[Docket No. APHIS-2013-0064] Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy
[Federal Register Volume 79, Number 190 (Wednesday, October 1, 2014)]
[Notices] [Pages 59207-59208] From the Federal Register Online via the
Government Printing Office [www.gpo.gov] [FR Doc No: 2014-23407]
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Federal Register / Vol. 79, No. 190 / Wednesday, October 1, 2014 /
Notices
[[Page 59207]]
DEPARTMENT OF AGRICULTURE
Animal and Plant Health Inspection Service
[Docket No. APHIS-2013-0064]
Concurrence With OIE Risk Designations for Bovine Spongiform
Encephalopathy
AGENCY: Animal and Plant Health Inspection Service, USDA.
ACTION: Notice.
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SUMMARY: We are advising the public of our decision to concur with the
World Organization for Animal Health's (OIE) bovine spongiform encephalopathy
(BSE) risk designations for 15 regions. The OIE recognizes these regions as
being of either negligible risk for BSE or of controlled risk for BSE. We are
taking this action based on our review of information supporting the OIE's risk
designations for these regions.
FOR FURTHER INFORMATION CONTACT: Dr. Silvia Kreindel, Senior Staff
Veterinarian, Regionalization Evaluation Services, National Import Export
Services, VS, APHIS, 4700 River Road Unit 38, Riverdale, MD 20737-1231; (301)
851-3300.
SUPPLEMENTARY INFORMATION: The regulations in 9 CFR part 92 subpart B,
``Importation of Animals and Animal Products; Procedures for Requesting BSE Risk
Status Classification With Regard to Bovines'' (referred to below as the
regulations), set forth the process by which the Animal and Plant Health
Inspection Service (APHIS) classifies regions for bovine spongiform
encephalopathy (BSE) risk. Section 92.5 of the regulations provides that all
countries of the world are considered by APHIS to be in one of three BSE risk
categories: Negligible risk, controlled risk, or undetermined risk. These risk
categories are defined in Sec. 92.1. Any region that is not classified by APHIS
as presenting either negligible risk or controlled risk for BSE is considered to
present an undetermined risk. The list of those regions classified by APHIS as
having either negligible risk or controlled risk can be accessed on the APHIS
Web site at http://www.aphis.usda.gov/
importexport/animals/ animaldiseasestatus.shtml. The list can also be obtained
by writing to APHIS at National Import Export Services, 4700 River Road Unit 38,
Riverdale, MD 20737. Under the regulations, APHIS may classify a region for BSE
in one of two ways. One way is for countries that have not received a risk
classification from the World Organization for Animal Health (OIE) to request
classification by APHIS. The other way is for APHIS to concur with the
classification given to a country by the OIE. If the OIE has recognized a
country as either BSE negligible risk or BSE controlled risk, APHIS will seek
information to support our concurrence with the OIE classification. This
information may be publicly available information, or APHIS may request that
countries supply the same information given to the OIE. APHIS will announce in
the Federal Register, subject to public comment, its intent to concur with an
OIE classification. In accordance with that process, we published a notice \1\
in the Federal Register on December 4, 2013 (78 FR 72859-72860, Docket No.
APHIS-2013-0064), in which we announced our intent to concur with the OIE risk
designations for 15 regions. In the notice we mistakenly stated that we intended
to concur with the risk designations for 14 regions; the correct number is 15.
The regions listed in the notice, however, were correct. The OIE recognizes
these regions as being of either negligible risk for BSE or of controlled risk
for BSE. We solicited comments on the notice for 60 days ending on February 3,
2014. We received three comments by that date, from two private citizens and a
foreign industry association.
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\1\ To view the notice and the comments we received, go to http://www.regulations.gov/#!docketDetail;D=APHIS-2013-0064.
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One commenter expressed general concern that the risk designations did not
accurately reflect the actual risk of BSE, but the commenter did not address the
specific details of the OIE process or of any region's designation. Another
commenter expressed concern that the OIE process is not transparent and there is
insufficient detail in the OIE summaries to make an adequate determination of
BSE risk. This commenter stated that APHIS should undertake its own assessment
of BSE status rather than accepting the OIE risk designation. The summaries are
the only information the OIE makes publicly available. Countries may make their
BSE dossiers publicly available, in whole or in part, or they may share their
dossiers with other countries upon request. For this reason, before announcing
our intent to concur with the OIE classification, APHIS verifies that the
information can be provided to us, or is publicly available, for review to
support our concurrence with the OIE classification. APHIS' intention is to
follow the OIE's BSE guidelines while ensuring that OIE-recognized countries
apply adequate BSE risk mitigation measures assuring that bovines and bovine
commodities destined for export pose a negligible risk for BSE, and that the
country complies with OIE requirements for the specific BSE country recognition.
If the information is not publicly available and the country does not provide
the information, then we will not recognize the country's BSE status. APHIS thus
has greater confidence in the outcomes of the evaluations and will have the
necessary documentation to support or defend recognition decisions. The process
we use is described in the regulations in Sec. 92.5. The information provided in
the OIE dossier is more comprehensive than what appears in the summaries of the
OIE Scientific Commission, and includes information about the likelihood that
the disease could have been introduced into the country though the importation
of bovine or bovine commodities in the last 7 years, the likelihood that the
agent could have been recycled in as meat-and-bone meal or greaves for the last
8 years, the awareness, notification and laboratory capabilities of the region,
BSE surveillance in the region, and the history of BSE in the region. One
commenter stated that, according to the OIE summary reports, the evaluation for
Brazil was provided by the OIE in February 2012. The commenter also stated that
in December
[[Page 59208]]
2012, it was learned that a cow from Brazil that was sampled for testing in
December 2010 tested positive for BSE. The commenter noted that
immunohistochemistry (IHC) tests were not completed until June 2012, and it was
another 6 months before a confirmatory test was completed at the Community
Reference Laboratory in Weybridge, United Kingdom. The commenter stated that the
lack of specific information regarding the OIE evaluation of the surveillance
system made it difficult to determine if this was a one-time error or a failure
of the system. APHIS agrees that the delays in the testing and reporting of the
atypical BSE case detected in Brazil were problematic. In response to these
concerns, the OIE Scientific Commission requested that Brazil provide all
relevant information for their meeting in February 2013. At that meeting, the
OIE Scientific Commission affirmed that the identification of this single case
of BSE did not put Brazil's or its trading partners' animal and public health at
risk because the animal was destroyed and no parts of it had entered the food or
feed chain. However, the OIE was also concerned about the delay before Brazil
sent the clinical samples for a confirmatory diagnosis and requested more
detailed information on the procedures for processing samples and the
improvement of the surveillance system in the country, so that they could
further monitor compliance by Brazil with international standards.\2\ At a
subsequent meeting in September 2013, the OIE assessed the additional
information provided by Brazil.\3\ The OIE was satisfied with the evidence
submitted but also concluded that Brazil should submit the results of the
proficiency tests conducted for 2013 to the OIE as soon as they became
available.
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\2\ The report of the OIE scientific commission meeting in February 2013
can be viewed at http://www.oie.int/fileadmin/Home/eng/InternationaStandardSetting/docs/pdf/SCAD/ASCADFeb2013.pdf.
The discussion of the BSE case in Brazil appears on pages 13-14. \3\ The report
of the OIE scientific commission meeting in September 2013 can be viewed at http://www.oie.int/fileadmin/Home/eng/InternationaStandardSetting/docs/pdf/SCAD/ASCADSept2013.pdf.
The discussion of the BSE case in Brazil appears on page 7.
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In addition, representatives of APHIS and the United States Department of
Agriculture's Food Safety and Inspection Service visited Brazil in February 2013
to evaluate the BSE laboratory infrastructure, emergency response, and
BSE-related mitigations at the slaughter level. APHIS' review of the
epidemiological and laboratory reports, including the report from the
confirmatory tests conducted at Weybridge, shows that Brazil's first BSE case
was most consistent with the atypical form of the disease. In addition, as a
result of the delays in testing and reporting of this case, Brazil's
Minist[eacute]rio da Agricultura, Pecu[aacute]ria e Abastecimento conducted
audits of the laboratories to identify areas for change and improvement, and has
implemented several new procedures to assure the timely testing of samples and
reporting of results. Corrective actions include addition of a second lab to
conduct IHC tests, expansion of testing capabilities to include Western Blot,
and the development of an inter-laboratory data management system which will
issue reports, record improper samples, and flag delays in sample receipt,
completion, and notification of test results. Samples will be forwarded for IHC
testing immediately after the immunofluorescence test for rabies is completed,
rather than waiting for the animal inoculation tests to be completed. We note
that Brazil detected a suspected case of BSE in a 12-year- old cow in April
2014. The Brazilian authorities carried out the required epidemiological
investigation in accordance with OIE guidelines. In May 2014, tests at the OIE
reference laboratory in Weybridge confirmed that it was an atypical case of BSE.
Brazil still meets the criteria for a negligible risk region. In Article 11.5.3
of the Terrestrial Animal Health Code, the OIE requires, among other things,
that if there has been an indigenous case of BSE in a region, every indigenous
case was born more than 11 years ago. The cow in which BSE was detected was over
11 years of age. Therefore, this most recent case will not affect Brazil's
negligible risk status. One commenter stated that India should be included in
the list of regions of negligible risk for BSE. Our review of information in
support of concurrence with the OIE designation for India is ongoing; we have
requested the OIE dossier but have not yet received it. When our review is
complete, if the findings support concurrence with the OIE designation, we will
publish a notice in the Federal Register announcing our preliminary concurrence
with the OIE's designation for India and provide the public with an opportunity
to comment. One commenter stated that the United States should be included on
this list of regions of negligible risk for BSE because some raw material may be
exported from the United States and then reimported after processing abroad.
When APHIS assesses the disease status of a region, it is to determine whether
imports can be safely allowed from that region. For this reason we do not
typically include the United States in the lists of regions recognized for any
given disease status. In the event that raw material was exported for
processing, we could allow it to be reimported under conditions that would be
specified on the import permit. Therefore, in accordance with the regulations in
Sec. 92.5, we are announcing our decision to concur with the OIE risk
classifications of the following countries: Regions of negligible risk for BSE:
Austria, Belgium, Brazil, Colombia, Israel, Italy, Japan, the Netherlands,
Singapore, Slovenia. Regions of controlled risk for BSE: Bulgaria, Costa Rica,
Croatia, Nicaragua, Taiwan.
Authority: 7 U.S.C. 1622 and 8301-8317; 21 U.S.C. 136 and 136a; 31 U.S.C.
9701; 7 CFR 2.22, 2.80, and 371.4.
Done in Washington, DC, this 26th day of September 2014. Kevin Shea,
Administrator, Animal and Plant Health Inspection Service. [FR Doc. 2014-23407
Filed 9-30-14; 8:45 am] BILLING CODE 3410-34-P
From: Terry S. Singeltary Sr. Sent: Monday, September 29, 2014 9:28 PM To:
Louis.Gagnon@fao.org Cc: FAO-Newsroom@fao.org ; kkm@onehealthinitiative.com ;
globalhealth@hhs.gov Subject: FAO joins new global efforts targeting Ebola and
other infectious diseases
Greetings Honorable FAO Director-General José Graziano da Silva et al,
I wish to kindly, and urgently address something I did not see in these
reports, a long incubating, 100% fatal once clinical disease i.e. the
Transmissible Spongiform Encephalopathy TSE Prion diseases aka mad cow type
disease. They have been conveniently ignored, or covered up, take your pick, for
way too long. I urge you to take further actions to address this issue as soon
as possible. The INDUSTRY FRIENDLY trade agreements between Countries, via the
OIE, is a sham, when considering the TSE prion disease, BSE, Scrapie, CWD, TME,
FSE, and other animal TSE not yet documented such as canine spongiform
encephalopathy CSE, and all the human TSE prion disease, and the many different
names that follow, just making things much more complicated. the ramifications
from friendly fire, or the iatrogenic modes from all the above is great. the
longer global recognition, and surveillance there from is ignored, the worse it
will get, and this is what the mad cow debacle has shown us, and please spare us
what I term the UKBSEnvCJD only theory. that dog don’t hunt no more.
