). The latter finding suggests that specific prion strains can overrule the codon 170 homology requirement.
http://www.jci.org/articles/view/42051?key=456180f4a34aad821c6f#B87
see also ;
Monday, June 14, 2010
A molecular switch controls interspecies prion disease transmission in mice
http://chronic-wasting-disease.blogspot.com/2010/06/molecular-switch-controls-interspecies.html
Friday, May 14, 2010
Prion Strain Mutation Determined by Prion Protein Conformational Compatibility and Primary Structure Published Online May 13, 2010 Science DOI: 10.1126/science.1187107 Science Express Index
http://chronic-wasting-disease.blogspot.com/2010/05/prion-strain-mutation-determined-by.html
http://chronic-wasting-disease.blogspot.com/
Saturday, June 5, 2010
Research Project: Transmissible Spongiform Encephalopathies: Identification of atypical scrapie in Canadian sheep
http://nor-98.blogspot.com/2010/06/research-project-transmissible.html
Saturday, June 12, 2010 PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse
http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html
Wednesday, June 16, 2010
Defining sporadic Creutzfeldt-Jakob disease strains and their transmission properties
http://creutzfeldt-jakob-disease.blogspot.com/2010/06/defining-sporadic-creutzfeldt-jakob.html
Tuesday, June 1, 2010
USA cases of dpCJD rising with 24 cases so far in 2010
http://cjdtexas.blogspot.com/2010/06/usa-cases-of-dpcjd-rising-with-24-cases.html
Wednesday, June 02, 2010 CJD Annex H UPDATE AFTER DEATH PRECAUTIONS Published: 2 June 2003
Updated: May 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/06/cjd-annex-h-update-after-death.html
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
>>>Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=19:cjd-english-info&catid=9:cjd-ingles&Itemid=8
>>>Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
http://creutzfeldt-jakob-disease.blogspot.com/2010/03/irma-linda-andablo-cjd-victim-she-died.html
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
http://cjdtexas.blogspot.com/2010/03/cjd-texas-38-year-old-female-worked.html
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.
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
Tuesday, June 1, 2010
USA cases of dpCJD rising with 24 cases so far in 2010
http://cjdtexas.blogspot.com/2010/06/usa-cases-of-dpcjd-rising-with-24-cases.html
14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)
18.173 page 189
Experimental Challenge of Cattle with H-type and L-type Atypical BSE
A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada
Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.
Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.
Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.
http://www.isid.org/14th_icid/
http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf
http://www.isid.org/publications/ICID_Archive.shtml
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
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.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
please see full text ;
Wednesday, March 31, 2010
Atypical BSE in Cattle
http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html
END...TSS
----- Original Message -----
From: Williams, Monica
To: flounder9@verizon.net
Cc: Williams, Monica
Sent: Friday, June 18, 2010 9:59 AM
Subject: Freedom of Information Act
Mr. Terry Singeltary, Sr.:
This is in response to your May 10, 2010, Freedom of Information Act (FOIA) request concerning the results of Project Number 3625-32000-086-05, Study of Atypical BSE, and whether it is necessary to change SRM removal due to any different tissue infectivity distribution. Your request was logged in and assigned FOIA No. 10-93.
In searching for records responsive to your request, we discovered that our Agricultural Research Information System (ARIS) database contained incorrect information. The ARIS database incorrectly linked the same progress report to Project Numbers 3625-32000-086-05S and 3625-32000-086-04S, which resulted in inaccurate information being reported for the Study of Atypical BSE. This discrepancy was reported to the managing office and has been resolved.
We are providing the link to our website for the correct progress report for Project Number 3625-32000-086-05, Study of Atypical BSE, which documents research conducted under a Specific Cooperative Agreement between the Agricultural Research Service and the Italian BSE Reference Laboratory. Additional details of research can be found in the report for the parent Project 3625-32000-086-00D, Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies.
To view the progress report, click or copy and paste the URL into your browser window:
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490&showpars=true&fy=2009.
We hope this information is helpful. If you need further assistance, please contact me at 301-504-1640 or via e-mail at monica.williams@ars.usda.gov.
