[Federal Register Volume 81, Number 73 (Friday, April 15, 2016)] [Notices]
[Page 22208] From the Federal Register Online via the Government Publishing
Office [www.gpo.gov] [FR Doc No: 2016-08651]
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Notices Federal Register
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This section of the FEDERAL REGISTER contains documents other than rules or
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Federal Register / Vol. 81, No. 73 / Friday, April 15, 2016 / Notices
[[Page 22208]]
DEPARTMENT OF AGRICULTURE
Animal and Plant Health Inspection Service
[Docket No. APHIS-2016-0029]
Secretary's Advisory Committee on Animal Health; Meeting
AGENCY: Animal and Plant Health Inspection Service, USDA.
ACTION: Notice of meeting.
-----------------------------------------------------------------------
SUMMARY: This is a notice to inform the public of the next meetings of the
Secretary's Advisory Committee on Animal Health. The meetings are being
organized by the Animal and Plant Health Inspection Service to discuss matters
of animal health.
DATES: The meetings will be held May 2, 2016, and June 16, 2016, from 11
a.m. to 1:30 p.m. eastern standard time.
ADDRESSES: The meetings will be conducted as multisite teleconferences.
Opportunities for public attendance are described in the Supplementary
Information section of this document.
FOR FURTHER INFORMATION CONTACT: Mrs. R.J. Cabrera, Designated Federal
Officer, VS, APHIS, 4700 River Road, Unit 34, Riverdale, MD 20737; (301)
851-3478; email: SACAH.Management@aphis.usda.gov.
SUPPLEMENTARY INFORMATION: The Secretary's Advisory Committee on Animal
Health (the Committee) advises the Secretary of Agriculture on matters of animal
health, including means to prevent, conduct surveillance on, monitor, control,
or eradicate animal diseases of national importance. In doing so, the Committee
will consider public health, conservation of natural resources, and the
stability of livestock economies.
Tentative topics for discussion during the May 2, 2016, meeting
include:
One Health [cir] U.S. Department of Agriculture Antimicrobial Resistance
Action Plan; and [cir] Zoonotic Diseases.
Tentative topics for discussion during the June 16, 2016, meeting
include:
Emerging Disease Response; and Comprehensive Integrated Animal Health
Surveillance.
A final agenda will be posted on the Committee Web site 2 weeks prior to
each scheduled meeting.
Those wishing to listen in on the meetings should complete a brief
registration form by clicking on the ``SACAH Meeting Sign-up'' button on the
Committee's Web site (http://www.aphis.usda.gov/animalhealth/sacah).
Members of the public may join the teleconference in ``listen- only'' mode by
dialing 1-800-619-4086 and then entering the public passcode, 4414646# for the
May 2 meeting, and 9786716# for the June 16 meeting.
Questions and written statements for the Committee's consideration may be
submitted up to 5 working days before each scheduled meeting. They may be sent
to SACAH.Management@aphis.usda.gov or mailed to the person listed in this notice
under FOR FURTHER INFORMATION CONTACT. Statements filed with the Committee must
include the name of the individual listed under FOR FURTHER INFORMATION CONTACT,
the docket number listed in this notice, and specify the meeting to which they
pertain.
This notice of meeting is given pursuant to section 10 of the Federal
Advisory Committee Act (5 U.S.C. App. 2).
Done in Washington, DC, this 11th day of April 2016. Kevin Shea,
Administrator, Animal and Plant Health Inspection Service. [FR Doc. 2016-08651
Filed 4-14-16; 8:45 am] BILLING CODE 3410-34-P
Greetings APHIS et al, I kindly wish to comment on APHIS [Docket No.
APHIS-2016-0029] Secretary's Advisory Committee on Animal Health, and my
comments are as follows, and thanks you kindly for allowing me to comment again.
I previously wrote back in February of 2016, but with great urgency, I must
write a follow up with very disturbing findings. More cases of CWD in TEXAS,
ARKANSAS explodes with CWD cases, WISCONSIN CWD is out of control, Europe Norway
just discovered it’s first case of Chronic Wasting disease CWD TSE Prion in a
wild Reindeer, and FDA et al are bringing up again FEED controls of animal
protein in an old DOCKET and reviving it; something I have been begging them to
do since 2003. however, it’s still NONBINDING. this DOCKET, ‘Docket No.
FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal
Feed’ MUST BE MADE MANDATORY.
THIS LOOPHOLE MUST BE CLOSED!
IF LEFT AS NON-BINDING LIKE THE LAST 15 YEARS, IT WILL BE AS WORTHLESS AS
THE LAST 15 YEARS, NOTHING BUT INK ON PAPER!
SEE MARCH 2016 UPDATE OF THIS VERY IMPORTANT DOCKET ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al,
I would kindly like to comment on ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
#158
Guidance for Industry
Use of Material from Deer and Elk in Animal Feed
This version of the guidance replaces the version made available
September15, 2003.
This document has been revised to update the docket number, contact
information, and standard disclosures. Submit comments on this guidance at any
time.
Submit electronic comments to http://www.regulations.gov. Submit written
comments to the Division of Dockets Management (HFA-305), Food and Drug
Administration, 5630 Fishers Lane, Rm. 1061, Rockville, MD 20852. All comments
should be identified with the Docket No. FDA-2003-D-0432 (formerly 03D-0186).
For further information regarding this guidance, contact Burt Pritchett,
Center for Veterinary Medicine (HFV-222), Food and Drug Administration, 7519
Standish Place, Rockville, MD 20855, 240-402-6276, E-mail:
burt.pritchett@fda.hhs.gov.
Additional copies of this guidance document may be requested from the
Policy and Regulations Staff (HFV-6), Center for Veterinary Medicine, Food and
Drug Administration, 7519 Standish Place, Rockville, MD 20855, and may be viewed
on the Internet at either http://www.fda.gov/AnimalVeterinary/default.htm
or http://www.regulations.gov.
U.S. Department of Health and Human Services Food and Drug Administration
Center for Veterinary Medicine March 2016
Contains Nonbinding Recommendations
2
Guidance for Industry Use of Material from Deer and Elk in Animal Feed
This guidance represents the current thinking of the Food and Drug
Administration (FDA or Agency) on this topic. It does not establish any rights
for any person and is not binding on FDA or the public. You can use an
alternative approach if it satisfies the requirements of the applicable statutes
and regulations. To discuss an alternative approach, contact the FDA office
responsible for this guidance as listed on the title page.
I. Introduction
Under FDA’s BSE feed regulation (21 CFR 589.2000) most material from deer
and elk is prohibited for use in feed for ruminant animals. This guidance
document describes FDA’s recommendations regarding the use in all animal feed of
all material from deer and elk that are positive for Chronic Wasting Disease
(CWD) or are considered at high risk for CWD. The potential risks from CWD to
humans or non-cervid animals such as poultry and swine are not well understood.
However, because of recent recognition that CWD is spreading rapidly in
white-tailed deer, and because CWD’s route of transmission is poorly understood,
FDA is making recommendations regarding the use in animal feed of rendered
materials from deer and elk that are CWD-positive or that are at high risk for
CWD.
In general, FDA’s guidance documents do not establish legally enforceable
responsibilities. Instead, guidances describe the Agency’s current thinking on a
topic and should be viewed only as recommendations, unless specific regulatory
or statutory requirements are cited. The use of the word should in Agency
guidances means that something is suggested or recommended, but not required.
II. Background
CWD is a neurological (brain) disease of farmed and wild deer and elk that
belong in the animal family cervidae (cervids). Only deer and elk are known to
be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer, white-tailed deer, North American elk, and in farmed
black-tailed deer. CWD belongs to a family of animal and human diseases called
transmissible spongiform encephalopathies (TSEs). These include bovine
spongiform encephalopathy (BSE or “mad cow” disease) in cattle; scrapie in sheep
and goats; and classical and variant Creutzfeldt-Jakob diseases (CJD and vCJD)
in humans. There is no known treatment for these diseases, and there is no
vaccine to prevent them. In addition, although validated postmortem diagnostic
tests are available, there are no validated diagnostic tests for CWD that can be
used to test for the disease in live animals.
