Sunday, August 26, 2012

Detection of PrPSc in peripheral tissues of clinically affected cattle after oral challenge with BSE

Detection of PrPSc in peripheral tissues of clinically affected cattle after oral challenge with BSE




Martin Franz1, Martin Eiden1, Anne Balkema-Buschmann1, Justin Greenlee2, Hermann M Schaetzl3, Christine Fast1, Juergen Richt4, Jan-Peter Hildebrandt5 and Martin Groschup1,6


+ Author Affiliations


1 Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany; 2 National Animal Disease Center, ARS-USDA, Ames, IA, USA; 3 Depts of Veterinary Sciences and Molecular Biology, University of Wyoming, Laramie, WY, USA; 4 Kansas State University, College of Veterinary Medicine, Manhattan, KS, USA; 5 University Greifswald, Germany


↵6 E-mail: martin.groschup@fli.bund.de


Received 6 June 2012. Accepted 20 August 2012.



Abstract



Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative prion disease that mainly affects cattle. Transmission of BSE to humans caused a variant form of Creutzfeldt-Jakob disease (vCJD). Following infection the protease-resistant, disease-associated isoform of prion protein (PrPSc) accumulates in the central nervous system and in other tissues. Many countries have defined bovine tissues that may contain prions as specified risk materials (SRMs), which must not enter the human or animal food chains and therefore must be discarded. Ultrasensitive techniques such as the protein misfolding cyclic amplification (PMCA) have been developed to detect PrPSc when present in miniscule amounts that are not readily detected by other diagnostic methods such as immunohistochemistry or western blot. This study was conducted to determine when and where PrPSc can be found by PMCA in cattle orally challenged with BSE. A total of 48 different tissue samples from 4 orally BSE-infected cattle at clinical stages of disease were examined using a standardized PMCA protocol. The protocol used brain homogenate from bovine PrP transgenic mice (Tgbov XV) as substrate and three consecutive rounds of PMCA. Using this protocol PrPSc was found in brain, spinal cord, nerve ganglia, optic nerve, and Peyer’s patches. We could confirm the presence of PrPSc in adrenal gland as well as in mesenteric lymph node – a finding, which was recently reported by another group. Interestingly, additional positive results were obtained for the first time in oesophagus, abomasum, rumen, and rectum of clinically affected cattle.








Wednesday, May 2, 2012


ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND ANIMAL HEALTH






Wednesday, July 28, 2010


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


see full text ;



Wednesday, July 28, 2010


re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010








USDA TRIPLE BSE MAD COW FIREWALL, SRM, FEED, AND SURVEILLANCE


2012


***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...







MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...


***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model






***Infectivity in skeletal muscle of BASE-infected cattle






***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries.






***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.







The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission.


In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.








Friday, May 11, 2012


Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits



***support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE










Thursday, June 21, 2012


Clinical and Pathologic Features of H-Type Bovine Spongiform Encephalopathy Associated with E211K Prion Protein Polymorphism


Justin J. Greenlee1*, Jodi D. Smith1, M. Heather West Greenlee2, Eric M. Nicholson1


1 National Animal Disease Center, United States Department of Agriculture, Agricultural Research Service, Ames, Iowa, United States of America, 2 Iowa State University, Ames, Iowa, United States of America


Abstract


The majority of bovine spongiform encephalopathy (BSE) cases have been ascribed to the classical form of the disease. Htype and L-type BSE cases have atypical molecular profiles compared to classical BSE and are thought to arise spontaneously. However, one case of H-type BSE was associated with a heritable E211K mutation in the prion protein gene. The purpose of this study was to describe transmission of this unique isolate of H-type BSE when inoculated into a calf of the same genotype by the intracranial route. Electroretinograms were used to demonstrate preclinical deficits in retinal function, and optical coherence tomography was used to demonstrate an antemortem decrease in retinal thickness. The calf rapidly progressed to clinical disease (9.4 months) and was necropsied. Widespread distribution of abnormal prion protein was demonstrated within neural tissues by western blot and immunohistochemistry. While this isolate is categorized as BSE-H due to a higher molecular mass of the unglycosylated PrPSc isoform, a strong labeling of all 3 PrPSc bands with monoclonal antibodies 6H4 and P4, and a second unglycosylated band at approximately 14 kDa when developed with antibodies that bind in the C-terminal region, it is unique from other described cases of BSE-H because of an additional band 23 kDa demonstrated on western blots of the cerebellum. This work demonstrates that this isolate is transmissible, has a BSE-H phenotype when transmitted to cattle with the K211 polymorphism, and has molecular features that distinguish it from other cases of BSE-H described in the literature.


