Importation of Sheep, Goats, and Certain Other Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10
Importation of Sheep, Goats, and Certain Other Ruminants [Docket No.
APHIS-2009-0095]RIN 0579-AD10
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS,
are working to further legalize the trading of Transmissible Spongiform
Encephalopathy TSE Pion disease around the globe.
THIS is absolutely insane. it’s USDA INC.
Importation of Sheep, Goats, and Certain Other Ruminants [Docket No.
APHIS-2009-0095]RIN 0579-AD10
[Federal Register Volume 81, Number 137 (Monday, July 18, 2016)]
[Proposed Rules]
[Pages 46619-46639]
From the Federal Register Online via the Government Publishing Office
[www.gpo.gov][FR Doc No: 2016-16816] --
---------------------------------------------------------------------
DEPARTMENT OF AGRICULTURE
Animal and Plant Health Inspection Service
9 CFR Parts 93, 94, 95, 96, and 98
[Docket No. APHIS-2009-0095]RIN 0579-AD10
Importation of Sheep, Goats, and Certain Other Ruminants
AGENCY: Animal and Plant Health Inspection Service, USDA.
ACTION: Proposed rule.
-----------------------------------------------------------------------
SUMMARY: We are proposing to amend the regulations that govern the
importation of animals and animal products to revise the conditions for the
importation of live sheep, goats, and certain other non-bovine ruminants, and
products derived from sheep and goats, with regard to transmissible spongiform
encephalopathies such as bovine spongiform encephalopathy (BSE) and scrapie. We
are proposing to remove BSE-related import restrictions on sheep and goats and
most of their products, and to add import restrictions related to transmissible
spongiform encephalopathies for certain wild, zoological, or other non-bovine
ruminant species. The conditions we are proposing for the importation of
specified commodities are based on internationally accepted scientific
literature and will in general align our regulations with guidelines set out in
the World Organization for Animal Health's Terrestrial Animal Health Code.
DATES: We will consider all comments that we receive on or before September
16, 2016.
ADDRESSES: You may submit comments by either of the following methods:
Federal eRulemaking Portal: Go to
Postal Mail/Commercial Delivery: Send your comment to Docket No.
APHIS-2009-0095, Regulatory Analysis and Development, PPD, APHIS, Station
3A-03.8, 4700 River Road, Unit 118, Riverdale, MD 20737-1238. Supporting
documents and any comments we receive on this docket may be viewed at
or in our reading room, which is located in room 1141 of the USDA South
Building, 14th Street and Independence Avenue SW., Washington, DC. Normal
reading room hours are 8 a.m. to 4:30 p.m., Monday through Friday, except
holidays. To be sure someone is there to help you, please call (202) 799-7039
before coming.
FOR FURTHER INFORMATION CONTACT: For information concerning live animals,
contact Dr. Oriana Beemer, Veterinary Medical Officer, Animal Permitting and
Negotiating Services, National Import Export Services, VS, APHIS, 4700 River
Road, Unit 39, Riverdale, MD 20737-1231; (301) 851-3300.
For information regarding ruminant products and for other information
regarding this proposed rule, contact Dr. Christopher Robinson, Director, Animal
Products Permitting and Negotiation Services, National Import Export Services,
VS, APHIS, 4700 River Road, Unit 38, Riverdale, MD 20737-1231; (301)
851-3300.
SUPPLEMENTARY INFORMATION:
I. Executive Summary
Need for the Regulatory Action
snip...
The changes we are proposing with regard to sheep and goats and BSE are
consistent with the approach taken by the OIE. The OIE, of which the United
States is a Member country, is the internationally recognized standard-setting
body that develops science-based recommendations for the safe trade of animals
and animal products. The World Trade Organization has recognized the OIE as the
international forum for setting animal health standards, reporting global animal
disease events, and presenting guidelines and recommendations on sanitary
measures relating to animal health.
snip...
Based on the evidence discussed above, we believe it is not warranted to
continue to prohibit or restrict trade of live sheep and goats and the products
of sheep and goats due to BSE, other than processed animal protein. We continue
to consider processed animal protein containing materials derived from sheep and
goats to be a BSE risk due to the possibility that such material has been
commingled with bovine materials, and because one significant use of these
materials is in animal feed. For these reasons, we would continue to restrict
the importation of these commodities.
snip...
Over the years, the OIE Member countries, including the United States, have
agreed to amend the OIE guidelines for BSE based on increased scientific
evidence regarding the disease. Current OIE recommendations regarding BSE in
ruminants do not include any BSE-related measures for sheep and goats other than
the general requirements applied to all ruminant meat and bone meal (processed
animal proteins).
snip...
Sec. 93.435 Sheep and goats: This section would be revised to contain
provisions for importing sheep and goats from anywhere in the world. The
provisions for sheep and goats imported for immediate slaughter and restricted
feeding for slaughter would be similar to the existing requirements for sheep
and goats imported for those purposes from Canada, currently contained in Sec.
93.419. The requirements for importing sheep and goats for other purposes,
currently contained in Sec. 93.435, would be updated to make them in general
consistent with international standards, by limiting imports for these purposes
to animals from classical scrapie-free countries or flocks, except as permitted
by the Administrator under paragraph (a)(5) of Sec. 93.404. This would allow for
the importation of animals that are very low risk due to their genotype or other
factors. We would also revise this section to establish a notice-based approach
for recognizing regions as free of classical scrapie. The regulations would
provide the Web address and a contact for requesting copies of the list[[Page
46624]]of classical scrapie-free regions by mail, fax, or email. The regulations
also would explain APHIS' process for adding or removing a region to or from the
list.
snip...
Currently, non-bovine ruminants other than sheep and goats from regions not
listed in Sec. 94.24(a) are not subject to any import restrictions with regard
to BSE. We believe, however, that there is a certain category of ruminants that
present enough of a potential risk of spreading TSEs that their importation
should be prohibited unless certain risk mitigation measures are in place. This
category of ruminants includes certain ruminants held in zoological facilities
and certain wild ruminants. For the purposes of discussion, we will refer to
such animals as zoological ruminants to distinguish them from domesticated
sheep, goats, and bovines.
