June 23, 2013
National Animal Health Laboratory Network Reorganization Concept Paper
(Document ID APHIS-2012-0105-0001)
I kindly wish to submit my comments on the National Animal Health
Laboratory Network Reorganization Concept Paper (Document ID
APHIS-2012-0105-0001). I write in urgent regards as to the continued spread of
the Transmissible Spongiform Encephalopathy TSE prion disease in cervids in
North America, the reduced testing to numbers so low, it would almost be
impossible to detect a TSE BSE prion type disease in the USA bovine, the
continued build of of captive shooting pens aka game farms, restrictions on CWD
testing there from to only 16 months and older, should be ALL cervids tested on
ALL game farms, once a year, and every dead or bought or sold cervid , and CWD
risk factors there from. the lack of Testing for the TSE prion mad cow type
disease in the USA bovine, the continued failed ruminant protein feed ban
violations, and surveillance of the BSE TSE prion type mad cow disease, of all
strains and phenotypes, and finally, the failures of the O.I.E. and the
U.S.D.A., in regards to all of the above. CJD in young and old have been rising
in the USA and Canada, with a new strain of CJD they are now calling VPSPr type
CJD.
By the stripping of funding for the entire Transmissible Spongiform
Encephalopathy TSE prion type disease in all species, including humans, by NOT
having CJD TSE prion disease in humans OF ALL AGE groups, being a reportable
disease, you therefore risk further spreading the TSE prion type disease from a
multitude of proven iatrogenic routes and sources, from all these different TSE
prion strains in different species for consumption here in the USA and North
America. I urge once again not to kid yourself, and continue to blind yourself
with the greed of the industries involved, and continue to ignore this slow
incubating, yet 100% fatal disease once clinical, continue to ignoring all risk
facts and continue business as nothing ever happened, continue letting the junk
science by the USDA and the OIE in regards to the TSE prion disease and
regulations put forth, therefrom, will just continue to spread and load up the
environment, and your industries worst nightmare could come true, i.e.
horizontal and or vertical transmissions of the TSE prion disease in the bovine,
from either a strain of CWD in cervids back into the bovine as another TSE prion
disease that spreads like CWD, or like Scrapie or any of the atypicals
therefrom. it’s your game of chance you have been playing with humans and
animals, it’s your call.
I strenuously urge the National Animal Health Laboratory Network
Reorganization Concept Paper (Document ID APHIS-2012-0105-0001) to include a 5
year enhanced program of BSE TSE prion testing in the bovine, sheep, goat, and
cervids, to include 1 million tests for each species, using the enhanced testing
techniques, not the OBEX ONLY CRITERIA THE USDA OIE USED FOR YEARS, missing who
knows how many cases. seems it was so bad in the bovine testing for BSE in the
USA, some 9,200+ test were questioned, and Texas has since issued a warning on
this with their testing for CWD in cervids. too bad Texas did not do this for
their mad cows, when they were still testing for them.
I also strenuously urge the National Animal Health Laboratory Network
Reorganization Concept Paper (Document ID APHIS-2012-0105-0001), to plead with
the USDA INC., and the OIE, to recall the EXEMPTION OF THE ATYPICAL SCRAPIE from
the OIE TSE prion trading policies, and to CEASE all further attempts to make
typical scrapie as well, a legal trading commodity, by exempting it too from the
TSE Prion trading protocols of the OIE and the USDA INC. by making these foolish
exemptions, you will only further spread the TSE prion disease in to different
species, including man, but also, continue to load the environment with the TSE
prion disease. ...
Chronic Wasting Disease CWD, and other TSE prion disease, these TSE prions
know no borders.
these TSE prions know NO age restrictions.
The TSE prion disease survives ashing to 600 degrees Celsius, that’s around
1112 degrees Fahrenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a
mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the
environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of
protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple
autoclave will not kill this TSE prion agent.