Contains Nonbinding Recommendations
III. Use in animal feed of material from CWD-positive deer and elk
Material from CWD-positive animals may not be used in any animal feed or
feed ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and
Cosmetic Act, animal feed and feed ingredients containing material from a
CWD-positive animal would be considered adulterated. FDA recommends that any
such adulterated feed or feed ingredients be recalled or otherwise removed from
the marketplace.
IV. Use in animal feed of material from deer and elk considered at high
risk for CWD Deer and elk considered at high risk for CWD include: (1) animals
from areas declared by State officials 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 immediately before the time of slaughter were in a captive herd that
contained a CWD-positive animal.
FDA recommends that materials from deer and elk considered at high risk for
CWD no longer be entered into the animal feed system. Under present
circumstances, FDA is not recommending that feed made from deer and elk from a
non-endemic area be recalled if a State later declares the area endemic for CWD
or a CWD eradication zone. In addition, at this time, FDA is not recommending
that feed made from deer and elk believed to be from a captive herd that
contained no CWD-positive animals be recalled if that herd is subsequently found
to contain a CWD-positive animal.
V. Use in animal feed of material from deer and elk NOT considered at high
risk for CWD FDA continues to consider materials from deer and elk NOT
considered at high risk for CWD to be acceptable for use in NON-RUMINANT animal
feeds in accordance with current agency regulations, 21 CFR 589.2000. Deer and
elk not considered at high risk include: (1) deer and elk from areas not
declared by State officials to be endemic for CWD and/or to be CWD eradication
zones; and (2) deer and elk that were not at some time during the 60-month
period immediately before the time of slaughter in a captive herd that contained
a CWD-positive animal.
3
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al,
MY comments and source reference of sound science on this very important
issue are as follows ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
I kindly wish to once again submit to Docket No. FDA-2003-D-0432 (formerly
03D-0186) Use of Material from Deer and Elk in Animal Feed.
Thank you kindly for allowing me to comment again, ...and again...and
again, on a topic so important, why it is ‘NON-BINDING’ is beyond me.
this should have been finalized and made ‘BINDING’ or MANDATORY OVER A
DECADE AGO.
but here lay the problem, once made ‘BINDING’ or ‘MANDATORY’, it is still
nothing but ink on paper.
we have had a mad cow feed ban in place since August 1997, and since then,
literally 100s of millions of pounds BANNED MAD COW FEED has been sent out to
commerce and fed out (see reference materials).
ENFORCEMENT OF SAID BINDING REGULATIONS HAS FAILED US TOO MANY TIMES.
so, in my opinion, any non-binding or voluntary regulations will not work,
and to state further, ‘BINDING’ or MANDATORY regulations will not work unless
enforced.
with that said, we know that Chronic Wasting Disease CWD TSE Prion easily
transmits to other cervid through the oral route.
the old transmission studies of BSE TSE floored scientist once they figured
out what they had, and please don’t forget about those mink that were fed 95%+
dead stock downer cow, that all came down with TME. please see ;
It is clear that the designing scientists must also have shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
SEE MAD COW FEED VIOLATIONS AFER MAD COW FEED VIOLATIONS ;
SEE WHAT DEFRA MAFF ET AL SAID JUST LAST MONTH ABOUT THIS ;
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Sheep and cattle may be exposed to CWD via common grazing areas with
affected deer but so far, appear to be poorly susceptible to mule deer CWD
(Sigurdson, 2008).
***In contrast, cattle are highly susceptible to white-tailed deer CWD and
mule deer CWD in experimental conditions but no natural CWD infections in cattle
have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how
susceptible humans are to CWD but given that the prion can be present in muscle,
it is likely that humans have been exposed to the agent via consumption of
venison (Sigurdson, 2008). Initial experimental research, however, suggests that
human susceptibility to CWD is low and there may be a robust species barrier for
CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD
is affecting wild and farmed cervid populations in endemic areas with some deer
populations decreasing as a result.
snip...
For the purpose of the qualitative risk assessment developed here it is
necessary to estimate the probability that a 30-ml bottle of lure contains urine
from an infected deer. This requires an estimate of the proportion of deer herds
in the USA which are infected with CWD together with the within herd
prevalence.
The distribution map of CWD in US shows it is present mainly in central
states (Figure 1). However, Virginia in the east of the country has recorded
seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take
steps to prevent urine being taken from infected animals eg by sourcing from
farms where the deer are randomly tested for CWD (Anon 2015a). However, if
disease is already present and testing is not carried out regularly, captive
populations are not necessarily disease free (Strausser 2014). Urine-based deer
lures have been known to be collected from domestic white-tailed deer herds and
therefore there is a recognised risk. This is reflected by 6 US States which
have
14
banned the use of natural deer urine for lures, as the deer urine may be
sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For
example, the US State of Virginia is banning the use of urine-based deer lures
on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska
banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned
urine-based deer lures and acknowledged that there is no way to detect their use
(Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it
appears that up to 50% of deer herds can be infected with 80-90% of animals
infected within some herds.
*** It is therefore assumed that probability that a 30-ml bottle of deer
urine lure imported from the USA is sources from an infected deer is
medium.
SNIP...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. ***For elk and deer
considered at high risk for CWD, the FDA recommends that these animals do not
enter the animal feed system. ***However, this recommendation is guidance and
not a requirement by law.
***Animals considered at high risk for CWD include:
***1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
***2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
***Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants. The
amount of animal PAP that is of deer and/or elk origin imported from the USA to
GB cannot be determined, however, as it is not specified in TRACES. It may
constitute a small percentage of the very low tonnage of non-fish origin
processed animal proteins that were imported from US into GB.
*** Overall, therefore, it is considered there is a greater than negligible
risk that (non-ruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB. There is uncertainty associated with this estimate
given the lack of data on the amount of deer and/or elk protein possibly being
imported in these products.
SNIP...
Summary and MORE HERE ;
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids, as well as non-ruminants such as cats and dogs as
well, as soon as possible for the following reasons...
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
I previously wrote ;
Sent: Saturday, February 06, 2016 12:11 PM To:
SACAH.Management@aphis.usda.gov Subject: Secretary's Advisory Committee on
Animal Health; Meeting [Docket No. APHIS-2016-0007] Singeltary Submission
SNIP...
I have wasted (it seems) a lifetime (17+ years), just about every day since
December 14, 1997, trying to warn the world about the Transmissible Spongiform
Encephalopathy TSE Prion disease aka mad cow type disease. from state to state,
county to county, country to country, the TSE Prion disease know no borders,
they know no borders, and or know no age groups. from mad cow disease BSE in the
bovine, or back to sheep or humans or deer, the same for sheep scrapie, and or
chronic wasting disease cwd of cervid, and or all the atypical strains, and yes
there are more than one strain of cwd in cervid. that’s what makes the tse prion
disease so very difficult to understand, that and the incubation period, but
once these tse prion disease start to mutate, it’s a whole new ball game. I
don’t nor have I ever stated or portrayed myself as any expert with TSE prion
disease, but I have followed the science day by day as these mad cow follies
played out starting back in 1997, when I watched my mother die from the
Heidenhain Variant of Creutzfeldt Jakob Disease, a terrible horrible thing to
see a loved one die from, and then have the feds tell you it’s not here, it’s
all spontaneous or sporadic, while watching Oprah on T.V. fighting Cactus cattle
feeders over what she had said. I about fell about of bed that night back then.