Scientific literature indicates that at least certain zoological ruminants
are susceptible to TSEs caused by the BSE agent. In association with the BSE
epidemic in domestic cattle in Europe, TSEs have been diagnosed in several
species of zoo animals, all from the families Bovidae and Felidae. Sixteen cases
of TSEs have been recorded from antelope in U.K. zoos including one nyala
(Tragelaphus angasi), six eland (Taurotragus oryx), six greater kudu
(Tragelaphus strepsiceros), one gemsbok (Oryx gazelle), one Arabian oryx (Oryx
leucoryx), and one scimitar-horned oryx (Oryx dammah) (Travis and Miller 2003).
The first recorded case was a nyala euthanized at a wildlife park in England in
1986, the same year that the first BSE cases in cattle were recognized (Wells,
Scott et al. 1987; Jeffrey and Wells 1988). Reported cases of TSEs in zoo bovids
peaked around 1991, and no additional cases in zoo antelope have been reported
since 1996 (Kirkwood 2000).
Several lines of evidence support the hypothesis that at least some, if not
all, of the spongiform encephalopathy cases diagnosed in zoo bovids were caused
by the BSE agent. First, the cases in zoos coincide geographically and
temporally with the BSE epidemic in Great Britain. Second, epidemiologic
investigations indicated that all affected animals, or the herds into which they
were born or moved, could have been exposed to feeds containing ruminant-derived
protein or other potentially contaminated material (Kirkwood and Cunningham
1994). Finally, comparable patterns of incubation periods and pathologic effects
were seen in mice inoculated with brain tissue homogenate from the affected
nyala, an affected kudu, and BSE-affected cattle (Jeffrey, Scott et al. 1992).
The greater kudu, a non-domestic African antelope, appears to be
particularly susceptible to BSE. Six of eight kudu that died in a small herd at
the London Zoo from 1989 through 1992 were diagnosed with spongiform
encephalopathy (Kirkwood and Cunningham 1994). The disease is presumed to have
been introduced to the kudu herd through feeds containing ruminant-derived
protein around the time of the BSE epidemic in U.K. cattle. However, some of the
affected kudu were born after the elimination of the potentially contaminated
feed from the premises, and one case occurred in a kudu born at another zoo and
introduced to the affected herd (Kirkwood, Cunningham et al. 1994). Because most
of the affected kudu did not consume feed containing ruminant-derived protein,
it was postulated that the disease may have spread naturally in the herd, either
by transmission between individuals or through contamination of the environment
(Kirkwood, Cunningham et al. 1993).
The epidemiology of the TSE cases in kudu contrasts with BSE in cattle in
several respects. The attack rate in the London Zoo kudu herd is notably higher
than the attack rate seen in BSE affected cattle herds. The pattern of disease
in antelope also differs from cattle affected with BSE, characterized by a
younger average age of onset and a shortened clinical course (Kirkwood and
Cunningham 1999). Additionally, infectivity in greater kudu with TSE is
distributed in a wider range of tissues than in cattle with BSE (Cunningham,
Kirkwood et al. 2004).
Information about the infectivity of tissues from TSE-affected zoological
ruminants is limited to studies of tissue from four London Zoo kudus with
spongiform encephalopathy. Fifteen of 32 kudu tissue homogenates transmitted BSE
to mice. Of these, fresh central nervous, lymphoreticular, and distal ileum
tissue indicated moderate or high levels of spongiform encephalopathy
infectivity. Traces of infectivity were demonstrated in kudu spleen, lung, skin,
conjunctiva, and salivary gland (Cunningham, Kirkwood et al. 2004).
A wide range of species in zoological collections were probably exposed to
BSE-contaminated feed; new cases in other captive zoological species may emerge,
or it is possible that some species may carry and transmit the disease without
showing clinical signs. The possibility of transmission of BSE-related
encephalopathy between[[Page 46625]]members, or from mother to offspring, within
herds of zoological ruminants, as suspected with the London Zoo kudus, cannot be
ruled out. Although there is currently no evidence that TSEs exist in
free-living zoological ruminants (veterinary authorities in southern African
countries conducting passive surveillance in wildlife have not encountered any
clinical cases or histopathological lesions compatible with TSEs (Horn, Bobrow
et al.), active surveillance has not been implemented in any region of the world
for TSEs in antelope or free-living Caprinae.
Many of the non-domestic ruminants are endangered species. The
scimitar-horned oryx, for example, is listed as ``Extinct in the Wild'' on the
International Union for Conservation of Nature Red List (http://www.iucnredlist.org/), and 13
species of the Caprinae subfamily are listed as threatened on the Red List. In
order to maintain genetic diversity in these very small populations, animals
must be moved between zoological collections, both domestically and
internationally (Shackleton 1997). Movement of animals may also be a goal of
conservation programs seeking to reintroduce captive-bred endangered species
into the wild. Both types of movement carry the risk of inadvertent introduction
of infectious diseases that may have serious consequences for conservation
efforts. The management of animal genetic resources must include a consideration
of the potential risk of importing undetected prion diseases with rare breeding
stock.
Although each of the cases to date of ruminant TSEs possibly connected to
BSE in zoo animals was diagnosed in a region known to be affected with BSE, we
believe that even zoological ruminants in regions not categorized as
BSE-affected or as posing undue risk of BSE could be at risk for BSE-related
TSEs, due to possible origin in a BSE-affected region or feeding with
BSE-contaminated protein. Even in countries that have enforced a ban on the
feeding of ruminant protein to domestic ruminants for an identifiable period of
time, it can be difficult in some cases to determine when and if a country
ceased feeding ruminant protein to zoo ruminants.
Because of the potential variety of practices in the feeding of zoo
ruminants, as well as the potential that certain zoo ruminants may have
originated in BSE-affected countries, we believe it is necessary to consider on
a case-by-case basis the potential spongiform encephalopathy risk of zoological
ruminants. As noted above, a ruminant may not be imported into the United States
unless the importer has first applied for and obtained a permit from APHIS for
such importation. In the case of zoological ruminants, the Administrator will
consider the disease risk of each animal and the ability of the receiving zoo to
manage the risks before deciding whether to issue an import permit.
Paragraph (a)(3) of Sec. 93.404 currently provides that an application for
a permit to import ruminants may be denied due to, among other reasons, the lack
of satisfactory information necessary to determine that the importation will not
be likely to transmit any communicable disease to livestock or poultry of the
United States.
Even with zoological ruminants that would otherwise be denied importation
into the United States, however, we believe that, in most cases, adequate
mitigation measures with respect to potential TSE risks can be taken to allow
the animal to be safely imported into the United States.
