SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary: The transmissible spongiform encephalopathies (also
called prion diseases) are fatal neurodegenerative diseases that affect animals
and humans. The agent of prion diseases is a misfolded form of the prion protein
that is resistant to breakdown by the host cells. Since all mammals express
prion protein on the surface of various cells such as neurons, all mammals are,
in theory, capable of replicating prion diseases. One example of a prion
disease, bovine spongiform encephalopathy (BSE; also called mad cow disease),
has been shown to infect cattle, sheep, exotic undulates, cats, non-human
primates, and humans when the new host is exposed to feeds or foods contaminated
with the disease agent. The purpose of this study was to test whether non-human
primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.
After an incubation period of approximately 10 years a macaque developed
progressive clinical signs suggestive of neurologic disease. Upon postmortem
examination and microscopic examination of tissues, there was a widespread
distribution of lesions consistent with a transmissible spongiform
encephalopathy. This information will have a scientific impact since it is the
first study that demonstrates the transmission of scrapie to a non-human primate
with a close genetic relationship to humans. This information is especially
useful to regulatory officials and those involved with risk assessment of the
potential transmission of animal prion diseases to humans. Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease
that also causes variant Creutzfeldt-Jakob disease in humans. Over the past
decades, c-BSE's zoonotic potential has been the driving force in establishing
extensive protective measures for animal and human health.
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated.
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains.
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01 Most doctors believe that sCJD is caused by a prion protein
deforming by chance into a killer. But Singeltary thinks otherwise. He is one of
a number of campaigners who say that some sCJD, like the variant CJD related to
BSE, is caused by eating meat from infected animals. Their suspicions have
focused on sheep carrying scrapie, a BSE-like disease that is widespread in
flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb...
2001
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01
Like lambs to the slaughter
31 March 2001
by Debora MacKenzie Magazine issue 2284.
FOUR years ago, Terry Singeltary watched his mother die horribly from a
degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary
was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded
an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number of
campaigners who say that some sCJD, like the variant CJD related to BSE, is
caused by eating meat from infected animals. Their suspicions have focused on
sheep carrying scrapie, a BSE-like disease that is widespread in flocks across
Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no
evidence that it poses a risk to human health. But if the French finding means
that scrapie can cause sCJD in people, countries around the world may have
overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD. They
injected the brains of macaque monkeys with brain from BSE cattle, and from
French and British vCJD patients. The brain damage and clinical symptoms in the
monkeys were the same for all three. Mice injected with the original sets of
brain tissue or with infected monkey brain also developed the same
symptoms.
As a control experiment, the team also injected mice with brain tissue from
people and animals with other prion diseases: a French case of sCJD; a French
patient who caught sCJD from human-derived growth hormone; sheep with a French
strain of scrapie; and mice carrying a prion derived from an American scrapie
strain. As expected, they all affected the brain in a different way from BSE and
vCJD. But while the American strain of scrapie caused different damage from
sCJD, the French strain produced exactly the same pathology.
"The main evidence that scrapie does not affect humans has been
epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute
for Animal Health in Edinburgh, who was a member of the same team as Deslys.
"You see about the same incidence of the disease everywhere, whether or not
there are many sheep, and in countries such as New Zealand with no scrapie." In
the only previous comparisons of sCJD and scrapie in mice, Bruce found they were
dissimilar.
But there are more than 20 strains of scrapie, and six of sCJD. "You would
not necessarily see a relationship between the two with epidemiology if only
some strains affect only some people," says Deslys. Bruce is cautious about the
mouse results, but agrees they require further investigation. Other trials of
scrapie and sCJD in mice, she says, are in progress.
People can have three different genetic variations of the human prion
protein, and each type of protein can fold up two different ways. Kretschmar has
found that these six combinations correspond to six clinical types of sCJD: each
type of normal prion produces a particular pathology when it spontaneously
deforms to produce sCJD.
But if these proteins deform because of infection with a disease-causing
prion, the relationship between pathology and prion type should be different, as
it is in vCJD. "If we look at brain samples from sporadic CJD cases and find
some that do not fit the pattern," says Kretschmar, "that could mean they were
caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence
elsewhere. Singeltary and other US activists think that some of these people
died after eating contaminated meat or "nutritional" pills containing dried
animal brain. Governments will have a hard time facing activists like Singeltary
if it turns out that some sCJD isn't as spontaneous as doctors have
insisted.