Sincerely,
Monica Williams
FOIA Office, REE USDA
5601 Sunnyside Avenue
Building 1-2248, Mail Stop #5128
Beltsville, MD 20705-5128
monica.williams@ars.usda.gov
Telephone: 301-504-1640
Facsimile: 301-504-1647
===============================================================
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *It also suggests a similar cause or source for atypical BSE in these countries.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Thursday, November 18, 2010
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS
http://bse-atypical.blogspot.com/2010/11/united-states-of-america-vs-galen-j.html
Monday, November 22, 2010
Atypical transmissible spongiform encephalopathies in ruminants: a challenge for disease surveillance and control
REVIEW ARTICLES
http://transmissiblespongiformencephalopathy.blogspot.com/2010/11/atypical-transmissible-spongiform.html
TSS
Subject: re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE
Greetings again Ms Williams et al at FOIA USDA,
Thank You again for your kind reply on this important information. However, I am concerned that you may not be aware of new transmission studies. You (USDA et al) state Ma'am ;
================================================
The SCA with Italy was mainly to confirm our respective country’s diagnostic tests would detect the various atypical BSE cases as seen in each country), in the meantime, the Italians have published their transmissibility and pathogenesis work on their BASE cases in the following article:
Lombardi G, Casalone C, A DA, Gelmetti D, Torcoli G, Barbieri I, Corona C, Fasoli E, Farinazzo A, Fiorini M, Gelati M, Iulini B, Tagliavini F, Ferrari S, Caramelli M, Monaco S, Capucci L, Zanusso G (2008) Intraspecies transmission of BASE induces clinical dullness and amyotrophic changes. PLoS Pathog 4:e1000075
The above mentioned paper concludes, “In all experimentally infected animals, no PrP**TSE was detected in peripheral tissues, including cervical and mesenteric lymph nodes, spleen, thymus, liver, lung, peripheral nerves and forelimb and limb muscles, either by standard Western blot analysis or following phosphotungstic acid precipitation.“
It is not necessary to change SRM removal due to any different tissue infectivity distribution between classical BSE and atypical BSE. At this time, there is no scientific evidence to suggest a need for expanding the list of tissues included in the Specified Risk Material (SRM) ban as a result of published studies on atypical BSE.
snip...
Moreover, in the paper by Buschmann A, Groschup MH (2005,) Highly bovine spongiform encephalopathy-sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle. J Infect Dis 192:934-942; the authors, when speaking about the classical BSE food-borne epidemic in Europe, concluded their “results provide further indication that the pathogenesis of BSE in cattle is fundamentally different from that in sheep and mice, due to an exclusive intraneuronal spread of infectivity from the gut to the central nervous system.”
end...
================================================
Again, in my opinion, the USDA is cherry picking the science they want to use, and in doing so, I believe they are putting human lives at risk.
I disagree for the following reasons. New studies indeed show that ;
July 10, 2010
Conclusions We report accumulation of L-type atypical BSE prions in peripheral nerve tissues sampled from intracerebrally challenged cattle. Our study demonstrated that almost all of the peripheral nerve tissues tested became PrPres positive in a time-dependent manner, whereas no PrPres was detectable in lymphoid tissues, even in cattle with fatal atypical BSE. Our results suggest the possibility that, like classical BSE prions, L-type BSE prions propagated in the central nervous system and were spread centrifugally by nerve pathways (11,12). In Italy, L-type BSE prions have been characterized in detail by using cattle challenged intracerebrally. However, PrPres was not detected in their peripheral tissues, including the peripheral nerves (13). The reason for the discrepancy in PrPres detection is unclear. In view of the similarities between the L-type and BSE/JP24 prion characteristics (9), this discrepancy may result from differences in the methods used for PrPres detection.