Although the precise measures APHIS considers necessary could vary on a
case-by-case basis, such measures could include the following:
That the animal be held at approved permanent post-entry quarantine
facilities;
That any movement of the animal out of or among such facilities occur only
in accordance with a compliance agreement between APHIS and the owners of
approved facilities; and That, upon the death of the animal, the APHIS Service
Center Director be notified, and the carcass be tested for TSEs and be
completely destroyed in a manner acceptable to the Administrator.
Any conditions for the importation of a zoological ruminant would be
spelled out in the import permit for that animal. Any such conditions could also
be applied to any progeny of the animal, as well to as any ruminants housed with
either the animal or its progeny. In the event that the conditions of
importation of a zoological ruminant were applied to its progeny or contact
animals, the Administrator could require that a zoo enter into a cooperative,
compliance, or other agreement that sets out specific requirements for releasing
the progeny or contact animals based on postmortem testing of the imported
animal with negative results.
snip...
Ruminants From Regions Where BSE Exists
As noted above, the current regulations contain broad prohibitions and
restrictions regarding the importation of non-bovine ruminants other than sheep
and goats from regions listed in Sec. 94.24(a). The prohibitions apply to
zoological ruminants as well as to domesticated ruminants. However, the
regionally based prohibitions do not address individual situations where a
ruminant that would otherwise be denied entry from a region listed in Sec.
94.24(a) could be safely entered into the United States, provided certain risk
mitigation measures are taken.
Section 93.401 of the regulations contains general prohibitions on the
importation of ruminants. We would amend paragraph (a) of this section by
revising the second sentence to remove the reference to Sec. 94.24(a). That
section contains a list of regions in which BSE is known to exist, but is no
longer needed since we have changed the way we recognize regions for BSE risk.
We are proposing to amend the second sentence to read ``Notwithstanding any
other provision of this subpart, the importation of any ruminant that is not a
bovine, camelid, cervid, sheep, or goat is prohibited.'' This change would
remove BSE restrictions on the importation of many non-bovine ruminants, but
would continue to protect against the introduction of TSEs into the United
States.
Currently Sec. 93.401(a) also provides that the Administrator may, upon
request in specific cases, allow ruminants or products to be brought into or
through the United States under such conditions as he or she may prescribe, when
he or she determines in the specific case that such action will not endanger the
livestock or poultry of the United States. Providing for the importation of
specific animals in individual cases has great value for conservation efforts.
In order to maintain genetic diversity in species with very small populations,
animals must be moved between zoological collections, both domestically and
internationally.
In the preceding section of this document, we discussed the type of
mitigation measures that could be used to adequately mitigate TSE risk from zoo
ruminants from regions other than those listed in Sec. 94.24(a). We believe that
the same types of mitigation measures can be employed to safely import
zoological ruminants from regions listed in Sec. 94.24(a).
In this document, therefore, we are proposing to add a new paragraph (a)(5)
to the import permit provisions in Sec. 93.404 to address such situations. The
new paragraph would provide that, in specific cases, a permit may be issued for
ruminants that would otherwise be prohibited importation due to TSEs pursuant to
part 93 subpart D if the Administrator determines that the disease risk posed by
the animals can be
[[Page 46626]]
adequately mitigated through pre-entry or post-entry mitigation measures,
or through combinations of such measures. Such measures would be specified in
the permit. If it is determined prior to or after importation that any pre-entry
or post-entry requirements were not met, or that the ruminants are affected with
or have been exposed to TSEs, the ruminants, their progeny, and any other
ruminants that have been housed with or exposed to the ruminants will be
disposed of or otherwise handled as directed by the Administrator.
snip...
Restrictions on the Importation of Meat and Edible Products Due to BSE
The regulations in Sec. 94.24 restrict the importation of meat and edible
products, including gelatin, from ovines and caprines due to BSE, those in Sec.
94.25 restrict the importation from Canada of meat and edible products from
ovines and caprines other than gelatin, and those in Sec. 94.26 apply to gelatin
derived from horses or swine or from ovines or caprines that have not been in a
region restricted because of BSE. While there is no BSE risk associated with
gelatin or meat and other edible products derived from sheep and goats, these
restrictions also function as protection against the introduction of other TSEs,
such as scrapie.
We are proposing to remove Sec. Sec. 94.24 and 94.25. This will remove both
the prohibition on the importation of meat and other edible products ovines and
caprines from regions in which BSE is known to exist, and the requirement that
meat and edible products from sheep and goats from Canada, other than gelatin,
be derived only from animals less than 12 months of age. These restrictions were
related to concerns about BSE risk and are no longer warranted since there is no
scientific evidence that BSE is circulating in sheep or goats.
We are proposing to amend Sec. 94.26 by removing the references to ovines
and caprines that have not been in a region restricted because of BSE from the
section heading and the regulatory text. In place of those references we would
add a reference to non-bovine ruminants. Gelatin derived from non-bovine
ruminants, like gelatin derived from horses and swine, does not present a risk
for BSE since there is no scientific evidence that BSE is circulating in sheep
or goats.
snip...
Restrictions on Importation of Byproducts Derived From Ruminants Due to BSE
Part 95 of the regulations prohibits or restricts the importation of
products other than meat and other edible products to prevent the introduction
of certain animal diseases. We are proposing to amend Sec. 95.1 by removing the
definitions for positive for a transmissible spongiform encephalopathy and
suspect for a transmissible spongiform encephalopathy because those terms no
longer appear in the regulations.
Section 95.4 contains restrictions on the importation of processed animal
protein, offal, tankage, fat, glands, certain tallow other than tallow
derivatives, and serum due to bovine spongiform encephalopathy. We are proposing
to amend this section first by revising the section heading to remove the
exception for certain tallow derivatives. We would also revise paragraph (b)(1)
to remove the exception for tallow derivatives from that paragraph. We are
making these changes in order to be consistent with our requirements for
bovine-derived tallow derivatives, which are subject to restrictions set out in
Sec. 95.9.
Paragraph (a) contains a list of regions in which BSE is known to exist. We
would revise the paragraph to remove this list, which is no longer needed since
we have changed the way we recognize regions for BSE risk.