Deslys's work on macaques also provides further proof that the human
disease vCJD is caused by BSE. And the experiments showed that vCJD is much more
virulent to primates than BSE, even when injected into the bloodstream rather
than the brain. This, says Deslys, means that there is an even bigger risk than
we thought that vCJD can be passed from one patient to another through
contaminated blood transfusions and surgical instruments.
Then follow up with PNAS studies from which new scientist article written
from;
Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human health
THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,
Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp
[Dagger
] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique
Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible for
French iatrogenic growth hormone-linked CJD taken as a control is very different
from vCJD but is similar to that found in one case of sporadic CJD and one sheep
scrapie isolate;
CWD to CJD in humans (why not?), as easy as BSE/Scrapie;
The EMBO Journal, Vol. 19, No. 17 pp. 4425-4430, 2000
© European Molecular Biology Organization
Evidence of a molecular barrier limiting susceptibility of humans, cattle
and sheep to chronic wasting disease
G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O?Rourke3,
L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M.
Smits2
and B. Caughey1,7
1NIAID/NIH Rocky Mountain Laboratories, Hamilton, MT 59840,
3USDA/ARS/ADRU, Pullman, WA 99164-7030, 4USDA/ARS/ABADRL,
Laramie, WY 82071, 5Colorado Division of Wildlife, Wildlife Research
Center, Fort Collins, CO 80526-2097, 6Department of Veterinary
Sciences,
University of Wyoming, Laramie, WY 82070, USA and 2ID-Lelystad,
Institute for Animal Science and Health, Lelystad, The Netherlands
7Corresponding author e-mail: bcaughey@nih.gov Received June 7, 2000;
revised July 3, 2000; accepted July 5, 2000.
Abstract
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy
(TSE) of deer and elk, and little is known about its transmissibility to other
species. An important factor controlling interspecies TSE susceptibility is
prion protein (PrP) homology between the source and recipient species/genotypes.
Furthermore, the efficiency with which the protease-resistant PrP (PrP-res) of
one species induces the in vitro conversion of the normal PrP (PrP-sen) of
another species to the protease-resistant state correlates with the
cross-species transmissibility of TSE agents. Here we show that the
CWD-associated PrP-res (PrPCWD) of cervids readily induces the conversion of
recombinant cervid PrP-sen molecules to the protease-resistant state in
accordance with the known transmissibility of CWD between cervids. In contrast,
PrPCWD-induced conversions of human and bovine PrP-sen were much less efficient,
and conversion of ovine PrP-sen was intermediate. These results demonstrate a
barrier at the molecular level that should limit the susceptibility of these
non-cervid species to CWD.
snip...
Clearly, it is premature to draw firm conclusions about CWD passing
naturally into humans, cattle and sheep, but the present results suggest that
CWD transmissions to humans would be as limited by PrP incompatibility as
transmissions of BSE or sheep scrapie to humans. Although there is no evidence
that sheep scrapie has affected humans, it is likely that BSE has caused variant
CJD in 74 people (definite and probable variant CJD cases to date according to
the UK CJD Surveillance Unit). Given the presumably large number of people
exposed to BSE infectivity, the susceptibility of humans may still be very low
compared with cattle, which would be consistent with the relatively inefficient
conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently
been infected by BSE, it would seem prudent to take reasonable measures to limit
exposure of humans (as well as sheep and cattle) to CWD infectivity as has been
recommended for other animal TSEs.
snip...
Scrapie to Humans USA?
1: Neuroepidemiology. 1985;4(4):240-9. Related Articles,
Links
Sheep consumption: a possible source of spongiform encephalopathy in
humans.
Davanipour Z, Alter M, Sobel E, Callahan M.
A fatal spongiform encephalopathy of sheep and goats (scrapie) shares many
characteristics with Creutzfeldt-Jakob disease (CJD), a similar dementing
illness of humans. To investigate the possibility that CJD is acquired by
ingestion of contaminated sheep products, we collected information on
production, slaughtering practices, and marketing of sheep in Pennsylvania. The
study revealed that sheep were usually marketed before central nervous system
signs of scrapie are expected to appear; breeds known to be susceptible to the
disease were the most common breeds raised in the area; sheep were imported from
other states including those with a high frequency of scrapie; use of veterinary
services on the sheep farms investigated and, hence, opportunities to detect the
disease were limited; sheep producers in the area knew little about scrapie
despite the fact that the disease has been reported in the area, and animal
organs including sheep organs were sometimes included in processed food.