Please see ;
Volume 16, Number 7–July 2010
Dispatch
Accumulation of L-type Bovine Prions in Peripheral Nerve Tissues
Yoshifumi Iwamaru, Morikazu Imamura, Yuichi Matsuura, Kentaro Masujin, Yoshihisa Shimizu, Yujing Shu, Megumi Kurachi, Kazuo Kasai, Yuichi Murayama, Shigeo Fukuda, Sadao Onoe, Ken'ichi Hagiwara, Yoshio Yamakawa, Tetsutaro Sata, Shirou Mohri, Hiroyuki Okada, and Takashi Yokoyama Author affiliations: National Institute of Animal Health, Tsukuba, Ibaraki, Japan (Y. Iwamaru, M. Imamura, Y. Matsuura, K. Masujin, Y. Shimizu, Y. Shu, M. Kurachi, K. Kasai, Y. Murayama, S. Mohri, H. Okada, T. Yokoyama); Hokkaido Animal Research Center, Hokkaido, Japan (S. Fukuda, S. Onoe); and National Institute of Infectious Diseases, Tokyo, Japan (K. Hagiwara, Y. Yamakawa, T. Sata)
Suggested citation for this article
Abstract We recently reported the intraspecies transmission of L-type atypical bovine spongiform encephalopathy (BSE). To clarify the peripheral pathogenesis of L-type BSE, we studied prion distribution in nerve and lymphoid tissues obtained from experimentally challenged cattle. As with classical BSE prions, L-type BSE prions accumulated in central and peripheral nerve tissues.
Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative disorder of cattle characterized by accumulation of a protease-resistant form of a normal cellular prion protein (PrPres) in the central nervous system. The scientific literature in general has assumed that BSE in cattle is caused by a uniform strain (classical BSE). However, different neuropathologic and molecular phenotypes of BSE (atypical BSEs) have recently been reported from various countries (1). Recent data from Western blot analyses of field cases of atypical BSEs are characterized by a higher (H-type BSE) or lower (L-type BSE) molecular mass of the unglycosylated form of PrPres than is classical BSE (2). The origins of atypical BSEs remain obscure; unlike classical BSE, atypical BSE has been detected mainly in aged cattle and suggested a as possible sporadic form of BSE (3).
Several lines of evidence demonstrate that classical BSE and a variant form of Creutzfeldt-Jacob disease are most likely caused by the same agent (4,5). Transmission of classical BSE to humans has been proposed to result from ingestion of contaminated food. Whether atypical BSEs are transmissible to humans remains uncertain; however, human susceptibility to L-type BSEs is suggested by recent experimental transmission in primates (6) and mice transgenic for human prion protein (PrP) (7) by using the most effective route of intracerebral inoculations of prions. The L-type BSE prion is much more virulent in primates and in humanized mice than is the classical BSE prion, which suggests the possibility of zoonotic risk associated with the L-type BSE prion. These findings emphasize the critical importance of understanding tissue distribution of L-type BSE prions in cattle because, among the current administrative measures for BSE controls, the specified risk materials removal policy plays a crucial role in consumer protection.
In Japan, atypical BSE was detected in an aged Japanese Black cow (BSE/JP24) (8). We recently reported the successful transmission of BSE/JP24 prions to cattle and showed that the characteristics of these prions closely resemble those of L-type BSE prions found in Italy (9). In this study, we report the peripheral distribution of L-type BSE prions in experimentally challenged cattle.
The Study
snip...
Conclusions We report accumulation of L-type atypical BSE prions in peripheral nerve tissues sampled from intracerebrally challenged cattle. Our study demonstrated that almost all of the peripheral nerve tissues tested became PrPres positive in a time-dependent manner, whereas no PrPres was detectable in lymphoid tissues, even in cattle with fatal atypical BSE. Our results suggest the possibility that, like classical BSE prions, L-type BSE prions propagated in the central nervous system and were spread centrifugally by nerve pathways (11,12). In Italy, L-type BSE prions have been characterized in detail by using cattle challenged intracerebrally. However, PrPres was not detected in their peripheral tissues, including the peripheral nerves (13). The reason for the discrepancy in PrPres detection is unclear. In view of the similarities between the L-type and BSE/JP24 prion characteristics (9), this discrepancy may result from differences in the methods used for PrPres detection.