In paragraph (c), we would remove the reference to paragraph (a)(4) from
paragraph (c)(1)(iv), and remove paragraphs (c)(2) and (c)(3). These revisions
would remove BSE-related restrictions from these products when derived from
sheep and goats. We would also amend paragraphs (c)(1)(ii) and (iv) to add the
words ``and the material is not ineligible for importation under the conditions
of Sec. 95.5'' after the words ``cervids and camelids'' and ``ovines and
caprines,'' respectively. These would not be new requirements; the regulations
in Sec. 95.5 have always applied to products derived from all ruminant species,
due to concerns about commingling or cross-contamination. However, this change
would clarify that the restrictions in that section continue to apply to
products derived from cervids, camelids, ovines, and caprines. Paragraphs (c)(4)
through (c)(8) would be redesignated as paragraphs (c)(2) through (c)(6),
respectively.
In newly redesignated paragraph (c)(3), we would amend the first sentence
to remove the requirement that facilities that process or handle any material
derived from mammals be inspected at least annually for compliance with the
provisions of this section, either by a representative of the government agency
responsible for animal health in the region, or by APHIS. Instead, we would
require only facilities that process or handle processed animal protein be
inspected at least annually. The rendering process
[[Page 46627]]
used to make processed animal protein creates a material that cannot be
differentiated by species without a polymerase chain reaction test, and much
rendering is performed involving multiple species. As a result, there is a risk
of cross-contamination with processed animal protein that does not exist with
the other products. For this reason we would continue to require inspections for
facilities that process or handle processed animal proteins.
Paragraphs (d) and (e) contain restrictions on serum, serum albumin,
serocolostrum, amniotic liquids or extracts, and placental liquids derived from
ovines and caprines due to BSE. We are proposing to remove both of these
paragraphs because BSE-related restrictions on these products are no longer
warranted. These products present a risk of introducing other diseases, however,
and would continue to be prohibited importation into the United States, except
for scientific, educational, or research purposes if the Administrator
determines that the importation can be made under conditions that will prevent
the introduction of animal diseases into the United States.
Paragraph (g) contains restrictions on offal derived from ovines and
caprines. These restrictions are no longer warranted and paragraph (g) would be
removed.
Section 95.40 contains additional certification requirements for certain
materials derived from sheep and goats, including processed animal protein,
tankage, offal, glands and unprocessed fat tissue, and derivatives of those
products. These additional certification requirements were established due to
BSE concerns and are no longer warranted; therefore, we are proposing to remove
Sec. 95.40.
Restrictions on the Importation of Foreign Animal Casings
snip...
the sheer ignorance of all this is just to long to post, please see link
and full text below...GOD HELP US!
From: Terry S. Singeltary Sr.
Sent: Saturday, May 14, 2016 10:16 AM
To: m.eloit@oie.int
Subject: OIE Director General, Dr Monique Eloit USA TSE PRION EMERGENCY
URGENT PLEA
OIE Director General, Dr Monique Eloit USA TSE PRION EMERGENCY URGENT
PLEA
Greetings Dr. Eloit Director General Ma’am,
a warm greetings from sunny Bacliff, Texas.
I wish to make an urgent request to you (I accidently sent the email just
before this by mistake, before I had added my plea, sorry).
I have been begging the OIE et al, for going on 18 years now, most every
year, about risk factors that were being ignored by the OIE, thanks to the USDA
et al, and the BSE MRR blunder. I have wasted 18 years of my life doing this,
because I have failed in getting anything done. I have corresponded with OIE
Doctors on several occasions voicing my concerns about all the TSE Prion
disease, with them seemingly to agree with my concerns, yet nothing has been
done. I wish to pass this information to you, and I only hope that you take the
time to read what I have come to know, and understand I am a meat eater. I am
not anti trade, anti beef, etc........... what I am though is, I am anti stupid,
and there has been so much stupid to go around the last say 3 plus decades with
the Transmissible Spongiform Encephalopathy TSE Prion disease, that I am not
sure we can ever recover. due to the BSE MRR taking over the BSE GBRs, that
fateful year when USDA inc covered up for the second time a mad cow, let it set
up on a shelf somewhere for 7 months, when they had a positive hit on a rapid
test, it took not only letters from me, but letters from scientist around the
world to write to the OIE, and finally the Honorable Phyllis Fong of the OIE
made the USDA send that sample to Weybridge, did that cow become positive. if
not for those letters, that cow would have been toast, never confirmed, another
mad cow cover up. it’s not the first time that has happened either. all the
while this cover up was going on, the BSE MRR was ratified. yes Ma’am, that
fateful day December 23, 2003, the day usda inc lost it’s gold card, BSE FREE
status, the BSE TSE mad cow science changed forever, and BSE TSE Prion became a
legal trading commodity.
I have been begging the OIE for over a decade, to please don’t wait until
corporate science allows you to acknowledge the CWD TSE Prion in Cervids, for
what it is, mad deer disease, and to please take action, and classify this
Chronic Wasting Disease CWD TSE Prion as a Zoonotic disease. again, OIE Doctors
seemed concerned, it was brought up several times in meetings, but nothing done.
a terrible mistake, and please see the latest science on the CWD TSE Prion below
from the Prion 2016 TOKYO Conference and It’s Zoonotic potential. You must take
action Ma’am, especially due to the exposure factor, and iatrogenic transmission
from friendly fire there from via surgical, medical, dental, blood, tissue...the
list is endless.
I have been begging the OIE about the risk factors of Scrapie to man, and
that it too should be a Zoonotic disease, especially after the OIE and the USDA
inc chose to drop Scrapie and Atypical Scrapie from the list of Zoonotic disease
concerns. I am not for sure how that turned out yet.
BUT my main concern, even if all the above was taken up and ratified (yet
to late imo), even if all this was taken up, my main concern is the lack of
validation or reporting of TSE PRION disease from countries, especially the USA.
If a country submits false and fraudulent reports on it’s TSE Prion status via
the BSE MRR, yet the OIE knowingly accepts this, something is then wrong Ma’am
with the OIE. I know I have sad many bad things about the OIE over the past 18
years or so, but things need to change there about how risk factors are
evaluated with the TSE Prion disease.
I lost my Mother to the Heidenhain Variant of Creutzfeldt Jakob Disease
hvCJD December 14, 1997, and just made a promise to her. never forget, and never
let them forget.
PLEASE read this Dr. Eloit, please read it very carefully, and then at the
bottom, I will at my correspondence with the OIE Doctors about my concerns over
the year, but first the latest about the USA CWD and the latest science.
I cannot urge you enough Ma’am, to act now, we have floundered for too
long, due to corporate junk science, and the incubation period, all for trade.
...
thank you,
with kindest regards,
terry
references...snip...end
From: OIE.