I am not anti-meat, anti-gun, anti-hunt, what I am is anti-stupid, and
there has been enough stupid to go around for everybody over the past 3 or 4
decades in handling this TSE Prion disease due to the money factor, God protect
the industry at all cost mentality. you don’t think this happens, and this is
just another conspiracy theory, then just think back to Tobacco and Asbestos,
and that long incubating killer disease, and then think if it can happen or not,
hell, it already has. this is just another fine example of lobbied corporate
politics making bad terrible bad policy, just to save the industry, to hell with
human and animal health. it’s true, I am not making this up, the BSE MRR policy
will come back to haunt every country that wanted it, and rightfully so. I know
I have been a thorn in USDA, APHIS, FSIS, FDA, CDC et al behind, but it was for
a reason, no one should have to die or be at risk from the Transmissible
Spongiform Encephalopathy TSE Prion disease, just because of corporate interest
or special interest group, because it’s a long incubation disease and to date
it’s hard for trace back or friendly fire i.e. iatrogenic, the pass if forward
mode of transmission. oh, it’s real too, just not documented much, again, due to
long incubation. the risk factors from BSE, Scrapie, and CWD are all and have
been proven to be a risk factor for humans now. all one has to to is sit down
and read the history of the science, and the most update science. or, you can
let the industry fed junk science rule the day, which is what’s happening right
now in TEXAS with CWD (like BSE in cattle in Texas), where TEXAS will change the
science to suit their need $$$ i.e. if CWD live testing is approved before the
CWD test itself is validated at 100 % validated, by validated TSE prion
scientist around the world, not the industry itself. remember, in Texas, if
you’re in the cervid business, even if you own your own game farm, you can
validate yourself via a short program, to take your own samples from suspect CWD
deer to be tested i.e., thus the OBEX only testing in Texas is very handy, to
discard some very suspect CWD positive deer, which is the case now with two
suspect cwd in captive, that were deemed not positive, due to not confirmed in
both the Obex and Lymphnoids, so it is not conclusive. case closed. hmmm, where
did I hear this before in Texas. OH YES, that was the infamous 2nd Texas mad cow
that was covered up, until scientist from around the world, and myself, wrote
the OIG the Honorable Phyllis Fong. Finally, 7 months later, that Texas mad cow
was finally confirmed, only after the BSE MRR policy was ratified, the legal
trading of the TSE Prion globally. oh, I am not making this up either ;
Thursday, October 22, 2015
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk
mad cow disease USDA and what really happened ***
if we don’t get serious about the TSE Prion disease, all of them, and what
we really need to do, and do it, it may be too late.
some of the industry claims that cwd has been here a long time and will
just die out.
I don’t believe that, and how did that work our for Scrapie (same as cwd).
if we continue to ignore the CWD TSE prion, it will only get worse.
all hunter kill cervid must be tested for CWD, this should be mandatory in
every state, and it should say it on your tags.
you can’t have one state making up a set of cwd tse prion rules based on
how they might read the science and policy there from, and not have the rest of
the states reading the science the same way and making the same policy making
decisions for the cwd tse prion, and then import and export between them. it
just does not work.
the states must get on the same page, and the only way that will happen is
to have it mandatory and regulated by the feds, however, we must make sure the
feds are on the same page with sound science, and in doing this, we must have
sound cwd tse prion policy making, from science by scientist, not by paid
lobbyist, politicians, or scientist they have in their pockets$
stop all transport of cervid and cervid carcasses from state to state, any
and all parts, and even between counties in one state where cwd risk factor is.
trucking cwd tse prion around is a real risk factor, down to the dirt on
the tires, and dirt on the clothes or shoes of any person or animal that has
been exposed to cwd tse prion.
cwd tse prion has the capabilities of exposing water tables, land, the
surrounding environment, fence line, furniture, and plants, down to the knife
and equipment you use to clean a deer or elk.
stop baiting period. the congregation of cervid by unnatural means whether
or not it’s a pile of corn or a field of planted lettuce and such, bottom line,
you congregate cervid in one place, and over time, the shedding of the CWD TSE
Prion will load up the environment, and given enough time, everything will be
exposed or contaminated.
stop urine use for scents.
stop the use of mineral blocks.
stop the feeding grounds at state parks.
stop the loophole that still allows animal protein being fed to cervid.
cwd tse prion testing must be enhanced in all states, with a large increase
in all cwd tse prion testing across the board.
scorched earth policy must be adhered to. kill everything, and test it with
validated cwd tse prion test, until a live validated test is ready, one that can
guaranty without any doubt, to be 100% in all cervid, of all age groups.
killing and field dressing a cervid in the wild has it’s risk factors for
the cwd tse prion to spread, due to environmental risk factors, if that cervid
is infected with CWD tse prion. proper carcass disposal is critical.
game farms help spread cwd, simple fact. it’s been proven. game farms are
not the only risk factor though, however, they are a big part of the problem,
history shows this.
the quarantine of cwd tse prion infected game farms must be extended to 16
years now.
the CWD LOTTO ENTITLEMENT of captive game farms where the states pays game
farms for CWD MUST BE STOPPED. if the cwd infected farm does not buy insurance
for any and all loss from CWD for them and any party that does business with
them, and or any loss to the state, and or any products there from, that’s to
bad, they should never be allowed to be permitted. in fact, for any state that
does allow game farming, urine mills, sperm mills, antler mills, velvet mills,
big high fence ranch, little low fence farm, in my opinion, it’s that states
responsibility to protect that state, thus, any states that allow these farms
and business there from, it should be mandatory before any permit is allowed,
that game farm must have enough personal insurance that would cover that farm,
any farm that does business with them, and or any products there from, and the
state, before such permit is issued. personally, I am sick and tired of all the
big ag entitlement programs, and that’s all cwd indemnity is. in fact, the USDA
CWD INDEMNITY PROGRAM, should read, THE USDA CWD ENTITLEMENT PROGRAM.
we cannot, and must not, let the industry regulate itself, especially with
the junk science they try to use. it’s just not working, and it’s been going on
long enough.
if they are not going to be science based, they must be banned.
science has told us for 3 decade or longer, that these are the things that
_might_ work, yet thanks to the industry, and government catering to industry,
regulations there from have failed, because of catering to the industry, and the
cwd tse prion agent has continued to spread during this time. a fine example is
Texas.
snip...see full text of my previous comment with source references ; From:
Terry S. Singeltary Sr. Sent: Saturday, February 06, 2016 12:11 PM To:
SACAH.Management@aphis.usda.gov Subject: Secretary's Advisory Committee on
Animal Health; Meeting [Docket No. APHIS-2016-0007] Singeltary Submission
Hello Mrs. R.J. Cabrera and USDA et al,
I would kindly like to submit and comment on the Secretary's Advisory
Committee on Animal Health; Meeting [Docket No. APHIS-2016-0007] ;
WITH GREAT URGENCY, I MUST UPDATE MY COMMENT PLEASE, AS FOLLOWS ;
Arkansas CWD outbreak
Since this last comment, Arkansas has had a great outbreak of Chronic
Wasting disease CWD, and this is very disturbing as to how many cases of CWD
that have been found, in such a small sample survey. see ;
“At this time, 61 out of the 266 random samples taken by the AGFC from the
focal area have tested positive,” Baxter said. “That’s a prevalence rate of 22
percent from the results we’ve received.”
Texas more CWD cases found
Saturday, April 02, 2016
TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER
BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Friday, February 05, 2016
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER
RELEASE SITE
Friday, April 08, 2016
Arkansas AGFC Chronic Wasting Disease CWD TSE Prion Confirms 23 Additional
Cases Total At 79 To Date
Friday, April 01, 2016
ARKANSAS CHRONIC WASTING DISEASE CWD TSE PRION CASES EXPLODE BY 27 NEW
CASES WITH 50 CASES TOTAL TO DATE
WISCONSIN CWD CASES OUT OF CONTROL
Wednesday, March 16, 2016 Wisconsin CWD sample survey 2015 confirms 290
cases of Chronic Wasting Disease TSE Prion
KANSAS CWD CASES ALARMING
Wednesday, March 02, 2016 Kansas Chronic Wasting Disease CWD TSE Prion 52
cases 2015 updated report 'ALARMING'
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive for CWD in the Oswego
zone of Kendall County
I could go on, for more see ;
Thursday, March 31, 2016
*** Chronic Wasting Disease CWD TSE Prion Roundup USA April 1, 2016
***
NOW, THE GREAT URGENCY PART ;
EUROPE NORWAY DETECTS FIRST CASE OF CHRONIC WASTING DISEASE CWD TSE PRION
IN WILD REINDEER
The first detection of Chronic Wasting Disease (CWD) in Europe Published:
04/04/2016 6:27 pm Last modified: 05/04/2016 4:00 pm
The first detection of Chronic Wasting Disease (CWD) in Europe Reinsdyr.
Foto: Colourbox.
The Norwegian Veterinary Institute has diagnosed Chronic Wasting Disease
(CWD) in a free-ranging reindeer from the Nordfjella population in South-Norway.