We detected infectivity in the nerve tissue samples (including samples from the obex, sciatic nerve, adrenal gland, brachial nerve plexus, and vagus nerve) obtained 10, 12, and 16 mpi. On the basis of the incubation time of 223 ± 25 (mean ± SD) days in mice injected with a 1,000-fold dilution of the obex homogenate, infectious titers in peripheral nerve tissues appeared to be 1,000 × lower than those estimated in the obex during endpoint titration of infectivity.
Our results demonstrate that L-type atypical BSE prions can be distributed in the peripheral nerve tissues of intracerebrally challenged cattle. These findings are useful for understanding L-type BSE pathogenesis and accurately assessing the risks associated with this disease. Investigations of prion distribution in cattle that have been orally challenged with L-type BSE prions are critical.
full text ;
http://www.cdc.gov/eid/content/16/7/pdfs/1151.pdf
http://www.cdc.gov/eid/content/16/7/1151.htm
*****URGENT NOTE HERE ABOUT OIE AND THEIR JUNK SCIENCE ABOUT ATYPICAL BSE*****
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.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
snip...
please see full text ;
Thursday, June 24, 2010
Accumulation of L-type Bovine Prions in Peripheral Nerve Tissues
Volume 16, Number 7–July 2010
http://bse-atypical.blogspot.com/2010/06/accumulation-of-l-type-bovine-prions-in.html
ALSO, please note, atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype ;
P26
TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS
Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA
Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C. The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.
III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)
http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf
BUT yet, USDA scientist even managed to change that science around too, by having the only cow known in the world to date that is familial BSE $ PLEASE NOTE, this so-called BSE with mutated bovine PrP gene (termed BSE-M) that was found in 2006 in the USA. a supposedly new strain of familial BSE ? takes me back to the infamous sporadic FFI, that's not familial ? they don't have a clue, in my opinion. but yet the USDA officials will blame it on anything and everything, but the most likely cause i.e. MAD COW FEED IN COMMERCE. instead, we have another new strain of mad cow disease, only this is in the USA, and it is just a spontaneous old cow disease i.e. 'familial h-BSEalabama'.
''We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in “the approximately 10-year-old cow” carrying the E221K mutation.''
WHAT a hoot. They have now taken the same strain of mad cow disease (h-BSE), that Kong et al in 2009 showed was transmissible to humans via human TG mice, and termed it another new mad cow disease, termed ‘‘U.S. BSE Alabama’’ as being another spontaneous happening from nothing. I swear, this just get's better and better. what about IBNC BSE, no cases yet in the USA ? and just what is IBNC BSE ? (more on that later).
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
Wednesday, March 31, 2010
Atypical BSE in Cattle / position: Post Doctoral Fellow
http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html
Wednesday, February 24, 2010
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th
ICID International Scientific Exchange Brochure -
http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html
Tuesday, July 27, 2010
Spontaneous generation of mammalian prions
http://madcowspontaneousnot.blogspot.com/2010/07/spontaneous-generation-of-mammalian.html
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse
http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html
Thank You Ms Williams, I hope you can understand my disgust. ...
Kind Regards,
Terry S. Singeltary SR.
P.O. Box 42
Bacliff, Texas USA
----- Original Message -----
From: Williams, Monica
To: flounder9@verizon.net
Sent: Wednesday, July 28, 2010 9:26 AM
Subject: Freedom of Information Act
Mr. Terry Singeltary, Sr:
This is a follow up to your Freedom of Information Act (FOIA) request with regard to our response to you on June 18, 2010, concerning the results of Project Number: 3625-32000-086-05, Study of Atypical BSE, and whether it is necessary to change SRM removal due to any different tissue infectivity distribution. Your request was assigned FOIA No. 10-93.
In speaking with our National Animal Disease Center (NADC), we are providing the following clarification responsive to your request:
The Italians submitted the manuscript which is still in review at the journal and we do not have an idea when the manuscript will be accepted or published. Our hope is later this calendar year. Also, the manuscript in review does not contain information relating to transmission or tissue distribution. The Italians have already published their work on the topic. Our animal studies at the National Animal Disease Center (NADC) only started in February and will take many years to complete. We have no way of predicting the time of onset of disease and it could be several years, if ever, before the cattle become diseased.