snip...


Most significantly it must be determined if the molecular phenotype of this cattle TSE remains stable when transmitted to cattle without the E211K polymorphism as several other isolates of atypical BSE have been shown to adopt a molecular profile consistent with classical BSE after passage in transgenic mice expressing bovine PrPC [40] or multiple passages in wild type mice [23]. Results of ongoing studies, namely passage of the E211K Htype isolate into wild-type cattle, will lend further insight into what role, if any, genetic and sporadic forms of BSE may have played in the origins of classical BSE. Atypical cases presumably of spontaneous or, in the case of E211K BSE-H, genetic origins highlight that it may not be possible to eradicate BSE entirely and that it would be hazardous to remove disease control measures such as prohibiting the feeding of meat and bone meal to ruminants.







Saturday, May 26, 2012


Are USDA assurances on mad cow case 'gross oversimplification'?


SNIP...


What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”


The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”


“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.


In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the origins of atypical cases of BSE,” she said


The argument about feed is critical because if feed is the cause, not a spontaneous mutation, the California cow could be part of a larger outbreak.


SNIP...






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


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


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


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


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


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






Friday, December 05, 2008


Detection of Prion Infectivity in Fat Tissues of Scrapie-Infected Mice


Brent Race1#, Kimberly Meade-White1#, Michael B. A. Oldstone2, Richard Race1, Bruce Chesebro1*






Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿


Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro*






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.






Monday, July 9, 2012


Spread of Classic BSE Prions from the Gut via the Peripheral Nervous System to the Brain


Study Finds "Mad Cow Disease" in Cattle Can Spread Widely in Autonomic Nervous System before Detectable in the Central Nervous System






Response to Public Comments


on the


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:






Suppressed peer review of Harvard study October 31, 2002.


October 31, 2002 Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Conducted by the Harvard Center for Risk Analysis, Harvard School of Public Health and Center for Computational Epidemiology, College of Veterinary Medicine, Tuskegee University Final Report Prepared for U.S. Department of Agriculture Food Safety and Inspection Service Office of Public Health and Science Prepared by RTI Health, Social, and Economics Research Research Triangle Park, NC 27709 RTI Project Number 07182.024






Owens, Julie


From: Terry S. Singeltary Sr. [flounder9@verizon.net]


Sent: Monday, July 24, 2006 1:09 PM


To: FSIS RegulationsComments


Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)



Page 1 of 98 8/3/2006



Greetings FSIS,




I would kindly like to comment on the following ;



snip...




HOWEVER, JAPAN has already shown infectivity in tissues other than CNS in there atypical TSE in cattle, so why should we wait, and expose many to this agent needlessly, since the last two mad cows in the USA were also atypical TSE ?


PrPSc distribution of a natural case of bovine spongiform encephalopathy


Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori- kazu Imamura, Takashi Yokoyama and Morikazu Shinagawa Priori Disease Research Center, National Institute of Animal Health, 3-1-5 Kannondai, Tsukuba 305-0856 Japan gan@affrc.go.jp


Abstract


Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes progressive neurodegeneration of the central nervous system. Infectivity of BSE agent is accompanied with an abnormal isoform of prion protein (PrPSc).