I lost my mother to the Heidenhain Variant of Creutzfeldt Jakob disease aka
hvCJD aka sporadic CJD (just another name of the same disease), and no, please,
how can a supposedly genetic TSE prion disease, such as FFI or GSS, suddenly
become a sporadic disease, such as now sporadic FFI, or sporadic GSS, or VPSPr,
but not be connected to any family genetically? please tell me this.
I have wasted almost 18 years of my life, daily, searching for answers, as
are many others, to what the government calls a spontaneous event. ...that dog
don’t hunt no more either.
THE TSE prion disease, aka mad cow type disease, they are more of a
political disease than anything else$
I just mad a promise to mom, never forget, and never let them forget.
I submit the following information on the USA and it’s state of the TSE
prion disease aka mad cow type disease. for what’s it worth, please use as you
wish.
I kind submitt ;
FAO joins new global efforts targeting Ebola and other infectious
diseases
In talks hosted by U.S. President Barack Obama, FAO Director-General
outlines FAO's role in Global Health Security Agenda
Photo: ©FAO
FAO Director-General José Graziano da Silva speaks at the Global Health
Security Summit at the White House.
26 September 2014, Washington, D.C. - FAO Director-General José Graziano da
Silva today stressed the need for controls on animal health to help curb the
spread of Ebola and other infectious diseases dangerous to humans, during
discussions hosted by U.S. President Barack Obama.
The FAO chief joined leaders of the World Health Organization (WHO), the
World Organisation for Animal Health (OIE) and representatives from more than 40
countries at the Global Health Security Agenda (GHSA) event held at the White
House in Washington, D.C.
President Obama underscored the importance of dealing with the breakout of
infectious diseases collectively, highlighting that in a world that is deeply
interconnected, outbreaks have the potential to impact every country. "No nation
can meet this challenge on its own. Nobody is that isolated," he said, stressing
the need for global cooperation.
The U.S. government-initiated GHSA is an international partnership to
strengthen health systems with the objective to prevent, detect and respond to
emerging disease threats. It is estimated that 70 percent of new infectious
diseases that have emerged in humans over recent decades have animal origin,
mostly from wildlife.
Graziano da Silva underlined that "controlling zoonotic diseases and
emerging threats at the human, animal and ecosystems interface needs an
integrated and multidisciplinary approach that brings different sectors to work
closely together to attain the health of people, animals and the environment."
He noted how this is echoed in the One Health agenda which has seen FAO, as
part of its tripartite partnership (FAO-WHO-OIE), integrate this approach in its
vision for sustainable livestock development "to attain a healthier and more
prosperous world."
By focusing on prevention, countries can minimize loss of human life when
diseases cross over from animal to human populations and thus become harder to
manage - a fact illustrated by the current Ebola outbreak in West Africa, the
FAO Director-General said.
He expressed "great concern" over the possible impact of this epidemic on
"food security and livelihoods of affected communities, with a potential to
cause long-term food insecurity in West Africa, as a result of prolonged
disruption of crop harvesting and subsequent planting."
The FAO Director-General in his address also mentioned other recent
emerging diseases of animal origin that affect humans such as H5N1 avian
influenza, Severe Acute Respiratory Syndrome (SARS) and Middle East respiratory
syndrome (MERS).
"There is a need to set up global preparedness, surveillance and response
programmes," Graziano da Silva told participants at the White House event. He
welcomed the GHSA's focus on prevention, detection and response, and noted how
FAO shared this approach.
Graziano da Silva reiterated FAO's commitment, alongside WHO and OIE, to
further support countries in tackling threats to health from animal sources. FAO
works with country and regional partners to assist them to develop preparedness
and contingency plans for animal health-related events, and these capacities
serve both public health and food security aims.
FAO also contributes to health protection through its work on the Joint
FAO/WHO Codex Alimentarius Commission, that provides guidance on food safety and
public health taking into account the entire food chain.
The Director-General, in his address at the White House event, emphasized
the strong link between nutrition and human health. He noted how the upcoming
Second International Conference on Nutrition (ICN2), jointly organized by FAO
and WHO, will establish a framework of actions on nutrition that will be part of
the Post-2015 Agenda.
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Laura H Kahn, MD,MPH, MPP Bruce Kaplan, DVM Thomas P. Monath, MD
email: kkm@onehealthinitiative.com
>>> It is estimated that 70 percent of new infectious diseases
that have emerged in humans over recent decades have animal origin, mostly from
wildlife.
USA 4TH CASE VCJD (aka nvCJD) HUMAN MAD COW, THE SILENCE IS DEAFENING BSE,
CWD, AND SCRAPIE TSE PRION DISEASE
Greetings DSHS, Dr. Fishcer, et al,
I know that most in the USA could care less about the CJD TSE prion disease
aka mad cow type disease. but there are some of us here that will never forget.
you can cover up what ever you want. we all know. I have seen it happen too
many times here in Texas with BSE TSE prion, either the typical or the atypical
strains, or with the feed, or, with cwd, or scrapie as that goes, but we are
still here, and we will never forget...
kind regards, terry
Creutzfeld-Jacob Disease (CJD) Emerging & Acute Infectious Disease
Branch Michael Fischer
Marilyn Felkner
512-776-7676
512-776-7676
Chronic Wasting Disease Zoonosis Control Branch Eric Fonken
512-776-2155
Lab tests have confirmed a diagnosis of variant Creutzfeldt-Jakob Disease
(CJD) in a patient who recently died in Texas. Variant CJD is a rare, fatal
brain disorder, first described in 1996 in the United Kingdom and associated
with beef consumption overseas.
This is the fourth case ever reported in the United States. In each of the
three previous cases, infection likely occurred outside the United States,
including the United Kingdom and Saudi Arabia. The history of this fourth
patient includes extensive travel to Europe and the Middle East, and infection
likely occurred outside the United States. The CDC and DSHS continue to
investigate the case.
There are no Texas public health concerns or threats associated with this
case.
CDC Confirmation Information: http://www.cdc.gov/ncidod/dvrd/vcjd/other/confirmed-case-in-texas.htm
CDC Fact Sheet: http://www.cdc.gov/ncidod/dvrd/vcjd/factsheet_nvcjd.htm
Texas CJD Information: http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/
Last updated June 02, 2014
CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
Monday, June 02, 2014 Confirmed Variant CJD Case in Texas
SO, 4 months after the fact and still no word on this case. no information
what so ever. the silence is deafening $$$
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Transmissible Spongiform Encephalopathy TSE Prion Disease have now been
discovered in a wide verity of species across North America. typical C-BSE,
atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine,
typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98
Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD
in cervid is slowly spreading without any stopping it in Canada and the USA and
now has mutated into many different strains. Transmissible Mink Encephalopathy
TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease
have been silently mutating and spreading in different species in North America
for decades.
The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion
Firewall, of which we now know without a doubt, that it was nothing but ink on
paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of
banned mad cow feed has been put out into commerce, never to return, as late as
December of 2013, serious, serious breaches in the FDA mad cow feed ban have
been documented. The 2004 enhanced BSE surveillance program was so flawed, that
one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown,
who is preparing a scientific paper based on the latest two mad cow cases to
estimate the maximum number of infected cows that occurred in the United States,
said he has "absolutely no confidence in USDA tests before one year ago" because
of the agency's reluctance to retest the Texas cow that initially tested
positive.
see ;
The BSE surveillance and testing have also been proven to be flawed, and
the GAO and OIG have both raised serious question as to just how flawed it has
been (see GAO and OIG reports). North America has more documented TSE prion
disease, in different documented species (excluding the Zoo BSE animals in the
EU), then any other place on the Globe. This does not include the very
likelihood that TSE prion disease in the domestic feline and canine have been
exposed to high doses of the TSE prion disease vid pet food. To date, it’s still
legal to include deer from cwd zone into pet food or deer food. Specified Risk
Material i.e. SRM bans still being breach, as recently as just last month.
nvCJD or what they now call vCJD, another case documented in Texas last
month, with very little information being released to the public on about this
case? with still the same line of thought from federal officials, ‘it can’t
happen here’, so another vCJD blamed on travel of a foreign animal disease from
another country, while ignoring all the BSE TSE Prion risk factors we have here
in the USA and Canada, and the time that this victim and others, do spend in the
USA, and exposed to these risk factors, apparently do not count in any way with
regard to risk factor. a flawed process of risk assessment.
sporadic CJD, along with new TSE prion disease in humans, of which the
young are dying, of which long duration of illness from onset of symptoms to
death have been documented, only to have a new name added to the pot of prion
disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a
familial type disease could be sporadic with no genetic link to any family
member? when the USA is the only documented Country in the world to have
documented two different cases of atypical H-type BSE, with one case being
called atypical H-G BSE with the G meaning Genetic, with new science now showing
that indeed atypical H-type BSE is very possible transmitted to cattle via oral
transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada,
USA, and the UK, with the same old excuse, better surveillance. You can only use
that excuse for so many years, for so many decades, until one must conclude that
CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a
blip or a reason of better surveillance, it is a mathematical rise in numbers.
More and more we are seeing more humans exposed in various circumstance in the
Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same
time in North America, more and more humans are becoming exposed to the TSE
prion disease via consumption of the TSE prion via deer and elk, cattle, sheep
and goats, and for those that are exposed via or consumption, go on to further
expose many others via the iatrogenic modes of transmission of the TSE prion
disease i.e. friendly fire. I pondered this mode of transmission via the victims
of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone
sub-clinical with sFFI or sGSS ? what if?
Two decades have passed since Dr. Ironside first confirmed his first ten
nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first
ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is
transmissible. yet all these TSE prion disease and victims in the USA and Canada
are being pawned off as a spontaneous event, yet science has shown, the
spontaneous theory has never been proven in any natural case of TSE prion
disease, and scientist have warned, that they have now linked some sporadic CJD
cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about
this in the public domain. We must make all human and animal TSE prion disease
reportable in every age group, in ever state and internationally, we must have a
serious re-evaluation and testing of the USA cattle herds, and we must ban
interstate movement of all cervids. Any voluntary effort to do any of this will
fail. Folks, we have let the industry run science far too long with regards to
the TSE prion disease. While the industry and their lobbyist continues to funnel
junk science to our decision policy makers, Rome burns. ...end
REFERENCES
Sunday, June 29, 2014
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Tuesday, August 12, 2014
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST
2014
Singeltary Response to USDA, and USDA
RESPONSE TO SINGELTARY ON HARVARD BSE RISK ASSESSMENT
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE) Page 1 of 98
FSIS, USDA, REPLY TO SINGELTARY
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
Monday, November 30, 2009
*** USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL
HEALTH CODE, DOES NOT SURPRISE ME $
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to the Central Bureau,
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States'
risk classification for mad cow disease to "negligible" from "controlled", and
risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further
exposing the globe to the TSE prion mad cow type disease
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010 ***
Sunday, October 13, 2013
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
*** When people talk about 1 per million, often they interpret that as
thinking it is incredibly rare. They think they have a 1-in-a-million chance of
developing this disease. You haven’t. You’ve got about a 1-in-30,000 chance of
developing it.