Sent: Tuesday, May 17, 2016 9:23 AM
To: flounder9@verizon.net
Subject: TR: OIE Director General, Dr Monique Eloit USA TSE PRION EMERGENCY
URGENT PLEA
Dear Mr Singeltary,
Thank you for your email, and your extensive dossier on TSEs.
OIE is committed to ensuring that our standards are based on and
incorporate the latest scientific knowledge. Our practice of bringing together
subject matter experts from around the globe on an on-going basis to inform our
standard development and revision process is a key part of achieving that. That
process continues with respect to BSE.
Further our whole standard development and revision process is designed to
be consultative and transparent. All comments and submissions on draft new or
revised standards are considered by our Specialist Commissions and subject
matter experts, as appropriate. Finally all OIE standards must be adopted by the
democratic process of our World Assembly of Delegates.
Please let me assure you that your submissions have been, and will
continue to be, considered in the development of our TSE standards.
Thank you for your on-going interest and support for OIE.
Yours sincerely,
OIE Office
============================
From: information.dept
Sent: Monday, April 25, 2016 8:57 AM
To: Terry S. Singeltary Sr.
Cc: Marija Popovic ; Neo Joel Mapitse ; Paolo Tizzani
Subject: RE: The first detection of Chronic Wasting Disease (CWD) in
Europe
Dear Terry,
I respond on behalf of Paula who is on a mission.
Thank you for sharing the blog with us regarding the occurrence of scrapie
in the United States of America.
The OIE does recognize the importance of scrapie worldwide and as such,
scrapie is one of the OIE-listed diseases. I like to refer you to the criteria
that allows for a disease, infection or infestation to become listed in the OIE
Terrestrial Animal Health Code :http://www.oie.int/index.php?id=169&L=0&htmfile=chapitre_criteria_diseases.htm
. As a result countries are obliged to notify the presence or absence of this
disease to the OIE. In addition, the disease is reported present regularly in
the reports sent by the United States of America.
Best regards,
Dr Neo MAPITSE Deputy Head of World Animal Health Information and Analysis
Department
Adjoint au Chef du Service d’information et d’analyse de la santé animale
mondiale
Jefe Adjunto del departamento de Información y Análisis de Sanidad animal
mundial
12 rue de Prony 75017 Paris, France Tel: +33 - 1 44 15 19 70 Fax: +33 - 1
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From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: vendredi 22 avril 2016 23:11
To: information.dept Cc: Marija Popovic; Neo Joel Mapitse;
information.dept; Paolo Tizzani
Subject: Re: The first detection of Chronic Wasting Disease (CWD) in Europe
Thank You Dr. Caceres-Soto kindly for taking the time and acknowledging my
note about CWD in Norway.
sadly, more bad news here in the USA. I know the OIE does not care now
about Scrapie, and that the USDA does not care either about Scrapie, but you all
better start caring, IMO.
Friday, April 22, 2016
Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected
in a Mule Deer
I have a bad report coming out about Colorado later, if you are
interested......
with kindest regards, terry
=======================
we have heard nothing from the OIE about this ;
Thursday, July 07, 2016
Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd
Norwegian moose
14/06/2016 - Norway reports a third case
IT is of my opinion, that the OIE and the USDA et al, are the soul reason,
and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion
diseases, including typical and atypical BSE, typical and atypical Scrapie, and
all strains of CWD, and human TSE there from, spreading around the globe.
I have lost all confidence of this organization as a regulatory authority
on animal disease, and consider it nothing more than a National Trading
Brokerage for all strains of animal TSE, just to satisfy there commodity. AS i
said before, OIE should hang up there jock strap now, since it appears they will
buckle every time a country makes some political hay about trade protocol,
commodities and futures. IF they are not going to be science based, they should
do everyone a favor and dissolve there organization.
JUST because of low documented human body count with nvCJD and the long
incubation periods, the lack of sound science being replaced by political and
corporate science in relations with the fact that science has now linked some
sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of
CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call
for this organization to be dissolved. ...
Tuesday, July 17, 2012
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th
General Session, 20 - 25 May 2012
Thursday, December 20, 2012
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe
WITH BOVINE MAD COW DISEASE
Friday, February 04, 2011
NMLB and USDA allow scrapie prion infected mutton to enter food chain on
the Navajo Reservation in New Mexico
Scrapie-like disorder in a Nyala (Tragelaphus angasi)
IN CONFIDENCE
Spongiform encephalopathy has so far only been recorded in the sheep and
goat, man, mink, and several deer including the mule deer, black tailed deer and
the elk (most, if not all, of the deer incidents occurred in wild life parts in
Wyoming and Colorado). Clinical cases in deer all occurred from 3 1/2 to 5 years
old and usually 60-80% losses occurred over a 4 year period...
The clinical and neuropathological findings in F22 are consistent with the
spongiform encephalopathies of animals and man. The agents causing spongiform
encephalopathy in various species cannot be unequivocally distinguished and some
isolates of human agent cause neurologic disease in goats indistinguishable from
scrapie. The spongiform encephalopathies are invariably fatal once clinical
signs of disease are evident and as very high fatality rates (79% of 67 animals)
are recorded in Mule deer it is important that an awareness of the disease is
maintained at Marwell.
Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY
*** How Did CWD Get Way Down In Medina County, Texas?
DISCUSSION Observations of natural outbreaks of scrapie indicated that the
disease spread from flock to flock by the movement of infected, but apparently
normal, sheep which were incubating the disease.
There was no evidence that the disease spread to adjacent flocks in the
absent of such movements or that vectors or other host species were involved in
the spread of scrapie to sheep or goats; however, these possibilities should be
kept open...
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...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
Saturday, April 23, 2016
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.***
Saturday, February 11, 2012
PrPSc Detection and Infectivity in Semen from Scrapie-Infected Sheep
Friday, December 23, 2011
Detection of PrPres in Genetically Susceptible Fetuses from Sheep with
Natural Scrapie
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
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
Sunday, December 12, 2010
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2
December 2010
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
Thursday, December 23, 2010
Molecular Typing of Protease-Resistant Prion Protein in Transmissible
Spongiform Encephalopathies of Small Ruminants, France, 2002-2009
Volume 17, Number 1 January 2011
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Wednesday, April 4, 2012
20120402 - Breach of quarantine/Violation de la mise en quarantaine of an
ongoing Scrapie investigation
Michigan and California have had a high spike in Goat Scrapie cases,
compared to elsewhere ???