Therefore, it was concluded that in Pennsylvania there are some 'weak links'
through which scrapie-infected animals could contaminate human food, and that
consumption of these foods could perhaps account for spongiform encephalopathy
in humans. The weak links observed are probably not unique to
Pennsylvania.
PMID: 3915057 [PubMed - indexed for MEDLINE]
2015
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
Tuesday, December 16, 2014
*** Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE.
***The serial transmission of different scrapie isolates in these mice led
to the propagation of prions that are phenotypically identical to those causing
sporadic CJD (sCJD) in humans.
***These results demonstrate that scrapie prions have a zoonotic potential
and raise new questions about the possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
see more here ;
***The serial transmission of different scrapie isolates in these mice led
to the propagation of prions that are phenotypically identical to those causing
sporadic CJD (sCJD) in humans.***
***These results demonstrate that scrapie prions have a zoonotic potential
and raise new questions about the possible link between animal and human
prions.***
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire).
Saturday, July 6, 2013
*** Small Ruminant Nor98 Prions Share Biochemical Features with Human
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive
Prionopathy
Research Article
Monday, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types
(hmmm, this is getting interesting now...TSS)
Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine
(reticular) deposits,
see also ;
All of the Heidenhain variants were of the methionine/ methionine type 1
molecular subtype.
see full text ;
Monday, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types
*** OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED, WISHES TO
CONTINUE SPREADING IT AROUND THE GLOBE
Monday, November 30, 2009
*** USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL
HEALTH CODE, DOES NOT SURPRISE ME $
Confucius confused again, and Ponders, what about those Libyan Jews and
sheep scrapie and codon 200 of the prion protein gene of the CJD Victims
therefrom?
Could it be not that the codon 200 of the prion protein gene made these
poor victims of CJD just more susceptible to the sheep scrapie agent?
Pondering Confucius...
European Journal of Epidemiology
September 1991, Volume 7, Issue 5, pp 490-493
First online:
Creutzfeldt-Jakob disease among libyan jews A. D. Korczyn
Abstract
The focus of CJD among Jews of Libyan origin has been recognized for two
decades, but the reasons underlying it were unknown. Prevailing views suggested
transmission from sheep infected with scrapie. However, recent data show that in
fact CJD in this ethnic group is a genetically determined disease due to a point
mutation on the codon 200 of the prion protein gene. The clinical
characteristics of CJD in this group, and particularly the less common periodic
activity in the EEG, are reviewed. New findings include peripheral neuropathy of
the demyelinating type in two cases, presumably due to involvement of Schwann
cells. The pathophysiology of the disease includes, presumably, a focal
post-translational modification of the prion protein, (predisposed by the
mutation). Later, the disease progresses through cell-to-cell transmission.
Key words Creutzfeldt-Jakob diseases – Prion disease – Jews – Libya –
Genetics – Pathophysiology
1: Cent Eur J Public Health 2003 Mar;11(1):19-22
Analysis of unusual accumulation of Creutzfeldt-Jakob disease cases in
Orava and Liptov regions (northern Slovak focus) 1983-2000.
Mad'ar R, Maslenova D, Ranostajova K, Straka S, Baska T.
Institute of Epidemiology, Jessenius Faculty of Medicine, Comenius
University, Sklabinska 26, Martin, 037 53 Slovakia. MADAR@jfmed.uniba.sk
While familial cases of Creutzfeldt-Jakob disease are extremely rare all
over the world, 3 familial clusters were observed between 1983-2000 in a
relatively small area situated in the North of Slovakia. Prevalence of CJD in
this area exceeded the overall prevalence in Slovakia more than 8 times. The
majority of CJD patients admitted consuming sheep brain. Most patients lived in
small secluded villages with rather common familial intermarriage. CJD affected
both sexes equally. All patients were prior to the disease mentally normal
individuals. Shortly after the onset of CJD their mental status deteriorated
remarkably with an average survival rate of 3.6 months.
PMID: 12690798
------------------------------------------------------------------------
1: Eur J Epidemiol 1991 Sep;7(5):520-3
"Clusters" of CJD in Slovakia: the first laboratory evidence of
scrapie.
Mitrova E, Huncaga S, Hocman G, Nyitrayova O, Tatara M.