CWD is a lethal disease in cervids. The disease is well known in North America;
however this is the first detection of CWD in Europe. Also, this is the first
detection of natural infection in reindeer worldwide. This news includes a video
with expert interviews.
-The sick female reindeer (Rangifer tarandus tarandus) was detected in the
middle of March 2016 in connection with capture for GPS-collaring using
helicopter performed by the Norwegian Institute for Nature Research (NINA. It
died and the carcass was submitted to the Norwegian Veterinary Institute in Oslo
for necropsy and laboratory examinations. It was an adult animal, says wildlife
pathologist Turid Vikøren at Norwegian Veterinary Institute, who performed the
necropsy.
The body condition of the reindeer was below medium, but it had still some
adipose tissue left. In cervids older than 18 months, we routinely collect
sample of the brain for CWD examination as part of the national surveillance
program for CWD, and that was also done in this reindeer, Vikøren
continues.
The head of the Norwegian Reference Laboratory for animal prion diseases at
Norwegian Veterinary Institute, Sylvie Benestad, states that the brain sample
from the reindeer was positive for the detection of prions both by the first
routine test (ELISA-test) and in two supplementary tests (Western Blotting,
Immunohistochemistry).
SEE VIDEO ;
The disease
Chronic Wasting Disease is a contagious neurological disease that attacks
the brain of cervids. CWD belongs to a group of diseases known as Transmissible
Spongiform Encephalopathies (TSEs), in which the infectious agents are known to
be the prion protein, a normal protein that misfolds and destroys the brain. The
development of the disease is slow and affected cervids show loss of body
condition and altered behaviour. Death is inevitable once clinical disease
occurs.
CWD is an endemic disease in North America, in which natural infections
occurs in mule deer (Odocoileus hemionus), white-tailed deer (O. virginianus),
elk (Cervus elaphus nelsoni) og moose (Alces alces shirasi).The reindeer from
Norway represents the first detection of CWD in Europe. Also, this is the first
detection of a natural infection in reindeer worldwide.
The brain from the reinsdeer. Photo: Sylvie Lafond Benestad, Norwegian
Veterinary Institute.
The brain from the reinsdeer. Photo: Sylvie Lafond Benestad, Norwegian
Veterinary Institute.
Prions from microscope. Photo: Sylvie Lafond Benestad, Norwegian Veterinary
Institute.
Prions from microscope. Photo: Sylvie Lafond Benestad, Norwegian Veterinary
Institute.
The Norwegian Veterinary Institute will take the initiative to follow-up
surveys of this disease in the Norwegian wild reindeer populations.
Contacts....
Turid Vikøren (Wildlife Health) turid.vikoren@vetinst.no
Kjell Handeland (Wildlife Health) kjell.handeland@vetinst.no
Sylvie Benestad (Prions Diseases) sylvie.benestad@vetinst.no
Jorun Jarp, Head of Dep. of Health Surveillance jorun.jarp@vetinst.no
Mobile: 90056216.
Asle Haukaas, Communication Director asle.haukaas@vetinst.no Mobile:
92080877.
Sunday, April 10, 2016
Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion
disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer
(Rangifer tarandus tarandus)
Saturday, April 9, 2016
The Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion
disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer
(Rangifer tarandus tarandus)
Department for Environment, Food and Rural Affairs
Thursday, January 29, 2015
Atypical H-TYPE BSE Case Confirmed in Norway
Monday, April 11, 2016
*** DECLARATION OF EXTRAORDINARY EMERGENCY DUE TO A FOREIGN ANIMAL DISEASE
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION CHRONIC WASTING DISEASE CWD IN
THE UNITED STATES AND NORTH AMERICA ?
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Sheep and cattle may be exposed to CWD via common grazing areas with
affected deer but so far, appear to be poorly susceptible to mule deer CWD
(Sigurdson, 2008).
***In contrast, cattle are highly susceptible to white-tailed deer CWD and
mule deer CWD in experimental conditions but no natural CWD infections in cattle
have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how
susceptible humans are to CWD but given that the prion can be present in muscle,
it is likely that humans have been exposed to the agent via consumption of
venison (Sigurdson, 2008). Initial experimental research, however, suggests that
human susceptibility to CWD is low and there may be a robust species barrier for
CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD
is affecting wild and farmed cervid populations in endemic areas with some deer
populations decreasing as a result.
snip...
For the purpose of the qualitative risk assessment developed here it is
necessary to estimate the probability that a 30-ml bottle of lure contains urine
from an infected deer. This requires an estimate of the proportion of deer herds
in the USA which are infected with CWD together with the within herd
prevalence.
The distribution map of CWD in US shows it is present mainly in central
states (Figure 1). However, Virginia in the east of the country has recorded
seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take
steps to prevent urine being taken from infected animals eg by sourcing from
farms where the deer are randomly tested for CWD (Anon 2015a). However, if
disease is already present and testing is not carried out regularly, captive
populations are not necessarily disease free (Strausser 2014). Urine-based deer
lures have been known to be collected from domestic white-tailed deer herds and
therefore there is a recognised risk. This is reflected by 6 US States which
have
14
banned the use of natural deer urine for lures, as the deer urine may be
sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For
example, the US State of Virginia is banning the use of urine-based deer lures
on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska
banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned
urine-based deer lures and acknowledged that there is no way to detect their use
(Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it
appears that up to 50% of deer herds can be infected with 80-90% of animals
infected within some herds.
*** It is therefore assumed that probability that a 30-ml bottle of deer
urine lure imported from the USA is sources from an infected deer is
medium.
SNIP...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. ***For elk and deer
considered at high risk for CWD, the FDA recommends that these animals do not
enter the animal feed system. ***However, this recommendation is guidance and
not a requirement by law.
***Animals considered at high risk for CWD include:
***1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
***2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
***Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants. The
amount of animal PAP that is of deer and/or elk origin imported from the USA to
GB cannot be determined, however, as it is not specified in TRACES. It may
constitute a small percentage of the very low tonnage of non-fish origin
processed animal proteins that were imported from US into GB.
*** Overall, therefore, it is considered there is a greater than negligible
risk that (non-ruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB. There is uncertainty associated with this estimate
given the lack of data on the amount of deer and/or elk protein possibly being
imported in these products.
SNIP...
Summary and MORE HERE ;
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission ***UPDATED MARCH 2016***
Tuesday, March 15, 2016
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information Singeltary Submission
***SO, my question, why is it the OIE and other trade officials and policy
making there from, knowing that the USA and Canada, with not a clue about
Mexico, why is it that nobody has Declared an EXTRAORDINARY EMERGENCY DUE TO A
FOREIGN ANIMAL DISEASE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION CHRONIC
WASTING DISEASE CWD IN THE UNITED STATES AND NORTH AMERICA ?
well, since no one else will, than I must.
Terry S. Singeltary Sr. Declares a DECLARATION OF EXTRAORDINARY EMERGENCY
DUE TO A FOREIGN ANIMAL DISEASE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE
PRION CHRONIC WASTING DISEASE CWD IN THE UNITED STATES AND NORTH AMERICA.
The elephant in the room I was speaking of that we all have missed was the
feed, yes we all know of ruminant and non ruminant protein and risk factors
there from with TSE Prion disease, but we missed the rest of the feed i.e. FEED
GRAINS. YES, science has shown in the past, and now recently, the shedding of
the CWD TSE Prion into the environment is indeed a risk factor, and for all the
grains and such that goes into feed, even hay, hell, Norway does not require any
APHIS-Veterinary Services certification for the import of hay/straw. see for
yourself ;
Hay/Straw
Norway does not require any APHIS-Veterinary Services certification for the
import of hay/straw.