I go from state to state trying to warn of the CWD and other TSE prion
disease in other species, I just made a promise to mom. back then, there was no
information.
so, I submit this to you all in good faith, and hope that you take the time
to read my research of the _sound_, peer review science, not the junk science
that goes with the politics $$$
right or left or teaparty or independent, you cannot escape the TSE prion
disease.
there is a lot of science here to digest, but better digesting this _sound_
science, instead of the junk political science you will hear from the shooting
pen industry.
the new BSE TSE PRION MAD COW risk category the OIE gave the USA, puts
everyone around the globe at more risk of a tse prion mad cow type disease now.
in my opinion, this new risk category was bought and paid for by your local
cattle dealer, via fraud.
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. ...
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,
in the links below, I supplied source reference materials, with the latest
peer review scientific studies on the TSE prion disease to date, and that I DO
NOT ADVERTISE, just made a promise way back in 1997, when there was very little
public information on the TSE prion disease. this scientific materials I have
collected and posted in the following links are for educational use.
...tss
USDA INC
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
sporadic CJD has now been linked to atypical BSE, atypical Scrapie, and
don’t count CWD, typical scrapie, or typical BSE (Collinge et al) out just yet.
...
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...
Rural and Regional Affairs and Transport References Committee
The possible impacts and consequences for public health, trade and
agriculture of the Government's decision to relax import restrictions on beef
Final report June 2010
2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr
Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric,
epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey
told the committee of his concerns regarding the lengthy incubation period for
transmissible spongiform encephalopathies, the inadequacy of current tests and
the limited nature of our current understanding of this group of
diseases.49
2.66 Dr Fahey also told the committee that in the last two years a link has
been established between forms of atypical CJD and atypical BSE. *** Dr Fahey
said that: They now believe that those atypical BSEs overseas are in fact
causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to
mad sheep disease or a different form. If you look in the textbooks it looks
like this is just arising by itself. But in my research I have a summary of a
document which states that there has never been any proof that sporadic
Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no
proof of that. The recent research is that in fact it is due to atypical forms
of mad cow disease which have been found across Europe, have been found in
America and have been found in Asia. These atypical forms of mad cow disease
typically have even longer incubation periods than the classical mad cow
disease.50
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set
out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE
which include the H-type and L-type atypical forms. This assumption is
scientifically not completely justified and accumulating evidence suggests that
this may in fact not be the case. Molecular characterization and the spatial
distribution pattern of histopathologic lesions and immunohistochemistry (IHC)
signals are used to identify and characterize atypical BSE. Both the L-type and
H-type atypical cases display significant differences in the conformation and
spatial accumulation of the disease associated prion protein (PrPSc) in brains
of afflicted cattle. Transmission studies in bovine transgenic and wild type
mouse models support that the atypical BSE types might be unique strains because
they have different incubation times and lesion profiles when compared to C-type
BSE.
When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE. 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.
This study will contribute to a correct definition of specified risk
material (SRM) in atypical BSE. The incumbent of this position will develop new
and transfer existing, ultra-sensitive methods for the detection of atypical BSE
in tissue of experimentally infected cattle.
add all the above up, and then ponder iatrogenic CJD there from $$$
Greetings Dr. Paul Van Buynder et al @ FraserHealth,
Sadly, in the year 2013, we are still going by science that is 3 decades
old, to manage risk factors from the many different strains of the TSE prion
disease.
Dr. Paul Van Buynder et al state ;
> I want to be clear there is absolutely no evidence that these three
confirmed or probable cases are linked to food consumption.
when in reality, you have no clue Sir.
sporadic CJD is not a single strain of the TSE prion sporadic phenotypes
(there are many, and they are mounting).
sporadic CJD has now been linked to atypical BSE, and atypical Scrapie, and
many reputable scientist around the globe are especially concerned with the CWD
of cervids, and it’s different strains, which we now know there are more
strains.
the UKBSEnvCJD only theory is a false myth, and proven to be so.
also, all iatrogenic CJD is, is sporadic CJD until route and source of the
TSE agent is confirmed.
what fuels this madness, and the spread of this disease, are Doctors and
officials that continue to spread this junk science.
you are part of the problem, in my opinion, and I mean no disrespect Sir.
if I still sound angry, I am, 15+ years later.