Institute of Preventive and Clinical Medicine, Bratislava.
Epidemic-like occurrence of Creutzfeldt-Jakob disease was observed in 1987
in Slovakia (Orava). Search for the cause of CJD focus indicated a coincidence
of genetic and environmental risks in clustering patients. Since Spongiform
Encephalopathies might be transmitted orally, (Bovine Spongiform
Encephalopathy), the possibility of zoonotic source of CJD cases in Orava was
also considered. A deficient knowledge about the occurrence of scrapie in
Slovakia stimulated an examination of sheep with signs of CNS disorders in two
flocks of Valasky breed in Orava. In one flock, neurohistopathological
examination revealed in sheep brains lesions characteristic for scrapie. Frozen
brain tissue of these animals were used for the detection of scrapie associated
fibrils. They were found in 2 animals from the same flock. This is the first
laboratory confirmation of scrapie in Czecho-Slovakia. The possible
epidemiological and economical implications are emphasized.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1761109&dopt=Abstract
Mutation of the prion protein in Libyan Jews with Creutzfeldt-Jakob disease
Article Abstract:
Creutzfeldt-Jakob disease (CJD) is a neurodegenerative disease of a class
referred to as the spongiform encephalopathies. The disease can be transmitted
experimentally and has also been transmitted accidentally. The causative agent
in these transmissions is unlike any well characterized infectious agent and is
referred to by many as a prion. Creutzfeldt-Jakob disease may occur in families,
but is usually sporadic. The incidence of Creutzfeldt-Jakob disease is about one
or two cases per million people. However, among Jews from Libya, the incidence
is 100 times higher. Many possible explanations have been put forward to account
for this unusually high incidence, but none has sustained any scrutiny. One of
the more popular notions was that the eating of sheep brains, a popular delicacy
in the region, infected people with scrapie, a prion disease of sheep similar to
CJD. However, the eating of sheep brain is popular throughout the Mediterranean,
and cannot explain the specificity of the increased incidence to Libyan Jews.
Mediterranean sheep, if anything, have a lower rate of scrapie than other areas
of Europe and North America. A study was undertaken to determine if the
increased incidence of CJD among these people might be accounted for by genetic
factors. The prion protein genes were analyzed in 11 Libyan Jews with
Creutzfeldt-Jakob disease. Investigation of one patient revealed that a mutation
had occurred in the 200th codon of the gene, that is, the 200th set of three DNA
bases. The net result of this change would be to substitute a lysine for
glutamine in the resulting protein. After this mutation was identified, it was
confirmed in the other 10 Libyan patients. It is interesting to note that the
mutation was not present in a Moroccan Jew with CJD. The results suggest that
the increased incidence of Creutzfeldt-Jakob disease in this population is the
result of a gene carried by this group. In eight of the present cases, a family
history of CJD could be confirmed. Although not all families were cooperative in
providing information of the ancestral heritage, all the families for which such
information was available could be traced to Djerba, which is an island off the
coast of Tunisia. (Consumer Summary produced by Reliance Medical Information,
Inc.)
author: Scarlato, Guglielmo, Prusiner, Stanley B., Hsiao, Karen, Meiner,
Zeev, Kahana, Esther, Cass, Carin, Kahana, Irit, Avrahami, Dana, Abramsky, Oded,
Gabizon, Ruth Publisher: Massachusetts Medical Society Publication Name: The New
England Journal of Medicine Subject: Health ISSN: 0028-4793 Year: 1991
Epidemiology of Scrapie in the United States 1977
Monday, March 28, 2016
National Scrapie Eradication Program February 2016 Monthly Report
Comment from Terry Singeltary This is a Comment on the Animal and Plant
Health Inspection Service (APHIS) Proposed Rule: Scrapie in Sheep and
Goats
For related information, Open Docket Folder Docket folder icon
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Comment View document:Indeed, much science has changed about the Scrapie
TSE prion, including more science linking Scrapie to humans. sadly, politics,
industry, and trade, have not changed, and those usually trump sound science, as
is the case with all Transmissible Spongiform Encephalopathy TSE Prion disease
in livestock producing animals and the OIE. we can look no further at the legal
trading of the Scrapie TSE prion both typical and atypical of all strains, and
CWD all stains. With as much science of old, and now more new science to back
this up, Scrapie of all types i.e. atypical and typical, BSE all strains, and
CWD all strains, should be regulated in trade as BSE TSE PRION. In fact, I urge
APHIS et al and the OIE, and all trading partners to take heed to the latest
science on the TSE prion disease, all of them, and seriously reconsider the
blatant disregards for human and animal health, all in the name of trade, with
the continued relaxing of TSE Prion trade regulations through the 'NEGLIGIBLE
BSE RISK' PROGRAM, which was set up to fail in the first place. If the world
does not go back to the 'BSE RISK ASSESSMENTS', enhance, and or change that
assessment process to include all TSE prion disease, i.e. 'TSE RISK ASSESSMENT',
if we do not do this and if we continue this farce with OIE and the USDA et al,
and the 'NEGLIGIBLE BSE RISK' PROGRAM, we will never eradicate the TSE prion aka
mad cow type disease, they will continue to mutate and spread among species of
human and animal origin, and they will continue to kill. ...