you add up all the other grains in feed, and then wonder about exposure to
the CWD TSE PRION from cervid and risk factor from the CWD there from via
shedding or right down to the soil these grains were grown in, and you have a
world of problems. see ;
Feed Grains Data: Yearbook Tables Created March 10, 2016 Updates of this
data, and data covering more years and countries, can be found at
U.S. Acreage, Production, Yield, and Farm Price Table 1--Corn, sorghum,
barley, and oats: Planted acreage, harvested acreage, production, yield, and
farm price World Production, Supply, and Disappearance
Table 2--Foreign coarse grains: Supply and disappearance
Table 3--Feed grains (corn, sorghum, barley, and oats): Supply and
disappearance U.S. Supply and Disappearance
Table 4--Corn: Supply and disappearance
Table 5--Sorghum: Supply and disappearance
Table 6--Barley: Supply and disappearance
Table 7--Oats: Supply and disappearance U.S. Production, Yield, and Stocks
Table 8--Hay: Production, harvested acreage, yield, and stocks Domestic and
International Prices
Table 9--Corn and sorghum: Average prices received by farmers, United
States
Table 10--Barley and oats: Average prices received by farmers, United
States
Table 11--Hay: Average prices received by farmers, United States
Table 12--Corn: Cash prices at principal markets
Table 13--Sorghum: Cash prices at principal markets
Table 14--Barley and oats: Cash prices at principal markets
Table 15--Feed-price ratios for livestock, poultry, and milk Table
16--Byproduct feeds: Average wholesale price, bulk, specified markets Table
17--Processed corn products: Quoted market prices Exports and Imports Table
18--U.S. corn and sorghum exports Table 19--U.S. barley and oats exports Table
20--U.S. corn and sorghum imports Table 21--U.S. barley and oats imports Table
22--U.S. corn and sorghum exports by selected destinations Table 23--U.S. barley
and oats exports by selected destinations Table 24--U.S. corn and sorghum
imports by selected sources Table 25--U.S. barley and oats imports by selected
sources Table 26--U.S. white corn exports by selected destinations Table
27--World coarse grain trade: Selected exporters and importers by commodity Rail
rates and shipments Table 28--Rail rates and grain shipments Processed feeds and
animal unit indexes Table 29--Processed feeds: Quantities fed and feed per
grain-consuming animal unit Table 30--Indexes of feed consuming animal units
Feed, seed, and industrial uses Table 31—Corn: Feed, seed, and industrial uses
Exports and imports for ethyl alcohol and brewers’ and distillers’ dregs and
waste Table 32—U.S. exports of ethyl alcohol by selected destinations Table
33—U.S. imports of ethyl alcohol by selected sources Table 34—U.S. exports of
brewers’ and distillers’ dregs and waste by selected commodities Table 35—U.S.
imports of brewers’ and distillers’ dregs and waste by selected sources Contact:
Thomas Capehart at tcapehart+A25@ers.usda.gov
‘’The statement you were concerned about was corrected to "One sorghum DDGS
out of 168 DG samples was contaminated with animal protein prohibited for use in
ruminant feed and was channeled to poultry feed."
From: Terry S. Singeltary Sr.
Sent: Thursday, October 01, 2015 9:18 PM
To: parias@ksat.com
Subject: Re: TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE
PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
***UDATED CORRECTION BY AUTHOR...SEE EMAIL TO ME...terry
From: Kyung-Min Lee Sent: Thursday, October 01, 2015 1:39 PM
To: Terry S. Singeltary Sr. ; BSE-L@LISTS.AEGEE.ORG
Cc: CJD-L@LISTS.AEGEE.ORG ; cjdvoice@yahoogroups.com ;
bloodcjd@yahoogroups.com ; jcattanach@foodprotection.org ; cnc3@psu.edu ;
dloynachan@foodprotection.org ; lhovey@foodprotection.org ; Timothy J. Herrman
Subject: RE: TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE
PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
Dear Terry S. Singeltary Sr.
Thank for your interest and concern about our published article entitled
“Evaluation of Selected Nutrients and Contaminants in Distillers Grains from
Ethanol Production in Texas”. I should apologize you and others that there were
some errors and misleading statements in this article due to inappropriate
terminology. The statement you were concerned about was corrected to "One
sorghum DDGS out of 168 DG samples was contaminated with animal protein
prohibited for use in ruminant feed and was channeled to poultry feed." We
requested the journal editor to correct some errors and the relevant statements,
or to withdraw the article from the journal.
Again I sincerely apologize for any confusion and inconvenience this may
cause. Thanks.
best wishes,
Kyung-Min
Kyung-Min Lee, Ph. D. Research Scientist Office of the Texas State
Chemist
Texas A&M AgriLife Research P.O. Box 3160, College Station, TX
77841-3160 Phone: 979-845-4113 (ext 132) Email:kml@otsc.tamu.edu Fax:
979-845-1389
snip...end...tss
my link corrected
Sunday, September 27, 2015
TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE
SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
kind regards, terry
From: Terry S. Singeltary Sr.
Sent: Monday, September 28, 2015 8:30 PM
To: parias@ksat.com
Subject: Fw: TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE
PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
From: Terry S. Singeltary Sr.
Sent: Sunday, September 27, 2015 4:39 PM
Cc: CJD-L@LISTS.AEGEE.ORG ; cjdvoice@yahoogroups.com ;
bloodcjd@yahoogroups.com ; jcattanach@foodprotection.org ; cnc3@psu.edu ;
dloynachan@foodprotection.org ; lhovey@foodprotection.org ; kml@otsc.tamu.edu
Subject: TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE
PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
TEXAS One sorghum DDGS sample out of 168 DG samples was contaminated with
bovine spongiform encephalopathy, but the transmission route of the bovine
spongiform encephalopathy agent could not be clearly defined.
J Food Prot. 2015 Oct;78(10):1861-9. doi: 10.4315/0362-028X.JFP-15-157.
Evaluation of Selected Nutrients and Contaminants in Distillers Grains from
Ethanol Production in Texas.
Lee KM1, Herrman TJ2. Author information 1Office of the Texas State
Chemist, Texas A&M AgriLife Research, Texas A&M University System,
College Station, Texas 77841, USA. kml@otsc.tamu.edu. 2Office of the Texas State
Chemist, Texas A&M AgriLife Research, Texas A&M University System,
College Station, Texas 77841, USA.
Abstract
This study evaluated distillers grain (DG) by-products produced in
different ethanol plants and supplemented in animal diets in Texas, based on
samples analyzed from 2008 to 2014. The samples were assessed for concentration,
occurrence, and prevalence of selected nutrients and contaminants. Protein and
sulfur contents of DG were largely different between corn and sorghum
by-products as well as wet distillers grain with solubles and dry distillers
grain with solubles (DDGS), indicating a significant effect of grain feedstock
and dry-grind process stream on DG composition and quality. Salmonella was
isolated in 4 DDGS samples out of a total of 157 DG samples, a percentage (2.5%)
that is much lower than the percentage of Salmonella-positive samples found in
other feed samples analyzed during the same period. A small amount of
virginiamycin residue was found in 24 corn DDGS, 1 corn wet distillers grain
with solubles, and 2 sorghum DDGS samples out of 242 samples in total. One
sorghum DDGS sample out of 168 DG samples was contaminated with bovine
spongiform encephalopathy, but the transmission route of the bovine spongiform
encephalopathy agent could not be clearly defined. The concentrations of
aflatoxin and fumonisin DG by-products averaged 3.4 ÎĽg/kg and 0.7 mg/kg,
respectively. Among contaminated corn DG samples, five DDGS samples for
aflatoxin contained a higher concentration than the U.S. Food and Drug
Administration action level for use in animal feed, whereas no sample for
fumonisin was found above the action level. The study results raised some
important issues associated with the quality and use of DG by-products,
suggesting several approaches and strategies for their effective and safe use as
a feed ingredient to promote animal and human health and welfare.
PMID: 26408135 [PubMed - in process]
Terry S. Singeltary Sr. Declares a DECLARATION OF EXTRAORDINARY EMERGENCY
DUE TO A FOREIGN ANIMAL DISEASE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE
PRION CHRONIC WASTING DISEASE CWD IN THE UNITED STATES AND NORTH AMERICA.
it’s time someone steps up to the plate (OIE ...LMAO!), and declare an
extraordinary emergency for foreign animal disease due to Chronic Wasting
Disease or Cervid Spongiform Encephalopathy TSE Prion disease from the United
States of America, Canada, and Mexico i.e. North America, before this damn
disease is spread to hell and back, and you can just throw in there BSE and
Scrapie just for grins. ...and I ain’t grinning Sad smile OIE, you have
floundered too long with mad cow type TSE Prion disease...