The SCA with Italy was mainly to confirm our respective country’s diagnostic tests would detect the various atypical BSE cases as seen in each country), in the meantime, the Italians have published their transmissibility and pathogenesis work on their BASE cases in the following article:
Lombardi G, Casalone C, A DA, Gelmetti D, Torcoli G, Barbieri I, Corona C, Fasoli E, Farinazzo A, Fiorini M, Gelati M, Iulini B, Tagliavini F, Ferrari S, Caramelli M, Monaco S, Capucci L, Zanusso G (2008) Intraspecies transmission of BASE induces clinical dullness and amyotrophic changes. PLoS Pathog 4:e1000075
The above mentioned paper concludes, “In all experimentally infected animals, no PrP**TSE was detected in peripheral tissues, including cervical and mesenteric lymph nodes, spleen, thymus, liver, lung, peripheral nerves and forelimb and limb muscles, either by standard Western blot analysis or following phosphotungstic acid precipitation.“
It is not necessary to change SRM removal due to any different tissue infectivity distribution between classical BSE and atypical BSE. At this time, there is no scientific evidence to suggest a need for expanding the list of tissues included in the Specified Risk Material (SRM) ban as a result of published studies on atypical BSE.
Moreover, in the paper by Buschmann A, Groschup MH (2005,) Highly bovine spongiform encephalopathy-sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle. J Infect Dis 192:934-942; the authors, when speaking about the classical BSE food-borne epidemic in Europe, concluded their “results provide further indication that the pathogenesis of BSE in cattle is fundamentally different from that in sheep and mice, due to an exclusive intraneuronal spread of infectivity from the gut to the central nervous system.”
We hope this information is helpful.
Sincerely,
Monica Williams
FOIA Office, REE, USDA
5601 Sunnyside Avenue
Room 1-2248, Mail Stop 5128
Beltsville, MD 20705-5128
monica.williams@ars.usda.gov
Telephone: 301-504-1640
----- Original Message -----
From: Terry S. Singeltary Sr.
To: BSE-L@LISTS.AEGEE.ORG
Sent: Friday, June 18, 2010 11:48 AM
Subject: Re: [BSE-L] Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE
Greetings Ms Williams, ARS, USDA, ET AL,
Thank you for your kind reply and correction of the information in your data base on the Project Number 3625-32000-086-05, Study of Atypical BSE, and whether it is necessary to change SRM removal due to any different tissue infectivity distribution. Your request was logged in and assigned FOIA No. 10-93.
Ms Williams ARS USDA et al stated ;
>>>In searching for records responsive to your request, we discovered that our Agricultural Research Information System (ARIS) database contained incorrect information. The ARIS database incorrectly linked the same progress report to Project Numbers 3625-32000-086-05S and 3625-32000-086-04S, which resulted in inaccurate information being reported for the Study of Atypical BSE. This discrepancy was reported to the managing office and has been resolved. To view the progress report, click or copy and paste the URL into your browser window:
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490&showpars=true&fy=2009
<<<> 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
http://www.ushrl.saa.ars.usda.gov/research/projects/projects.htm?accn_no=408490
my FOIA, two questions still have not been answered. There have been 5 years gone by now
>>> Start Date: Sep 15, 2004 End Date: Sep 14, 2009
<<<> 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
THE STUDY objective specifically said ;
>>> 1a.Objectives (from AD-416) The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species. <<<
>>> 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
http://www.ushrl.saa.ars.usda.gov/research/projects/projects.htm?accn_no=408490
Ms Williams et al at ARS USDA, please tell me via FOIA or not, what the results of the tissue distribution and transmissibility of atypical BSE isolates and comparisons were as stated ;
>>> 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
The study plainly stated that during the 5 years study in question, that Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species would be done ;
>>> Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal. <<<
http://foiamadsheepmadrivervalley.blogspot.com/2010/02/final-report-of-testing-of-belgian.html
http://foiamadsheepmadrivervalley.blogspot.com/
Thank You, Kindly
still waiting
FOIA request answers Project Number 3625-32000-086-05, Study of Atypical BSE, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY UPDATE
June 16, 2010 J Clin Invest. doi:10.1172/JCI42051. Copyright © 2010, The American Society for Clinical Investigation.