Tuesday, April 01, 2014
*** Questions linger in U.S. CJD cases 2005, and still do in 2014 ***
Sent: Sunday, September 28, 2014 5:14 PM
Cc: michael.fischer@dshs.state.tx.us ;
marilyn.felkner@dshs.state.tx.us ;
rita.cantu@dshs.state.tx.us
Subject: USA 4TH CASE VCJD (aka nvCJD) HUMAN MAD COW, THE
SILENCE IS DEAFENING BSE, CWD, AND SCRAPIE TSE PRION
DISEASE
USA 4TH CASE VCJD (aka nvCJD) HUMAN MAD COW, THE SILENCE IS DEAFENING BSE,
CWD, AND SCRAPIE TSE PRION DISEASE
Greetings DSHS, Dr. Fishcer, et al,
I know that most in the USA could care less about the CJD TSE prion disease
aka mad cow type disease. but there are some of us here that will never forget.
you can cover up what ever you want. we all know. I have seen it happen too
many times here in Texas with BSE TSE prion, either the typical or the atypical
strains, or with the feed, or, with cwd, or scrapie as that goes, but we are
still here, and we will never forget...
kind regards, terry
Creutzfeld-Jacob Disease (CJD) Emerging & Acute Infectious Disease
Branch Michael Fischer
Marilyn Felkner
512-776-7676
512-776-7676
Chronic Wasting Disease Zoonosis Control Branch Eric Fonken
512-776-2155
Lab tests have confirmed a diagnosis of variant Creutzfeldt-Jakob Disease
(CJD) in a patient who recently died in Texas. Variant CJD is a rare, fatal
brain disorder, first described in 1996 in the United Kingdom and associated
with beef consumption overseas.
This is the fourth case ever reported in the United States. In each of the
three previous cases, infection likely occurred outside the United States,
including the United Kingdom and Saudi Arabia. The history of this fourth
patient includes extensive travel to Europe and the Middle East, and infection
likely occurred outside the United States. The CDC and DSHS continue to
investigate the case.
There are no Texas public health concerns or threats associated with this
case.
CDC Confirmation Information: http://www.cdc.gov/ncidod/dvrd/vcjd/other/confirmed-case-in-texas.htm
CDC Fact Sheet: http://www.cdc.gov/ncidod/dvrd/vcjd/factsheet_nvcjd.htm
Texas CJD Information: http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/
Last updated June 02, 2014
CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
Monday, June 02, 2014 Confirmed Variant CJD Case in Texas
SO, 4 months after the fact and still no word on this case. no information
what so ever. the silence is deafening $$$
SO, 4 months after the fact and still no word on this case.
no information what so ever. the silence is deafening $$$
*** CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
Monday, June 02, 2014 Confirmed Variant CJD Case in Texas
MAD DEER AND ELK DISEASE
CHRONIC WASTING DISEASE CWD
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE
PRION DISEASE
*** 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.
NOW, what is the latest on human risk factors to CWD strains ???
*** 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.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
***These results indicate that the CWD prion may have the potential to
infect human peripheral lymphoid tissues.
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of
the ability of sheep, cattle and deer prion disease isolates to convert normal
human prion protein to its pathological isoform in a cell-free system
***However, they also show that there is no absolute barrier to conversion of
human prion protein in the case of chronic wasting disease.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood,
and mother to offspring transmission
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
there is in fact evidence that the potential for cwd transmission to humans
can NOT be ruled out.
I thought your readers and hunters and those that consume the venison,
should have all the scientific facts, personally, I don’t care what you eat, but
if it effects me and my family down the road, it should then concern everyone,
and the potential of iatrogenic transmission of the TSE prion is real i.e.
‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there
from...like deer antler velvet and TSE prions and nutritional supplements there
from, all a potential risk factor that should not be ignored or silenced. ...
the prion gods at the cdc state that there is ;
''no strong evidence''
but let's see exactly what the authors of this cwd to human at the cdc
state ;
now, let’s see what the authors said about this casual link, personal
communications years ago. 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 ;
***********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 ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb**************
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
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer
and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 –0500
EMC 1 Terry S. Singeltary Sr. Vol #: 1
*** We hypothesize that both BSE prions and CWD prions passaged through
felines will seed human recPrP more efficiently than BSE or CWD from the
original hosts, evidence that the new host will dampen the species barrier
between humans and BSE or CWD. The new host effect is particularly relevant as
we investigate potential means of trans-species transmission of prion disease.
Monday, August 8, 2011
*** Susceptibility of Domestic Cats to CWD Infection ***
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M.
Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K.
Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness.
*** Two of these cats have developed rear limb ataxia. Although the limited
data from this ongoing study must be considered preliminary, they raise the
potential for cervid-to-feline transmission in nature.
AD.63:
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado
State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN
USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to
the domestic cat, thus raising the issue of potential cervid-to- feline
transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
FELINE SPONGIFORM ENCEPHALOPATHY FSE
Sunday, November 10, 2013
LARGE CJD TSE PRION POTENTIAL CASE STUDY AMONG HUMANS WHO TAKE DEER ANTLER
VELVET WILL BE ONGOING FOR YEARS IF NOT DECADES, but who's cares $
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose
DOCUMENT ID: APHIS-2006-0118-0411
***Singeltary submission
Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program
Standards
>>>The CWD herd certification program is a voluntary, cooperative
program that establishes minimum requirements for the interstate movement of
farmed or captive cervids, provisions for participating States to administer
Approved State CWD Herd Certification Programs, and provisions for participating
herds to become certified as having a low risk of being infected with
CWD<<<
Greetings USDA/APHIS et al,
I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting
Disease Herd Certification Program and Interstate Movement of Farmed or Captive
Deer, Elk, and Moose; Program Standards.
I believe, and in my opinion, and this has been proven by scientific facts,
that without a validated and certified test for chronic wasting disease cwd,
that is 100% sensitive, and in use, any voluntary effort will be futile. the
voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow
surveillance program has failed terribly, as well as the testing for bse tse
prion in cattle, this too has failed terrible. all this has been proven time and
time again via OIG reports and GOA reports.
I believe that until this happens, 100% cwd testing with validated test,
ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO
INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.
In my opinion, and the opinions of many scientists and DNR officials, that
these so called game farms are the cause of the spreading of chronic wasting
disease cwd through much negligence. the game farms in my opinion are not the
only cause, but a big factor. I kindly wish to submit the following to show what
these factors are, and why interstate movement of cervids must be banned.
...
snip...see full text and PDF ATTACHMENT HERE ;
Sunday, June 23, 2013
National Animal Health Laboratory Network Reorganization Concept Paper
(Document ID APHIS-2012-0105-0001)
***Terry S. Singeltary Sr. submission
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population CWD TSE PRION
disease in cervids
***SINGELTARY SUBMISSION
The Scottish Parliament’s Rural Affairs, Climate Change and Environment
Committee has been looking into deer management, as you can see from the
following press release,
***and your email has been forwarded to the committee for information:
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population
Sunday, July 21, 2013
Welsh Government and Food Standards Agency Wales Joint Public Consultation
on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations
2013
*** Singeltary Submission WG18417
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets?
=============================================================================
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM ***
=============================================================================
Ronnie Dunn Cross Examination, slaughtering cattle, or killing deer ?
IN THE UNITED STATES DISTRICT COURT FOR THE NORTHERN DISTRICT OF INDIANA
SOUTH BEND DIVISION UNITED STATES OF AMERICA, vs. RUSSELL G. BELLAR, Defendant.
___________________________
)))))))))
Cause No.: 3:04cr00068-AS South Bend, Indiana January 4, 2005 9:30 a.m.
TRANSCRIPT EXCERPT OF JURY TRIAL (TESTIMONY OF: RONNIE DUNN AND RUSTY CAMP)
BEFORE THE HONORABLE ALLEN SHARP
snip...
Ronnie Dunn Cross Examination
Q. Mr. Dunn, at one point I believe you told the federal agents that Mr.
Bellar told you that this was a private deer farm and shooting deer on that farm
was like slaughtering cattle; is that correct?
A. I don't know if I used the word "slaughter," but it was, yeah, like
that.
Q. You don't know if that was your word, "slaughtering cattle"?
A. I don't know that.
Q. Well, did he give you the idea of killing cattle?
A. Yes, it was the same principle.
snip...
see full text ;
BUCK FEVER
Thursday, September 18, 2014
*** Risk behaviors in a rural community with a known point-source exposure
to chronic wasting disease
Saturday, September 20, 2014
*** North Carolina Captive cervid licenses and permits Senate Bill 744
Singeltary Submission
Description The proposed changes to 15A NACA 10H .0301 would allow the
Commission to issue new captivity licenses and permits for the purpose of
holding cervids in captivity and allow certified herd owners to sell or transfer
cervids to any licensed facility. Also, mandatory testing for CWD will be raised
from all cervids that die at age 6 months or older to all cervids that die at
age 12 months or older.
Rule Text Click here http://www.ncwildlife.org/Portals/0/ProposedRegulations/15A%20NCAC%2010H%20.0301%20for%20web%20posting.pdf
North Carolina Captive cervid licenses and permits Senate Bill 744
Singeltary Submission
*** p.s. please add this to my submission, very important
information...
Saturday, February 04, 2012
*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of fawns
sampled were between the ages of 5 to 9 months, though some were as young as 1
month.
*** Two of the six fawns with CWD detected were 5 to 6 months old.
All six of the positive fawns were taken from the core area of the CWD
eradication zone where the highest numbers of positive deer have been
identified.
Saturday, February 04, 2012
*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
*** Conclusion. CWD prions (as inferred by prion seeding activity by
RT-QuIC) are shed in urine of infected deer as early as 6 months post
inoculation and throughout the subsequent disease course. Further studies are in
progress refining the real-time urinary prion assay sensitivity and we are
examining more closely the excretion time frame, magnitude, and sample variables
in relationship to inoculation route and prionemia in naturally and
experimentally CWD-infected cervids.
SNIP...SEE FULL TEXT ;
Saturday, September 20, 2014
*** North Carolina Captive cervid licenses and permits Senate Bill 744
Singeltary Submission
Thursday, September 11, 2014
Missouri Nixon's Veto Stands Overide Fails on Agriculture Legislation
How they voted: attempt to override veto of ag bill fails in the
House
Wednesday, September 17, 2014
Wyoming GAME AND FISH CONTINUES CWD SAMPLING
Pennsylvania
>>> Thank you for your comments, which I will share with the Board
Thank You kindly !
>>> Please note that in Pennsylvania, the responsibility for
regulating captive cervids falls to the Pennsylvania Department of
Agriculture.
please note;
*** 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. ...
also, see where even decades back, the USDA had the same thought as they do
today with CWD, not their problem...see page 27 below as well, where USDA stated
back then, the same thing they stated in the state of Pennsylvania, not their
damn business, once they escape, and they said the same thing about CWD in
general back then ;
”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.
”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.
sound familiar $$$
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
Saturday, June 29, 2013
PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN
INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd
Pennsylvania Update May 28, 2013
*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana,
quarantine began on October 18, 2012, still ongoing, Lake Charles premises.
Thursday, September 11, 2014
*** TEXAS ANIMAL HEALTH COMMISSION 390th COMMISSION MEETING AGENDA (CWD
movement restriction zone) September 16, 2014 8:30 A.M.
Wednesday, September 17, 2014
*** Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant
Health Inspection Service Veterinary Services ***
Friday, September 05, 2014
*** CFIA CWD and Grain Screenings due to potential risk factor of spreading
via contamination of grain, oil seeds, etc. ***
Wednesday, September 17, 2014
*** Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant
Health Inspection Service Veterinary Services ***
Sunday, September 21, 2014
INFORM: Cervid Health and States Indemnity FY 2015
Wednesday, September 17, 2014
Cost benefit analysis of the development and use of ante-mortem tests for
transmissible spongiform encephalopathies
Sunday, August 24, 2014
*** USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program
Goals TSE PRION October 17 – 23, 2013
*** Ronnie Dunn Cross Examination, slaughtering cattle, or killing deer ?
***
IN THE UNITED STATES DISTRICT COURT FOR THE NORTHERN DISTRICT OF INDIANA
SOUTH BEND DIVISION UNITED STATES OF AMERICA, vs. RUSSELL G. BELLAR, Defendant.
___________________________
)))))))))
Cause No.: 3:04cr00068-AS South Bend, Indiana January 4, 2005 9:30 a.m.
TRANSCRIPT EXCERPT OF JURY TRIAL (TESTIMONY OF: RONNIE DUNN AND RUSTY CAMP)
BEFORE THE HONORABLE ALLEN SHARP
snip...
