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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