I have wasted 15 years daily following the science as it emerges with the
TSE prion disease, and documenting it. I hope you take the time to read some of
it.
no need to reply, most never do, but I urge you to educate yourself on this
topic of the TSE prion disease, and cease spreading the false science that
continues to fuel the spread of this TSE prion disease. ...
thank you, kind regards,
terry
Saturday, June 15, 2013
Canada Fraser Health Statement on Creutzfeldt-Jakob Disease outbreak
Sunday, June 09, 2013
Missouri House forms 13-member Interim Committee on the Cause and Spread of
Chronic Wasting Disease CWD
Thursday, June 20, 2013
atypical, BSE, CWD, Scrapie, Captive Farmed shooting pens (livestock), Wild
Cervids, Rectal Mucosa Biopsy 2012 USAHA Proceedings, and CJD TSE prion Update
Thursday, June 13, 2013
*** Experimental interspecies transmission studies of the transmissible
spongiform encephalopathies to cattle: comparison to bovine spongiform
encephalopathy in cattle
Tuesday, June 11, 2013
Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant
deviations from requirements in FDA regulations that are intended to reduce the
risk of bovine spongiform encephalopathy (BSE) within the United States
Thursday, June 6, 2013
BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI
ratings as at June 5, 2013
2012 California atypical L-type BASE BSE mad cow disease ;
Saturday, May 26, 2012
Are USDA assurances on mad cow case 'gross oversimplification'?
SNIP...
What irks many scientists is the USDA’s April 25 statement that the rare
disease is “not generally associated with an animal consuming infected feed.”
The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown,
one of the world’s experts on this type of disease who retired recently from the
National Institutes of Health.
"(The agency) has no foundation on which to base that statement.”
“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an
official with the USDA during the Clinton Administration now at Mississippi
State.
In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the
origins of atypical cases of BSE,” she said
The argument about feed is critical because if feed is the cause, not a
spontaneous mutation, the California cow could be part of a larger outbreak.
SNIP...
==============================================
Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
=============================================
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE
INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
Sunday, August 26, 2012
Detection of PrPSc in peripheral tissues of clinically affected cattle
after oral challenge with BSE
Thursday, June 20, 2013
*** atypical, BSE, CWD, Scrapie, Captive Farmed shooting pens (livestock),
Wild Cervids, Rectal Mucosa Biopsy 2012 USAHA Proceedings, and CJD TSE prion
Update
Thursday, May 02, 2013
Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TEXTING
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA
Final report
IN CONFIDENCE BSE ATYPICAL LESION DISTRIBUTION
http://web.archive.org/web/20041226015813/http://www.bseinquiry.gov.uk/files/yb/1993/03/14001001.pdf
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only)
diagnostic criteria CVL 1992
Sunday, August 26, 2012
Detection of PrPSc in peripheral tissues of clinically affected cattle
after oral challenge with BSE
Tuesday, May 21, 2013
*** Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a
common origin and why the SSS policy is in full force $$$
CFIA, USDA, AND OIE SHOOT, SHOVEL, AND SHUT THE HELL UP SSS BSE TSE PRION
MAD COW TYPE POLICY $$$, and the media is buying it hook, line, and sinker $$$
EDMONTON - Some of former Alberta premier Ralph Klein's most colourful
quotes — and the reactions they elicited:
SNIP...
"This all came about through the discovery of a single, isolated case of
mad cow disease in one Alberta cow on May 20th.
The farmer — I think he was a Louisiana fish farmer who knew nothing about
cattle ranching.
*** I guess any self-respecting rancher would have shot, shovelled and shut
up, but he didn't do that." — Klein recalls how the mad cow crisis started and
rancher Marwyn Peaster's role.