please see ;
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
please see file attachment for full submission and recent science and my
deep concerns on the TSE Prion disease... No documents available.
AttachmentsView All (1) scrapie-usa-blogspot-com View Attachment:
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
Comment from Terry S. Singeltary Sr. Return to Docket Folder Summary This
is a Comment on the Food and Drug Administration (FDA) Notice: Risk Assessment
of Foodborne Illness Associated With Pathogens From Produce Grown in Fields
Amended With Untreated Biological Soil Amendments of Animal Origin; Request for
Scientific Data, Information, and Comments
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Comment View document:Greetings FDA et al, I kindly would like to make
comment submission to ;
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information
A Notice by the Food and Drug Administration on 03/04/2016
MY comment as follows,
There has been proven documented risk for Untreated Biological Soil
Amendments of Animal Origin and risk of transmitting Transmissible Spongiform
Encephalopathy TSE Prion disease aka mad cow type disease such as the typical
and atypical Bovine Spongiform Encephalopathy strains, typical and atypical
Scrapie strains, typical and atypical Chronic Wasting Disease CWD strains, and
even the Transmissible Mink Encephalopathy TME Prion disease.
Science has shown that infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces thereby leading to
transmission by direct contact and environmental contamination.
Ingestion of prion contaminated leaves and roots produced disease with a
100% attack rate and an incubation period not substantially longer than feeding
animals directly with scrapie brain homogenate.
Plants can uptake prions from contaminated soil and transport them to
different parts of the plant tissue (stem and leaves) [please see data from Soto
et al Prion2015 Conference below in Science reference data].
Also, Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area is very concerning.
Science has shown that soil plays a role in the spreading and transmission
of the CWD and Scrapie TSE prion agent.
For these reason and more (see reference materials) I urge the FDA to stop
this practice of Untreated Biological Soil Amendments of Animal Origin,
including blood, for use on our produce grown in fields, for the following
reasons,
please see attachments and updated TSE Prion science on these very
important matters here (I do not advertise or make money the science is there
for educational use for Transmissible Spongiform Encephalopathy TSE Prion
disease.
just made a promise to mom dod 12/14/97 confirmed Heidenhain Variant
Creutzfeldt Jakob Disease, hvCJD. ... AttachmentsView All (1) Comment from Terry
S Singeltary Sr View Attachment:
Tuesday, March 15, 2016
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information Singeltary Submission
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
Friday, April 22, 2016
Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in
a Mule Deer
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Title: Scrapie transmits to
white-tailed deer by the oral route and has a molecular profile similar to
chronic wasting disease Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Sheep and cattle may be exposed to CWD via common grazing areas with
affected deer but so far, appear to be poorly susceptible to mule deer CWD
(Sigurdson, 2008).
***In contrast, cattle are highly susceptible to white-tailed deer CWD and
mule deer CWD in experimental conditions but no natural CWD infections in cattle
have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how
susceptible humans are to CWD but given that the prion can be present in muscle,
it is likely that humans have been exposed to the agent via consumption of
venison (Sigurdson, 2008). Initial experimental research, however, suggests that
human susceptibility to CWD is low and there may be a robust species barrier for
CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD
is affecting wild and farmed cervid populations in endemic areas with some deer
populations decreasing as a result.
snip...
For the purpose of the qualitative risk assessment developed here it is
necessary to estimate the probability that a 30-ml bottle of lure contains urine
from an infected deer. This requires an estimate of the proportion of deer herds
in the USA which are infected with CWD together with the within herd
prevalence.