Research Article A molecular switch controls interspecies prion disease transmission in mice
Christina J. Sigurdson1,2,3, K. Peter R. Nilsson3, Simone Hornemann4, Giuseppe Manco3, Natalia Fernández-Borges5, Petra Schwarz3, Joaquín Castilla5,6, Kurt Wüthrich4,7 and Adriano Aguzzi3 1Department of Pathology and Department of Medicine, University of California, San Diego, La Jolla, California, USA. 2Department of Pathology, Immunology, and Microbiology, University of California, Davis, Davis, California, USA. 3UniversitätsSpital Zürich, Institute of Neuropathology, Zürich, Switzerland. 4Institut für Molekularbiologie und Biophysik, ETH Zürich, Zürich, Switzerland. 5CIC BioGUNE, Parque tecnológico de Bizkaia, Bizkaia, Spain. 6Ikerbasque, Basque Foundation for Science, Bizkaia, Spain. 7Department of Molecular Biology and Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California, USA. Address correspondence to: Adriano Aguzzi, UniversitätsSpital Zürich, Institute of Neuropathology, Department of Pathology, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland. Phone: 41.44.255.2107; Fax: 41.44.255.4402; E-mail: adriano.aguzzi@usz.ch. Or to: Christina Sigurdson, Department of Pathology, University of California, San Diego, 9500 Gilman Dr., La Jolla, California 92093, USA. Phone: 858.534.0978; Fax: 858.246.0523; E-mail: csigurdson@ucsd.edu. Published June 14, 2010 Received for publication December 15, 2009, and accepted in revised form April 28, 2010.
Transmissible spongiform encephalopathies are lethal neurodegenerative disorders that present with aggregated forms of the cellular prion protein (PrPC), which are known as PrPSc. Prions from different species vary considerably in their transmissibility to xenogeneic hosts. The variable transmission barriers depend on sequence differences between incoming PrPSc and host PrPC and additionally, on strain-dependent conformational properties of PrPSc. The ß2-a2 loop region within PrPC varies substantially between species, with its structure being influenced by the residue types in the 2 amino acid sequence positions 170 (most commonly S or N) and 174 (N or T). In this study, we inoculated prions from 5 different species into transgenic mice expressing either disordered-loop or rigid-loop PrPC variants. Similar ß2-a2 loop structures correlated with efficient transmission, whereas dissimilar loops correlated with strong transmission barriers. We then classified literature data on cross-species transmission according to the 170S/N polymorphism. Transmission barriers were generally low between species with the same amino acid residue in position 170 and high between those with different residues. These findings point to a triggering role of the local ß2-a2 loop structure for prion transmissibility between different species.
snip...
These observations suggest striking differences in the ß-sheet alignment of PrPSc aggregates between prion-infected 170S and 170N animals and may provide a plausible starting point for clarifying the structural basis of prion species barriers that are highly relevant to public health, including the potential transmissibility of bovine and cervid prions to humans. snip... As a possible exception to these observations, cattle may be susceptible to CWD from white-tailed deer (86). The latter finding suggests that specific prion strains can overrule the codon 170 homology requirement.