The premier was speaking at the Western Governors Association meeting in
Big Sky, Mont. September 2004.
Wednesday, December 22, 2010.
Manitoba veterinarian has been fined $10,000 for falsifying certification
documents for U.S. bound cattle and what about mad cow disease?
CENSORSHIP IS A TERRIBLE THING $$$.
Canada has had a COVER-UP policy of mad cow disease since about the 17th
case OR 18th case of mad cow disease. AFTER THAT, all FOIA request were ignored
$$$.
THIS proves there is indeed an epidemic of mad cow disease in North
America, and it has been covered up for years and years, if not for decades, and
it’s getting worse $$$.
Thursday, February 10, 2011.
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011
and how to hide mad cow disease in Canada Current as of: 2011-01-31.
Thursday, January 17, 2013.
Canada, U.S. agree on animal-disease measures to protect trade, while
reducing human and animal health protection.
Wednesday, August 11, 2010.
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA.
Thursday, August 19, 2010.
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA.
Friday, March 4, 2011.
Alberta dairy cow found with mad cow disease.
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, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Wednesday, April 4, 2012
20120402 - Breach of quarantine/Violation de la mise en quarantaine of an
ongoing Scrapie investigation
Michigan and California have had a high spike in Goat Scrapie cases,
compared to elsewhere ???
Tuesday, February 01, 2011
Sparse PrP-Sc accumulation in the placentas of goats with naturally
acquired scrapie
(Figure 6) including five goat cases in FY 2008 that originated from the
same herd in Michigan. This is highly unusual for goats, and I strenuously urge
that there should be an independent investigation into finding the common
denominator for these 5 goats in the same herd in Michigan with Scrapie. ...
Thursday, February 23, 2012
Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012
RESEARCH
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A.
Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins,
Melanie J. Chaplin, and John Spiropoulos
To investigate the possibility of oral transmission of atypical scrapie in
sheep and determine the distribution of infectivity in the animals’ peripheral
tissues, we challenged neonatal lambs orally with atypical scrapie; they were
then killed at 12 or 24 months. Screening test results were negative for
disease-specifi c prion protein in all but 2 recipients; they had positive
results for examination of brain, but negative for peripheral tissues.
Infectivity of brain, distal ileum, and spleen from all animals was assessed in
mouse bioassays; positive results were obtained from tissues that had negative
results on screening. These fi ndings demonstrate that atypical scrapie can be
transmitted orally and indicate that it has the potential for natural
transmission and iatrogenic spread through animal feed. Detection of infectivity
in tissues negative by current surveillance methods indicates that diagnostic
sensitivity is suboptimal for atypical scrapie, and potentially infectious
material may be able to pass into the human food chain.
SNIP...
Although we do not have epidemiologic evidence that supports the effi cient
spread of disease in the fi eld, these data imply that disease is potentially
transmissible under fi eld situations and that spread through animal feed may be
possible if the current feed restrictions were to be relaxed. Additionally,
almost no data are available on the potential for atypical scrapie to transmit
to other food animal species, certainly by the oral route. However, work with
transgenic mice has demonstrated the potential susceptibility of pigs, with the
disturbing fi nding that the biochemical properties of the resulting PrPSc have
changed on transmission (40). The implications of this observation for
subsequent transmission and host target range are currently unknown.
How reassuring is this absence of detectable PrPSc from a public health
perspective? The bioassays performed in this study are not titrations, so the
infectious load of the positive gut tissues cannot be quantifi ed, although
infectivity has been shown unequivocally. No experimental data are currently
available on the zoonotic potential of atypical scrapie, either through
experimental challenge of humanized mice or any meaningful epidemiologic
correlation with human forms of TSE. However, the detection of infectivity in
the distal ileum of animals as young as 12 months, in which all the tissues
tested were negative for PrPSc by the currently available screening and confi
rmatory diagnostic tests, indicates that the diagnostic sensitivity of current
surveillance methods is suboptimal for detecting atypical scrapie and that
potentially infectious material may be able to pass into the human food chain
undetected.