The distribution map of CWD in US shows it is present mainly in central
states (Figure 1). However, Virginia in the east of the country has recorded
seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take
steps to prevent urine being taken from infected animals eg by sourcing from
farms where the deer are randomly tested for CWD (Anon 2015a). However, if
disease is already present and testing is not carried out regularly, captive
populations are not necessarily disease free (Strausser 2014). Urine-based deer
lures have been known to be collected from domestic white-tailed deer herds and
therefore there is a recognised risk. This is reflected by 6 US States which
have
14
banned the use of natural deer urine for lures, as the deer urine may be
sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For
example, the US State of Virginia is banning the use of urine-based deer lures
on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska
banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned
urine-based deer lures and acknowledged that there is no way to detect their use
(Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it
appears that up to 50% of deer herds can be infected with 80-90% of animals
infected within some herds.
*** It is therefore assumed that probability that a 30-ml bottle of deer
urine lure imported from the USA is sources from an infected deer is
medium.
SNIP...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. ***For elk and deer
considered at high risk for CWD, the FDA recommends that these animals do not
enter the animal feed system. ***However, this recommendation is guidance and
not a requirement by law.
***Animals considered at high risk for CWD include:
***1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
***2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
***Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants. The
amount of animal PAP that is of deer and/or elk origin imported from the USA to
GB cannot be determined, however, as it is not specified in TRACES. It may
constitute a small percentage of the very low tonnage of non-fish origin
processed animal proteins that were imported from US into GB.
*** Overall, therefore, it is considered there is a greater than negligible
risk that (non-ruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB. There is uncertainty associated with this estimate
given the lack of data on the amount of deer and/or elk protein possibly being
imported in these products.
SNIP...
Summary and MORE HERE ;
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21
CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from
deer and elk is prohibited for use in feed for ruminant animals. With regards to
feed for non-ruminant animals, under FDA law, CWD positive deer may not be used
for any animal feed or feed ingredients. For elk and deer considered at high
risk for CWD, the FDA recommends that these animals do not enter the animal feed
system.
***However, this recommendation is guidance and not a requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
BSE: TIME TO TAKE H.B. PARRY SERIOUSLY
If the scrapie agent is generated from ovine DNA and thence causes disease
in other species, then perhaps, bearing in mind the possible role of scrapie in
CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the
notifiable disease. ...
Thursday, August 20, 2015 Doctor William J. Hadlow
William J. Hadlow Dr. Hadlow (Ohio State ’48), 94, Hamilton, Montana, died
June 20, 2015.
Biological Warfare, or another happenstance of bad luck ???
The Alfords believe their son's illness was caused by eating sheep's brains
while he was serving in Oman. Medical experts say they don't know the cause.
snip... "In June of 2003 they told us he wouldn't see his 25th birthday; then in
August they were absolutely certain he wouldn't be here at Christmas.
"Here we are at his fourth birthday since he was diagnosed. I'm not ready
to say anything about having a fourth Christmas with him, but we're headed in
that direction."
Alford was assigned to the U.S. Army's 5th Special Forces Group. His
illness was chronicled in a front-page story in The Tennessean in November
2003.
According to the Creutzfeldt-Jakob Foundation, the incidence of CJD in the
United States is one case per 9,000 adults age 55 and older; it occurs much less
frequently in people 30 and younger.
The disease can be contracted by contamination during surgery or inherited
at birth, but 85 percent of cases are of the "sporadic" variety, meaning the
cause for the disease is unknown, the CJD Foundation reported. That's the case
in Alford's situation.
Because he was so well traveled as a Special Forces soldier, his family
said he may have eaten contaminated beef in England, where more than 125 persons
have contracted the disease after eating beef from cows that were fed products
rendered from scrapie-infected sheep. Scrapie is a form of a brain disorder
found in sheep.
The soldier also told his family that in 2001 he ate a sheep's brain while
stationed in Oman. However, while the disease is linked to cattle that have
eaten sheep-byproducts, there has been no evidence of direct transfer from sheep
to humans, according to the CJD Foundation.
At the time of infection, it is believed that Jamie contracted it from
eating sheep's brain with tribesmen in Oman. This was something that he HAD to
do in order to win the respect of the Omani tribesmen. Oman is a key territory
in the War on Terror.
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. | 9:57 AM
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