Saturday, April 9, 2016
The Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion
disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer
(Rangifer tarandus tarandus)
Department for Environment, Food and Rural Affairs
NORTH AMERICA IS ALREADY RESPONSIBLE FOR SHIPPING CWD TO KOREA, HOW MANY
MORE COUNTRIES MUST FALL DUE TO THE OIE AND THE USDA $$$
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
Potential role of soil properties in the spread of CWD in western
Canada
Alsu Kuznetsova, Debbie McKenzie, Pamela Banser, Tariq Siddique & Judd
M. Aiken
Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted
Infectivity from Complex Solutions (BASICS)
Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted
Infectivity from Complex Solutions (BASICS) A. Christy Wyckoff, Krista L.
Lockwood, Crystal Meyerett-Reid, Brady A. Michel, Heather Bender, Kurt C.
VerCauteren, Mark D. Zabel PLOS x Published: March 4, 2013 http://dx.doi.org/10.1371/journal.pone.0058630
Behavior of Prions in the Environment: Implications for Prion Biology
Shannon L. Bartelt-Hunt1*, Jason C. Bartz2*
Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of
Prion Infection A. Christy Wyckoff1, 2 n1 , Nathan Galloway3 n1 , Crystal
Meyerett-Reid1 , Jenny Powers4 , Terry Spraker1 , Ryan J. Monello4 , Bruce
Pulford1 , Margaret Wild4 , Michael Antolin3 , Kurt VerCauteren2 […] & Mark
Zabel1 - Show fewer authors Scientific Reports 5, Article number: 8358 (2015)
doi:10.1038/srep08358 Download Citation
Molecular ecology Proteins Statistics Received: 27 June 2014
CELL REPORTS
Report
Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions
PRION UPDATE VIA VEGETABLE PLANTS FROM THE SOIL
56. Members considered that there is no evidence that crops grown on the
land which received composted excreta from BSE-challenged animals pose a TSE
risk to humans or animals. One member suggested that, as some of these animals
are orally challenged with high doses of BSE-infected materials, and the
distribution of infectivity in the digestive system is not completely
understood, it might be premature to conclude that there is no infective agent
in the manure.
Furthermore, an unpublished study had indicated low level absorption of PrP
from soil by tomato plants although it should be noted that this study had not
been repeated. Details of this work would be sent to the SEAC Secretary. Dr
Matthews explained that most of the manure from animals challenged with high
doses of BSE had already been composted and used for coppicing. Members agreed
that the risks from disposal of residual manure from experimental animals would
be much less than historic risks of on farm contamination from naturally
infected animals at the height of the BSE epidemic. ...SNIP...END
SRM are certain cattle tissues capable of transmitting BSE. There is no
human health risk assessment to indicate the absence of human health concerns
associated with use of composted SRM domestically. To date, scientific evidence
has not been able to demonstrate that composting destroys prions. Although
domestic use would pose a negligible risk to livestock, there is a potential
risk to humans via direct ingestion of the compost or of compost particles
adhered to skin or plant material (e.g. carrots). Another potential route of
exposure is by ingestion of prions that have been taken up by plants. It has
been proven that bacteria are readily taken up by some plants (e.g. E. coli in
lettuce) thus the uptake of prions by plants cannot be precluded or dismissed at
this time. As a science-based regulator, the CFIA cannot change the policy on
this issue without a risk assessment demonstrating that the use of composted SRM
poses an acceptable risk to humans.
The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester
Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE
BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences &
Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s
Hospital London and William Harvey Hospital Ashford April 1999
snip...
88. Natural decay: Infectivity persists for a long time in the
environment. A study by Palsson in 1979 showed how scrapie was contracted by
healthy sheep, after they had grazed on land which had previously been grazed by
scrapie-infected sheep, even though the land had lain fallow for three years
before the healthy sheep were introduced. Brown also quoted an early experiment
of his own (1991), where he had buried scrapie-infected hamster brain and found
that he could still detect substantial infectivity three years later near where
the material had been placed. 89. Potential environmental routes of infection:
Brown discusses the various possible scenarios, including surface or subsurface
deposits of TSE-contaminated material, which would lead to a build-up of
long-lasting infectivity. Birds feeding on animal remains (such as gulls
visiting landfill sites) could disperse infectivity. Other animals could become
vectors if they later grazed on contaminated land. "A further question concerns
the risk of contamination of the surrounding water table or even surface water
channels, by effluents and discarded solid wastes from treatment plants. A
reasonable conclusion is that there is a potential for human infection to result
from environmental contamination by BSE-infected tissue residues. The potential
cannot be quantified because of the huge numbers of uncertainties and
assumptions that attend each stage of the disposal process". These comments,
from a long established authority on TSEs, closely echo my own statements which
were based on a recent examination of all the evidence. 90. Susceptibility: It
is likely that transmissibility of the disease to humans in vivo is probably
low, because sheep that die from scrapie and cattle that die from BSE are
probably a small fraction of the exposed population. However, no definitive data
are available.
91. Recommendations for disposal procedures: Brown recommends that
material which is actually or potentially contaminated by BSE should be: 1)
exposed to caustic soda; 2) thoroughly incinerated under carefully inspected
conditions; and 3) that any residue should be buried in landfill, to a depth
which would minimise any subsequent animal or human exposure, in areas that
would not intersect with any potable water-table source.
92. This review and recommendations from Brown have particular importance.
Brown is one of the world's foremost authorities on TSEs and is a senior
researcher in the US National Institutes of Health (NIH). It is notable that
such a respected authority is forthright in acknowledging the existence of
potential risks, and in identifying the appropriate measures necessary to
safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M
Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will,
"Geographical distribution of variant CJD in the UK (excluding Northern
Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41
(02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD
(variant CJD) might live closer to rendering factories than would be expected by
chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were
studied. The incubation period of vCJD is not known but by analogy with other
human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure
to rendering products, such exposure might plausibly have occurred 8-10 years
before the onset of symptoms. The authors were able to obtain the addresses of
all rendering plants in the UK which were in production in 1988. For each case
of vCJD, the distance from the place of residence on 1st January 1998 to the
nearest rendering plant was calculated
snip...
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naĂŻve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Sheep and cattle may be exposed to CWD via common grazing areas with
affected deer but so far, appear to be poorly susceptible to mule deer CWD
(Sigurdson, 2008).
***In contrast, cattle are highly susceptible to white-tailed deer CWD and
mule deer CWD in experimental conditions but no natural CWD infections in cattle
have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how
susceptible humans are to CWD but given that the prion can be present in muscle,
it is likely that humans have been exposed to the agent via consumption of
venison (Sigurdson, 2008). Initial experimental research, however, suggests that
human susceptibility to CWD is low and there may be a robust species barrier for
CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD
is affecting wild and farmed cervid populations in endemic areas with some deer
populations decreasing as a result.
snip...
For the purpose of the qualitative risk assessment developed here it is
necessary to estimate the probability that a 30-ml bottle of lure contains urine
from an infected deer. This requires an estimate of the proportion of deer herds
in the USA which are infected with CWD together with the within herd
prevalence.
The distribution map of CWD in US shows it is present mainly in central
states (Figure 1). However, Virginia in the east of the country has recorded
seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take
steps to prevent urine being taken from infected animals eg by sourcing from
farms where the deer are randomly tested for CWD (Anon 2015a). However, if
disease is already present and testing is not carried out regularly, captive
populations are not necessarily disease free (Strausser 2014). Urine-based deer
lures have been known to be collected from domestic white-tailed deer herds and
therefore there is a recognised risk. This is reflected by 6 US States which
have
14
banned the use of natural deer urine for lures, as the deer urine may be
sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For
example, the US State of Virginia is banning the use of urine-based deer lures
on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska
banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned
urine-based deer lures and acknowledged that there is no way to detect their use
(Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it
appears that up to 50% of deer herds can be infected with 80-90% of animals
infected within some herds.
*** It is therefore assumed that probability that a 30-ml bottle of deer
urine lure imported from the USA is sources from an infected deer is
medium.
SNIP...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. ***For elk and deer
considered at high risk for CWD, the FDA recommends that these animals do not
enter the animal feed system. ***However, this recommendation is guidance and
not a requirement by law.
***Animals considered at high risk for CWD include:
***1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
***2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
***Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants. The
amount of animal PAP that is of deer and/or elk origin imported from the USA to
GB cannot be determined, however, as it is not specified in TRACES. It may
constitute a small percentage of the very low tonnage of non-fish origin
processed animal proteins that were imported from US into GB.