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire).
Saturday, May 2, 2009
APHIS AND WHO PLAN TO EXEMPT THE ATYPICAL SCRAPIE NOR-98 FROM REGULATIONS
AT MEETING THIS MONTH
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH
CODE
Thursday, December 20, 2012
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe
WITH BOVINE MAD COW DISEASE
Wednesday, April 24, 2013
Chimpanzees Released After 30 Years Of Testing, Brace Yourself For Smiles
THE OIE, USDA, CFIA, DEFRA, MAFF, $$$ POLICY OF SPREADING THE TSE PRION
DISEASE GLOBALLY, THE LEGAL TRADING OF ATYPICAL AND POSSIBLY TYPICAL SCRAPIE AS
A COMMODITY. ...
absolutely insane, crazy, absurd, NEGLIGENT, take your pick. ... tss
Tuesday, April 30, 2013
Transmission of classical scrapie via goat milk
Veterinary Record2013;172:455 doi:10.1136/vr.f2613
Tuesday, May 7, 2013
Feds want five-year paper trail for livestock NAIS COOL
Thursday, May 30, 2013
Statement from Agriculture Secretary Tom Vilsack Regarding World
Organization for Animal Health (OIE) Upgrade of United States' BSE Risk Status
Release No. 0106.13 Contact: USDA Office of Communications (202) 720-4623
Tuesday, May 21, 2013
Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common
origin and why the SSS policy is in full force $$$
Tuesday, March 05, 2013
*** A closer look at prion strains Characterization and important
implications Prion
7:2, 99–108; March/April 2013; © 2013 Landes Bioscience
Monday, June 3, 2013
*** Unsuccessful oral transmission of scrapie from British sheep to cattle
Sunday, March 31, 2013
Creutzfeldt Jakob Disease CJD worlds youngest documented victim, 11 years
old, shall we pray
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
Monday, July 23, 2012
The National Prion Disease Pathology Surveillance Center July 2012
2011 Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
Wednesday, June 29, 2011
TSEAC Meeting August 1, 2011 donor deferral Saudi Arabia vCJD risk blood
and blood products
Wednesday, June 29, 2011 TSEAC JUNE 2, 1999 Welcome to the FDA traveling
road show From: TSS
Subject: TSEAC JUNE 2, 1999 Welcome to the FDA traveling road show
Date: October 15, 2007 at 3:18 pm PST
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE MEETING
Thursday, June 2, 1999
Wednesday, March 2, 2011
Transmissible Spongiform Encephalopathies Advisory Committee Meeting
Transcript Posted: 3/2/2011 Posted: 3/2/2011
October 28, 2010
Transmissible Spongiform Encephalopathies Advisory Committee Meeting
Transcript Posted: 3/2/2011
Monday, February 7, 2011
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of
Transmission of CJD and vCJD by Blood and Blood Products 2011 ???
October 29, 2010
Transmissible Spongiform Encephalopathies Advisory Committee Meeting
Transcript Posted: 3/2/2011
Monday, October 18, 2010
TSEAC Transmissible Spongiform Encephalopathies Advisory Committee Draft
Agenda and Meeting Materials,
Posted: 10/18/2010
Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee
Center Date Time Location
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of
Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
Saturday, September 5, 2009
TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June
12, 2009 (Singeltary submission)
TO : william.freas@fda.hhs.gov
May 8, 2009
Greetings again Dr. Freas, TSEAC et al,
I would kindly, once again, wish to comment at this meeting about the
urgent actions that need to be taken asap, to the Meeting of the Transmissible
Spongiform Encephalopathies Committee On June 12, 2009. Due to my disability
from my neck injury, I will not be attending this meeting either, however I hope
for my submission to be read and submitted. ...