Tuesday, February 01, 2011
Sparse PrP-Sc accumulation in the placentas of goats with naturally
acquired scrapie
(Figure 6) including five goat cases in FY 2008 that originated from the
same herd in Michigan. This is highly unusual for goats, and I strenuously urge
that there should be an independent investigation into finding the common
denominator for these 5 goats in the same herd in Michigan with Scrapie. ...
Thursday, February 23, 2012
Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012
RESEARCH
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A.
Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins,
Melanie J. Chaplin, and John Spiropoulos
To investigate the possibility of oral transmission of atypical scrapie in
sheep and determine the distribution of infectivity in the animals’ peripheral
tissues, we challenged neonatal lambs orally with atypical scrapie; they were
then killed at 12 or 24 months. Screening test results were negative for
disease-specifi c prion protein in all but 2 recipients; they had positive
results for examination of brain, but negative for peripheral tissues.
Infectivity of brain, distal ileum, and spleen from all animals was assessed in
mouse bioassays; positive results were obtained from tissues that had negative
results on screening. These fi ndings demonstrate that atypical scrapie can be
transmitted orally and indicate that it has the potential for natural
transmission and iatrogenic spread through animal feed. Detection of infectivity
in tissues negative by current surveillance methods indicates that diagnostic
sensitivity is suboptimal for atypical scrapie, and potentially infectious
material may be able to pass into the human food chain.
SNIP...
Although we do not have epidemiologic evidence that supports the effi cient
spread of disease in the fi eld, these data imply that disease is potentially
transmissible under fi eld situations and that spread through animal feed may be
possible if the current feed restrictions were to be relaxed. Additionally,
almost no data are available on the potential for atypical scrapie to transmit
to other food animal species, certainly by the oral route. However, work with
transgenic mice has demonstrated the potential susceptibility of pigs, with the
disturbing fi nding that the biochemical properties of the resulting PrPSc have
changed on transmission (40). The implications of this observation for
subsequent transmission and host target range are currently unknown.
How reassuring is this absence of detectable PrPSc from a public health
perspective? The bioassays performed in this study are not titrations, so the
infectious load of the positive gut tissues cannot be quantifi ed, although
infectivity has been shown unequivocally. No experimental data are currently
available on the zoonotic potential of atypical scrapie, either through
experimental challenge of humanized mice or any meaningful epidemiologic
correlation with human forms of TSE. However, the detection of infectivity in
the distal ileum of animals as young as 12 months, in which all the tissues
tested were negative for PrPSc by the currently available screening and confi
rmatory diagnostic tests, indicates that the diagnostic sensitivity of current
surveillance methods is suboptimal for detecting atypical scrapie and that
potentially infectious material may be able to pass into the human food chain
undetected.
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
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).
Monday, June 20, 2016
Specified Risk Materials SRMs BSE TSE Prion Program
Sunday, May 27, 2012
CANADA PLANS TO IMPRISON ANYONE SPEAKING ABOUT MAD COW or ANY OTHER DISEASE
OUTBREAK, CENSORSHIP IS A TERRIBLE THING
BSE, SCRAPIE, CWD, TSE, PRION, and the legal trading therefrom, thanks to
the USDA and OIE et al
thanks to the OIE and the USDA inc. mad cow disease of all types have been
spread globally thanks to the BSE MRR policy, the legal trading of all strains
of TSE Prion aka mad cow type disease. can you say pass the prions
please...
BSE, SCRAPIE, CWD, TSE, PRION, and the legal trading therefrom, thanks to
the USDA and OIE et al
Tuesday, May 31, 2016
Priority Interim Position Paper PROTECTING THE FOOD CHAIN FROM PRIONS
Perspectives
Tuesday, June 07, 2016
Comparison of two US sheep scrapie isolates supports identification as
separate strains
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
CHRONIC WASTING DISEASE TSE PRION
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Prion 2016
Purchase options Price * Issue Purchase USD 198.00
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting
disease (CWD) is the prion disease affecting deer, elk and moose, and it is a
widespread and expanding epidemic affecting 22 US States and 2 Canadian
provinces so far. CWD poses the most serious zoonotic prion transmission risks
in North America because of huge venison consumption (>6 million deer/elk
hunted and consumed annually in the USA alone), significant prion infectivity in
muscles and other tissues/fluids from CWD-affected cervids, and usually high
levels of individual exposure to CWD resulting from consumption of the affected
animal among often just family and friends. However, we still do not know
whether CWD prions can infect humans in the brain or peripheral tissues or
whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no
essays to reliably detect CWD infection in humans. We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) CWD transmission to humans has already occurred. We will test these
hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in
vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain
or peripheral lymphoid tissues at low levels by conducting systemic bioassays in
a set of "humanized" Tg mouse lines expressing common human PrP variants using a
number of CWD isolates at varying doses and routes. Experimental "human CWD"
samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission
barrier is dependent on prion strain and influenced by the host (human) PrP
sequence by examining and comparing the transmission efficiency and phenotypes
of several atypical/unusual CWD isolates/strains as well as a few prion strains
from other species that have adapted to cervid PrP sequence, utilizing the same
panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD
infection in humans by examining in details the clinical, pathological,
biochemical and in vitro seeding properties of existing and future experimental
"human CWD" samples generated from Aims 1-2 and compare them with those of
common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining
a significant number of brain samples from prion-affected human subjects in the
USA and Canada who have consumed venison from CWD-endemic areas utilizing the
criteria and essays established in Aim 3. The findings from this proposal will
greatly advance our understandings on the potential and characteristics of
cervid prion transmission in humans, establish reliable essays for CWD zoonosis
and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure
to cervid prions because chronic wasting disease (CWD, a widespread and highly
infectious prion disease among deer and elk in North America) continues
spreading and consumption of venison remains popular, but our understanding on
cervid-to-human prion transmission is still very limited, raising public health
concerns. This proposal aims to define the zoonotic risks of cervid prions and
set up and apply essays to detect CWD zoonosis using mouse models and in vitro
methods. The findings will greatly expand our knowledge on the potentials and
characteristics of cervid prion transmission in humans, establish reliable
essays for such infections and may discover the first case(s) of CWD infection
in humans.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 1R01NS088604-01A1
Application # 9037884
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2015-09-30
Budget End 2016-07-31
Support Year 1
Fiscal Year 2015
Total Cost $337,507
Indirect Cost $118,756
Institution
Name Case Western Reserve University
Department Pathology
Type Schools of Medicine
DUNS # 077758407
City Cleveland
State OH
Country United States
Zip Code 44106
===========================================================
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) *** CWD transmission to humans has already occurred. *** We will test
these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary
in vitro approaches.