Ronnie Dunn Cross Examination
Q. Mr. Dunn, at one point I believe you told the federal agents that Mr.
Bellar told you that this was a private deer farm and shooting deer on that farm
was like slaughtering cattle; is that correct?
A. I don't know if I used the word "slaughter," but it was, yeah, like
that.
Q. You don't know if that was your word, "slaughtering cattle"?
A. I don't know that.
Q. Well, did he give you the idea of killing cattle?
A. Yes, it was the same principle.
snip...
see full text ;
BUCK FEVER
Thursday, September 18, 2014
*** Risk behaviors in a rural community with a known point-source exposure
to chronic wasting disease
*** We conclude that TSE infectivity is likely to survive burial for long
time periods with minimal loss of infectivity and limited movement from the
original burial site. However PMCA results have shown that there is the
potential for rainwater to elute TSE related material from soil which could lead
to the contamination of a wider area. These experiments reinforce the importance
of risk assessment when disposing of TSE risk materials.
*** The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute
and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental
routes, and there are also concerns about BSE infection remaining in the
environment after carcass burial or waste 3disposal. In two demonstration
experiments we are determining survival and migration of TSE infectivity when
buried for up to five years, as an uncontained point source or within bovine
heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters
containing either sandy or clay soil. Migration from the boluses is being
assessed from soil cores taken over time. With the exception of a very small
amount of infectivity found 25 cm from the bolus in sandy soil after 12 months,
no other infectivity has been detected up to three years. Secondly, ten bovine
heads were spiked with TSE infected mouse brain and buried in the two soil
types. Pairs of heads have been exhumed annually and assessed for infectivity
within and around them. After one year and after two years, infectivity was
detected in most intracranial samples and in some of the soil samples taken from
immediately surrounding the heads. The infectivity assays for the samples in and
around the heads exhumed at years three and four are underway. These data show
that TSE infectivity can survive burial for long periods but migrates slowly.
Risk assessments should take into account the likely long survival rate when
infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
*** Susceptibility of UK red deer (Cervus alaphus elaphus) to oral BSE
transmission Project Code: M03024 ***
02/08/2011
The project confirmed that U.K red deer are susceptible to both oral and
intra-cerebral inoculation with the cattle BSE agent. Six clinically positive
(from 26-42 months post inoculation) i.c inoculated and one (56 months post
inoculation) orally dosed deer that tested positive for TSE by
immunohistochemistry and Western blotting using several primary antibodies
demonstrated widespread accumulation of disease specific prion protein in the
central nervous system, peripheral nervous system and enteric nervous system but
none in lymphoreticular system. All showed several brain sites positive for
disease specific prion protein and presented immunohistochemistry and Western
blotting phenotypes with similarities to BSE in sheep, goats and cattle but
unlike those seen in chronic wasting disease (CWD) in elk or scrapie in sheep.
The vacuolar pathology and distribution of disease specific prion protein in red
deer resembled that of CWD in most major respects however we have shown that BSE
can be clearly differentiated from CWD by existing immunohistochemical and
biochemical methods that are in routine use.
The knowledge gained as a result of this work will permit rapid and
accurate diagnosis should a TSE ever be detected in European red deer and will
also enable effective disease control methods to be quickly put in place.
Results
We confirmed that U.K red deer are susceptible to both oral and
intra-cerebral inoculation with the cattle BSE agent. Six clinically positive
(from 26-42mpi) i.c inoculated and one (56mpi) orally dosed deer that tested
positive for TSE by IHC and WB using several primary antibodies demonstrated
widespread accumulation of disease specific PrP in CNS, PNS and ENS but none in
LRS. All showed several brain sites positive for disease specific PrP and
presented IHC and WB phenotypes with similarities to BSE in sheep, goats and
cattle but unlike those seen in CWD in elk or scrapie in sheep. The vacuolar
pathology and distribution of PrPd BSE in red deer resembled that of CWD in most
major respects however we have shown that BSE can be clearly differentiated from
CWD by existing immunohistochemical and biochemical methods that are in routine
use.
Final technical report MO3024 01/04/2003 – 31/03/2010 Susceptibility of UK
red deer (Cervus elaphus elaphus) to oral BSE transmission. Stuart Martin - VLA
Lasswade Pentlands Science Park Bush Loan Penicuik EH26 0PZ Page 2 of 21 Further
work undertaken August 2009 – March 2010. Genetic analysis - Wilfred Goldmann;
Roslin NPD.
Negative controls and the remaining 5 orally dosed deer culled at 72mpi
tested negative by IHC and Western blot however analysis of the PrP ORF of these
deer (kindly carried out by Wilfred Goldmann of the Roslin NPD) identified a Q
to E polymorphism at codon 226 that may influence the efficiency of oral
transmission (not published).
In the experimental BSE challenge of red deer six out of six deer succumbed
to BSE when challenged by intracerebral routes but only one of six deer
challenged by the oral route succumbed to infection. Deer killed at 190 days or
365 days post oral challenge showed no evidence of abnormal PrP accumulation
when tested by immunocytochemistry. The PrP gene of red deer includes a Q to E
polymorphism at codon 226. The table shows the distribution of these codon 226
polymorphisms within experimental challenge groups.
snip...
Research article Open Access
Immunohistochemical and biochemical characteristics of BSE and CWD in
experimentally infected European red deer (Cervus elaphus elaphus)
Stuart Martin*1, Martin Jeffrey1, Lorenzo González1, Sílvia Sisó1, Hugh W
Reid2, Philip Steele2, Mark P Dagleish2, Michael J Stack3, Melanie J Chaplin3
and Aru Balachandran4 Address: 1Veterinary Laboratories Agency (VLA-Lasswade),
Pentlands Science Park, Bush Loan, Penicuik, Midlothian, EH26 0PZ, UK, 2Moredun
Research Institute, Pentlands Science Park, Bush Loan, Penicuik, Midlothian,
EH26 0PZ, UK, 3VLA-Weybridge, Addlestone, Surrey, KT15 3NB, UK and 4Animal
Diseases Research Institute, Canadian Food Inspection Agency, Ottawa, Ontario,
K2H 8P9, Canada
Abstract
Background: The cause of the bovine spongiform encephalopathy (BSE)
epidemic in the United Kingdom (UK) was the inclusion of contaminated meat and
bone meal in the protein rations fed to cattle. Those rations were not
restricted to cattle but were also fed to other livestock including farmed and
free living deer. Although there are no reported cases to date of natural BSE in
European deer, BSE has been shown to be naturally or experimentally
transmissible to a wide range of different ungulate species. Moreover, several
species of North America's cervids are highly susceptible to chronic wasting
disease (CWD), a transmissible spongiform encephalopathy (TSE) that has become
endemic. Should BSE infection have been introduced into the UK deer population,
the CWD precedent could suggest that there is a danger for spread and
maintenance of the disease in both free living and captive UK deer populations.
This study compares the immunohistochemical and biochemical characteristics of
BSE and CWD in experimentally-infected European red deer (Cervus elpahus
elaphus).
Results: After intracerebral or alimentary challenge, BSE in red deer more
closely resembled natural infection in cattle rather than experimental BSE in
small ruminants, due to the lack of accumulation of abnormal PrP in lymphoid
tissues. In this respect it was different from CWD, and although the
neuropathological features of both diseases were similar, BSE could be clearly
differentiated from CWD by immunohistochemical and Western blotting methods
currently in routine use.
Conclusion: Red deer are susceptible to both BSE and CWD infection, but the
resulting disease phenotypes are distinct and clearly distinguishable.
SNIP...
Results
Clinical disease
All six deer challenged i.c. with BSE developed clinical disease between
794 and 1260 days post-inoculation with a mean incubation period of 1027 days. A
detailed description of the clinical signs was provided in an earlier report
[8]. Briefly, affected deer showed variable degrees of ataxia, anorexia,
circling and apparent blindness, together with failure of seasonal change of
coat, weight loss and 'panic attacks'. In addition, one of six red deer orally
dosed with BSE developed clinical disease 1740 days after challenge, and this
animal presented with a short clinical duration of two days; the other five deer
from this group remain healthy at the time of writing (65 months after
challenge). Sequential rectal biopsies taken at five different time points from
orally and i.c. inoculated deer were negative for PrPd.
All four deer orally challenged with CWD started to show behavioural
changes between 577 and 586 days post challenge;
these progressed to definite neurological disease between 742 and 760 days
post-challenge (Table 1).
Clinical signs were similar to the BSE challenged deer and included
nervousness, weight loss, excessive salivation, roughness of coat, and
progressive ataxia. All these CWD inoculated deer showed PrPd accumulation in
the secondary follicles of rectal biopsies taken at 7 months post
infection.
Conclusion
European red deer are susceptible to infection with the cattle BSE agent,
not only by the intra-cerebral but also by the oral route, and although the
clinical signs and spong- iform change are similar to those of CWD in the same
species, these two infections can be easily differentiated. The lack of lymphoid
involvement, the PrPd truncation pattern both "in vivo" and "in vitro", and the
predominantly intracellular accumulation of PrPd are features of deer BSE that
are in contrast with those of deer CWD. However, only one of six deer developed
disease after alimentary exposure to 25 g of a BSE brain pool homogenate after
an incubation period of nearly 5 years; this suggests a strong species barrier
but if a TSE in European red deer should ever be identified then BSE/CWD
discrimination would be an urgent priority. To determine whether there are
potential naturally occurring BSE-like strains and to determine the degree to
which there is strain variation, it would be necessary to examine many more
naturally occurring CWD cases. These results will support the ongoing European
surveillance for natural TSEs in red deer and the further assessment of
potential risk to human health.
Published: 27 July 2009 BMC Veterinary Research 2009, 5:26
doi:10.1186/1746-6148-5-26 Received: 12 February 2009 Accepted: 27 July 2009
This article is available from: http://www.biomedcentral.com/1746-6148/5/26
© 2009 Martin et al; licensee BioMed Central Ltd. This is an Open Access article
distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium,
provided the original work is properly cited.
Monday, May 05, 2014
*** Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing ***
snip...
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
*** Overall, therefore, it is considered there is a __greater than
negligible risk___ that (nonruminant) animal feed and pet food containing deer
and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In
Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #: 1
see my full text submission here ;
Sunday, December 15, 2013
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Tuesday, September 16, 2014
mad cow scaremongers consumerfreedom.com December 20, 2003 article and a
2014 review
The detection of low levels of BSE-PrPSc in the presence of an excess of
scrapie-PrPSc
It was previously thought that any given prion disease had a very limited
natural host range. However, the BSE agent has affected species other than
cattle. This study aims to provide a novel, high sensitivity assay to monitor
for the presence of very low levels of BSE in small ruminants, even with
concurrent scrapie infections. Study Duration: October 2012 to December 2013
Contractor: ADAS Project Code: FS101077 Background Research Approach Background
Prion diseases are fatal brain diseases with no effective treatment. Until the
emergence of BSE in the mid-1980s it was thought that any given prion disease
had a very limited natural host range. For example, scrapie affecting
sheep/goats and Creutzfeldt Jakob disease (CJD) affecting humans. However, the
BSE agent not only affected cattle, but was also the causal agent of feline
spongiform encephalopathy and human variant CJD (vCJD), both arising from the
consumption of BSE contaminated bovine products.
BSE-contaminated bovine-derived meat and bone meal was extensively fed not
only to cows, giving rise to the UK cattle BSE epidemic, but also to small
ruminants. Yet extensive surveillance has failed to uncover BSE infections in
sheep populations throughout Europe, including the UK. This is surprising given
that sheep are susceptible to BSE when fed the agent under experimental
conditions. Two cases of BSE infections have been identified in goats. The UK
small ruminant population has had endemic scrapie and whilst the incidence of
this disease has been significantly reduced, it is estimated that approximately
67,000 scrapie infected animals still enter the human food chain each year. One
concern is that low levels of BSE cases may be harboured within the small
ruminant population and be masked by concurrent scrapie infections.