*** Overall, therefore, it is considered there is a greater than negligible
risk that (non-ruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB. There is uncertainty associated with this estimate
given the lack of data on the amount of deer and/or elk protein possibly being
imported in these products.
SNIP...
Summary and MORE HERE ;
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21
CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from
deer and elk is prohibited for use in feed for ruminant animals. With regards to
feed for non-ruminant animals, under FDA law, CWD positive deer may not be used
for any animal feed or feed ingredients. For elk and deer considered at high
risk for CWD, the FDA recommends that these animals do not enter the animal feed
system.
***However, this recommendation is guidance and not a requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
Monday, March 28, 2016
National Scrapie Eradication Program February 2016 Monthly Report
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al,
I would kindly like to comment on ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
#158
Guidance for Industry
Use of Material from Deer and Elk in Animal Feed
This version of the guidance replaces the version made available
September15, 2003.
This document has been revised to update the docket number, contact
information, and standard disclosures. Submit comments on this guidance at any
time.
Submit electronic comments to http://www.regulations.gov. Submit written
comments to the Division of Dockets Management (HFA-305), Food and Drug
Administration, 5630 Fishers Lane, Rm. 1061, Rockville, MD 20852. All comments
should be identified with the Docket No. FDA-2003-D-0432 (formerly 03D-0186).
For further information regarding this guidance, contact Burt Pritchett,
Center for Veterinary Medicine (HFV-222), Food and Drug Administration, 7519
Standish Place, Rockville, MD 20855, 240-402-6276, E-mail:
burt.pritchett@fda.hhs.gov.
Additional copies of this guidance document may be requested from the
Policy and Regulations Staff (HFV-6), Center for Veterinary Medicine, Food and
Drug Administration, 7519 Standish Place, Rockville, MD 20855, and may be viewed
on the Internet at either http://www.fda.gov/AnimalVeterinary/default.htm
or http://www.regulations.gov.
U.S. Department of Health and Human Services Food and Drug Administration
Center for Veterinary Medicine March 2016
Contains Nonbinding Recommendations
2
Guidance for Industry Use of Material from Deer and Elk in Animal Feed
This guidance represents the current thinking of the Food and Drug
Administration (FDA or Agency) on this topic. It does not establish any rights
for any person and is not binding on FDA or the public. You can use an
alternative approach if it satisfies the requirements of the applicable statutes
and regulations. To discuss an alternative approach, contact the FDA office
responsible for this guidance as listed on the title page.
I. Introduction
Under FDA’s BSE feed regulation (21 CFR 589.2000) most material from deer
and elk is prohibited for use in feed for ruminant animals. This guidance
document describes FDA’s recommendations regarding the use in all animal feed of
all material from deer and elk that are positive for Chronic Wasting Disease
(CWD) or are considered at high risk for CWD. The potential risks from CWD to
humans or non-cervid animals such as poultry and swine are not well understood.
However, because of recent recognition that CWD is spreading rapidly in
white-tailed deer, and because CWD’s route of transmission is poorly understood,
FDA is making recommendations regarding the use in animal feed of rendered
materials from deer and elk that are CWD-positive or that are at high risk for
CWD.
In general, FDA’s guidance documents do not establish legally enforceable
responsibilities. Instead, guidances describe the Agency’s current thinking on a
topic and should be viewed only as recommendations, unless specific regulatory
or statutory requirements are cited. The use of the word should in Agency
guidances means that something is suggested or recommended, but not required.
II. Background
CWD is a neurological (brain) disease of farmed and wild deer and elk that
belong in the animal family cervidae (cervids). Only deer and elk are known to
be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer, white-tailed deer, North American elk, and in farmed
black-tailed deer. CWD belongs to a family of animal and human diseases called
transmissible spongiform encephalopathies (TSEs). These include bovine
spongiform encephalopathy (BSE or “mad cow” disease) in cattle; scrapie in sheep
and goats; and classical and variant Creutzfeldt-Jakob diseases (CJD and vCJD)
in humans. There is no known treatment for these diseases, and there is no
vaccine to prevent them. In addition, although validated postmortem diagnostic
tests are available, there are no validated diagnostic tests for CWD that can be
used to test for the disease in live animals.
Contains Nonbinding Recommendations
III. Use in animal feed of material from CWD-positive deer and elk
Material from CWD-positive animals may not be used in any animal feed or
feed ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and
Cosmetic Act, animal feed and feed ingredients containing material from a
CWD-positive animal would be considered adulterated. FDA recommends that any
such adulterated feed or feed ingredients be recalled or otherwise removed from
the marketplace.
IV. Use in animal feed of material from deer and elk considered at high
risk for CWD Deer and elk considered at high risk for CWD include: (1) animals
from areas declared by State officials 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 immediately before the time of slaughter were in a captive herd that
contained a CWD-positive animal.
FDA recommends that materials from deer and elk considered at high risk for
CWD no longer be entered into the animal feed system. Under present
circumstances, FDA is not recommending that feed made from deer and elk from a
non-endemic area be recalled if a State later declares the area endemic for CWD
or a CWD eradication zone. In addition, at this time, FDA is not recommending
that feed made from deer and elk believed to be from a captive herd that
contained no CWD-positive animals be recalled if that herd is subsequently found
to contain a CWD-positive animal.
V. Use in animal feed of material from deer and elk NOT considered at high
risk for CWD FDA continues to consider materials from deer and elk NOT
considered at high risk for CWD to be acceptable for use in NON-RUMINANT animal
feeds in accordance with current agency regulations, 21 CFR 589.2000. Deer and
elk not considered at high risk include: (1) deer and elk from areas not
declared by State officials to be endemic for CWD and/or to be CWD eradication
zones; and (2) deer and elk that were not at some time during the 60-month
period immediately before the time of slaughter in a captive herd that contained
a CWD-positive animal.
3
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al,
MY comments and source reference of sound science on this very important
issue are as follows ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
I kindly wish to once again submit to Docket No. FDA-2003-D-0432 (formerly
03D-0186) Use of Material from Deer and Elk in Animal Feed.
Thank you kindly for allowing me to comment again, ...and again...and
again, on a topic so important, why it is ‘NON-BINDING’ is beyond me.
this should have been finalized and made ‘BINDING’ or MANDATORY OVER A
DECADE AGO.
but here lay the problem, once made ‘BINDING’ or ‘MANDATORY’, it is still
nothing but ink on paper.
we have had a mad cow feed ban in place since August 1997, and since then,
literally 100s of millions of pounds BANNED MAD COW FEED has been sent out to
commerce and fed out (see reference materials).
ENFORCEMENT OF SAID BINDING REGULATIONS HAS FAILED US TOO MANY TIMES.
so, in my opinion, any non-binding or voluntary regulations will not work,
and to state further, ‘BINDING’ or MANDATORY regulations will not work unless
enforced.
with that said, we know that Chronic Wasting Disease CWD TSE Prion easily
transmits to other cervid through the oral route.
the old transmission studies of BSE TSE floored scientist once they figured
out what they had, and please don’t forget about those mink that were fed 95%+
dead stock downer cow, that all came down with TME. please see ;
It is clear that the designing scientists must also have shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies
and discuss the implications of such extended incubation periods on risk
assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
*** Title: Transmission of scrapie prions to primate after an extended
silent incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary: The transmissible spongiform encephalopathies (also
called prion diseases) are fatal neurodegenerative diseases that affect animals
and humans. The agent of prion diseases is a misfolded form of the prion protein
that is resistant to breakdown by the host cells. Since all mammals express
prion protein on the surface of various cells such as neurons, all mammals are,
in theory, capable of replicating prion diseases. One example of a prion
disease, bovine spongiform encephalopathy (BSE; also called mad cow disease),
has been shown to infect cattle, sheep, exotic undulates, cats, non-human
primates, and humans when the new host is exposed to feeds or foods contaminated
with the disease agent. The purpose of this study was to test whether non-human
primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.
***After an incubation period of approximately 10 years a macaque developed
progressive clinical signs suggestive of neurologic disease.