============================================================
Key Molecular Mechanisms of TSEs
Zabel, Mark D.
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs),
are fatal neurodegenerative diseases affecting humans, cervids, bovids, and
ovids. The absolute requirement of PrPC expression to generate prion diseases
and the lack of instructional nucleic acid define prions as unique infectious
agents. Prions exhibit species-specific tropism, inferring that unique prion
strains exist that preferentially infct certain host species and confront
transmission barriers to heterologous host species. However, transmission
barriers are not absolute. Scientific consensus agrees that the sheep TSE
scrapie probably breached the transmission barrier to cattle causing bovine
spongiform encephalopathy that subsequently breached the human transmission
barrier and likely caused several hundred deaths by a new-variant form of the
human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human
health, emotion and economies can still be felt in areas like farming, blood and
organ donations and the threat of a latent TSE epidemic. This precedent raises
the real possibility of other TSEs, like chronic wasting disease of cervids,
overcoming similar human transmission barriers. A groundbreaking discovery made
last year revealed that mice infected with heterologous prion strains facing
significant transmission barriers replicated prions far more readily in spleens
than brains6. Furthermore, these splenic prions exhibited weakened transmission
barriers and expanded host ranges compared to neurogenic prions. These data
question conventional wisdom of avoiding neural tissue to avoid prion
xenotransmission, when more promiscuous prions may lurk in extraneural tissues.
Data derived from work previously funded by NIH demonstrate that Complement
receptors CD21/35 bind prions and high density PrPC and differentially impact
prion disease depending on the prion isolate or strain used. Recent advances in
live animal and whole organ imaging have led us to generate preliminary data to
support novel, innovative approaches to assessing prion capture and transport.
We plan to test our unifying hypothesis for this proposal that CD21/35 control
the processes of peripheral prion capture, transport, strain selection and
xenotransmission in the following specific aims. 1. Assess the role of CD21/35
in splenic prion strain selection and host range expansion. 2. Determine whether
CD21/35 and C1q differentially bind distinct prion strains 3. Monitor the
effects of CD21/35 on prion trafficking in real time and space 4. Assess the
role of CD21/35 in incunabular prion trafficking
Public Health Relevance Transmissible spongiform encephalopathies, or prion
diseases, are devastating illnesses that greatly impact public health,
agriculture and wildlife in North America and around the world. The impact to
human health, emotion and economies can still be felt in areas like farming,
blood and organ donations and the threat of a latent TSE epidemic. This
precedent raises the real possibility of other TSEs, like chronic wasting
disease (CWD) of cervids, overcoming similar human transmission barriers. Early
this year Canada reported its first case of BSE in over a decade audits first
case of CWD in farmed elk in three years, underscoring the need for continued
vigilance and research. Identifying mechanisms of transmission and zoonoses
remains an extremely important and intense area of research that will benefit
human and other animal populations.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Allergy and Infectious Diseases (NIAID)
Type High Priority, Short Term Project Award (R56)
Project # 1R56AI122273-01A1
Application # 9211114
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Beisel, Christopher E
Project Start 2016-02-16
Project End 2017-01-31
Budget Start 2016-02-16
Budget End 2017-01-31
Support Year 1
Fiscal Year 2016
Total Cost
Indirect Cost Institution Name Colorado State University-Fort Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
PMCA Detection of CWD Infection in Cervid and Non-Cervid Species
Hoover, Edward Arthur
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Chronic wasting disease (CWD) of deer and elk is an emerging highly
transmissible prion disease now recognized in 18 States, 2 Canadian provinces,
and Korea. We have shown that Infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces, and in the tissues
generating those body fluids and excreta, thereby leading to facile transmission
by direct contact and environmental contamination. We have also shown that CWD
can infect some non-cervid species, thus the potential risk CWD represents to
domestic animal species and to humans remains unknown. Whether prions borne in
blood, saliva, nasal fluids, milk, or excreta are generated or modified in the
proximate peripheral tissue sites, may differ in subtle ways from those
generated in brain, or may be adapted for mucosal infection remain open
questions. The increasing parallels in the pathogenesis between prion diseases
and human neurodegenerative conditions, such as Alzheimer's and Parkinson's
diseases, add relevance to CWD as a transmissible protein misfolding disease.
The overall goal of this work is to elucidate the process of CWD prion
transmission from mucosal secretory and excretory tissue sites by addressing
these questions: (a) What are the kinetics and magnitude of CWD prion shedding
post-exposure? (b) Are excreted prions biochemically distinct, or not, from
those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the
source of excreted prions? and (d) Are excreted prions adapted for horizontal
transmission via natural/trans-mucosal routes? The specific aims of this
proposal are: (1) To determine the onset and consistency of CWD prion shedding
in deer and cervidized mice; (2); To compare the biochemical and biophysical
properties of excretory vs. CNS prions; (3) To determine the capacity of
peripheral tissues to support replication of CWD prions; (4) To determine the
protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To
compare the mucosal infectivity of excretory vs. CNS prions. Understanding the
mechanisms that enable efficient prion dissemination and shedding will help
elucidate how horizontally transmissible prions evolve and succeed, and is the
basis of this proposal. Understanding how infectious misfolded proteins (prions)
are generated, trafficked, shed, and transmitted will aid in preventing,
treating, and managing the risks associated with these agents and the diseases
they cause.