Research Approach The presence of mixed strains of prion agents within an
individual host is known to exist for both natural infections and experimental
models. Importantly, it is also known that hosts with mixed infections
displaying a single pathology can harbour low levels of a distinct strain which
can emerge upon further passage. There are limited studies on mixed infections
with BSE and scrapie, however within a mouse model this scenario led to the
presentation of a scrapie-associated pathology, even when the inoculum had much
greater levels of BSE agent compared to scrapie agent. Together, data suggests
that similar mixed infections of sheep or goats may present as scrapie even
though the BSE agent is present.
An in vitro prion amplification assay will be applied to the detection of
very low levels of BSE agent in the presence of an excess of scrapie agent. The
contractor has previously demonstrated that this assay is exquisitely sensitive
for the BSE agent and does not amplify any scrapie agents. The aim of this study
is to establish this novel amplification-assay for the detection of BSE in the
presence of scrapie agent and to compare this method with conventional BSE tests
applied in routine surveillance. The aim is to provide a novel, high sensitivity
assay to monitor for the presence of very low levels of BSE in small ruminants,
even with concurrent scrapie infections. It will help to inform policy as to the
potential risk of BSE agent being present in sheep or goats but not being
detected when measured by conventional assays.
Overall, all Nor98 isolates contained highly PK resistant PrPres
aggregates, with the main PrPres being a non-glycosylated internal fragment,
cleaved at both the N and C termini, which represent the distinctive biochemical
feature of Nor98. This biochemical signature, unique among animal TSEs, is
reminiscent of PrPres observed in human prion disorders such as GSS and
VPSPr.
snip...
At present the only epidemiological link between animal and human TSEs has
been demonstrated for classical BSE and variant CJD [16], [78], showing for the
first time the zoonotic potential of TSEs. Since then, the implementation of
active surveillance in livestock has led to the identification of Nor98 and
other previously unrecognised animal prion strains, mainly with a sporadic
occurrence, whose origin and zoonotic potential are still poorly understood
[79]. It has been previously shown that peripheral tissues of sheep with Nor98
might harbour detectable levels of infectivity [49], [50], indicating that
infectious material might enter the food chain. On the other hand, the well
known genetic aetiology of GSS suggests that the similar PrPSc conformations
found in Nor98 and GSS P102L are unlikely to indicate a common infectious
source, but might derive from a similar molecular mechanisms involved in
PrPC-to-PrPSc conversion.
snip...
Citation: Pirisinu L, Nonno R, Esposito E, Benestad SL, Gambetti P, et al.
(2013) Small Ruminant Nor98 Prions Share Biochemical Features with Human
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive
Prionopathy. PLoS ONE 8(6): e66405. doi:10.1371/journal.pone.0066405
Editor: Corinne Ida Lasmezas, The Scripps Research Institute Scripps
Florida, United States of America
Received: January 24, 2013; Accepted: May 6, 2013; Published: June 24,
2013
Copyright: © 2013 Pirisinu et al. This is an open-access article
distributed under the terms of the Creative Commons Attribution License, which
permits unrestricted use, distribution, and reproduction in any medium, provided
the original author and source are credited.
Funding: This work was supported by grants from the Italian Ministry of
Health (RF-2009-1474624); the European Union (Neuroprion Network of Excellence
CT-2004–506579); the National Institutes of Health (NIH) NS062787, NIH AG-08012,
AG-14359; Alliance BioSecure, as well as the Center for Disease Control and
Prevention Contract UR8/CCU515004. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
Competing interests: The authors have declared that no competing interests
exist.
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98.
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion
poker goes up again $
OR-10: Variably protease-sensitive prionopathy is transmissible in bank
voles
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1
Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan
Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome,
Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna,
Italy; 3Case Western Reserve University; Cleveland, OH USA
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently
described “sporadic”neurodegenerative disease involving prion protein
aggregation, which has clinical similarities with non-Alzheimer dementias, such
as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in
Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the
prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is
the electrophoretic pattern of PrPSc after digestion with proteinase K (PK).
After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern
similar to that described in GSS cases. The clinical and pathological features
of VPSPr raised the question of the correct classification of VPSPr among prion
diseases or other forms of neurodegenerative disorders. Here we report
preliminary data on the transmissibility and pathological features of VPSPr
cases in bank voles.
Materials and Methods. Seven VPSPr cases were inoculated in two genetic
lines of bank voles, carrying either methionine or isoleucine at codon 109 of
the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases
selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical
diagnosis in voles was confirmed by brain pathological assessment and western
blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission
in BvM109. Overall, 3 voles were positive with survival time between 290 and 588
d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form
of the typical PrP27–30, which was indistinguishable to that previously observed
in BvM109 inoculated with sCJDMM1 cases.
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until
now. Overall, 5 voles were positive with survival time between 281 and 596
d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like
PrPSc electrophoretic pattern, characterized by low molecular weight PrPres.
These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative
with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus
and the N-terminus. Second passages are in progress from these first successful
transmissions.
Conclusions. Preliminary results from transmission studies in bank voles
strongly support the notion that VPSPr is a transmissible prion disease.
Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of
voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
The discovery of previously unrecognized prion diseases in both humans and
animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion
diseases might be wider than expected and raises crucial questions about the
epidemiology and strain properties of these new forms. We are investigating this
latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
Wednesday, March 28, 2012
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion
poker goes up again $
Thursday, October 10, 2013
CJD REPORT 1994 increased risk for consumption of veal and venison and lamb
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98.
Increased Atypical Scrapie Detections
Press reports indicate that increased surveillance is catching what
otherwise would have been unreported findings of atypical scrapie in sheep. In
2009, five new cases have been reported in Quebec, Ontario, Alberta, and
Saskatchewan. With the exception of Quebec, all cases have been diagnosed as
being the atypical form found in older animals. Canada encourages producers to
join its voluntary surveillance program in order to gain scrapie-free status.
The World Animal Health will not classify Canada as scrapie-free until no new
cases are reported for seven years. The Canadian Sheep Federation is calling on
the government to fund a wider surveillance program in order to establish the
level of prevalence prior to setting an eradication date. Besides long-term
testing, industry is calling for a compensation program for farmers who report
unusual deaths in their flocks.
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
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011 However, work with transgenic mice has
demonstrated the potential susceptibility of pigs, with the disturbing finding
that the biochemical properties of the resulting PrPSc have changed on
transmission (40).
Monday, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types
(hmmm, this is getting interesting now...TSS)
Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine
(reticular) deposits,
see also ;
All of the Heidenhain variants were of the methionine/ methionine type 1
molecular subtype.
see full text ;
Monday, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types
P03.141
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National
Veterinary Insitute, Sweden; 2National Veterinary Institute,
Norway Nor98 is a prion disease of old sheep and goats. This atypical form
of scrapie was first described in Norway in 1998. Several features of Nor98 were
shown to be different from classical scrapie including the distribution of
disease associated prion protein (PrPd) accumulation in the brain. The
cerebellum is generally the most affected brain area in Nor98. The study here
presented aimed at adding information on the neuropathology in the cerebellum of
Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A
panel of histochemical and immunohistochemical (IHC) stainings such as IHC for
PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers
for phagocytic cells were conducted. The type of histological lesions and tissue
reactions were evaluated. The types of PrPd deposition were characterized. The
cerebellar cortex was regularly affected, even though there was a variation in
the severity of the lesions from case to case. Neuropil vacuolation was more
marked in the molecular layer, but affected also the granular cell layer. There
was a loss of granule cells. Punctate deposition of PrPd was characteristic. It
was morphologically and in distribution identical with that of synaptophysin,
suggesting that PrPd accumulates in the synaptic structures. PrPd was also
observed in the granule cell layer and in the white matter. The pathology
features of Nor98 in the cerebellum of the affected sheep showed similarities
with those of sporadic Creutzfeldt-Jakob disease in humans.
***The pathology features of Nor98 in the cerebellum of the affected sheep
showed similarities with those of sporadic Creutzfeldt-Jakob disease in
humans.
PR-26
NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS
R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B.
Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto
Superiore di Sanità, Department of Food Safety and Veterinary Public Health,
Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna,
Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo,
Norway
Molecular variants of PrPSc are being increasingly investigated in sheep
scrapie and are generally referred to as "atypical" scrapie, as opposed to
"classical scrapie". Among the atypical group, Nor98 seems to be the best
identified. We studied the molecular properties of Italian and Norwegian Nor98
samples by WB analysis of brain homogenates, either untreated, digested with
different concentrations of proteinase K, or subjected to enzymatic
deglycosylation. The identity of PrP fragments was inferred by means of
antibodies spanning the full PrP sequence. We found that undigested brain
homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11),
truncated at both the C-terminus and the N-terminus, and not N-glycosylated.
After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and
N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11.
Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are
mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at
the highest concentrations, similarly to PrP27-30 associated with classical
scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment
of 17 kDa with the same properties of PrP11, that was tentatively identified as
a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in
2% sodium laurylsorcosine and is mainly produced from detergentsoluble,
full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a
sample with molecular and pathological properties consistent with Nor98 showed
plaque-like deposits of PrPSc in the thalamus when the brain was analysed by
PrPSc immunohistochemistry. Taken together, our results show that the
distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids
~ 90-155. This fragment is produced by successive N-terminal and C-terminal
cleavages from a full-length and largely detergent-soluble PrPSc, is produced in
vivo and is extremely resistant to PK digestion.
*** Intriguingly, these conclusions suggest that some pathological features
of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
119
A newly identified type of scrapie agent can naturally infect sheep with
resistant PrP genotypes
Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne
Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?,
Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author
Affiliations
*Virologie Immunologie Moléculaires and ?Génétique Biochimique et
Cytogénétique, Institut National de la Recherche Agronomique, 78350
Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la
Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte
Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire
des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon,
France; **Pathologie Infectieuse et Immunologie, Institut National de la
Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology,
National Veterinary Institute, 0033 Oslo, Norway
***Edited by Stanley B. Prusiner, University of California, San Francisco,
CA (received for review March 21, 2005)
Abstract Scrapie in small ruminants belongs to transmissible spongiform
encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative
disorders that affect humans and animals and can transmit within and between
species by ingestion or inoculation. Conversion of the host-encoded prion
protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP
(PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified
surveillance of scrapie in the European Union, together with the improvement of
PrPSc detection techniques, has led to the discovery of a growing number of
so-called atypical scrapie cases. These include clinical Nor98 cases first
identified in Norwegian sheep on the basis of unusual pathological and PrPSc
molecular features and "cases" that produced discordant responses in the rapid
tests currently applied to the large-scale random screening of slaughtered or
fallen animals. Worryingly, a substantial proportion of such cases involved
sheep with PrP genotypes known until now to confer natural resistance to
conventional scrapie. Here we report that both Nor98 and discordant cases,
including three sheep homozygous for the resistant PrPARR allele (A136R154R171),
efficiently transmitted the disease to transgenic mice expressing ovine PrP, and
that they shared unique biological and biochemical features upon propagation in
mice. *** These observations support the view that a truly infectious TSE agent,
unrecognized until recently, infects sheep and goat flocks and may have
important implications in terms of scrapie control and public health.
Monday, December 1, 2008
When Atypical Scrapie cross species barriers
Authors
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon
S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J.
M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France;
ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex,
France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway,
INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.
Content
Atypical scrapie is a TSE occurring in small ruminants and harbouring
peculiar clinical, epidemiological and biochemical properties. Currently this
form of disease is identified in a large number of countries. In this study we
report the transmission of an atypical scrapie isolate through different species
barriers as modeled by transgenic mice (Tg) expressing different species PRP
sequence.
The donor isolate was collected in 1995 in a French commercial sheep flock.
inoculation into AHQ/AHQ sheep induced a disease which had all
neuro-pathological and biochemical characteristics of atypical scrapie.
Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate
retained all the described characteristics of atypical scrapie.