IN reply to ;
snip...see full text ;
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June
12, 2009 (Singeltary submission)
TO : william.freas@fda.hhs.gov
Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October
31, 2005 INTRODUCTION The United States Department of Agriculture’s Food Safety
and Inspection Service (FSIS) held a public meeting on July 25, 2006 in
Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine
Spongiform Encephalopathy Update, October 31, 2005 (report and model located on
the FSIS website:
Comments on technical aspects of the risk assessment were then submitted to
FSIS. Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary. This document provides itemized replies to the public comments
received on the 2005 updated Harvard BSE risk assessment. Please bear the
following points in mind:
From: Terry S. Singeltary Sr.
To: FREAS@CBER.FDA.GOV
Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov
Sent: Friday, December 01, 2006 2:59 PM
Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS
SUBMISSION
snip...
ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear
with me)
THE USA is in a most unique situation, one of unknown circumstances with
human and animal TSE. THE USA has the most documented TSE in different species
to date, with substrains growing in those species (BSE/BASE in cattle and CWD in
deer and elk, there is evidence here with different strains), and we know that
sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie
documented and also BSE is very likely to have passed to sheep. all of which
have been rendered and fed back to animals for human and animal consumption, a
frightening scenario. WE do not know the outcome, and to play with human life
around the globe with the very likely TSE tainted blood from the USA, in my
opinion is like playing Russian roulette, of long duration, with potential long
and enduring consequences, of which once done, cannot be undone.
These are the facts as i have come to know through daily and extensive
research of TSE over 9 years, since 12/14/97. I do not pretend to have all the
answers, but i do know to continue to believe in the ukbsenvcjd only theory of
transmission to humans of only this one strain from only this one TSE from only
this one part of the globe, will only lead to further failures, and needless
exposure to humans from all strains of TSE, and possibly many more needless
deaths from TSE via a multitude of proven routes and sources via many studies
with primates and rodents and other species. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
snip... 48 pages...
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...
Tuesday, February 8, 2011
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Saturday, June 22, 2013
Characterization of variant Creutzfeldt-Jakob disease prions in prion
protein-humanized mice carrying distinct codon 129 genotypes
Saturday, June 15, 2013
Canada Fraser Health Statement on Creutzfeldt-Jakob Disease outbreak
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set
out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE
which include the H-type and L-type atypical forms. This assumption is
scientifically not completely justified and accumulating evidence suggests that
this may in fact not be the case. Molecular characterization and the spatial
distribution pattern of histopathologic lesions and immunohistochemistry (IHC)
signals are used to identify and characterize atypical BSE. Both the L-type and
H-type atypical cases display significant differences in the conformation and
spatial accumulation of the disease associated prion protein (PrPSc) in brains
of afflicted cattle. Transmission studies in bovine transgenic and wild type
mouse models support that the atypical BSE types might be unique strains because
they have different incubation times and lesion profiles when compared to C-type
BSE.
When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE. 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.
This study will contribute to a correct definition of specified risk
material (SRM) in atypical BSE. The incumbent of this position will develop new
and transfer existing, ultra-sensitive methods for the detection of atypical BSE
in tissue of experimentally infected cattle.
*** 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.
The chances of a person or domestic animal contracting CWD are “extremely
remote,” Richards said. The possibility can’t be ruled out, however. “One could
look at it like a game of chance,” he explained. “The odds (of infection)
increase over time because of repeated exposure. That’s one of the downsides of
having CWD in free-ranging herds: We’ve got this infectious agent out there that
we can never say never to in terms of (infecting) people and domestic
livestock.”
*** 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 $
CANADA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic
CJD’s). ...tss
PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD)
in Canada is also on a steady increase.
please see ;
> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is
pending.