Public Health Relevance Chronic wasting disease (CWD) of deer and elk is an
emergent highly transmissible prion disease now recognized throughout the USA as
well as in Canada and Korea. We have 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. In
that our studies have also shown that CWD can infect some non-cervid species,
the potential risk CWD may represents to domestic animal species and humans
remains unknown. The increasing parallels in the development of major human
neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and
prion diseases add relevance to CWD as a model of a transmissible protein
misfolding disease. Understanding how infectious misfolded proteins (prions) are
generated and transmitted will aid in interrupting, treating, and managing the
risks associated with these agents and the diseases they cause.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 4R01NS061902-07
Application # 9010980
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May Project Start 2009-09-30
Project End 2018-02-28
Budget Start 2016-03-01
Budget End 2017-02-28
Support Year 7
Fiscal Year 2016
Total Cost $409,868
Indirect Cost $134,234 Institution Name Colorado State University-Fort
Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid
prion protein (PrP) sequence through passage in cervidized transgenic mice
efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion
strain-dependent and humans can be vulnerable to novel cervid prion strains.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on the
existence of different CWD strains.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** now, let’s see what the authors said about this casual link, personal
communications years ago, and then the latest on the zoonotic potential from CWD
to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS
casual evidence ???? “Our conclusion stating that we found no strong evidence of
CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** NIH awards $11 million to UTHealth researchers to study deadly CWD
prion diseases Claudio Soto, Ph.D. ***
Public Release: 29-Jun-2016
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
CWD TSE PRION CHRONIC WASTING DISEASE UPDATE
Friday, July 01, 2016
*** TEXAS Thirteen new cases of chronic wasting disease (CWD) were
confirmed at a Medina County captive white-tailed deer breeding facility on June
29, 2016
*** Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force
Base Scrapie Experiment 1964 ***
How Did CWD Get Way Down In Medina County, Texas?
Confucius ponders...
Could the Scrapie experiments back around 1964 at Moore Air Force near
Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides
the CWD cases that have waltzed across the Texas, New Mexico border near WSMR
Trans Pecos region since around 2001)?
Epidemiology of Scrapie in the United States 1977
snip...
Scrapie Field Trial Experiments Mission, Texas
A Scrapie Field Trial was developed at Mission, Texas, to provide
additional information for the eradication program on the epidemiology of
natural scrapie. The Mission Field Trial Station is located on 450 acres of
pastureland, part of the former Moore Air Force Base, near Mission, Texas. It
was designed to bring previously exposed, and later also unexposed, sheep or
goats to the Station and maintain and breed them under close observation for
extended periods to determine which animals would develop scrapie and define
more closely the natural spread and other epidemiological aspects of the
disease.
The 547 previously exposed sheep brought to the Mission Station beginning
in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were
purchased as field outbreaks occurred, and represented 21 bloodlines in which
scrapie had been diagnosed. Upon arrival at the Station, the sheep were
maintained on pasture, with supplemental feeding as necessary. The station was
divided into 2 areas: (1) a series of pastures and-pens occupied by male animals
only, and (2) a series of pastures and pens occupied by females and young
progeny of both sexes. ...
snip...see full text ;
Thursday, June 09, 2016
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base
Scrapie TSE Prion Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was
detected in a Mule Deer
Wednesday, March 18, 2015
Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015
Wednesday, March 25, 2015
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
very important ;
Sunday, July 10, 2016
>>>*** Primary transmission of CWD versus scrapie prions from
small ruminants to ovine and cervid PrP transgenic mice ***<<<
Saturday, July 09, 2016
*** Texas Intrastate – within state movement of all Cervid or Trucking
Chronic Wasting Disease CWD TSE Prion Moratorium
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
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
Monday, May 09, 2016
A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation
2001 Deepthroat to Singeltary
The most frightening thing I have read all day is the report of Gambetti's
finding of a new strain of sporadic cjd in young people.........Dear God, what
in the name of all that is holy is that!!! If the US has different strains of
scrapie.....why???? than the UK...then would the same mechanisms that make
different strains of scrapie here make different strains of BSE...if the
patterns are different in sheep and mice for scrapie.....could not the BSE be
different in the cattle, in the mink, in the humans.......I really think the
slides or tissues and everything from these young people with the new strain of
sporadic cjd should be put up to be analyzed by many, many experts in
cjd........bse.....scrapie Scrape the damn slide and put it into
mice.....wait.....chop up the mouse brain and and spinal cord........put into
some more mice.....dammit amplify the thing and start the damned
research.....This is NOT rocket science...we need to use what we know and get
off our butts and move....the whining about how long everything takes.....well
it takes a whole lot longer if you whine for a year and then start the
research!!! Not sure where I read this but it was a recent press release or
something like that: I thought I would fall out of my chair when I read about
how there was no worry about infectivity from a histopath slide or tissues
because they are preserved in formic acid, or formalin or formaldehyde.....for
God's sake........ Ask any pathologist in the UK what the brain tissues in the
formalin looks like after a year.......it is a big fat sponge...the agent
continues to eat the brain ......you can't make slides anymore because the agent
has never stopped........and the old slides that are stained with Hemolysin and
Eosin......they get holier and holier and degenerate and continue...what you
looked at 6 months ago is not there........Gambetti better be photographing
every damned thing he is looking at.....
Okay, you need to know. You don't need to pass it on as nothing will come
of it and there is not a damned thing anyone can do about it. Don't even hint at
it as it will be denied and laughed at.......... USDA is gonna do as little as
possible until there is actually a human case in the USA of the nvcjd........if
you want to move this thing along and shake the earth....then we gotta get the
victims families to make sure whoever is doing the autopsy is credible,
trustworthy, and a saint with the courage of Joan of Arc........I am not
kidding!!!! so, unless we get a human death from EXACTLY the same form with
EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any
action........it is ALL gonna be sporadic!!!
And, if there is a case.......there is gonna be every effort to link it to
international travel, international food, etc. etc. etc. etc. etc. They will go
so far as to find out if a sex partner had ever traveled to the UK/europe, etc.
etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth.
They have all the cards, all the money, and are willing to threaten and carry
out those threats....and this may be their biggest downfall...
Thanks as always for your help.
(Recently had a very startling revelation from a rather senior person in
government here..........knocked me out of my chair........you must keep
pushing. If I was a power person....I would be demanding that there be a least a
million bovine tested as soon as possible and agressively seeking this disease.
The big players are coming out of the woodwork as there is money to be made!!!
In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the
burden to bare if there is any coverup!"
again it was said years ago and it should be taken seriously....BSE will
NEVER be found in the US! As for the BSE conference call...I think you did a
great service to freedom of information and making some people feign
integrity...I find it scary to see that most of the "experts" are employed by
the federal government or are supported on the "teat" of federal funds. A scary
picture! I hope there is a confidential panel organized by the new government to
really investigate this thing.
You need to watch your back........but keep picking at them.......like a
buzzard to the bone...you just may get to the truth!!! (You probably have more
support than you know. Too many people are afraid to show you or let anyone else
know. I have heard a few things myself... you ask the questions that everyone
else is too afraid to ask.)
==============end...TSS=============
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
posted by Terry S. Singeltary Sr. | 8:39 AM
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