Surprisingly the TSE agent characteristics were dramatically different
v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and
biochemical characteristics similar to those of atypical BSE L in the same mouse
model. Moreover, whereas no other TSE agent than BSE were shown to transmit into
Tg porcine mice, atypical scrapie was able to develop into this model, albeit
with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion showed
similar biological and biochemical characteristics than BSE adapted to this
porcine mouse model. Altogether these data indicate.
(i) the unsuspected potential abilities of atypical scrapie to cross
species barriers
(ii) the possible capacity of this agent to acquire new characteristics
when crossing species barrier
These findings raise some interrogation on the concept of TSE strain and on
the origin of the diversity of the TSE agents and could have consequences on
field TSE control measures.
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire).
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. Subscribe and get 4 free issues. 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.
Sunday, December 12, 2010
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2
December 2010
Wednesday, January 18, 2012
Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural
Scrapie Isolates Similar to CH1641 Experimental Scrapie
Journal of Neuropathology & Experimental Neurology: February 2012 -
Volume 71 - Issue 2 - p 140–147
Thursday, July 14, 2011
Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical
Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)
Wednesday, January 18, 2012
BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE
February 1, 2012
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, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types
(hmmm, this is getting interesting now...TSS)
Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine
(reticular) deposits,
see also ;
All of the Heidenhain variants were of the methionine/ methionine type 1
molecular subtype.
see full text ;
Monday, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types
Thursday, July 21, 2011
A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V
Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology
& Experimental Neurology:
August 2011 - Volume 70 - Issue 8 - pp 698-702
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep
Wednesday, January 19, 2011
EFSA and ECDC review scientific evidence on possible links between TSEs in
animals and humans Webnachricht 19 Januar 2011
Monday, June 27, 2011
Comparison of Sheep Nor98 with Human Variably Protease-Sensitive
Prionopathy and Gerstmann-Sträussler-Scheinker Disease
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep
Wednesday, November 13, 2013
Atypical Scrapie Prions from Sheep and Lack of Disease in Transgenic Mice
Overexpressing Human Prion Protein
REPORT OF THE COMMITTEE 344 Ewes were experimentally inoculated with brain
homogenate obtained from a U.S. sheep with clinical Nor98-like scrapie.
Recipient ewes are bred annually to examine the placenta for evidence of a
transmissible agent. Placentas shed 2009-2013 were negative.
*** In 2013, one recipient ewe developed an unrelated disease. At
postmortem examination, abundant accumulation of PrPSc was observed only in the
cerebellum of this ewe with much less accumulation in the hindbrain obex. This
confirms that initial inoculation of these ewes has been successful. Monitoring
continues in the remaining ewes of this study.
PROCEEDINGS ONE HUNDRED AND SEVENTEENTH ANNUAL MEETING of the UNITED STATES
ANIMAL HEALTH ASSOCIATION Town and Country Hotel San Diego, California October
17 – 23, 2013
snip...see ;
Sunday, August 24, 2014
USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program
Goals TSE PRION October 17 – 23, 2013
*** OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED, WISHES TO
CONTINUE SPREADING IT AROUND THE GLOBE
Monday, November 30, 2009
*** USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL
HEALTH CODE, DOES NOT SURPRISE ME $
Sunday, September 1, 2013
Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy
We previously described the biochemical similarities between PrPres derived
from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations
suggest a link between these two uncommon prion phenotypes in a primate model
(it is to note that such a link has not been observed in other models less
relevant from the human situation as hamsters or transgenic mice overexpressing
ovine PrP [28]). We speculate that a group of related animal prion strains
(L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion
diseases in humans with a type 2 PrPres molecular signature (and more
specifically type 2B for vCJD)
snip...
Together with previous experiments performed in ovinized and bovinized
transgenic mice and hamsters [8,9] indicating similarities between TME and
L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME
outbreaks in North America and Europe during the mid-1900s.
Tuesday, July 21, 2009
Transmissible mink encephalopathy - review of the etiology
http://transmissible-mink-encephalopathy.blogspot.com/2009/07/transmissible-mink-encephalopathy.html
Saturday, December 01, 2007
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and
L-type Bovine Spongiform Encephalopathy in a Mouse Model
Sunday, December 10, 2006
Transmissible Mink Encephalopathy TME
TSE have been around for decades.
it’s not out of the question to think that CWD might have been here much
sooner than it was documented.
have cwd and these other TSE been around for eons, or forever, I cannot
answer that.
I know scarpie was first documented around 1947 here in the USA, how long
it was here before that, I don’t know, some say over 250 years.
TME in mink was documented in the early 1960s. it was first thought that
the TME out break was from scrapie infected sheep, until a investigation was
done on feed practices at these mink facilities, and it was later found that the
mink had been fed 95%+ dead stock downer cows. and later, the Late Richard Marsh
tried to warn the feds of the pending mad cow debacle. they refused to listen.
...
some interesting reading on pages 26 to 33
1979
TME originates from feeding mink, scrapie infected materials...
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 ***
Wednesday, September 10, 2014
Creutzfeldt-Jakob disease (CJD) biannual update (August 2014), with updated
guidance on decontamination of gastrointestinal endoscopy equipment
Research and analysis
CWD STRAINS TO HUMANS ???
*** 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).
as I said, what if ?
*** our results raise the possibility that CJD cases classified as VV1 may
include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne
infection by type 1 prions from animals, e.g., chronic wasting disease prions in
cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have
been reported (40, 41). The results of the present study emphasize the need for
traceback studies and careful re-examination of the biochemical properties of
sCJD-VV1 prions. ***
===========================================
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
WHAT IF ?
Saturday, April 19, 2014
Exploring the zoonotic potential of animal prion diseases: In vivo and in
vitro approaches
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010 ***
Sunday, October 13, 2013
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
Tuesday, April 01, 2014
*** Questions linger in U.S. CJD cases 2005, and still do in 2014
Monday, March 29, 2010
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN
AND SPINAL CORD MATTER
URGENT, PLEASE NOTE ;
>>> Up until about 6 years ago, the pt worked at Tyson foods where
she worked on the assembly line, slaughtering cattle and preparing them for
packaging. She was exposed to brain and spinal cord matter when she would
euthanize the cattle. <<<
CJD NE TEXAS CLUSTER
Creutzfeldt-Jakob Disease in Northeast Texas
J.A. Rawlings,*1 K.A. Hendricks1, O.M. Nuno1, D.A. Brown1, D.A. Evans2,
Texas Department of Health, 1Austin and 2Tyler, Texas Creutzfeldt-Jacob Disease
(CJD), a transmissible spongiform encephalopathy, is caused by prions composed
of proteinaceous material devoid of nucleic acid. CJD occurs sporadically
(generally 1 case/1,000,000 population per year) in older patients (average age
of 65) and is characterized by rapidly progressive dementia, accompanied by
severe muscle spasms and incoordination. Death usually occurs within 3 to 12
months (average 7 months). CJD activity in Texas, which has a population of
nearly 19 million, appeared to be typical. The statewide death rate for 1995 and
1996 was just under 1/1,000,000. In April of 1997, the Texas Department of
Health became aware of an increased number of possible CJD cases in a 23-county
area of NE Texas with a population of just over one million. After review of
medical and pathology records, four patients were identified with definite
classic CJD and three were identified with probable CJD. Dates of death for the
eight patients were from April, 1996 through mid-July 1997. The patients were
from 46 through 65 years of age; four were male and three were female. A
case-control study to identify risks for CJD in NE Texas has been initiated. http://www.jifsan.umd.edu/tse/Rawlings.htm
we get them young cases of tse prion disease in Texas, that is not related
to anything $$$ money and politics will buy anything, especially junk science...
sporadic ffi and sporadic gss ;
NOT THIS CASE !!! but another one a while back in Texas...see ;
We report a case of a 33-year-old female who died of a prion disease for
whom the diagnosis of sFI or FFI was not considered clinically. Following death
of this patient, an interview with a close family member indicated the patient's
illness included a major change in her sleep pattern, corroborating the reported
autopsy diagnosis of sFI.
sporadic FFI or nvCJD Texas style ???
Creutzfeldt-Jakob Disease Surveillance in Texas
Sunday, July 11, 2010
CJD or prion disease 2 CASES McLennan County Texas population 230,213 both
cases in their 40s
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
Thursday, August 12, 2010
Seven main threats for the future linked to prions
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
snip...
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
*** but the possibility that a small proportion of human cases so far
classified as "sporadic" CJD are of zoonotic origin could not be excluded.
Moreover, transmission experiments to non-human primates suggest that some TSE
agents in addition to Classical BSE prions in cattle (namely L-type Atypical
BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential.
snip...
***In addition, non-human primates are specifically susceptible for
atypical BSE as demonstrated by an approximately 50% shortened incubation time
for L-type BSE as compared to C-type. Considering the current scientific
information available, it cannot be assumed that these different BSE types pose
the same human health risks as C-type BSE or that these risks are mitigated by
the same protective measures.
Monday, May 19, 2014
Variant CJD: 18 years of research and surveillance
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health
Crisis
full text with source references ;
re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
Views & Reviews
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in
the United States
Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and
Lawrence B. Schonberger, MD
+ Author Affiliations
From the Division of Viral and Rickettsial Diseases (Drs. Belay and
Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers
for Disease Control and Prevention, Atlanta, GA; and National Prion Disease
Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology,
Institute of Pathology, Case Western Reserve University, Cleveland, OH.
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600
Clifton Road, Mailstop A-39, Atlanta, GA 30333.
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al.
JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL
TEXT
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as
well
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North
America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember,
the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been
documented in North America, along with the typical scrapie's, and atypical
Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these
TSE in different species have been rendered and fed to food producing animals
for humans and animals in North America (TSE in cats and dogs ?), and that the
trading of these TSEs via animals and products via the USA and Canada has been
immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances
and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD
only theory in 2009. With all the science to date refuting it, to continue to
validate this old myth, will only spread this TSE agent through a multitude of
potential routes and sources i.e. consumption, medical i.e., surgical, blood,
dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and
the urgent need to make all human TSE in the USA a reportable disease, in every
state, of every age group, and to make this mandatory immediately without
further delay. The ramifications of not doing so will only allow this agent to
spread further in the medical, dental, surgical arena's. Restricting the
reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO
age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al
and many more, that the world of TSE Transmissible Spongiform Encephalopathy is
far from an exact science, but there is enough proven science to date that this
myth should be put to rest once and for all, and that we move forward with a new
classification for human and animal TSE that would properly identify the
infected species, the source species, and then the route.
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
I kindly disagree with your synopsis for the following reasons ;
snip...
I would kindly like to add to my initial concerns, something I brought up
years ago, and I believe that still hold true today, more so even than when I
first stated these concerns in 2003 ;
routine passive mortality CJD surveillance USA ?
THIS has been proven not to be very useful in the U.K.;
THE EPIDEMIOLOGY OF CJD RG WILL 1984 (182 PAGES)
snip...
One reason for this was the _inaccuracy_ in coding of cases correctly
certified as CJD Coding is carried out by staff who are not medically qualified
and it is not surprising that coding errors occur in the processing of large
numbers of certificates. In 1982, 12,000 certificates per week were processed at
the office of population censuses and surveys by 15 coders and 6 checkers
(Alderson et al., 1983). The occurrence of both inter- and intra-observer coding
errors has been described (Curb et al., 1983) and the _inaccuracies_ of BOTH
certification and coding discovered in this study _support_ the introduction of
a more accurate system of death certificates and a more detailed and specific
coding system...
snip...
Draft Proposal For The Monitoring of Creutzfeldt-Kakob Disease 1989 Dr. R.
Will
snip...
IDENTIFICATION OF CASES
Cases of CJD may be identified from death certificates, but this alone is
unlikely to provide adequate monitoring. ERRORS are made in certification and
diagnosis; in the Oxford study death certificates were obtained on a series of
known confirmed cases and CJD was mentioned in only 66% of certificates. In
another series of 175 certified cases, 42 patients were judged not to have
suffered from CJD after examination of case notes (7)...
full text;
http://web.archive.org/web/20050526035006/http://www.bseinquiry.gov.uk/files/yb/1989/05/00005001.pdf
snip...see my full text submission here ;
re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
2001-2002ish
greetings TSE PRION WORLD,
i am reminded of a few things deep throat told me years ago;
*** 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 at least a million bovine tested as soon as possible and
agressively seeking this disease. The big players are coming out of the wood
work 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 agreat 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.)