CJD Deaths Reported by CJDSS1, 1994-20122
As of May 31, 2012
Deaths of Definite and Probable CJD
Year Sporadic Iatrogenic Familial GSS FFI vCJD Total
1994 2 0 0 1 0 0 3
1995 3 0 0 0 0 0 3
1996 13 0 0 0 0 0 13
1997 16 0 1 1 0 0 18
1998 22 1 0 1 0 0 24
1999 26 2 2 1 0 0 31
2000 32 0 0 3 0 0 35
2001 27 0 2 1 0 0 30
2002 31 0 2 2 0 1 36
2003 27 1 1 0 0 0 29
2004 42 0 1 0 0 0 43
2005 42 0 0 2 0 0 44
2006 39 0 1 3 1 0 44
2007 35 0 0 4 0 0 39
2008 48 0 1 0 0 0 49
2009 48 0 3 2 0 0 53
2010 34 0 3 0 0 0 37
2011 37 0 2 1 0 1 41
2012 1 0 0 0 0 0 1
Total 525 4 19 22 1 2 573
1. CJDSS began in 1998
2. Data before 1998 are retrospective and partial, data from 1998 to 2008
are complete, and data for 2009 - 2012 are provisional
3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is
pending.
CJD Deaths Reported by CJDSS1, 1994-20122
As of May 31, 2012
SEE DECEMBER 2012 CANADA
USA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic
CJD’s). ...tss
National Prion Disease Pathology Surveillance Center
Cases Examined1
(May 18, 2012)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 50 32 28 4 0 0
1997 114 68 59 9 0 0
1998 88 52 44 7 1 0
1999 123 74 65 8 1 0
2000 145 103 89 14 0 0
2001 210 120 110 10 0 0
2002 248 149 125 22 2 0
2003 266 168 137 31 0 0
2004 326 187 164 22 0 13
2005 344 194 157 36 1 0
2006 382 196 166 28 0 24
2007 377 213 185 28 0 0
2008 396 232 206 26 0 0
2009 423 256 212 43 1 0
2010 413 257 216 41 0 0
2011 410 257 213 43 0 0
2012 153 82 51 15 0 0
TOTAL 44685 26406 2227 387 6 3
1 Listed based on the year of death or, if not available, on year of
referral;
2 Cases with suspected prion disease for which brain tissue and/or blood
(in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi
Arabia in the other case;
5 Includes 14 cases in which the diagnosis is pending, and 18 inconclusive
cases;
6 Includes 17 (16 from 2012) cases with type determination pending in which
the diagnosis of vCJD has been excluded. The Sporadic cases include 16 cases of
sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive
Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).
Rev 5/18/2012
> 6 Includes
> 17 (16 from 2012) cases with type determination pending in which the
diagnosis of vCJD has been excluded.
> The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI)
and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases
of sporadic Creutzfeldt-Jakob disease (sCJD).
WELL, it seems the USA mad cow strains in humans classified as type
determination pending tdpCJD, VPSPr, sFFI, and sCJD) have steadily increased
over the years, and the same old song and dance continues with sporadic CJD
cases $$$
CJD CANADA WINTER 2012
*** 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.
there has never been a proven case of any spontaneous TSE prion disease in
the wild.
85%+, of all human TSE prion disease i.e. sporadic CJD, is NOT a
happenstance of bad luck, from a twisted up funked out protein, that just
happens to get all twisted up over nothing...
lost my mom to the hvCJD confirmed...just made a promise to her way
back...DOD 12/14/97 layperson
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
Thank you for submitting a comment on the following Notice:
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For related information,
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Notice of Availability of a National Animal Health Laboratory Network Reorganization Concept Paper
Action
Notice of availability and
request for comments.
Summary
We are advising the public that
the Animal and Plant Health Inspection Service is making available a concept
paper that describes a revised structure for the National Animal Health
Laboratory Network (NAHLN) for public review and comment. The NAHLN is a
nationally coordinated network and partnership of Federal, State, and
university-associated animal health laboratories working to protect animal and
public health and the nation's food supply by providing diagnostic testing aimed
at detecting biological threats to the nation's food animals. The concept paper
we are making available for comment presents a structure we believe will give
the NAHLN increased capacity and flexibility to detect and respond to emerging
and zoonotic diseases.
Dates
We will consider all comments
that we receive on or before June 24, 2013.