The specified risk materials (SRM) are tissues potentially carrying BSE infectivity. The following tissues are designated as SRM in Japan: the skull including the brain and eyes but excluding the glossa and the masse- ter muscle, the vertebral column excluding the vertebrae of the tail, spinal cord, distal illeum. For a risk management step, the use of SRM in both animal feed or human food has been prohibited. However, detailed PrPSc distribution remains obscure in BSE cattle and it has caused controversies about definitions of SRM. Therefore we have examined PrPSc distribution in a BSE cattle by Western blotting to reassess definitions of SRM.


The 11th BSE case in Japan was detected in fallen stock surveillance. The carcass was stocked in the refrigerator. For the detection of PrPSc, 200 mg of tissue samples were homogenized. Following collagenase treatment, samples were digested with proteinase K. After digestion, PrPSc was precipitated by sodium phosphotungstate (PTA). The pellets were subjected to Western blotting using the standard procedure. Anti-prion protein monoclonal antibody (mAb) T2 conjugated horseradish peroxidase was used for the detection of PrPSc.


PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal ganglia, sublingual ganglion, retina. In addition, PrPSc was also detected in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve).





Our results suggest that the currently accepted definitions of SRM in BSE cattle may need to be reexamined.





T. Kitamoto (Ed.)PRIONSFood and Drug Safety




================





ALSO from the International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004; Bovine spongiform encephalopathy (BSE) in Japan


snip...


"Furthermore, current studies into transmission of cases of BSE that are atypical or that develop in young cattle are expected to amplify the BSE prion"


NO. Date conf. Farm Birth place and Date Age at diagnosis


1. 8. 2003.10.6. Fukushima Tochigi 2001.10.13. 23


2. 9. 2003.11.4. Hiroshima Hyogo 2002.1.13. 21


Test results


# 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology negative


b = atypical BSE case


c = case of BSE in a young animal


b,c, No PrPSc on IHC, and no spongiform change on histology


International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004.


Page 6 of 98


8/3/2006


Tetsuyuki Kitamoto Professor and Chairman Department of Prion Research Tohoku University School of Medicine 2-1 SeiryoAoba-ku, Sendai 980-8575, JAPAN TEL +81-22-717-8147 FAX +81-22-717-8148 e-mail; kitamoto@mail.tains.tohoku.ac.jp Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656 e-mail: kvomi-sasaki@mail.tains.tohoku.ac.ip




=================================













Sunday, February 14, 2010


[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)











Friday, February 11, 2011


Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues








Monday, January 2, 2012


EFSA Minutes of the 6th Meeting of the EFSA Scientific Network on BSE-TSE Brussels, 29-30 November 2011








UPDATE CALIFORNIA JULY 2012 ATYPICAL L-TYPE BASE BSE MAD COW


Saturday, May 26, 2012


Are USDA assurances on mad cow case 'gross oversimplification'?


SNIP...


What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”


The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”


“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.


In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the origins of atypical cases of BSE,” she said


The argument about feed is critical because if feed is the cause, not a spontaneous mutation, the California cow could be part of a larger outbreak.


SNIP...






==============================================



Saturday, August 4, 2012


*** Final Feed Investigation Summary - California BSE Case - July 2012






=============================================




SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012


Summary Report BSE 2012


Executive Summary






Saturday, August 4, 2012


Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation






in the url that follows, I have posted


SRM breaches first, as late as 2011.


then


MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until 2007, when they ceased posting them.


then,


MAD COW SURVEILLANCE BREACHES.




Friday, May 18, 2012


Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States Friday May 18, 2012






October 2009 O.11.3



Infectivity in skeletal muscle of BASE-infected cattle




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


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


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


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


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










Sunday, November 13, 2011


California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock








Wednesday, August 22, 2012


USDA, McDonald's suspend slaughterhouse buys from Central Valley Meat Co. over deadstock downer cows








Wednesday, August 01, 2012


Behavioural and Psychiatric Features of the Human Prion Diseases: Experience in 368 Prospectively Studied Patients








Monday, August 06, 2012


Atypical neuropathological sCJD-MM phenotype with abundant white matter Kuru-type plaques sparing the cerebellar cortex








Monday, July 23, 2012


The National Prion Disease Pathology Surveillance Center July 2012









layperson



Terry S. Singeltary SR. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net

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