================================================
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 SINGELTARY
HACKS IN (DEEP THROAT ABOVE HELPED ME GET IN)
Mad cow disease: Could it be here?
Man's stubborn crusade attracts experts' notice By Carol Christian | August
5, 2001
yes, cjd is popping up in more and more places it seems. I think in 55 year
and older, it's now 1 in 9,000.
see ;
lifetime risk of developing sporadic CJD is about 1 in 30,000, jumps to 1
in 9,000 in 50 years of age and above
IN REALITY, sporadic CJD is 1 in 9,000 in 50 years of age and above, and
that's with a inadequate or what I call passive surveillance system. see below
;
Dr. William Shulaw, a veterinarian with The Ohio State University extension
service, is involved in a nationwide program to eradicate scrapie, the form of
BSE found in sheep.
Shulaw said the chances of a person getting sporadic Creutzfeldt- Jakob
disease is about one in a million. But that's the total population, infants,
children, adults and the elderly.
Chances increase to one in 9,000 when the group is restricted to those age
50 and older.
Monday, June 02, 2014
Confirmed Human BSE aka mad cow Variant CJD vCJD or nvCJD Case in Texas
fact is, BSE cases in Europe of the past years have dropped dramatically
due to feed ban that was enforced, and extensive BSE testing, in large numbers.
just the opposite has happened in the USA. it’s all been documented. there is
ample evidence that there is as much of a chance (if not more), that this victim
contracted human mad cow disease from sources right here in the USA. this PR
push to alienate a USA source factor for human BSE in the USA is a PR stunt by
the USDA inc., and not justified now, in my opinion. compare BSE testing figures
in the EU compared to the USA, compare mad cow feed ban breaches, and you will
see. hell, the 2004 enhanced BSE surveillance program was flawed so bad, the top
Prion God at the NIH TSE prion expert Paul Brown, says he does not trust
anything from the USDA since Texas covered up a mad cow for 7 months, on a 48
hour confirmation turn around. it’s all documented below in link. USDA inc shut
down the mad cow testing after so many atypical BSE cases started showing up.
yes, another foreigner comes to the USA, or another USA citizens does some
traveling, and all of a sudden, it’s a foreign disease. evidently, these folks
never eat anything in the USA, and contracts nvcjd. right. just like the last
one in 2005. really? here are the facts of the TEXAS MAD COW, MAD COW FEED in
Texas, CJD CLUSTER in Texas, CJD CASE IN 38 YEAR OLD WOMAN THAT APPARENTLY
WORKED ON THE SLAUGHTER LINE FOR TYSON in Texas, AND OTHER STRANGE TSE PRION
DISEASE IN VERY YOUNG VICTIMS HERE IN TEXAS with long duration of illness from
onset of clinical symptoms to death, CALLED SPORADIC FFI (except it is not
linked to any genetic make up of that family), another nvcjd victim back in 2005
in Texas, apparently another UK victim that had moved to Texas, and never ate
anything. these are the facts as I have come to know them (official documents),
since hvcjd took my mom in December of 1997. just made a promise to mom, never
forget, and never let them forget, the rest of the story, the truth you don’t
hear about. ...our fine federal friends and the USDA inc, has lied to all of
us...
CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
Monday, June 02, 2014 Confirmed Variant CJD Case in Texas
Wednesday, September 10, 2014
*** Creutzfeldt-Jakob disease (CJD) biannual update (August 2014), with
updated guidance on decontamination of gastrointestinal endoscopy equipment
***
Research and analysis
Monday, July 28, 2014
Mitigating the Risk of Transmission and Environmental Contamination of
Transmissible Spongiform Encephalopathies 2013 Annual Report
Thursday, October 25, 2012
Current limitations about the cleaning of luminal endoscopes and TSE prion
risk factors there from
Article in Press
Saturday, January 16, 2010
Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to
Bramble et al
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr flounder@wt.net 1-24-3
Terry S. Singeltary Sr., P.O. BOX 42, Bacliff, Texas 77518 USA
Professor Michael Farthing wrote:
Louise Send this to Bramble (author) for a comment before we post. Michael
snip...
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr flounder@wt.net 1-24-3
I have researched human/animal TSEs now for over 5 years due to the death
of my Mother from the Heidenhain Variant Creutzfeldt Jakob disease, one of six -
known - variants of the infamous 'sporadic' CJD.
I did a little survey several years ago about CJD and ENDOSCOPY in 2001,
and then went there again when another article was released recently. However,
they seemed to only be concerned with the vCJD strain and risk from endoscopy
equipment.
My concerns are if vCJD can be transmitted by blood, and there are now 6
variants of the infamous sporadic CJDs that they are documenting to date, how do
they know that none of these 6 variants will not transmit the agent (prion) via
blood?...especially since the sporadic CJDs are the only ones documented to date
to transmit via the surgical arena and now that the CWD is spreading more and
more, who knows about the cattle?
I would always read this study and it would bring me back to reality as to
how serious/dangerous this agent is in the surgical/medical arena. You might
want to read this short abstract from the late, great Dr. Gibbs twice, and let
it really sink in. And please remember while reading some of these transmission
studies, that most all, if not ALL these agents transmit freely to primates.
Humans, of course, are primates.
Regarding claims that:
'Well, it has never been documented to transmit to humans."
There are two critical factors to think about:
A. CJD/TSEs in the USA are NOT reportable in most states and there is NO
CJD/TSE questionnaire for most victims and their families, and the one they are
now issuing asks absolutely nothing about route and source of the (prion) agent,
only how the disease was diagnosed. Furthermore, the elderly are only very
rarely autopsied, ie looking for Alzheimer's or 'FAST Alzheimer's' OR prion
disease-related factors and phenomena, such as heart failure caused by
disease.
B. It is unethical and against the law to do transmission studies of TSEs
to humans, they are 100% FATAL.
I suggest you read these case studies about medical arena CJD transmission
very carefully:
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD
20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
Tissue Infectivity and TSEs (brain = high / rectum = medium)
snip...see full text ;
Evidence For CJD TSE Transmission Via Endoscopes 1-24-3
re-Singeltary to Bramble et al
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr flounder@wt.net 1-24-3
Monday, August 18, 2014
Barriers to Creutzfeldt-Jakob Disease Autopsies, California and the
USA
Science and Technology Committee Oral evidence: Blood, tissue and organ
screening, HC 990 Wednesday 5 March 2014 SPORADIC CJD
Science and Technology Committee
Oral evidence: Blood, tissue and organ screening, HC 990 Wednesday 5 March
2014
Ordered by the House of Commons to be published on 5 March 2014.
Written evidence from witnesses:
– Prometic BioSciences Ltd
– Terumo BCT
– Prionics AG
– DuPont Chemicals and Fluoroproducts
Watch the meeting
Members present: Andrew Miller (Chair); Jim Dowd; David Heath; Stephen
Metcalfe; David Morris; Stephen Mosley; Pamela Nash; Sarah Newton; Graham
Stringer; David Tredinnick
snip...
Professor Collinge: I think there is some misunderstanding there. The
apparent incidence of sporadic CJD is increasing. There are about a hundred new
cases a year at the moment, and that has gone up substantially from the start of
surveillance. That is thought, principally, to reflect better diagnosis of the
disease, although that may not be all the explanation. It is possible, and we
can talk about that, that some of that may be BSE-related. However, I think that
the specific confusion there is that people talk about sporadic CJD occurring at
1 per million. That is not your individual risk. Your risk is 1 per million
every year. Actually, it is nearer 2 per million per year of the population will
develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about
1 in 30,000. So that has not really changed. When people talk about 1 per
million, often they interpret that as thinking it is incredibly rare. They think
they have a 1-in-a-million chance of developing this disease. You haven’t.
You’ve got about a 1-in-30,000 chance of developing it.
snip...
Q112 Graham Stringer: Professor Collinge, the last time you were here you
said that you believed that the risk of transmission of vCJD via surgical
instruments was a significant problem. If that is the case, why have no cases
been reported where vCJD has been transmitted in that particular way?
Professor Collinge: What I was trying to say is that there is clearly a
risk there. We have not been able to quantify that risk. It is correct that we
don’t know of any cases of secondary vCJD that can be attributed to surgical
instruments at this point in time, but it can’t be excluded that some of the
cases we have seen so far of vCJD have been related to that. It is a question of
how you would tell. That really comes from epidemiological studies. Since a
history of prior surgery—particularly a history of prior dental surgery—is so
common, and many patients you see will have had prior surgery and certainly
virtually all of them will have had dentistry, it is hard to make that link. The
link has been made with sporadic CJD where there have been clearly documented
instances of transmission of prions by surgical instruments, by neurosurgical
instruments. There is also epidemiological evidence from several countries now
that patients developing classical CJD are more likely to have had abdominal
surgery beforehand, for example. There are sufficient numbers where an
epidemiological link has been shown. You are right—we don’t have definite
evidence that a surgically transmitted case of vCJD has occurred, but that is,
perhaps, not surprising at this point in time.
What we do have is a great deal of scientific evidence that, first of all,
the infective agent in vCJD is much more widely distributed in the body than it
is in classical CJD, so there is more opportunity for it to contact surgical and
medical instruments. Of course, as you heard from the HPA study, there are,
potentially, quite a lot of people carrying the infection around. We also know,
experimentally, that it is relatively easy to transmit prions by binding them to
metal surfaces. In fact, it is something that we use experimentally now. It is a
very efficient way of transmitting the disease. Indeed, the blood test that we
talked about earlier exploits the affinity of prions on metal surfaces as a way
of concentrating the infective agent prior to detection. There is plenty of
scientific evidence that this would be an efficient route of transmission. There
is plenty of evidence that there are many people in the UK incubating the
disease and that the infection would be in tissues that come into contact with
surgical instruments. But you are right: so far, there is not a documented
example of that happening with vCJD.
Wednesday, December 11, 2013
*** Detection of Infectivity in Blood of Persons with Variant and Sporadic
Creutzfeldt-Jakob Disease ***
Sunday, March 09, 2014
*** A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of
Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease
FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
Thursday, February 20, 2014
*** Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS
Dr. Linda Detwiler 2014
Saturday, February 01, 2014
*** vCJD With Extremely Low Lymphoreticular Deposition of Prion Protein MAY
NOT HAVE BEEN DETECTABLE
Monday, October 14, 2013
*** Researchers estimate one in 2,000 people in the UK carry variant CJD
proteins ***
Wednesday, December 11, 2013
*** Detection of Infectivity in Blood of Persons with Variant and Sporadic
Creutzfeldt-Jakob Disease ***
Thursday, March 6, 2014
*** TEXAS RECALL LIST MASSIVE FROM DEAD STOCK DOWNER CANCER COWS OFFAL from
Class I Recall 002-2014 and 013-2014 Health Risk: High Jan 13, 2014 and Feb 8,
2014 shipped to Texas, Florida, and Illinois UPDATE FEBRUARY 14, 2014 ***
WHAT about the sporadic CJD TSE proteins ?
WE now know that some cases of sporadic CJD are linked to atypical BSE and
atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all
it’s sub-types $$$
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010 ***
Sunday, October 13, 2013
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type
prion disease, what it ???
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC)
recently delivered a scientific opinion on any possible epidemiological or
molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far *** but the
possibility that a small proportion of human cases so far classified as
"sporadic" CJD are of zoonotic origin could not be excluded. Moreover,
transmission experiments to non-human primates suggest that some TSE agents in
addition to Classical BSE prions in cattle (namely L-type Atypical BSE,
Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential.
snip...