***Upon postmortem examination and microscopic examination of tissues,
there was a widespread distribution of lesions consistent with a transmissible
spongiform encephalopathy.
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans.
***This information is especially useful to regulatory officials and those
involved with risk assessment of the potential transmission of animal prion
diseases to humans.
Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion
disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the
past decades, c-BSE's zoonotic potential has been the driving force in
establishing extensive protective measures for animal and human health.
***In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period.
***Neuropathologic examination revealed all of the features of a prion
disease: spongiform change, neuronal loss, and accumulation of PrPres throughout
the CNS.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated.
***Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains.
***Our study demonstrates susceptibility of adult cattle to oral
transmission of classical BSE. ***
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. ***
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants
and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and
humans at the molecular level, we investigated the ability of abnormal prion
protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical
scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to
proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding
cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from
transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc
seed from typical and atypical BSE- or typical scrapie-infected brain
homogenates from native host species. In the conventional PMCA, the conversion
of PrPC to PrPres was observed only when the species of PrPC source and PrPSc
seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA
and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested
prion strains. On the other hand, human PrPC was converted by PrPSc from typical
and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports
describing the lack of transmissibility of H-type BSE to ovine and human
transgenic mice,
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human.
Bioassay will be required to determine whether the PMCA products are
infectious to these animals.
================
==========================================
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
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 is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
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.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C.
Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡,
Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure.
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures
ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** 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).***
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary: The transmissible spongiform encephalopathies (also
called prion diseases) are fatal neurodegenerative diseases that affect animals
and humans. The agent of prion diseases is a misfolded form of the prion protein
that is resistant to breakdown by the host cells. Since all mammals express
prion protein on the surface of various cells such as neurons, all mammals are,
in theory, capable of replicating prion diseases. One example of a prion
disease, bovine spongiform encephalopathy (BSE; also called mad cow disease),
has been shown to infect cattle, sheep, exotic undulates, cats, non-human
primates, and humans when the new host is exposed to feeds or foods contaminated
with the disease agent. The purpose of this study was to test whether non-human
primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.
After an incubation period of approximately 10 years a macaque developed
progressive clinical signs suggestive of neurologic disease. Upon postmortem
examination and microscopic examination of tissues, there was a widespread
distribution of lesions consistent with a transmissible spongiform
encephalopathy. This information will have a scientific impact since it is the
first study that demonstrates the transmission of scrapie to a non-human primate
with a close genetic relationship to humans. This information is especially
useful to regulatory officials and those involved with risk assessment of the
potential transmission of animal prion diseases to humans. Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease
that also causes variant Creutzfeldt-Jakob disease in humans. Over the past
decades, c-BSE's zoonotic potential has been the driving force in establishing
extensive protective measures for animal and human health.
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated.
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains.
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
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
”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.
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
MAD COW DISEASE HAS BEEN IN THE USA FOR DECADES, AND I BELIEVE IT WAS IN
THE USA FIRST, PLEASE SEE ;
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...
Saturday, April 02, 2016
TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER
BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Friday, April 08, 2016
Arkansas AGFC Chronic Wasting Disease CWD TSE Prion Confirms 23 Additional
Cases Total At 79 To Date
Friday, April 01, 2016
ARKANSAS CHRONIC WASTING DISEASE CWD TSE PRION CASES EXPLODE BY 27 NEW
CASES WITH 50 CASES TOTAL TO DATE
Friday, April 01, 2016
Arkansas confirms six more cases of CWD bringing total to 56 since first
reported 2 months ago
Thursday, March 24, 2016
ARKANSAS FIRST BATCH OF TARGET TESTS REVEALS 19 ADDITIONAL CWD-POSITIVE
CERVIDS
Tuesday, March 29, 2016
Maryland Department of Natural Resources Five Deer Test Positive for
Chronic Wasting Disease ONE OUTSIDE CWD MANAGEMENT ZONE
Friday, March 18, 2016
Michigan confirms additional CWD-positive free-ranging, white-tailed deer,
bringing the total to seven
Wednesday, March 16, 2016
Wisconsin CWD sample survey 2015 confirms 290 cases of Chronic Wasting
Disease TSE Prion
Thursday, March 10, 2016
WYOMING RIDE EM COWBOY HELICOPTER WRANGLING RAMBO STYLE DEER BULLDOGGING
RODEO FOR CWD VIDEO
CHRONIC WASTING DISEASE: The Final Epidemic
Tuesday, March 08, 2016
Oklahoma Chronic Wasting Disease CWD of Deer and Elk Surveillance, Testing,
and Preparedness ???
Wednesday, March 02, 2016
Kansas Chronic Wasting Disease CWD TSE Prion 52 cases 2015 updated report
'ALARMING'
Sunday, March 06, 2016
Missouri 2015-2016 CWD Surveillance Summary to Date, with confirmed cases
mounting
TEXAS CWD TESTING TOTAL FIGURES ??? anyone’s guess to date. TAHC et al
should take up Arkansas reporting of test results to the public and open
discussion. ...
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Friday, February 26, 2016
Pennsylvania Monitoring the Growing Threat of Chronic Wasting Disease CWD
TSE Prion
Friday, February 05, 2016
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER
RELEASE SITE
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive for CWD in the Oswego
zone of Kendall County
Friday, February 05, 2016
IOWA Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee
County
Friday, January 29, 2016
NEBRASKA Three Positives for CWD Found in Recent Testing of Deer
Friday, November 20, 2015
ODNR Takes Action to Monitor Chronic Wasting Disease in Ohio's Deer Herd
Friday, October 23, 2015
Ohio Wildlife Council Passes Rule to Help Monitor CWD
Wednesday, August 05, 2015
Ohio confirms to me Chronic Wasting Disease CWD Spreads 19 confirmed cases
to date
Wednesday, February 11, 2015
World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with
two counts of tampering with evidence
Thursday, October 23, 2014
*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE
PRESERVE
Monday, June 11, 2012
*** OHIO Captive deer escapees and non-reporting ***
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild
Saturday, February 6, 2016
*** Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission
Friday, August 14, 2015
*** Susceptibility of cattle to the agent of chronic wasting disease from
elk after intracranial inoculation
Tuesday, March 15, 2016
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information Singeltary Submission
Friday, March 18, 2016 CFSAN
Constituent Update: FDA Announces Final Rule on Bovine Spongiform
Encephalopathy BSE MAD COW TSE PRION Center for Food Safety and Applied
Nutrition - Constituent Update
Thursday, March 24, 2016
FRANCE CONFIRMS BOVINE SPONGIFORM ENCEPHALOPATHY BSE MAD COW (ESB) chez une
vache dans les Ardennes
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
***so 20 cases of atypical BSE in France, compared to the remaining 40
cases in the remaining 12 Countries, divided by the remaining 12 Countries,
about 3+ cases per country, besides Frances 20 cases. you cannot explain this
away with any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain
location and PrPsc by PMCA only, how many cases have we missed?
Monday, January 4, 2016
Long live the OIE, or time to close the doors on a failed entity?
PLEASE REMEMBER, IN 55 YEARS AND OLDER, THE RATE OF DOCUMENTED CJD JUMPS TO
ONE IN 9,000. but officials don’t tell you that either. carry on...
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.
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?
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003
doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
Xavier Bosch
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is
one of a number of people who have remained largely unsatisfied after being told
that a close relative died from a rapidly progressive dementia compatible with
spontaneous Creutzfeldt—Jakob ...
Thursday, April 14, 2016
*** Arizona 22 year old diagnosed with Creutzfeldt Jakob Disease CJD
***
Terry S. Singeltary Sr. Declares a DECLARATION OF EXTRAORDINARY EMERGENCY
DUE TO A FOREIGN ANIMAL DISEASE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE
PRION CHRONIC WASTING DISEASE CWD IN THE UNITED STATES AND NORTH AMERICA.
Monday, April 11, 2016
DECLARATION OF EXTRAORDINARY EMERGENCY DUE TO A FOREIGN ANIMAL DISEASE
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION CHRONIC WASTING DISEASE CWD IN
THE UNITED STATES AND NORTH AMERICA ?
Saturday, February 6, 2016
Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission
Terry S. Singeltary Sr.
Bacliff, Texas USA 77518