http://www.jci.org/articles/view/42051?key=456180f4a34aad821c6f#B87
see also ;
Monday, June 14, 2010
A molecular switch controls interspecies prion disease transmission in mice
http://chronic-wasting-disease.blogspot.com/2010/06/molecular-switch-controls-interspecies.html
Friday, May 14, 2010
Prion Strain Mutation Determined by Prion Protein Conformational Compatibility and Primary Structure Published Online May 13, 2010 Science DOI: 10.1126/science.1187107 Science Express Index
http://chronic-wasting-disease.blogspot.com/2010/05/prion-strain-mutation-determined-by.html
http://chronic-wasting-disease.blogspot.com/
Saturday, June 5, 2010
Research Project: Transmissible Spongiform Encephalopathies: Identification of atypical scrapie in Canadian sheep
http://nor-98.blogspot.com/2010/06/research-project-transmissible.html
Saturday, June 12, 2010 PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse
http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html
Wednesday, June 16, 2010
Defining sporadic Creutzfeldt-Jakob disease strains and their transmission properties
http://creutzfeldt-jakob-disease.blogspot.com/2010/06/defining-sporadic-creutzfeldt-jakob.html
Tuesday, June 1, 2010
USA cases of dpCJD rising with 24 cases so far in 2010
http://cjdtexas.blogspot.com/2010/06/usa-cases-of-dpcjd-rising-with-24-cases.html
Wednesday, June 02, 2010 CJD Annex H UPDATE AFTER DEATH PRECAUTIONS Published: 2 June 2003
Updated: May 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/06/cjd-annex-h-update-after-death.html
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
>>>Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=19:cjd-english-info&catid=9:cjd-ingles&Itemid=8
>>>Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
http://creutzfeldt-jakob-disease.blogspot.com/2010/03/irma-linda-andablo-cjd-victim-she-died.html
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
http://cjdtexas.blogspot.com/2010/03/cjd-texas-38-year-old-female-worked.html
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.
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
Tuesday, June 1, 2010
USA cases of dpCJD rising with 24 cases so far in 2010
http://cjdtexas.blogspot.com/2010/06/usa-cases-of-dpcjd-rising-with-24-cases.html
14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)
18.173 page 189
Experimental Challenge of Cattle with H-type and L-type Atypical BSE
A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada
Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.
Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.
Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.
http://www.isid.org/14th_icid/
http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf
http://www.isid.org/publications/ICID_Archive.shtml
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
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.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
please see full text ;
Wednesday, March 31, 2010
Atypical BSE in Cattle
http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html
END...TSS
----- Original Message -----
From: Williams, Monica
To: flounder9@verizon.net
Cc: Williams, Monica
Sent: Friday, June 18, 2010 9:59 AM
Subject: Freedom of Information Act
Mr. Terry Singeltary, Sr.:
This is in response to your May 10, 2010, Freedom of Information Act (FOIA) request concerning the results of Project Number 3625-32000-086-05, Study of Atypical BSE, and whether it is necessary to change SRM removal due to any different tissue infectivity distribution. Your request was logged in and assigned FOIA No. 10-93.
In searching for records responsive to your request, we discovered that our Agricultural Research Information System (ARIS) database contained incorrect information. The ARIS database incorrectly linked the same progress report to Project Numbers 3625-32000-086-05S and 3625-32000-086-04S, which resulted in inaccurate information being reported for the Study of Atypical BSE. This discrepancy was reported to the managing office and has been resolved.
We are providing the link to our website for the correct progress report for Project Number 3625-32000-086-05, Study of Atypical BSE, which documents research conducted under a Specific Cooperative Agreement between the Agricultural Research Service and the Italian BSE Reference Laboratory. Additional details of research can be found in the report for the parent Project 3625-32000-086-00D, Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies.
To view the progress report, click or copy and paste the URL into your browser window:
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490&showpars=true&fy=2009.
We hope this information is helpful. If you need further assistance, please contact me at 301-504-1640 or via e-mail at monica.williams@ars.usda.gov.
Sincerely,
Monica Williams
FOIA Office, REE USDA
5601 Sunnyside Avenue
Building 1-2248, Mail Stop #5128
Beltsville, MD 20705-5128
monica.williams@ars.usda.gov
Telephone: 301-504-1640
Facsimile: 301-504-1647
===============================================================
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *It also suggests a similar cause or source for atypical BSE in these countries.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Thursday, November 18, 2010
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS
http://bse-atypical.blogspot.com/2010/11/united-states-of-america-vs-galen-j.html
Monday, November 22, 2010
Atypical transmissible spongiform encephalopathies in ruminants: a challenge for disease surveillance and control
REVIEW ARTICLES
http://transmissiblespongiformencephalopathy.blogspot.com/2010/11/atypical-transmissible-spongiform.html
TSS
Labels: ARS, atypical bse, PERIPHERAL NERVE TISSUES, PUBLICATION REQUEST, SRM
posted by Terry S. Singeltary Sr. at
9:07 PM
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