Thursday, August 12, 2010
Seven main threats for the future linked to prions First threat The TSE
road map defining the evolution of European policy for protection against prion
diseases is based on a certain numbers of hypotheses some of which may turn out
to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform
Encephalopathy), recently identified by systematic testing in aged cattle
without clinical signs, may be the origin of classical BSE and thus potentially
constitute a reservoir, which may be impossible to eradicate if a sporadic
origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
snip...
*** 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.
Monday, March 10, 2014
Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards
Singeltary Submission
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion
strains in transgenic mice expressing human prion protein
Variant Creutzfeldt–Jakob disease (vCJD) has been recognized to date only
in individuals homozygous for methionine at PRNP codon 129. Here we show that
transgenic mice expressing human PrP methionine 129, inoculated with either
bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the
neuropathological and molecular phenotype of vCJD, consistent with these
diseases being caused by the same prion strain. Surprisingly, however, BSE
transmission to these transgenic mice, in addition to producing a vCJD-like
phenotype, can also result in a distinct molecular phenotype that is
indistinguishable from that of sporadic CJD with PrPSc type 2. These data
suggest that more than one BSE-derived prion strain might infect humans; it is
therefore possible that some patients with a phenotype consistent with sporadic
CJD may have a disease arising from BSE exposure.
Wednesday, December 4, 2013
Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine
Products; Final Rule Federal Register / Vol. 78 , No. 233 / Wednesday, December
4, 2013
TO ALL IMPORTING COUNTRIES THAT IMPORTS FROM THE USA, BE WARNED, NEW MAD
COW BSE REGULATIONS USDA, AND OIE, not worth the paper the regulations were
wrote on, kind of like the mad cow feed ban of August 1997, nothing but ink on
paper $$$
full text ;
Monday, December 02, 2013
*** A parliamentary inquiry has been launched today into the safety of
blood, tissue and organ screening following fears that vCJD – the human form of
‘mad cow’ disease – may be being spread by medical procedures
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Aug. 5, 2001, 12:25AM
Mad cow disease: Could it be here?
Man's stubborn crusade attracts experts' notice
By CAROL CHRISTIAN Copyright 2001 Houston Chronicle
Like Paul Revere with e-mail, Terry Singeltary Sr. is on a mission to sound
an alarm: Beware of mad cow disease.
As is true of many crusaders, however, his pleas often fall on deaf ears.
Health officials here and abroad insist that bovine spongiform encephalopathy --
popularly known as mad cow disease, a fatal brain disorder that can make cows
shake uncontrollably -- has been kept out of this country through surveillance
of the cattle industry.
But since his mother's death in December 1997, the Galveston County man has
been obsessed with possible connections between her deadly brain disorder,
sporadic Creutzfeldt-Jakob Disease, and mad cow disease.
And after much persistence on his part, people are taking notice of this
former machinist and high school dropout who jokes that he has a Ph.D. -- a Pool
Hall Degree.
"They called me Chicken Little for four years," he said. "Now they're
calling back, asking for more information."
For the past year he has been U.S. co-coordinator of an international
monitoring group called CJD Watch. He regularly gets e-mail from scientists and
journalists around the world.
Debora MacKenzie, a reporter for the British magazine New Scientist,
described Singeltary, 47, as a "dogged unearther and tabulator of government
documents." Singeltary monitors "every word written about CJD/BSE," said Anita
Manning of USA Today, also by e-mail.
"He's passionate, opinionated and not always tactful, although I like him
because he's such a character and he is so transparent," Manning said. "He is
what he appears to be."
Science and environment writer Jonathan Leake of the Sunday Times in London
said Singeltary has helped him track down families of people with CJD along with
academic research papers.
"I strongly suspect he is right in thinking the USA has had BSE cases,"
Leake said by e-mail.
"The American government is making the same mistake as the British in
putting the short-term commercial interests of its farmers before health
considerations," he added.
"It should start formal and widespread testing of cattle plus compulsory
autopsies for all human CJD victims at the state's expense. If there is BSE,
then leaving it to spread will kill people -- and that would eventually destroy
the industry, too."
Texas Department of Health epidemiologist Julie Rawlings said Singeltary's
careful monitoring of the disease had proven useful.
"Terry has been helpful in providing contact information regarding suspect
CJD cases so that the Health Department can initiate case investigations and
learn more about CJD in Texas," she said.
Noting that the department cannot release records on individual patients,
she added, "I think we learn more from him than he does from us."
Mad cow disease surfaced in England in 1986 and quickly became an epidemic.
It since has been reported in 15 European countries, most recently Greece on
July 2, and the Czech Republic on June 14. Two German-born cows tested positive
for BSE in November.
Singeltary said he became convinced that BSE is here as he watched his
mother, Barbara Poulter of Crystal Beach, dying of sporadic Creutzfeldt-Jakob
Disease. The rare, fatal brain disease is sometimes accompanied by severe
jerking.
"She would jerk so bad at times, it would take three of us to hold her
down," Singeltary said. "They can call it whatever they want, but I know what I
saw, and what she went through. `Sporadic' simply means they don't know."
Poulter, a retired telephone-company field worker, had a form of sporadic
CJD -- Haidenhain variant -- that is even less common than the typical sporadic
case. One of its first symptoms is loss of vision.
She started seeing brown spots in September 1997 and was virtually blind
within two weeks. By the eighth week of the illness Poulter was bedridden, and
in the 10th week she died. Before that she had been in good health.
In many countries and most U.S. states, physicians are not required to
report CJD cases to health officials. Texas made the disease reportable in 1998.
Through 2000, there were 17 probable or confirmed cases, according to the Texas
Department of Health.
In mid-June, a case of sporadic CJD was confirmed through brain biopsy at
Christus Spohn Hospital Shoreline in Corpus Christi, said Jane Bakos, hospital
vice president. The patient has since died, the hospital reported.
CJD and mad cow disease leave their victims' brains full of holes like a
sponge.
Although not contagious, the illnesses are thought to be transmissible
through prions, or nearly indestructible abnormal proteins.
Because the prion protein is not killed by standard sterilization, sporadic
CJD can be spread by contaminated surgical instruments.
In March 1996, the British government announced the discovery of a new
variant of CJD, most likely explained by exposure to bovine spongiform
encephalopathy.
Through June, 101 cases of new-variant CJD have been reported in the United
Kingdom, three in France and one in Ireland. In contrast to sporadic CJD, the
new variant usually affects younger patients and lasts longer.
No cases of new-variant CJD or BSE have been reported in the United States.
No relationship has been shown between sporadic CJD and mad cow disease.
There is no indication that new-variant CJD can be spread through blood
transfusions, but a U.S. Food and Drug Administration advisory committee voted
in June to broaden the categories for excluding potential donors. The
recommendations have not yet been approved by the FDA.
The American Red Cross has announced that on Sept. 17 it will begin
rejecting potential blood donors who, since 1980, have spent at least three
months in the United Kingdom or at least six months in any European country or
combination of countries. Those who have received a blood transfusion in Britain
since 1980 also will be rejected.
The primary collector of local blood donations is the Gulf Coast Regional
Blood Center, which will follow the FDA's guidelines, said Bill Teague,
president and chief executive officer.
Singeltary said it's naive to think that U.S. prevention efforts have kept
mad cow and new-variant CJD out of the United States.
"They haven't found it," he said, "because they haven't looked."
For one thing, he said, too few cows are tested for the disease. In the
first six months of this year, the European Union tested more than 3.2 million
cows, David Byrne of the European Commission said in a speech last month.
By contrast, it took the U.S. Department of Agriculture nearly 10 years to
analyze about 13,000 cow brains, according to the department's Web site.
With more than 68 million cattle slaughtered since 1990 in the United
States, according to the USDA, checking about 13,000 falls far short, Singeltary
said.
Though not a scholar, Singeltary has collected voluminous material on mad
cow and CJD. Disabled from a neck injury, Singeltary never used a computer until
1998.
He now spends hours each day on the Internet while his wife, Bonnie
Singeltary, runs a flower shop in their home in Bacliff, in north Galveston
County.
His challenge to the CJD/BSE establishment is courageous and refreshing,
said Dr. Lynette Dumble, former visiting professor of surgery at University of
Texas Medical School at Houston and a former senior research fellow in the
history and philosophy of science at the University of Melbourne in
Australia.
"I certainly have no problem with Terry's ideas on BSE/CJD," said Dumble,
who coordinates the Global Sisterhood Network, a computer service that posts
media reports on developments affecting women. "His research skills are
excellent, and he is abreast of each and every development in the field."
Among Singeltary's worries now, he said, are widespread violations of an
August 1997 ban on feeding animal products to U.S. cattle. The FDA reported in
January that hundreds of feed manufacturers were not complying with regulations
designed to keep BSE out of this country.
(That same month, a Purina Mills feedlot near San Antonio told the FDA that
a "very low level" of cow parts had been found in cattle feed. The company
voluntarily removed 1,222 animals who had been fed the prohibited
materials.)
He obtained copies of FDA letters to various feed mills that had been found
in violation of the regulations and immediately sent them by e-mail to hundreds
of people around the world.
Singeltary might not be so zealous in getting the word out if he weren't
convinced that someone is covering up the truth.
"They used to say BSE would never transmit to humans," he said, "and it
has. They lied about the feed ban being in place.
"I've lost faith in the whole process. I've discovered too many things."
layperson
just made a promise, never forget, never let them forget...
MOM DOD 12/14/97 confirmed hvCJD Heidenhain Variant Creutzfeldt Jakob
Disease Case Report
snip...
Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'
DIVISION OF NEUROPATHOLOGY University of Texas Medical Branch 114 McCullough
Bldg. Galveston, Texas 77555-0785 FAX COVER SHEET DATE: 4-23-98 TO: Mr. Terry
Singeltary @ ------- FROM: Gerald Campbell FAX: (409) 772-5315 PHONE: (409)
772-2881 Number of Pages (including cover sheet): Message: *CONFIDENTIALITY
NOTICE* This document accompanying this transmission contains confidential
information belonging to the sender that is legally privileged. This information
is intended only for the use of the individual or entry names above. If you are
not the intended recipient, you are hereby notified that any disclosure, copying
distribution, or the taking of any action in reliances on the contents of this
telefaxed information is strictly prohibited. If you received this telefax in
error, please notify us by telephone immediately to arrange for return of the
original documents.
--------------------------
Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q
Patient Name: POULTER, BARBARA
Age: 63
YRS DOB: 10/17/34
Sex: F
Admitting Race: C
Attending Dr.: Date / Time Admitted : 12/14/97 1228
Copies to: UTMB University of Texas Medical Branch Galveston, Texas
77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY DIAGNOSIS
Autopsy' Office (409)772-2858 Autopsy NO.: AU-97-00435 AUTOPSY INFORMATION:
Occupation: Unknown Birthplace: Unknown Residence: Crystal Beach Date/Time
of Death: 12/14/97 13:30 Date/Time of Autopsy: 12/15/97 15:00
Pathologist/Resident: Pencil/Fernandez Service: Private Restriction:
Brain only FINAL AUTOPSY DIAGNOSIS I. Brain: Creutzfeldt-Jakob disease,
Heidenhain variant. snip...see full text ;
2001-2002ish
greetings TSE PRION WORLD,
i am reminded of a few things deep throat told me years ago;
*** 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 at least a million bovine tested as soon as possible and
agressively seeking this disease. The big players are coming out of the wood
work 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 agreat 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.)
Thursday, April 24, 2014
Brazil investigates possible BSE mad cow case
Monday, May 5, 2014
Brazil BSE Mad Cow disease confirmed OIE 02/05/2014
Thursday, September 26, 2013
Brazil evaluate the implementation of health rules on animal by-products
and derived products SRM BST TSE PRION aka MAD COW DISEASE
Friday, December 07, 2012
ATYPICAL BSE BRAZIL 2010 FINALLY CONFIRMED OIE 2012
Wednesday, December 19, 2012
Scientific Report of the European Food Safety Authority on the Assessment
of the Geographical BSE Risk (GBR) of Brazil
Terry S. Singeltary Sr. xxx Bacliff, Texas USA 77518
flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
10:04 AM
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