Addresses
You may submit comments by either
of the following methods:
- Federal eRulemaking Portal: Go to http://www.regulations.gov/#!documentDetail;D=APHIS-2012-0105-0001.
- Postal Mail/Commercial Delivery: Send your comment to Docket No.APHIS-2012-0105, Regulatory Analysis and Development, PPD, APHIS, Station 3A-03.8, 4700 River Road Unit 118, Riverdale, MD 20737-1238.
Supporting documents and any
comments we receive on this docket may be viewed at
http://www.regulations.gov/#!docketDetail;D=APHIS-2012-0105 or in our
reading room, which is located in Room 1141 of the USDA South Building, 14th
Street and Independence Avenue SW., Washington, DC. Normal reading room hours
are 8 a.m. to 4:30 p.m., Monday through Friday, except holidays. To be sure
someone is there to help you, please call (202) 799-7039 before
coming.
For Further Information Contact
Dr. Sarah Tomlinson, Associate
Coordinator, National Animal Health Laboratory Network, Veterinary Services,
APHIS, 2140 Centre Avenue, Building B, Fort Collins, CO 80526; (970)
494-7152.
Supplementary Information
Background
The National Animal Health
Laboratory Network (NAHLN) is a nationally coordinated network and partnership
of Federal, State, and university-associated animal health laboratories working
to protect animal and public health and the nation's food supply by providing
diagnostic testing aimed at detecting biological threats to the nation's food
animals. Participating NAHLN laboratories are currently designated as Core,
Member, Contract, or Adjunct laboratories, depending on their testing
capacities, geographical distribution, and degree of specialization. Oversight
and administration of the NAHLN is provided by the United States Department of
Agriculture (USDA) through the Animal and Plant Health Inspection Service
(APHIS). Input and leadership is provided to the NAHLN by a Coordinating Council
composed of USDA and State regulatory animal health officials and State employee
representatives of NAHLN laboratories.
Since its inception in 2002, the
NAHLN has expanded from 12 to over 50 current active participating laboratories,
each with varying diagnostic capacities. The need and available technology for
diagnostic testing has also changed. Stakeholder feedback indicates that the
NAHLN's structure also needs to change in order to expand detection of emerging
and zoonotic diseases. To address stakeholder feedback, APHIS is considering
certain elements that we believe will ensure continuation of the NAHLN's
founding principles while responding to the need for additional flexibility and
capacity to address identified gaps in the nation's surveillance, detection, and
response capabilities.
The concept paper describes the
roles and responsibilities of the NAHLN Coordinating Council and offers a
revised structure for the NAHLN that would clarify opportunities for
participation by State-based NAHLN laboratories. Inclusion of State-based
laboratories in the NAHLN allows for greater proximity to and linkages with
producers and veterinarians, which is critical to early detection of foreign
animal and emerging diseases. Possible criteria and designations for various
levels of participation, including participation by private laboratories, are
set forth in the concept paper. Instead of using Core, Member, Contract, or
Adjunct laboratory designations, participating laboratories would be designated
as Level 1, 2, or 3, Affiliate Laboratory, or Specialty Laboratory, depending on
the criteria met by each participating laboratory. To maintain designation,
qualifying laboratories would undergo annual reviews to demonstrate adherence to
established NAHLN policies and procedures.
APHIS will consider all comments
received on the concept paper in determining the appropriate structure and
governance for the NAHLN. The concept paper for the revised structure of the
NAHLN may be viewed on the Regulations.gov Web site or in our reading room
(seeADDRESSESabove for a link to Regulations.gov and information on the location
and hours of the reading room). You may request paper copies of the document by
calling or writing to the person listed underFOR FURTHER INFORMATION CONTACT.
Please refer to the title of this document when requesting
copies.
Done in Washington, DC, this 18th day of
April 2013.
Kevin Shea,
Acting Administrator, Animal and Plant
Health Inspection Service.
[FR Doc. 2013-09733 Filed 4-23-13; 8:45
am]
BILLING CODE
3410-34-P
TSS
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